NEET PG High Yield Topic Synopsis NEET 2019 PDF Version - Final

Anatomy
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1. SCAPULA
• Congenital elevation of scapula is called Sprengel shoulder.

• Winging of scapula is seen in paralysis of Serratus anterior muscle.
• Superior angle of scapula lies at T2 level.
• Inferior angle of scapula lies at T7.
• Superior border of scapula is non palpable.
• Protractor of scapula is Serratus anterior.
2. CLAVICLE
Clavicle
• First bone to ossify.

• Complete ossification at 21yr.
• Only long bone to ossify intramembranously.
• Most common bone to fracture during birth .
• Common injury in babies are clavicle #.
• Coracoclavicular ligament (at lateral end of clavicle which connects it with acromion of scapula to
form acromioclavicular joint).
• No medullary cavity.
• Clavicle fracture: Most common in middle 1/3rd of bone.
• The most common complication of clavicle fracture is Malunion.
• Treatment of fracture clavicle in an infant is best treated by Figure of 8 bandage.
• Missing clavicle seen in cleidocranial dysostosis.
• Shoulder stiffness can be managed by shoulder movement after patient is pain free.
3. SHOULDER JOINT
• The inferior part of shoulder joint capsule is the weakest area of shoulder joint capsule
• Long head of the biceps muscle crosses through the shoulder joint
• The tendon of the long head of biceps brachii muscle passes superiorly through the joint and
restricts upward movement of humeral head on glenoid cavity.
• Rotator cuff is called the dynamic stabiliser of the shoulder joint
4. HUMERUS BONE
• Humerus ossifies from 1 primary & 7 secondary centers.

• Multiplying factor for estimating stature from humerus in male is 5-6.
• Intertubercular sulcus (bicipital groove) separates lesser tubercle from greater tubercle and also
forms the lateral wall of axilla.
• Intertubercular sulcus of humerus gives attachment to pectoralis major, latissmus dorsi & teres
major.
• RADIAL Nerve passes through the Radial groove (spiral groove of humerus).
• Nerves of humerus are radial, ulnar & axillary nerve.
• Nerve injured in fracture of medial epicondyle of humerus is Ulnar nerve.
• Axillary nerve is damaged in fracture surgical neck of humerus.
• Most common complication of mid shaft humerus fracture is Radial nerve palsy.
• Distal (lower) end of Humerus ossifies from 4 secondary ossification centers.
• Most common nerve involved in supracondylar fracture of humerus is anterior interosseous branch
of median nerve is mostly affected.
5. RADIAL NERVE
• Radial nerve is Derived from C5,6,7,8, T1

• It is the branch of posterior cord of brachial plexus
• It lies in spiral groove of humerus
• The extensor compartment of arm & forearm is supplied by radial nerve
6. MOVEMENTS OF SHOULDER JOINT
• Movements that take place during abduction of shoulder are axial rotation of humerus at
acroclavicular joint ,elevation of humerus & movement at clavicular end of sternoclavicular joint.
• Movement in every direction (Flexion, extension, abduction, adduction, rotation, circumduction)
7. BRACHIAL ARTERY
• Bicipital aponeurosis passes superficial to the brachial artery and median nerve
• BP is measured in Brachial artery.
• In case of occlusion resulting from fracture of humerus immediate surgery is required.
8. AXILLARY ARTERY
• Cords of brachial plexus are named as per relation with axillary artery behind teres major
• Axillary artery is divided into 3 parts by pectoralis minor muscle
• Axillary artery extends from the outer border of the first rib to inferior border of teres major
muscle
• First part (1 branch) Superior thoracic artery
• Subscapular and scapular circumflex arteries are from the third part of the axillary artery, thus
providing a bypass for obstructions of the first or second parts of the axillary artery.
9. MUSCLES OF PECTORAL REGION
• Pectoralis major Forms anterior axillary fold

• Pectoralis major is not cut in posterio lateral thoractomy
• Pectoralis major insert into the intertubercular sulcus of the humerus
• Pectoralis major blood supply is mainly from pectoral branch of the thoracoacromial artery
• Pectoralis minor crosses in front of axillary artery and divides it into three parts.
• Removal of pectoralis minor and preservation of pectoralis major in Patey's mastectomy

• Pectoralis minor is the only shoulder girdle muscle which is not inserted on the bone in free upper
limb.
• Pectoralis minor inserts into the coracoid process of the scapula.
• Pectoralis minor draw scapula anterioinferiorly
• Serratus anterior is Cut in postero lateral thoractomy
• Serratus anterior protracts and rotates the scapula
• Serratus anterior attach to the costal (rib facing) surface of the medial border of the scapula
• Serratus anterior holds the scapula against the rib cage(forward).Helps in forced inspiration
• Serratus anterior is innervated by Long thoracic nerve(C5,6,7)
• Serratus anterior lesion results in Winging of the Scapula
• Pectoralis major muscle, it is never dissected in breast implant surgery
• Pectoralis major and minor muscles are the most common congenitally absent muscles in humans.
10. TRIGEMINAL (V) NERVE
• Spinal nuclei is nuclei of trigeminal nerve.

• Mesencephalic nuclei of trigeminal nerve give sensory supply to massetric muscle.
• The third branch of trigeminal nuclei emerges from foramen ovale.
• Sensation from skin of face is carried by trigeminal nerve fibers from mesencephalic nucleus.
• The third branch of trigeminal nerve gives motor supply.
• Corneal reflex is due to trigeminal nerve innervation.
• Afferent component in corneal reflex is mediated by - TRIGEMINAL NERVE (OPHTHALMIC
BRANCH).
• Efferent component in corneral reflex mediated by- FACIAL NERVE.
• CORNEAL REFLEX & JAW REFLEX are lost in trigeminal nerve injury.
• Unilateral trigeminal Nerve injury is tested by elevation & lowering of jaw.
• Anterior belly of digastric muscle is supplied by 3rd division of trigeminal nerve.
• Tensor tympani muscle is supplied by 3rd division of trigeminal nerve.
• Blood supply of trigeminal ganglion is from: Internal carotid artery, middle meningeal artery,
accessory meningeal artery & meningeal branch of ascending pharyngeal artery.
11. TRIGEMINAL NEURALGIA
TRIGEMINAL NEURALGIA Or TIC DOULOUREUX Or TRIFACIAL NEURALGIA Or FOTHERGILL’S NEURALGIA
• Trigeminal neuralgia characterized by intermittent, shooting pain in the face.

• Most debilitating form of neuralgia affecting the sensory branches of 5th C.N.
• Disorder of peripheral or central fibres of Trigeminal nerve.
• 95% of causes of trigeminal neuralgia are due to pressure on trigeminal nerve close to where it
enters the brain stem, past the Gasserian ganglion. In most cases, this pressure seems to be caused
by an artery or vein compressing trigeminal nerve.
DEFINITION:
• It is defined as Sudden, unilateral, intermittent paroxysmal, sharp, shooting, lancinating , shock like
pain, elicited by slight touching superficial ‘trigger points’ which radiates from that point, across the
distribution of one or more branches of the trigeminal nerve
• Trigeminal neuralgia also known as Prosopalgia or Fothergill’s disease is a neuropathic disorder
characterized by episodes of intense pain in the face, originating from trigeminal nerve.
ETIOLOGY:
• Vascular compression
• Usually idiopathic
• Demylination of the nerve
• Multiple sclerosis
• Petrous ridge compression
• Post – traumatic neuralgia
• Intracranial tumors
• Intracranial vascular abnormalities
• Viral etiology
CLINICAL SYMPTOMS:
• INCIDENCE 8:100000
• AGE-5th-6th decade of life
• SEX-female> male
• AFFLICTION FOR SIDE- right> left
• DIVISION OF TRIGEMINAL NERVE INVOLVEMENT- V2>V3>V1
• Manifests as a sudden, unilateral, intermittent paroxysmal, sharp, shooting, lancinating , shock
like pain, elicited by slight touching superficial ‘trigger points’ which radiates from that point,
across the distribution of one or more branches of the trigeminal nerve
• Pain is usually confined to one part of one division of trigeminal nerve
• Pain rarely crosses the midline.
• Attacks do not occur during sleep common during day time.
• Pain is of short duration, but may recur with variable frequency.
• In extreme cases, the patient will have a motionless face – the ‘frozen or mask like face’.
• Common trigger zone include- cutaneous( corner of the lips, cheek, ala of the nose, lateral brow);
intraoral( teeth, gingivae, tongue). Trigger area on the face are so sensitive that touching or even
air currents can trigger an episode.
• 10-12% of cases are bilateral, or occurring on both sides. This mainly seen in cases with systemic
involvement include multiple sclerosis or expanding cranial tumor.
DIAGNOSIS
• From a well taken history

• CT- scan
• MRI
• Diagnostic nerve block
DIFFERENTIAL DIAGNOSIS:
• MIGRAINE- severe type of periodic headache is persistent, at least over a period of hours and it has
no trigger zone.
• SINUSITIS- pain is not paroxysmal, in this pain is persistent, associated nasal symptoms.
• DENTAL PAIN- localized, related to biting or hot or cold foods, visible abnormalities on oral
examination.
• Tumors of nasopharynx- in this similar type of pain is produced, manifested in the lower jaw,
tongue and side of the head with associated middle ear deafness. This complex lesion is called
TROTTER’S syndrome. Patient exhibit asymmetry and defective mobility of the soft palate and
affected side. As the tumor progresses, trismus of internal pterygoid muscle develops, and patient
is unable to open the mouth. Here actual cause of pain is involvement of mandibular nerve in the
foramen ovale.
• Post herpetic neuralgia- pain is usually involved in ophthalmic division. The history of skin lesion
prior to onset of neuralgia, pain is persistent, associated nasal symptoms.
TREATMENT:
MEDICAL
• First line of treatment is CARBAMAZIPINE ( anticonvulsant)

• Second line of treatment is: BACLOFEN, LAMOTRIGINE, OXCARBAZEPINE, PHENYTOIN,
GABAPENTIN, PREGABALIN, SODIUM VALPROATE.
• Low dose of Antidepressants such as AMITRYPTILINE are thought to be effective in treating
neuropathic pain. Antidepressant are also used to counteract a medication side effect.
• DULOXETINE is helpful where neuropathic pain and depression are combined.
• Opiates such as MORPHINE and OXYCODONE, there is evidence of their effectiveness on
neuropathic pain, especially if combined with gabapentin, gallium maltoate in a cream or ointment
base has been reported to relieve refractory postherpetic TN
SURGICAL
• LONG ACTING ANESTHETIC AGENTS

• ALCOHOL INJECTION
• PERIPHERAL GLYCEROL INJECTION
• PERIPHERAL NEURECTOMY( NERVE AVULSION)
• OPEN PROCEDURES ( INTRACRANIAL PROCEDURES)
• MICROVASCULAR DECOMPRESSION
• PERCUTANEOUS RHIZOTOMIES
• STEREOTACTIC RADIOSURGERY(Gamma Knife, Cyber Knife)
12. MAXILLARY NERVE

• Maxillary nerve leaves the skull through the foramen rotundum
• Maxillary nerve lies in pterygopalatine fossa
• Maxillary nerve supplies nasopharynx
• Middle superior alveolar nerve is the branch of infraorbital branch of maxillary nerve
• Infraorbital nerve is the branch of maxillary nerve that lies in infraorbital canal
• Maxillary nerve with mandibular nerve supplies Middle cranial fossa
13. MANDIBULAR NERVE
• Mandibular nerve exits skull from foramen ovale.

• Middle cranial fossa is supplied by maxillary and mandibular nerve.
• Nervous spinosus (meningeal branch) enters the skull through foramen spinosum.
• Anterior division of mandibular nerve supplies Muscles of mastication, mylohyoid, anterior belly of
digastric,medial pterygoid , tensor tympani and tensor veli palatini & Skin and mucous membrane
of the cheek
• Anterior division of mandibular nerve have 4 branches Massetric,External Pterygoid, Deep
Temporal & Buccinator.
• Lingual nerve runs across the duct of the submandibular gland.
• The branch arising from the main trunk of mandibular nerve is Nerve to medial pterygoid.
14. OPHTHALMIC (V1) NERVE
• Varicella zoster virus lying dormant within the trigeminal ganglion can reactivate and spread
through the ophthalmic division of the trigeminal nerve.
• Largest branch of ophthalmic nerve is frontal nerve
• Most frequently involved in herpes zoster ophthalmicus branch of ophthalmic nerve is frontal
nerve.
• Anterior ethmoidal artery accompanies the Nasociliary nerve.
• If a patient has herpes zoster, tip of the nose is affected it means the nasociliary nerve is affected
and eye will definitely get involved. This is known as theHutchison’s rule.
• Supply the ethmoidal cells of ethmoidal sinus
• Anterior ethmoidal nerve supplies the ethmoid sinus, nasal cavity, and skin on the tip of the nose.
• Dura mater of anterior cranial fossa is supplied by anterior and posterior ethmoidal nerves.
• Function- General sensation (touch, pain & temperature).
• Cranial exit point- superior orbital fissure.
15. SCALP & SUPERFICIAL TEMPORAL REGIION
• Subcutaneous tissue is the highly vascular layer of scalp.

• Hemostasis in scalp wound is best achieved by direct pressure over wound.
• Lacerated wound appears as incised wound in scalp.
• Normal value of fetal scalp pH- 7.25-7.35.
• Fetal scalp blood Ph is used to determine Fetal hypoxia.
• EEG rhythm recorded from the surface of the scalp during REM sleep is Beta.
• Collection of sero-sanguineous fluid in the scalp is limited to individual bone.
• LOOSE SUBAPONEUROTIC TISSUE (Layer 4) is a "dangerous area" because it allows spread of
infection even, by way of the emissery veins, to intracranial structures.
SCALP: Soft tissue which covers the clavira of skull.
LAYERS OF SCALP: CONSISTS OF FIVE LAYERS
1. Skin:
• Thick and hairy.

• Adherent to the epicranial aponuerosis through the dense superficial fascia.
2. Close network of Connective tissue (superficial fascia):
• Contain vessels and nerves; highly vascular layer.

• The scalp gapes when cut, & blood vessels are held open by the dense connective tissue, resulting
in bleeding that should be arrested by pressure.
3. Aponuerosis (galea aponeurotica) with occipitofrontalis muscles:
• It is freely movable on the pericranium along with the overlying and adherent scalp and fascia.
• On each side it is attached to the superior temporal lines.
• Anteriorly, it receives the insertion of the frontalis.
• Posteriorly, receives insertion of the occipital bellies.
4. Loose areolar (Subaponuerotic) tissue:
• Containing the emissery veins & allowing free movement of layers 1 to 3 as a unit.
• Layer 4 is a "dangerous area" because it allows spread of infection even, by way of the emissery
veins, to intracranial structures.
5. Pericranium (outer periosteum of skull):
• Loosely attached to the surface of the bones, but is firmly adherent to the sutures where the
sutural ligaments bind the pericranium to the endocranium.
BLOOD SUPPLY:
ARTERIAL SUPPLY:
• IN FRONT OF AURICLE-
1. Supratrochlear
2. Supraorbital
3. Superficial temporal arteries
• BEHIND THE AURICLE-
1. Posterior auricular
2. Occipital arteries
VENOUS DRAINAGE:
• Supratrochlear+ supraorbital→ angular vein→ FACIAL VEIN.

• Superficial temporal+ Maxillary vein→ RETROMANDIBULAR VEIN→ divides
into anterior and posterior division.
• Anterior division+Facial vein→common facial veins→ INTERNAL JUGULAR VEIN.
• Posterior division+Posterior auricular vein→External jugular vein→SUBCLAVIAN VEIN.
• Occipital vein->suboccipital plexus
LYMPHATIC DRAINAGE:
• Lymph vessels from the frontal region above the root of the nose drain into the submandibular
nodes.
• Vessels from rest of the forehead,temporal region,upper half of the lateral auricular aspect and
anterior wall of the external acoustic meatus drain into superficial parotid nodes, just anterior to
the tragus ,on or deep to the parotid fascia.
• The occipital region of the scalp is drained by the occipital nodes,and partly by the vessel that runs
along the posterior borderof the sternocleidomastoid to the lower deep cervical nodes
• A strip of the scalp above the auricle drains to the upper deep cervical and retro auricular nodes.
• The retro auricular in turn drain to deep cervical.
NERVE SUPPLY:
• Scalp supplied by ten nerves on each side.

• Five nerves (4 sensory and one motor) enter scalp in front of the auricle.
• Remaining five (4 sensory one motor) enter behind the auricle.
IN FRONT OF AURICLE(SENSORY) BEHIND THE AURICLE(SENSORY)

SUPRATROCHLEAR branch of the Frontal (Opthalmic POSTERIOR DIVISION OFGREATER AURICULAR
div. of trigeminal nerve) (C2,C3) from cervical plexus
SUPRAORBITAL branch of Frontal (Opthalmic LESSER OCCIPITAL (C2), from cervical plexus
division of trigeminal nerve)
ZYGOMATICOTEMPORAL, branch of zygomatic GREATER OCCIPITAL (C2, dorsal ramus)
nerve (Maxillary division of trigeminal nerve)
AURICULOTEMPORAL branch of mandibular division THIRD OCCIPITAL (C3, dorsal ramus)
of trigeminal nerve.
(MOTOR) (MOTOR)
TEMPORAL BRANCH OF FACIAL NERVE POSTERIOR AURICULAR BRANCH OF

FACIAL NERVE
CLINICAL ANATOMY:
1. SEBACEOUS CYST- due to collection of sebum as a result of obstruction of sebaceous cyst, secondary
infection may sets in.
2. Scalp wounds bleed profusely- because elastic fibres of underlying galea aponuerotica prevent initial
vessel retraction, the wounds may be associated with significant blood loss which can result in clinical
shock.
3. Scalp flaps -used in craniofacial surgery for correction of congenital deformity,for release of
craniosynostosis, treatment of craniofacial fractures and for repair of scalp defects after excision of skin
tumors.
4. Hemostasis in scalp wound is best achieved by pressure over wound.
5. When suturing scalp lacerations, it is essential to control all bleeding points before repairing the scalp
itself.
6. It is necessary to tie off larger arterioles and veins and use bipolar diathermy to control smaller
arterioles and veins.
7. Repair of scalp require full thickness tension sutures because galea aponuerotica will otherwise gape as
the occipital and frontal bellies contract.
8. Lacerated wound appears as incised wound in scalp.
9. Failure to control bleeding points can result in significant hematomas, often subgaleal, leading to
breakdown of the orginal wound and sometimes necessitating surgical drainage.

16. MUSCLES OF FACIAL EXPRESSION
• Facial muscles develops from mesoderm.

• Facial muscles act as sphincter & dilator of orifice of face.
• Facial muscle develops from 2nd pharyngeal arch except levator palpebrae superioris.
• Lacrimal part of orbicularis oculi is k/as Horner's muscle.
• Levator Palpebrae superioris dilate palpebral aperture.
• Facial muscles are supplied by Facial nerve.
• Levator palpeberae superioris, only Facial muscle not supplied my facial nerve.
17. BELL'S PALSY
• Bell's palsy is due to paralysis of LMN VII nerve.

• Bell's palsy is most common facial palsy.
• Bells palsy is lower motor neuron facial palsy (LMN VII).
• Bells palsy is idiopathic ipsilateral paralysis of the facial nerve.
• Hyperacusis seen in Bells palsy.
• Hyperacusis occurs due to paralysis of Stapedius muscle supplied by facial nerve.
• 2 weeks after chemotherapy, if no improvement seen physiotherapy & electrical stimulation is
given.
18. MUSCLES OF MASTICATION
• The muscles of mastication are temporalis, masseter, medial pterygoid, lateral pterygoid
• Masseter originates from mesencephalic nucleus and the motor nucleus of trigeminal nerve
• All primary muscles of mastication are supplied by mandibular nerve
• Muscles that elevates mandible to close the mouth are temporalis, masseter & medial pterygoid
• The only primary muscle that depress mandible to open mouth is lateral pterygoid
• All Muscles of mastication are supplied by branches from Ant. div. of mandibular branch of
TRIGEMINAL NERVE except Medial Pterygoid.
TYPES:
• PRIMARY MUSCLES OF MASTICATION:
1. Temporalis: fan shaped & fills the temporal fossa

2. Masseter( quadrilateral): Covers lateral surface of ramus of Mandible & has 3 layers
3. Lateral Pterygoid: Short, conical & has upper 7 lower head
4. Medial pterygoid (quadrilateral):Has a small superficial & a large deep head
MUSCLE ORIGIN FIBERS INSERTION NERVE ACTION

SUPPLY &
NUCLEI
Masseter 1. superficial 1. superfici 1. Superfici Massetric Elevtaes
layer:Ant. al:down al:Lower nerve(C.N.V3 mandible to
2/3rd of lower & back part of ant. div.) close mouth
border of at 45o lateral
zygomatic 2. Middle surface (mesenceph
arch & & of ramus alic nucleus
zygomatic deep:ver 2. Middle: and the
process of tically middle motor
maxilla down part of nucleus
2. Middle layer: 3. 3 layers ramus of trigeminal
Ant. 2/3rd of seperate 3. Deep:Up nerve )
deep surface d by an per part
& post. 1/3rd artery & of ramus
of lower a nerve &
border of coronoid
zygomatic process
arch
3. deep
layer:Deep
surface of
zygomatic
arch
Temporalis 1. Temporal Converge & 1. Margins 2 deep 1. Elevat

fossa pass through & deep temporal es
excluding gap deep to surface branches(C.N mandi
zygomatic zygomatic arch of .V3 ant. div.) ble
bone coronoid 2. Retrac
2. Temporal process ts
fascia 2. Ant. Mandi
border ble
of ramus 3. Side
to side
grindi
ng
move
ment

Lateral 1. Upper Back & Lateral 1. Upper Lateral 1. Depre
Pterygoid Head:Infratem & converge for head:Pte pterygoid ss
poral surface& insertion rygoid branch (Ant. mandi
greater wing fovea at div. of ble
of sphenoid neck of C.N.V3) 2. Protru
2. Lower mandibl de
Head:Lateral e mandi
surface of 2. Lower ble
lateral head:Ant 3. grindi
pterygoid . margin ng
plate of move
articular ment
disc &
TMJ
capsule
Medial 1. Superficial Down, back & Roughened Nerve to 1. Elevat

Pterygoid Head: laterally area on medial Medial es
Tuberosity of surface of angle Pterygoid(M Mandi
maxilla & & adjoinig ain trunk of ble
adjoining ramus of C.N. V3) 2. Protu
bone mandible, de
2. Deep below & behind mandi
Head:Medial madibular ble
surface of foramen & 3. Grindi
lateral mylohyoid ng
pterygoid groove move
plate& ment
adjoining
process of
palatine bone
19. EXTRAOCULAR MUSCLES
• Superior oblique rotates the eye downward and away from midline.
• All the extra ocular muscles except inferior oblique arise from the apex of orbit.
• Anteroposterior stability of eyeball is provided by Superior oblique,Superior rectus & Orbital fat.
• The Superior oblique is the longest, thinnest extraocular muscle.
• Superior oblique muscle is involved in intorsion, depression and abduction of the eyeball.

• The superior oblique muscle is supplied by trochlear nerve.
• Superior rectus is supplied by superior division ofocculomotor nerve.
• Inferior rectus inserts 6.5 mm behind limbus
• Inferior rectus lies inferior to inferior oblique muscle.
• Inferior rectus is antagoinst to superior rectus.
• Inferior oblique is supplied by 3rd cranial nerve.
• Lateral rectus, Superior oblique are not supplied by occulomotor nerve.
• Downward and lateral gaze is action of superior oblique.
• Inferior oblique is the shortest extraocular muscle.
• The posterior end of inferior oblique Muscle lies near macula.
• The muscle which makes an angle of about 51° with the optical axis is superior oblique.
• The muscle which makes an angle of about 23° with the optical axis is Superior rectus.
• Lateral rectus is supplied by abducent nerve
• Action of superior rectus is elevtaion Adduction and intorsion.
• The extraocular muscles that does not arise from Annulus of Zinn is superior oblique.
• Muscle responsible for intorsion of the eye are superior oblique & superior rectus.
• Primary action of inferior oblique muscles are Extortion, Elevation, Abduction.
20. FACIAL (VII) NERVE
• Terminal branches of facial nerve are temporal, zygomatic, buccal, marginal mandibular & cervical
• Branch of facial nerve passing through pterygotympanic fissure is chorda tympani
• The arrangement of Branches of Facial nerve after exiting from Parotid gland is given the name
as Pes Anserinus
• Facial nerve is developmentally derived from the second pharyngeal arch
• Chorda tympani is a branch of facial nerve
• chorda tympani joins lingual nerve to supply submandibular gland and tongue
• chorda tympani carries secretomotor fibers to submandibular & sublingual gland
• Chorda tympani branch of facial nerve carries taste sensation from anterior 2/3rd of tongue
• Blood supply of facial nerve is by Anterior inferior cerebellar artery,Labyrinthine artery, Superficial
petrosal artery, Stylomastoid artery
• The terminal branches of facial nerve are Temporal, Zygomatic, Buccal, Marginal mandibular &
cervical
• Facial nerve supplies lacrimal, mucosal ,sublingual , submandibular glands but not parotid
• The muscles supplied by facial nerve include all muscles of face, scalp, auricle, eyelid, around
mouth, neck
• The intracranial branches of facial nerve are greater petrosal, stapedius, chorda tympani
• All the muscles of the face are supplied by facial nerve except levator palpebrae superioris
• Posterior belly of digastric is supplied by facial nerve
• Greater petrosal nerve is the First branch of facial nerve.
• stapedius is supplied by facial nerve

21. Facial Nerve: Functional Components
The general visceral afferent column is represented by part of the dorsal nucleus of the vagus nerve.
Dorsal vagal nucleus belongs to general visceral efferent component of vagus
Functional components of facial nerve are GSA, GVA,GVE,SVE,SVA (Facial nerve doesnot contain Somatic
Efferents).
22. GENICULATE GANGLION
• Lesion occurring at the level of geniculate ganglion will injure greater petrosal branch and will lead
to dryness of eyes
• The Ramsay Hunt Syndrome is caused by reactivation of Herpes Zoster in the geniculate ganglion
23. AZYGOUS VENOUS SYSTEM
• Azygos venous system arises from the supracardinal veins.

• Azygous vein drains into Superior vena cava.
• Azygous vein ascends through the aortic opening in the diaphragm.
• The azygous vien is formed by union of the lumbar azygous , right subcostal & right ascending
lumbar veins.
• The Last tributary of azygous vein is Right bronchial vein.
• Azygous vein & hemiazygous vein drain into Middle mediastinum.
• Hemiazygous vein crosses left to right at the level of T8.
24. WALLS OF ORBIT
• Haller cells are seen in Orbital Floor.

• Lines of Sebileau pass through Floor of orbit and maxillary antrum.
• Medial orbital wall is formed by frontal process of maxilla, lacrimal bone, ethmoid bone (orbital
plate) and body of sphenoid bone.
• Medial wall is the weakest wall and lateral wall is thickest.
• The thinnest portion of medial wall of orbit is the lamina papyracea which separates ethmoid
sinuses from orbit.
• Blowout fractures mainly involve orbital floor and medial wall (Most commonly Posterior-medial
wall of floor).
• Clinical Features of BLOWOUT FRACTURE are :

1. Enophthalmos,Diplopia,Restriction of eye movements.
2. Enophthalmos is caused by fracture of floor of orbit.
3. Escape (herniation) of orbital fat into maxillary sinus.
4. Forced duction test is positive in Blow out fracture due to restriction movements from entrapped
muscles.
5. Hanging drop or tear drop sign is seen in blow-out fracture of Orbit.
• The most common cause of fracture of roof of orbit is Blow on the forehead.
• Unilateral lacrimal gland destruction may be caused by fracture of roof of Orbit.
• Le Forte II facial fracture runs through zygomatic process of the maxilla, floor of orbit, root of nose
on both the sides.
• The walls of the orbit which are removed in the two wall decompression for proptosis of thyroid
ophthalmopathy include part of Orbital floor and medial wall.
• Inferior orbital fissure occupies the posterior part of function between lateral wall & floor.
• Superiororbital fissure occupies thew posterior part of the junction between the roof and lateral
wall.
• Optic canal lies at the junction of roof and medial wall, and is enclosed by lesser wing and body of
sphenoid.
25. TEMPOROMANDIBULAR JOINT
• Temporomandibular joint is a Condyloid and Synovial joint.

• The muscles acting upon the TM Joint are Temporalis,Masseter,Medial Pterygoid and Lateral
Pterygoid.
• In dislocation of the jaw, displacement of the articular disk beyond the articular tubercle of the
temporomandibular joint result from spasm or excessive contraction of Lateral pterygoid Muscle.
• Costen's syndrome refers to neurological pain associated with Temporomandibular joint.
• Blind nasal intubation is indicated in TM joint ankylosis.
• Referred pain in ear may occur due to TM joint Problems.
• Pantomography is done to visualise TM Joint.
26. SYNDROMES & DIAGNOSTIC TEST ASSOCIATED WITH FACIAL NERVE
• Facial Nerve stimulation during testing of nerve indicated by contraction of orbicularis oris muscle
• Facial nerve involvement in herpes zoster is known as Ramsay hunt syndrome
• Melkersson-Rosenthal syndrome consists of recurrent facial paralysis
• Schirmer's test is done to assess the function of Facial nerve
• Inability to close left eyelid, drooping of ipsilateral angle of mouth and inability to taste food.
History of discharge from his left ear are the symptoms of facial nerve palsy after herpes zoster
infection
• Prognosis of Ramsay hunt syndrome is poor than Bell's palsy
• Deviation of angle of mouth towards opposite side shows facial nerve palsy occurring due to lesion
at the outlet of stylomastoid.
• Frey's syndrome is caused by Post traumatic nerve fibres of facial nerve with parasympathetic of
auriculotemporal nerve
27. EXTERNAL CAROTID ARTERY
• The arterial supply to the parotid gland is from the external carotid artery and its branches within
and near the gland.
• The only medial branch of external carotid artery is Ascending pharyngeal
• Nasal mucosa is supplied by mainly external carotid artery.
• Superior thyroid artery originates from external carotid artery.
• Maxillary artery is the Larger terminal branch of external carotid artery.
• Maxillary artery develops from 1st branchial arch.
• Inferior alveolar artery which gives off its mylohyoid branch just prior to entering the mandibular
foramen.
• Sphenopalatine artery (Nasopalatine artery is the terminal branch of the Maxillary artery) major
blood supply to nasal mucosa.
• Middle meningeal artery is direct branch of Internal maxillary artery.
28. COMMON CAROTID ARTERY
• Common carotid artery ends at the level of upper border of the thyroid cartilage C4 (C3-C4
disc) where they bifurcate into internal & external carotid artery.
• The left common carotid arises directly from the aortic arch.
• Right common carotid artery arises from brachiocephalic trunk.
• Internal carotid artery at the bifurcation from the common carotid is Lateral to the external carotid.
• Common carotid artery can be compressed against anterior tubercle of transverse process of C6
vertebra, known as carotid tubercle (Chassaignac tubercle), at cricoid cartilage level.
• Common carotid artery can be felt along the anterior margin of sternocleidomastoid at the level of
laryngeal prominence.
• Common carotid artery is palpated at upper border of cricoid cartilage.
• The commonest variation in the arteries arising from the arch of aorta is Left common carotid
artery arising from brachiocephalic trunk.
• Hanging causes large amount of injury to common carotid artery.
• Dye is injected in common carotid in cerebral angiography.
• Right common carotid artery arises from brachiocephalic trunk.

29. INTERNAL CAROTID ARTERY
• Internal carotid artery Supplies duramater.

• Internal carotid artery lies in close relation of the optic nerve.
• Internal carotid artery at the bifurcation from the common carotid is Lateral to the external carotid
• Cavernous part of ICA runs through the medial wall of cavernous sinus.
• Internal carotid artery crosses Cavernous sinus.
BRANCHES:
1. Cervical Part:
• It ascends vertically in the neck from its origin to the base of skull to reach the lower end of the
carotid canal.
• This part is enclosed in carotid sheath along with internal jugular and vagus nerve.
• No branches arises from the internal carotid artery in the neck.
• Its initial part shows slight dilation, carotid sinus, which acts as a baroreceptor.
2. Petrous Part
• Within the petrous part of the temporal bone,in the carotid canal runs upward forward & medially
at rt. Angle.
• Branches:
1. Caroticotympanic- enter middle ear & anastomose with ant. & post. Tympanic branches
2. Artery of the Pterygoid Canal- anastomose with greater palatine artery
3. Cavernous Part
• Within the Cavernous Sinus

• Branches:
1. Cavernous branch
2. Superior & inferior Hypophyseal artery
3. Meningeal branch
4. Cerebral Part-
• Lies at the base of the brain after emerging from the cavernous sinus.
• Largest
• Branches:
1. Ophthalmic Artery
2. Anterior Cerebral Artery
3. Middle Cerebral Artery
4. Posterior Communicating Artery
5. Anterior choroidal Artery
30. CIRCLE OF WILLIS
• Berry aneurysms in Circle of Willis is commonly associated with adult polycystic kidney disease.
• Rupture of saccular aneurysm of Circle of Willis is the commonest cause of subarachnoid
haemorrhage.
• Most common site of saccular aneurysms is the anterior circulation on the circle of Willis.
• Vasospasm is the leading cause of morbidity and mortality following aneurysmal subarachnoid
hemorrhage.
• Distal part of the Circle of Willis requires access to the vertebral artery via Suboccipital triangle.
• Circle of Willis lies in subarachnoid space within the deep interpeduncular cistern.
• Anterior communicating arteries in the circle of Willis is derived from Anterior cerebral artery.
• Circle of willis is formed by Anterior cerebral artery (left and right), Anterior communicating artery,
Internal carotid artery (left and right), Posterior cerebral artery (left and right) & Posterior
communicating artery (left and right)
31. TROCHLEAR (IV) NERVE
• Trochlear nerve lies in lateral wall of cavernous sinus.

• Trochlear nerve has the longest intracranial course.
• Trochlear nerve arises from dorsum of brainstem.
• Trochlear nerve enters the orbit through lateral part of Superior orbital fissure.
• Trochlear nerve have 2 functional components somatic efferent & General somatic afferent.
• Trochlear nerve is the only cranial nerve to decussate prior to exiting the brainstem.
• Superior Oblique muscle is innervated by trochlear nerve.
32. PAROTID GLAND
• Secretomotor fiber to parotid salivary gland is supplied by otic ganglion.

• The arrangement of Branches of Facial nerve after exiting from Parotid gland is given the name
as Pes Anserinus.
• Parotid duct pierces buccinator muscle.
• Parotid gland is pierced but not innervated by facial nerve.
• The parasympathetic secretomotor fibres to parotid arises from the glossopharyngeal nerve
& reaches the gland via tympanic branch, the lesser petrosal nerve, the otic ganglion and the
auriculotemporal nerve.
• Parotid capsule is derived from deep cervical fascia.
• Postganglionic fibres to parotid gland is supplied by auriculotemporal nerve.
• Parotid duct is also k/as Stenson’s duct.
• The duct turns opens into the vestibule of the mouth (gingivo- buccal vestibule) opposite the crown
of the upper 2nd molar tooth
• Parotid duct pierces Buccal pad of fat, Buccalpharyngeal fascia & Buccinator.
33. CAVERNOUS SINUS
• Structures passing through cavernous sinus are internal carotid artery & abducent nerve.
• As afferents each CS receives spheno parietal sinus, frontal trunk of middle meningeal, superior &
inferior ophthalmic vein, superficial middle cerebral vein, inferior cerebral vein.
• III , IV, V1, V2, VI are the cranial nerves that travels through the cavernous sinus.
• Superior ophthalmic vein directly communicates with cavernous sinus.
• Abducent nerve & internal carotid artery Are the direct content of cavernous sinus
• Facial vein is connected to cavernous sinus via superior opthalmic vein.
• Veins communicating the cavernous sinus to pterygoid plexus pass through fossa of vesalius.
34. TONGUE
• Muscles of tongue develop from the occipital myotomes.

• Palatoglossus muscle does not develop from occipital myotomes.
• Anterior 2/3 of tongue develops from 2 lingual swellings and one tuberculum impar, i.e., from first
branchial arch supplied by lingual nerve (post-trematic) and chorda tympani (pre-trematic).

• Posterior 1/3 of tongue develops from the cranial half of the Hypobranchial eminence, i.e., from
the third arch supplied by glossopharyngeal nerve.
• Fungiform Papillae near tip & margins of tongue.
• Foliate Papillae form transverse mucosal folds on the lateral aspect of tongue.
• No taste buds are found in Filiform papillae.
• Referred otalgia from base of tongue or oropharynx is carried by Cranial nerve IX (Glossopharyngeal
nerve).
• Most common site of carcinoma tongue is middle of lateral border or the ventral aspect of the
tongue followed by tip and dorsum.
PART OF EMBRYO PART SENSORY(General TASTE MOTOR

TONGUE FROM WHICH sensation)
DERIVED
Epithelium Ist Lingual Chorda -
over Ant. nerve (Mandibular tympani branch of
2/3rd branch of Vth Cranial facial nerve(VII)
nerve)
Epithelium IIIrd Glossopharyngeal Glossopharyngeal -
over Post. Nerve nerve
1/3rd
Epithelium IVth Sup. Laryngeal branch Sup. Laryngeal -
over of Xth C.N nerve
Posterior
most
Muscles Occipital myotomes - - Hypoglossal
except nerve
Palatoglossal (XII) except
muscle Palatoglossal
nerve
35. MUSCLES OF TONGUE
• Tongue muscle derived from occipital myotomes.

• Motor supply to the muscles of the tongue is by Hypoglossal nerve
• Palatoglossus is only muscle of tongue not supplied by hypoglossal nerve.
• Platoglossus muscle supplied by vago-accessory complex i.e. through pharyngeal plexus of nerves.
• Genioglossus is the Safety muscle of tongue.
• Genioglossus- protude the tongue and deviates it to opposite side.
• Protrusion of tongue not possible in damage of Genioglossus muscle.
• Ipsilateral deviation of tongue in XIIth nerve palsy is due to unaltered action of contralateral
Genioglossus.

36. FACE
• Lymphatic drainage of lateral wall of nose Submandibular nodes, Retropharyngeal nodes & upper
deep cervical nodes.
• Angular vein communicares with Cavernous sinus.
• Dangerous area of face are upper lip & lower part of the nose.
• Angle of mandible supplied by Greater auricular nerve.
• Tip of nose is supplied by External nasal branch of Ophthalmic nerve.
• Muscles of face are supplied by Facial nerve except Levator palpebrae superioris.
• Levator palpebrae superioris muscle is supplied by sympathetic fibers & Occulomotor nerve.
• Complication of trauma to danger area of face- Cavernous sinus infection.
• Lymphatic drainage of lateral part of lower lip by Submandibular nodes.
37. OCCULOMOTOR (III) NERVE
• Nerve compressed by aneurysm of posterior communicating artery is occulomotor nerve.

• The muscles innervated by occulomotor nerve are superior rectus, levator palpebrae
superioris ,medial rectus, inferior rectus & inferior oblique.
• Occulomotor nerve Carries parasympathetic nerve fibres to eye.
• Causes constriction of pupil is caused by occulomotor nerve.
• Cross section of midbrain at the level of superior colliculus shows 3rd CN & red nucleus.
38. LARYNX
• Superiorly placed larynx in infants helps child to breathe & suckle at same time.
• Larynx is funnel shaped in infant
• Larynx is cylindrical shaped in adults
• Cricoid Cartilage is the narrowest part of infantile larynx.
• Laryngofissure is opening of larynx in midline.
39. CARTILAGE OF LARYNX
• Cunieform & corniculate cartilage of larynx are elastic in nature

• Cricoid is the narrowest part of infantile larynx
• Elastic cartilage are Found in inlet of larynx
• Cricoid cartilage encircles the larynx
• Thyroid is a hyaline cartilage
• The oesophgus commences at lower end of cricoid
• The narrowest part of trachea in a newborn is at the level of cricoid
40. LIGAMENTS OF LARYNX & EPIGLOTTIS
• Epiglottis is omega shaped in infants

• Epiglottis is common site of sarcoidosis in larynx
• Epiglottis lies separating the esophagus from the larynx
• Suprahyoid epiglottis with False cords- Arytenoids forms epilarynx
• Inlet of larynx is formed by aryepiglottis fold
• Epiglottis develops from 4th arch
• Epithelial lining of lingual surface of epiglottis is Stratified squamous epithelium
• Epiglottis is an unpaired cartilage of larynx
• Stratified squamous non-keratinized epithelium is Epithelial lining of glottis/ true vocal cords
41. LARYNGEAL MEMBRANE & MUCOSA
• Extrinsic membrane of larynx are thyrohyoid, hyoepiglottic & cricotracheal membrane.

• The laryngeal mucosa is supplied by internal laryngeal nerve.
42. MUSCLES OF LARYNX
• Posterior arytenoid is the abductor of vocal cord.

• Sternothyroid & thyrohyoid are attached to oblique line of thyroid.
• Tensor of vocal cord are Cricothyroid and internal thyroarytenoid.
• Cricothyroid is the only muscle that is located on the external aspect of larynx.
• Posterior cricoarytenoid is the Tensor of vocal cord during phonation
• Posterior cricoarytenoid is the Safety muscle of larynx.
• Lateral cricoarytenoid adduct vocal cord.
• Cricothyroid is the only Intrinsic muscle of larynx supplied by External laryngeal nerve.
• Thyrohyoid , Digastric ,Stylohyoid, Mylohyoid, Geniohyoid, Hyoglossus & Genioglossus are elevator
muscles of larynx.
• Sensory nerve supply of larynx below the level of vocal cord is recurrent laryngeal.
43. LARYNGEAL JOINTS & SPACES
• The anatomical location of Reinke's space of larynx is in True vocal cord

• Water can in the larynx (saccules) are present in laryngeal ventricle
• Vestibule,Ventricles,Reinke's space,External laryngeal spaces, Paraglottic space, Pre-epiglottic
Space, Tucker’s space & Boayer’s space Are the spaces found in larynx
44. MAXILLARY SINUS
• The maxillary sinus opens into middle meatus at the level of Hiatus semulinaris.
• Maxillary Sinus drains into middle meatus of nose.
• Osteomeatal complex (OMC) connects Nasal cavity with maxillary sinus.
• Maxillary sinus fully develops as the human being reaches the age of 16 at secondary dentition .
• Maxillary sinus is the first paranasal sinus to develop at birth.
• Antrum of Highmore is another name for maxillary sinus.
• Sudden death occur after maxillary sinus irrigation is due Air embolism.
45. FRONTAL SINUS
• Frontal sinus drains into anterior part of the corresponding middle nasal meatus of the nose.
• Frontal sinus is absent at birth.
• Frontal sinus is the Most superior sinus.
• Periodicity is a characteristic feature in frontal sinus infection.
• Mucocele is commonly seen in sinus.
• Most common site for osteoma is frontal sinus.
• The most common mucocele of the paranasal sinuses involving the orbit arises from frontal sinus.
46. NASAL SEPTUM/ MEDIAL NASAL WALL
• Kiesselbach's area or little's area involves 4 arteries anastomosis that are Anterior ethmoidal, Septal
branch of supeior labial, Septal branch of sphenopalotine & Septal branch of greater palatine
• Anterior ethmoidal artery supplying nasal septum is a branch of opthalmic artery.
• Kisselback's plexus is situated in anteroinferior part of the nasal septum.
• Structures that forms nasal septum are columella, Membranous septum, ethmoid, vomer
bone, septal cartilage, Crest of nasal bone, Nasal spine of frontal bone,Rostum of sphenoid, Crest of
palatine bone & Crest of maxilla and anterior nasal spine of maxilla
• Anterior half of the nasal septum drain to the submandibular node.
• Most common cause for nose bleeding is trauma to little's area.
• Most common site for nose bleeding in children is little's area.
• Apple jelly nodules on the nasal septum are found in cases of Lupus Vulgaris.

47. LATERAL NASAL WALL
LATERAL NASAL WALL
CONCHAE/ TURBINATES:
• Curved paired bony projection directed downward & medially:
1. Inferior conchae (Largest): Independant bone.

2. Middle conchae: projects from medial surface of ethmoidal labyrinth
3. Superior conchae (smallest): projects from medial surface of ethmoidal labyrinth.
→ Inferior turbinate is a maxilloturbinate because it is part of maxillary bone.
→ The inferior turbinate is a separate bone, while rest of the turbinates are a part of ethmoidal bone.
→ Sometimes fourth turbinate is also present just above superior turbinate known as Supreme turbinate.
→ The middle , superior & supreme turbinates are part of erhmoidal complex, they may be called
as "ethmoidal turbinates".
MEATUS:
• Passage beneath overlying conchae

• Communicates with nasal cavity proper
1. Inferior meatus (largest): Under inferior conchae
• Give opening to nasolacrimal duct (at junction of ant.1/3 & post. 2/3) guarded by Hasner's
valve or lacrimal fold.
2. Middle meatus: Under middle conchae.
• Structures present in it:
i). Ethmoidal bulla: round elevation produced by underlying ethmoidal sinus. Gives opening to middle
ethmoidal air sinus.
ii). Hiatus semilunaris: semicircular sulcus below bulla. Gives opening to:
• Ant.: frontal air sinus

• Post. maxillary sinus(2 openings)
• Anterior ethmoidal sinus
iii). Infundibulum: Passage at ant. end of hiatus

iv). Uncinate process of ethmoid: It partly covers the opening of maxillary sinus.
→ Atrium is a shallow depression in front of the middle turbinate.

→ Agger nasi is an elevation just anterior to the attachment of middle turbinate.
3. Superior meatus (shortest & shallowest): under superior conchae.
• Recives opening of posterior ethmoidal air sinus.
4. Sphenoethmoidal Recess:
• Triangular Fossa above superior conchae that recieves opening of sphenoidal air sinus.
48. FORAMENS OF SKULL
• Superior orbital fissure is formed by Greater wing of sphenoid and lesser wing of sphenoid.
• Optic canal is a part of lesser wing of sphenoid.
• Vertical crest in fundus of the internal carotid artery os known as Bill's bar.
• Gland derived from foramen caecum is Thyroid.
• Foramen transversarium transmit Vertebral artery.
STRUCTURES PASSING THROIGH FORAMINA

FORAMEN MAGNUM • Ant. Part: Apical ligament of dens, membrane tectoria, vertical
band of cruciate ligament.
• Post. Part: Lowest part of medulla oblongata, 3 meninges
(dura, arachnoid & pia mater)
• Subarachnoid space: spinal fibers of accessory nerve (XI),
vertebral artery, Lowest part of medulla oblongata
FORAMEN OVALE • Mandibular nerce

• Accessory meningeal artery [MALE]
• Lesser petrosal nerve
• Emissary vein
FORAMEN SPINOSUM • Middle meningeal artery

• Emissary vein [MEN]
• Nerve spinosus
FORAMEN LACERUM • Meningeal branch of ascending pharyngeal artery

• Nerve of pterygoid canal through its anterior wall.

FORAMEN ROTUNDUM • Maxillary nerve (V2)
STYLOMASTOID FORAMEN • Facial nerve (VII)
JUGULAR FORAMEN • Ant. Part: Inferior petrosal sinus

• Middle part: Glossopharyngeal nerve (IX), vagus
nerve (X), accessory nerve (XI)
• Posterior part: Internal jugular vein, sigmoid sinus, Occipital
artery
GREATER PALATINE FORAMEN • Greater palatine artery

• Greater palatine vein
• Anterior palatine nerves
LESSER PALATINE FORAMEN • Lesser palatine nerve, greater palatine nerve
INCISIVE FORAMEN • Terminal part of nasopalatine nerve (V2)

• Greater palatine vessels
MASTOID FORAMEN • Meningeal branch of occipital artery, emissary vein
SUPRAORBITAL FORAMEN • Supraorbital artery & nerve, frontal diploic vein
INFRAORBITAL FORAMEN • Infraorbital nerve & vessels
MENTAL FORAMEN • Mental Nerves and Vessels
FORAMEN OF WINSLOW • IVC
FORAMEN CECUM • Emissary veins to superior sagittal sinus from the upper part of
the nose
FORAMEN OF VESALIUS • Emissary vein connecting cavernous sinus with pterygoid

(Emissary sphenoidal venous plexus
foramen)
STRUCTURES PASSING THROIGH FORAMINA OF SKULL
CAROTID CANAL • Internal carotid artery with sympathetic plexus around

it
• Emissary vein (connecting cavernous sinus with IJV)
PTERYGOID CANAL • Vidian nerve

• Vidian artery
HYPOGLOSAL CANAL (Anterior • Hypoglossal nerve (XII)

condylar canal) • Meningeal branch of ascending pharyngeal artery
POSTERIOR CONDYLAR CANAL • Emissary vein (connecting sigmoid sinus with

suboccipital vein)
MASTOID CANALICULUS • Auricular branch of vagus nerve (entry) [Alderman’s

nerve or Arnold’s nerve]
TYMPANOMASTOID FISSURE • Auricular branch of vagus nerve (exit)
TYMPANIC CANALICULUS • Tympanic branch of Glossopharyngeal nerve (Jacobson

nerve)
OPTIC CANAL (Foramen) • Ophthalmic artery

• Optic nerve (II)
SUPERIOR ORBITAL FISSURE • Divided into 3 parts by common tendinous ring of Zinn:
Middle part- Upper & lower division of oculomotor nerve,

nasociliary nerve, Abducent nerve
Lateral part- Trochlear nerve, frontal nerve & Lacrimal nerve,

Superior ophthalmic vein
Medial part: Inferior ophthalmic vein, sympathetic nerves

around ICA
INFERIOR ORBITAL FISSURE • Zygomatic nerve and infraorbital nerve of maxillary

nerve (V2)
ANTERIOR ETHMOIDAL CANAL • Anterior ethmoidal nerve & vessels
POSTERIOR ETHMOIDAL CANAL • Posterior ethmoidal nerve & vessels
INTERNAL AUDITORY (Acoustic) • Facial nerve (VII), vestibulocochlear nerve (VIII)

MEATUS • Nervus intermedius of Wrisberg

49. PALATE
• Cranial part of accessory nerve supplies all palatal muscles, except tensor veli palatini
• The sensory supply of the palate is through Glossopharyngeal, maxillary nerve, facial nerve
• Pharyngeal plexus supply muscles of soft palate
• Tensor veli palatini is supplied by mandibular nerve
• Middle and posterior lesser palatine nerves supply soft palate and tonsil
• Pharyngeal plexus supply all muscles of soft palate except Tensor veli palatine
• Primary and secondary palates are divided by Incisive foramen
• Sensory fibres from the taste buds in the hard and soft palate travel along Facial nerve
• Tensor veli palatine, Levator veli palatini helps to open Eustachian tube while sneezing
• Palatoglossus is derived from the 6th arch
• Passavant ridge is formed by Superior constrictor and palatopharyngeus
50. PHARYNX
• Pharynx extends from base of skull to C6 vertebral level.

• Killian’s Dehiscence seen in cricopharynx.
• Killian’s Dehiscence is in Inferior constrictor.
• When a large bolus of food is swallowed, the hyoid bone moves anteriorly to open the pharynx,
mediated by geniohyoid.
• Geniohyoid is supplied by ansa cervicalis branch of C1.
• Pain sensation from oropharynx is carried by IX nerve
• All muscles of the pharynx are supplied by pharyngeal plexus, except stylopharyngeus.
• Pharyngeal diverticulum is a protustion of mucosa between the two parts of inferior constrictor
muslce of the pharynx.
• Nasopharynx is lined by which epithelium Ciliated columnar.
• Lymphatic drainage of orpharynx is mainly through Jugulodigastric nodes.
51. EXTERNAL EAR
• Pinna is ectodermal in origin

• Pinna is formed at birth
• Pinna is composed of a thin plate of yellow elastic cartilage, covered with integument
• Pinna develops from the cleft of Ist arch
• Sensory nerve supply of pinna is by V3
• Major part of the skin of pinna is supplied by Great auricular nerve
• Pinna is supplied by Vagus nerve, Auriculotemporal nerve, Greater auricular nerve
• Skin over pinna is fixed Loosely on medial side

52. Tympanic Membrane Of Ear/ EARDRUM
• Tympanic membrane represents all three layers of embryonic disc

• Handle of malleus is attached to the center of the tympanic membrane
• Nerve supply of the tympanic membrane is by Auriculotemporal
• Tympanic membrane is Pearly white in color
• The peripheral part of tympanic membrane is the most mobile part of the tympanic membrane
• Shrapnell’s membrane is another name for Pars flaccida of the tympanic membrane
• The distance between tympanic membrane and medial wall of middle ear at the level of center is
2mm
• Distance of promontory from tympanic membrane 2mm
• Surface area of tympanic membrane 90 mm2
• Effective area is 55 mm2(approximately 2/3 of the total area).
• Lateral wall of middle ear is formed by Tympanic membrane
53. MIDDLE EAR
• The chorda tympani nerve is related to the lateral wall of middle ear.
• The auditory tube connects the nasopharynx with the anterior wall of middle ear
• Tympanic plexus present in Medial projection of middle ear cavity
• The distance between tympanic membrane and medial wall of middle ear at the level of center is 2
mm
• Mesotympanum Narrowest part of middle ear
• Sensory nerve supply of middle ear cavity is provided by Glossopharyngeal nerve
• Tegmen seperates middle ear from the middle cranial fossa containing temporal lobe of brain by
roof of middle ear
• Floor of middle ear cavity is in relation with Bulb of the internal jugular vein
• Promontory seen in the middle ear is Basal turn of cochlea
• Lateral wall of middle ear is formed byTympanic membrane
• Scutum is present in Lateral wall of middle ear
• The middle ear cleft in the temporal bone includes Air cells,Mastoid Antrum,Aditus ad Antrum,Attic
(Epitympanum),Eustachian Tube,mesotympanum,Hypotympanum
54. CONTENTS OF TYMPANIC CAVITY/ MIDDLE EAR
• Stapes is a derivative of 2nd branchial arch

• Stapes foot plate covers Oval window
• Handle of the malleus is attached to the center of the tympanic membrane
• Tensor Tympani contract together with stapes to stiffen the ossicular chain and protect the inner
ear from noise damage
• The nerve supply to tensor tympani is by Branch of the nerve to medial pterygoid branch of V3
• Malleus and Incus are derived from First arch
• Foot plate of stapes is developed from Reicherts cartilage
• Superior maleolar ligament connects Head of malleus to roof of epitympanum
• Cone of light is due to Handle of malleus
• Stapedial reflex is a protective reflex against loud
• Body of incus ,Head of malleus,Chorda tympani are components of epitympanum
• Movement of stapes causes vibration in Scala vestibuli
• Bones of middle ear are responsible for Reduction of impedance to sound transmission
• Tendon of stapedius muscle passes through the pyramid in middle ear
• Fossa incudis is related to Short process of incus
55. MASTOID ANTRUM
• Mac Ewan's triangle is the landmark for mastoid antrum

• The suprameatal triangle overlies mastoid antrum
• Development of the mastoid air cell system does not occur until afterbirth
• Mastoid is not a pneumatic bone
• Suprameatal triangle forms lateral wall of mastoid antrum
• Shortest skull diameter is Bimastoid
• Lateral wall of mastoid antrum is related to External auditory canal
• Mastoid antrum is present in petrous part of temporal bone
56. INTERNAL EAR
• Otoacoustic emissions arise from Outer hair cells

• Shortest part of VIIth cranial nerve is labryinth canal
• Scala media of the cochlea is filled with a fluid similar to intracellular fluid with high K+ and low Na+
• Labyrinthine artery is a branch of Anterior inferior cerebellar artery
• Vestibule is the central chamber of internal ear
• Promontory seen in the middle ear is Basal turn of cochlea
• Inner ear bony labyrinth is Cartilaginous bone
• Cochlear aqueduct Connects internal ear with subarachnoid space
• Organ of corti is situated in Scala media
• Endolymphatic duct connects scala media to subdural space
• Bony labyrinth, sigmoid sinus, and superior petrosal sinus are the boundaries of Trautmann's
triangle
• Vestibule, Senicircular canal & cochlea are the structures included in bony labyrinth
• Modiolus is the Central(2, 3/4) pyramid of bone around which cochlea forms
• Sense organ for hearing is Organ of Corti
• Hair cell of organ of Corti is supported by Deiters & Hensen Cells

57. SEMICIRCULAR CANALS OF INNER EAR
• Semicircular canal perceives Angular acceleration

• Semicircular canal is responsible for detecting rotational acceleration
• Arcuate eminence of the petrous temporal bone is formed by Superior semicircular canal
• Horizontal semicircular canal is lateral
• Crus commune is a part of Semi circular canal
• Semicircular canals are stimulated by Rotation
• Horizontal semicircular canal responds to Rotational acceleration
• Angular movements are sensed by semicircular canal
• Semicircular canals are arranged at right angles to each other.
58. FLUID OF INNER EAR
• Endolymphatic duct drains into Subarachnoid space

• Endolymph in the inner ear Is secreted by Stria vascularis
• Scala media contains endolymph
• The function of stria vascularis is To maintain electric milieu of endolymph
• Endolymph is rich in K+
59. ANTERIOR TRIANGLE OF NECK
• Anterior triangles of neck are-Submental, Digastric, Carotid, Muscular.

• Submental lymph nodes drain superficial tissues beliw tge chin, central part of lower lip, adjoining
gums, anterior part if floor of mouth & tip of tongue.
• On both sides submental triangle is bounded by Anterior belly of diagastric.
• Posterior boundary of carotid triangle is formed by anterior border of sternocleidomastoid.
• Hypoglossal nerve is a content of both digastric & carotid triangles.
• Structure superficial to mylohyoid in anterior digastric triangle is Mylohyoid artery & nerve
• Floor of digastric triangle is formed by mylohyoid (anteriorly) & hyoglossus (posteriorly)
• Infrahyoid ribbon muscles are the chief contents of muscular triangle.
BORDERS
RIGHT BORDER • Formed by right atrium
LEFT BORDER (Obtuse margin) • Formed mainly by left ventricle & partly by left
auricle

INFERIOR BORDER (Acute • Formed mainly by right ventricle & partly by left
margin) ventricle near apex
UPPER BORDER • Mainly by left atrium & partly by right atrium where
SVC enters
APEX • Formed by left ventricle
SURFACES
ANTERIOR (Sternocostal Surface) • Formed mostly by right ventricle (major) &
right auricle & partly by left ventricle & left
auricle.
INFERIOR (Diaphragmatic Surface) • It is formed by left ventricle (left 2/3) & right
ventricle (right 1/3)
BASE (Posterior surface) • Formed mainly by left atrium & partly by right
atrium.
• It is separated from T5 to T8 vertebrae by
pericardium, oblique pericardial sinus,
esophagus & descending aorta.
RIGHT SURFACE • Mainly by right atrium
LEFT SURFACE • Mainly by left ventricle & partly by left auricle
61. HEART-ARTERIAL SUPPLY, NERVE SUPPLY, VEINS OF HEART
RIGHT CORONARY ARTERY LEFT CORONARY ARTERY

• Branch of anterior aortic sinus of • Larger than right coronary
ascending aorta. artery.
• Runs in the right anterior coronary • Arises from left posterior
sulcus (right atrioventricular groove) & aortic sinus of ascending
then winds round to inferior border to aorta.
run backards in the right posterior • It enters the
coronary sulcus & reaches the posterior atrioventricular groove &
interventricular groove where it ends gives anterior
by anastomosing with left coronary interventricular branch.
artery. • Further continuation of LCA
• Rt coronary artery (RCA)Diameter less known as circumflex artery.
than LCA
BRANCHES • Acute marginal (Right marginal) • Anterior interventricular

• Posterior (descending) artery
interventricular (descending) artery in • Circumflex artery
85-90% of cases. • Left diagonal
• Right conus (infundibular) • Obtuse marginal (left
artery (sometimes it arises directly from marginal)
anterio aortic sinus & is called third • Left conus artery
coronary artery) • Atrial branch, anterior
• Nodal branch to SA node (in 65% cases) ventricular branch &
• Atrial, anterior ventricular & posterior posterior ventricular branch
ventricular • Nodal (in 35%) for SA node.
ARTERIAL • Right atrium & a part of left atrium • Most of left atrium
SUPPLY • Most of the right ventricle (except the • Most of the left ventricle
area adjoining the anterior • Anterior 2/3 of ventricular
interventricular groove) & small part of septum
left ventricle adjoining posterior • Right bundle branch
interventricular groove • Left bundle branch
• Posterior interventricular septum • SA Node- 35% of cases
• Whole conducting system (except right
bundle branch & a part of left branch of
AV bundle).
• SA Node- (in 65%)

62. LIVER
• The physiological right & left lobes have separate biliary drainage & vascular supply, i.e. they are
supplied respectively by right & left branches of portal vein & hepatic artery & bile is conveyed by
the corresponding hepatic ducts (bile ducts).
SEGMENTAL ANATOMY OF THE LIVER
• Based on the distribution of portal vein & hepatic vein, Couinaud divided each physiological
(functional) lobe of liver into 4 segments each & hence liver is divided into 8 segments.
• The physiological left lobe is composed of 4 segments designated I to IV & is supplied by left
branch of hepatic artery, left branch of portal vein & drained by left hepatic duct.
• The physiological right lobe consists of segment V, VI, VII & VIII & is supplied by right hepatic
artery, right branch of portal vein & drained by right hepatic duct.
• Segment I corresponds to caudate lobe

• Segment IV to quadrate lobe
• RIGHT LOBE is subdivided into anterior & posterior segment & left lobe into medial & lateral
segments.
• Thus the segments of liver are:
1. Right anterior- V (Inferior), VII (Superior)

2. Right posterior- VI (Inferior), VII (Superior)
3. Left medial- IV (Quadrate lobe): divded into IV a (Superior) IV b (Inferior)
4. Left lateral- II (Superior), III (Inferior)
5. Caudate lobe (Segment I) is considered as posterior segment.
• Liver has dual blood supply & receives 20% of its blood supply through hepatic artery & 80%
through portal vein.
63. CHAMBERS OF HEART
• SA node is situated in the upper part of crista terminalis.

• Auricle lies in the superomedial portion.
• Floor of the fossa ovalis is formed by septum primum..
• Left atrium forms the base of the heart.
• Left atrium forms the anterior wall of oblique sinus of pericardium. It lies in front of esophagus.
• Left auricle projects anteriorly to overlap infundibulum of right ventricle.
• The anterior surface, or sternocostal surface, is mostly made up of the right ventricle.
• Torus aorticus is an impression in the cavity of Right atrium
• Superior vena cava- Has no valve.

64. SUPRAHYOID MUSCLES
• Digastric muscles refers to muscles with two bellies are Muscle fibers in the ligament of
Treitz, Omohyoid, Occipitofrontalis.
• Posterior belly of digastric is supplied by Facial nerve.
• Mylohyoid nerve - branch of CN V3 (Mandibular division of Trigeminal nerve) innervates anterior
belly of trigeminal nerve.
• Second branchial arch give rise to stylohyoid, posterior belly of digastric muscles.
• Stylohyoid & digastric are elevators of larynx.
• Stylohyoid muscle is supplied by Facial nerve.
• Submandibular gland is divided into superficial and deep parts by mylohyoid.
65. INFRAHYOID MUSCLES
• Sternothyroid & thyrohyoid are Attached to oblique line of thyroid cartilage.

• Omohyoid is a digastric muscle.
• Omohyoid is an important landmark for Anterior & posterior triangle.
• Sternthyroid, sternohyoid & omohyoid are the muscles innervated my ansa cervicalis.
• All infrahyoid muscles depresses larynx.
66. PERITONEAL FOLDS- LESSER OMENTUM & GREATER OMENTUM
PERITONEAL FOLD CONTENTS

Greater omentum Right & left gastroepiploic vessels
Lesser omentum
• Right free margin • Hepatic artery, portal vein, bile duct

• Along lesser curvature • Right & left gastric vessels
Mesentry Superior mesenteric artery

Transverse mesocolon Middle colic artery
Sigmoid misocolon Sigmoid & superior rectal vessels
• The greater omentum is folded back on itself and is therefore made up of four layers .
• Greater omentum is generally referred to as "policeman of abdomen".
• The blood supply to the greater omentum is derived from the right and left gastroepiploic arteries.
• Greater omentum develops from caudal part of dorsal mesogastrium.
• Lesser omentum develops from ventral mesogastrium (dorsal part).
67. Ventricular system
• Junction of the anterior horn and posterior horn of lateral ventricle is called as Trigone of lateral ventricle
• Drainage of CSF from lateral to third ventricle is through Foramen of munro
• Floor of 4th ventricle is formed by Sulcus limitans,Post. surface of pons & Post. surface of medulla
• Magendie foramen or the median aperture drains CSF from 4th ventricle to the cisterna magna
• Fourth ventricle develops from Rhombencephalon
• Infundibulum ,Mammillary body & Optic chiasma are seen in floor of 3rd ventricles
• Abducens nuclei, hypoglossal nuclei, vestibular nuclei & Dorsal vagal nuclei are found in floor of fourth
ventricles
• Cerebral aqueduct (Duct of Sylvius) connects III ventricle to IV ventricle.
• CSF is produced by modified ependymal cells of the choroid plexus
• Floor of fourth ventricle is formed by rhomboidal fossa.
• Ventricles of brain are lined by Ependymocytes
• Anterior horn of lateral ventricle is closed anteriorly by the genu and rostrum of corpus callosum.
68. INFERIOR VENA CAVA
• Ligamentum Venosum connects inferior vena cava to the left branch of the portal vein.
• Inferior vena cava forms the posterior wall of the epiploic foramen.
• The tributaries of the inferior vena cava include hepatic veins, inferior phrenic vein, right suprarenal
vein, renal veins, right gonadal vein, lumbar veins, common iliac vein
• Inferior vena cava is formed from vitelline vein .
• The most important structure involved in development of inferior vena cava is Supracardinal vein &
Subcardinal vein.
• The right suprarenal vein drains into the Inferior vena cava.
• Double inferior vena cava is formed due to Persistance of both supracardinal and subcardinal veins.
• Obstruction of Inferior vena cava presents Thoraco-epigastric dilation.
69. PERITONEAL CAVITY- LESSEER SAC & GREATER SAC
• The length of the epiploic foramen is 3 cm.

• Epiploic foramen provides communication between greater and lesser sacs.
• A posterior gastric ulcer may perforate into lesser sac.
• Omental bursa is site for abscess formation in posterior perforation of gastric ulcer and internal
hernia through epiploic foramen.
• Boundaries of lesser sac are:
• Anterior wall: Caudate lobe of liver, stomach, Lesser omentum & 2nd layer of greater omentum
• Posterior wall: 3rd layer of greater omentum, & structurres forming stomach bed
• Right border: Right free margin of greater omentum & floor of epiploic foramen.
• Left border: Left free mergin of greater omentum; gastrosplenic & gastrophrenic ligaments
• Upper border: Reflection of peritoneum from esophagus to diaphragm.
• Lower border: Continuation of 2nd & 3rd layers of greater omentum.
70. PORTAL VEIN
• Portal vein provides 80% blood supplies to Liver.

• Portal Vein is formed by the union of superior mesenteric vein and the splenic vein.
• The whole hepatic portal system is valveless
• The Normal Portal venous pressure is 5-10mm Hg
• Portal hypertension is defined as the elevation of the hepatic venous pressure gradient (HVPG) to
>5 mmHg.
• Left gastric vein drains into portal vein.
• Portal vein begins at L2 level.
• Two capillary beds connected by a larger blood vessel characterizes a portal system of blood
vessels.
• Portal vein is Situated deep to the hepatic artery and cystic duct
• Portal circulation is also seen in an endocrine gland i.e. hypophysis cerebri
• Veins draining into portal vein are Splenic vein, Superior mesenteric vein, Inferior mesenteric vein,
Gastric veins, Cystic vein.
• Portal hypertension is present if, portal venous pressure is more than 10-12mm Hg.
• Portal triad in liver is formed by Hepatic artery, Bile duct, Portal vein.
71. EXTRAHEPATIC BILIARY SYSTEM
• Segment I, the caudate lobe, has its own biliary drainage. Variations of this are common, and in
78% of individuals the caudate lobe drains into both the left and right hepatic duct.
• Pancreatic & bile duct open into duodenum at Ampulla of vater.
• Cell lining of common bile duct is Simple columnar.
• Common bile duct injuries are most commonly seen in Laparoscopic cholecystectomy operation.
• Onion skin" fibrosis of bile duct is seen in Primary sclerosing cholangitis.
• Cystic lymph node lies b/w cystic duct & common hepatic duct.
• Valves of Heister is seen in Cystic duct.
• Spiral valve is seen in Cystic duct.

72. INGUINAL CANAL
Deep ring (Internal ring):
• 'U' shaped defect in the fascia tranversalis which form the posterior wall of inguinal canal.
• It lies 1.25 cm above the midpoint of the inguinal ligament.
• Inferior epigastric vessels run upwards & medially along the medial margin of deep inguinal ring.
• Indirect inguinal hernia enters inguinal canal through it.
External ring (Superficial ring):
• Triangular defect in external oblique aponeurosis.

• It is bounded on lateral and medical crura formed by external oblique aponeurosis and the base is
formed by pubic crest.
• Superficial inguinal ring is situated superior and lateral to pubic tubercles.
INGUINAL CANAL BOUNDARIES:
• Anterior: Skin, superficial fascia, external oblique aponeurosis,fibers of internal oblique in lateral
1/3
• Posterior: Fascia transversalis, extraperitoneal connective tissue, parietal peritoneum, conjoint
tendon in medial 2/3, reflected part of inguinal ligament at medial end.
• Roof: Medial crus of aponeurosis of external oblique Musculoaponeurotic arches of internal oblique
and transverse abdominal
• Floor: Union of inguinal ligament with fascia transversalis, Lacunar ligament at medial end.
STRUCTURE PASSING THROUGH INGUINAL CANAL:
• Spermatic cord in males

• Internal spermatic fascia
• Round ligament of uterus in females
• Ilioinguinal nerve in both sexes.
STRUCTURE PASSING THROUGH DEEP INGUINAL RING:
• Same as above except ilioinguinal nerve, which enters between external and internal oblique
muscles and passes out through superficial inguinal ring.
INGUINAL TRIANGLE OF HASSELBACHS
• Peritoneal triangle in the posterior wall of the inguinal canal

• Boundaries are:
1. Laterally: inferior epigastric artery

2. Medially: lateral border of rectus abdominis
3. Inferiorly: medial half of inguinal ligament
• It is divided into two unequal portions by obliterated umbilical artery.

• Direct inguinal hernia enters the inguinal canal through this triangle.
73. INGUINAL LYMPH NODE
• Lymphatics from glans penis, women's clitoris,prostatic urethra, spongy urethra ,deep parts of
lower limb and superficial inguinal nodes drains into deep inguinal lymph nodes.
• Integument of the penis, Scrotum, Perineum ,Buttock, Abdominal wall below the level of the
umbilicus ,Back below the level of the iliac crest, Vulva, Anus (below the pectinate line) ,The thigh
and the medial side of the leg (the lateral leg drains to the popliteal lymph nodes first). drains into
superficial inguinal lymph nodes.
74. KIDNEY- STRUCTURE, RENAL FASCIA & VASCULATURE
• Right renal vein is shorter than the left

• Superior suprarenal artery originates from Inferior phrenic artery
• Initially when the kidneys are in pelvis, the renal arteries are branches of common iliac arteries
• Neonatal kidney is supplied by aorta.
• Right renal artery is longer and passes behind IVC
• There are 5 vascular segment in kidney:Posterior, apical, upper anterior, middle anterior and lower.
75. KIDNEY
• Right kidney is lower & distal than the left kidney

• Right kidney is related to duodenum
• The neonatal kidney achieves concentrating ability equivalent to adult's kidney by 1year
• Development of human kidney begins in Sacral region
• Between the renal pyramids are projections of cortex called renal columns (or Bertin columns).
• Extent of kidney is from T12-L3
• Kidney is supported by perirenal fat, renal fascia, and pararenal fat
• Renal angle lies between 12th rib and lateral border of sacrospinalis
• Excretory system of kidney is derived from Metanephros
• Kidney develops from Metanephros, Mesonephric duct(Mesonephros), Blastema.
• Collecting part of kidney develops from mesonephros or Ureteric bud
76. Hypoglossal Nerve
• Hypoglossal nerve supplies all muscles of tongue except palatoglossal

• Motor supply to the muscles of the tongue is by hypoglossal nerve
• Hypoglossal nerve is 12th cranial nerve
77. OPTIC (II) NERVE
• Onodi cells are seen in respect to optic nerve.

• Optic nerve serves as the afferent pathway for light pupillary reflex.
• Internal Carotid Artery is the nearest relation of the optic nerve.
• Optic nerve Arises from axons of bipolar neurons.
• Optic nerve consists of axons of ganglionic cells.
• Optic nerve is derived embryologically from the neuroectoderm.
• Longest part of optic nerve is Intraorbital.
78. GLOSSOPHARYNGEAL NERVE
• Pain sensation from ear in tonsillitis is due to glossopharyngeal nerve.

• Nerve supply of circumvallate papillae is glossopharyngeal nerve.
• Taste sensations from the posterior 1/3rd of tongue are carried by glossopharyngeal nerve.
• Glossopharyngeal nerve innervates the oral pharynx.
• Sensory supply to tongue is by glossopharyngeal nerve .
• Glossopharyngeal nerve travels through the jugular foramen in the base of the skull.
• Glossopharyngeal nerve supplies the posterior part of the tongue because it develops
from Hypobranchial eminence
• Stylopharyngeus Muscle supplied by glossopharyngeal nerve.
• Sensory nerve supply of the palatine tonsils is by glossopharyngeal nerve.
• General sensation from the posterior 1/3rd of tongue are carried by glossopharyngeal nerve.
79. LUMBAR PLEXUS
• Genital branch of the genitofemoral nerve is the content of spermatic cord.

• Obturator nerve innervates Obturator externus , Adductor longus , Adductor brevis , Gracilis ,
Pectineus ,Adductor magnus
• Ilioinguinal nerve serve as an afferent nerve while eliciting cremasteric reflex

• Iliohypogastric and the ilioinguinal nerves passes b/w posterior surface of kidney & quadratus
lumborum
• Urinary bladder is supplied by L1 & L 2 branches of lumbar plexus
• Femoral branch of genitofemoral nerve passes behind the inguinal ligament
• Cremasteric muscle is supplied by Genital branch of genitofemoral nerve
• Tibial part of sciatic nerve, Obturator nerve supply of adductor magnus .
• Saphenous nerve is a branch of femoral nerve
• Ilioinguinal nerve lies in inguinal canal
• Femoral nerve supplies Iliopsoas ,Pectineus , Sartorius , Quadriceps femoris ,Anterior cutaneous
branches ,Saphenous.
• Genital branch of genitofemoral nerve enters the inguinal canal through deep inguinal ring
• Iliohypogastric,Ilioinguinal,Genitofemoral,Lateral femoral cutaneous,Obturator,Femoral,Short,
direct muscular branches branch off from lumbar plexus.
80. SACRAL PLEXUS
• Nerves passing through lesser sciatic foramen are obturator internus & pudenal nerve
• Superior gluteal nerve supplies Gluteus medius, Gluteus minimus & Tensor fasia lata
• Pudendal nerve supplying motor part to external sphincter is derived from S2-S4 roots
• Gluteus medius is supplied by superior gluteal nerve
• Pudenal nerve is both sensory and motor
• Sacral plexus, Nervi erigentes (S2,3,4) & pudenal nerve are involved in process of erection of penis
• Pudendal nerve leaves pelvis and enters gluteal region through greater sciatic foramen
• Pudendal nerve leaves the gluteal region by passing through the lesser sciatic foramen and enters
the pudendal canal
• Anal canal Supplied by pudendal nerve
• Ischial spine is related to pudenal nerve
• Structures passing through lesser sciatic foramen:
1. Pudendal nerve( leaves gluteal region to enter pudenal canal) lies in relation to Ischial spine
2. Internal pudendal vessels
3. Nerve to obturator internus
4. Tendon of obturator internus
81. SCIATIC NERVE
• Sciatic nerve is the thickest nerve of body

• Nerve supply of adductor magnus is through sciatic & obturator nerve
• Sciatic nerve leaves pelvis & runs posteriorly in the thighs
• Sciatic nerve enters the gluteal region through greater sciatic foramen
• A posterior dislocation of the hip joint will generally injure the sciatic nerve
82. FEMORAL NERVE
• Skin overlying the region where a venous "cut-down" is made to access the Great saphenous vein is
supplied by Great saphenous vein is supplied by femoral nerve
• Femoral nerve supplies anterior thigh muscles that flex the hip joint (pectineus, iliacus, sartorius)
and extend the knee (quadriceps femoris: rectus femoris, vastus lateralis, vastus medialis and
vastus intermedius)
• Anterior division of femoral nerve gives Intermediate femoral cutaneous nerve (intermediate
cutaneous nerve of thigh), medial femoral cutaneous nerve (medial cutaneous nerve of thigh) and
muscular branch to sartorius.
83. Arterial Supply of Lower Limb
• Femoral artery is the Content of Adductor canal

• Popliteal artery is the deepest structure in the popliteal fossa so can't be palpated
• Main blood supply to the head and neck of femur comes from Medial circumflex femoral Artery
• The superficial external pudendal artery is a branch of the femoral artery
• Superficial circumflex iliac artery is a branch of femoral artery
• Blood supply of great toe is by dorsalis pedis artery
• Femoral artery lies midway between the ASIS & pubic symphysis
• Posterior tibial artery lies deep to flexor retinaculum
• Superficial epigastric artery is a branch of femoral artery
84. COMMON PERIONEAL NERVE / FIBULAR NERVE
• Structures lieing in relation to common peroneal nerve are Head & neck of femur, biceps
femoris, lateral head of the gastrocnemius,peroneus longus , head & neck of fibula
• Nerve that winds around neck of fibula is common peroneal nerve
• Muscles of the anterior compartment of the leg which are: tibialis anterior, extensor hallucis
longus, extensor digitorum longus, and the peroneus tertius are innervated by deep peroneal
• Deep peroneal provides sensory innervations to space between the first and second toe and a small
area just proximal to the first and second toe on the plantar aspect of the foot.
• Muscles of the anterior compartment of the leg are innervated primarily by deep peroneal nerve

85. TIBIAL NERVE
• Nerve supply of adductor magnus is through tibial nerve & obturator nerve
• Popliteus Muscle supplied by tibial nerve
86. VENOUS DRAINAGE OF LOWER LIMB
• Short saphenous vein is a tributary of lateral marginal vein.

• The femoral ring is bounded by femoral vein on one side.
• Greater saphenous vein can be located Anterior to the medial malleolus.
• Femoral vein passes behind the inguinal ligament.
• Great saphenous vein Starts as a continuation of medial marginal vein
• The most important perforator of the Lower limb is between Long saphenous and femoral vein
• Femoral vein contains valve.
• Sural nerve & Achillis tendon are the structures accompanying Small Saphenous Vein.
• Small Saphenous Vein lies behind lateral malleolus
• Femoral vein lies in femoral sheath
• Femoral vein lies in hunter canal.
87. MUSCULAR COMPARTMENT OF LEG
• Popliteus muscle is also called unlocker of knee

• Peroneus longus is inserted into medial cuneiform
• Peroneus longus causes eversion of ankle
• Gastrocnemius is used in normal walk during DIstance and swing
• Tibialis posterior passes deep to the flexor retinaculum
• Tibialis posterior is inserted in Calcaneus,Intermediate cuneiform & Cuboid
• Boundaries of Popliteal fossa is formed by Biceps femoris, Both heads of Gastrocnemius &
Adductor magnus
• Peroneus brevis is attached to the tuberosity of the 5th metatarsal
• Gastrocnemius & plantaris muscles acts both at knee and ankle joint
• Extensor digitorum longus, Extensor hallucis longus, Tibialis anterior & Peroneus tertius causes
dorsiflexion of ankle
• Plantaris , FHL , FDL, Soleus, popliteus, peroneus longus, peroneus brevis, Tibialis posterior all
causes Plantar flexion
• Tibialis anterior, Extensor DigitorumLongus , Extensor Hallucis Longus & Peroneus tertius are the
muscles of the anterior compartment of the leg
• Popliteus muscle is supplied by tibial nerve
• Soleus is also called peripheral heart
88. HIP JOINT MOIVEMENTS
• Gluteus maximus, piriformis, obturator internus, obturator externus, quadratus femoris, superior
gemellus, and inferior gemellus are responsible for external rotation of the hip
• Gluteus medius, gluteus minimus and the deep gluteals are abductors of thighs
• Tensor fasciae latae causes Abduction of hip , Flexion of hip, Extension of knee
• Iliopsoas, rectus femoris, sartorius are muscles causing flexion
• Iliofemoral ligaments limits extension at the hip joint
• Medial rotation and Abduction is caused by Gluteus medius and Gluteus minimus
89. FEMORAL SHEATH
• Femoral ring is bounded by inguinal ligament, Lacunar ligament,pectineus, septum, femoral vein
• Distance between femoral ring and saphenous opening is 1.25cm
• Structure forming medial boundary of femoral ring is Lacunar ligament
• Femoral artery lies outside the femoral sheath
90. OBTURATOR NERVE
• Adductor compartment is innervated by obturator nerve.

• Obturator nerve is the branch of anterior division of lumbar plexus .
• Tibial part of sciatic nerve ,Obturator nerve supply adductor magnus.
• The structure crossing dorsal surface of ischial spine is the Obturator nerve.
91. SAPHENOUS NERVE
• Saphenous nerve lies in adductor canal.

92. FEMORAL TRIANGLE
• Lymphatics is the medial most structure in femoral triangle

• Lateral margin of femoral triangle is formed by sartorius
• Femoral vessels lies in femoral triangle
• Femoral triangle floor is formed by pectineus and adductor longus muscles medially
and iliopsoas muscle laterally.
93. HIP JOINT
• Iliopsoas is the primary hip flexor muscle.

• Iliofemoral ligament, Ischiofemoral ligament, Pubofemoral ligament keeps the hip from hyper-
extension.
• Bigelow's ligament is a ligament of hip joint
• Medial rotation and Abduction is caused by Gluteus medius and Gluteus minimus
94. ADDUCTOR CANAL
• Adductor canal contains the femoral artery, femoral vein, nerve to the vastus medialis and the
saphenous nerve .
• Adductor canal is located in thighs.
95. BONES OF FOOT
• Talus bone do not gives muscle attachments.

• The 1st 3 metatarsal with talus cuneiform & calcaneus forms medial arch of foot
• Inferior Tibiofibular joint is anormally example of syndesmosis
• Calcaneus bone articulates with cuboid bone
• Talus bone articulates with both lateral & medial malleolus of tibia & fibula, calcaneus & Navicular
bone
• Length of tibia is 20% of height.
96. ANKLE JOINT- LIGAMENTS
• Deltoid ligament is attached to medial malleolus, Sustentaculum tali of

calcaneus, Calcaneonavicular ligament, Navicular tuberosity, Medial surface of talus
• Deltoid ligament strengthens ankle joints
• Ankle joint is more stable at dorsi-flexed position
• Deltoid ligament , Lateral ligament, Shape of the superior talar articular surface stablizes ankle joint
• Anterior talofibular ligament gets affected most commonly in injury of ankle
• Plantar calcaneonavicular ligament support head of talus.
97. MOVEMENTS OF FOOT & ANKLE
• Inversion of foot occurs at talocalcaneal joint

• Extensor digitorum , Peroneus tertius, Extensor hallucis longus, Tibialis anterior are the muscles
causing dorsiflexion of foot
• Gastrocnemius, Soleus, Plantaris, Tibialis posterior, Peroneus longus and brevis, Flexor digitorum
longus, and Flexor hallucis longus are the muscles responsible for plantar flexion
• Inversion of foot is carried out by tibialis anterior.
• The important movements of inversion and eversion of the foot take place at the subtalar and
transverse tarsal joints
98. MUSCLES OF FOOT
• Sesamoid bone present in tendon of Flexor hallucis brevis

• Lumbricals Originates from tendons of flexor digitorum profundus
• Popliteus is the unlocker of knee
• Peroneus longus is the Evertor of ankle inserted into the medial cuneiform
• Gastrocnemius Muscle is used in normal walk during DIstance and swing
• Tibialis posterior muscle passes deep to the flexor retinaculum
• Tibialis posterior is inserted into all tarsus bones except talus
• Peroneus brevis is inserted into proximal part of 5th metatarsal
• Gastrocnemius & plantaris acts both on knee & ankle
• Muscles causing dorsiflexion of foot are Extensor digitorum longus, Extensor hallucis longus &
Tibialis anterior
• Planter flaxion is brought about by Plantaris, FHL & Soleus
• Action of tibialis anterior is that in Non-weight-bearing leg tibialis anterior flexes the foot
dorsally and lift its medial edge (supination) & in Weight-bearing leg it brings the leg towards the
back of the foot, like in rapid walking.
• Tibilais anterior causes inversion of foot
• Soleus is k/as peripheral heart
• Flexor digiti minimi muscle is attached to hook of hamate.
• Action of popliteus muscle: unlock knee, flex knee.
99. LIGAMENTS OF KNEE JOINT
• Middle genicular artery is a branch of popliteal artery and supplies the cruciate ligaments & the
synovial membrane of knee joint
• Posterior cruciate ligament Prevents posterior dislocation of tibia
• Anterior cruciate ligament prevents Anterior dislocation of tibia
• Middle genicular artery pierces the oblique popliteal ligament of knee
• Posterior cruciate ligament Originates from Posterior part of intercondylar area of tibia
100. KNEE JOINT
• When a person gets up from sitting position the femur internally (medially) rotates on the fixed
tibia.
• Abduction of hip , Flexion of hip ,Extension of knee are the action of tensor fasciae latae
• Extension at the knee is caused by quadriceps femoris muscle
• Popliteus unlocks knee
• Chief extensor of knee joint in hip flexion is Rectus femoris
• Extension of knee joint is caused by Quadriceps femoris
• Flexion is coupled with lateral rotation
• In full extension collateral ligaments are taut
• Locking of knee joint can be caused by Osgood shalter & Loose body in knee joint
• Biceps femoris responsible for Lateral Rotaion of Flexed Knee Joint
101. SCIATIC FORAMEN
• The tendon of the Obturator internus, Internal pudendal vessels, Pudendal nerve, Nerve to the
obturator internus are the structures passing through lesser sciatic foramen.
• Structures passing through Greater sciatic foramen:
1. Sciatic Nerve
2. Superior Gluteal Nerve
3. Inferior Gluteal Nerve
4. Pudendal Nerve
5. Posterior Femoral Cutaneous Nerve
6. Nerve to Quadratus Femoris
7. Nerve to Obturator Internus
8. Superior Gluteal Artery & Vein
9. Inferior Gluteal Artery & vein,
10. Internal Pudendal Artery & vein
11. Piriformis muscle
102. GENITOURINARY EMBRYOLOGY
• METANEPHROS forms EXCRETORY UNIT of kidney i.e. Glomerulus , proximal convoluted tubule ,
loop of henle , distal convoluted tubule.
• URETERIC BUD forms COLLECTING PART of kidney i.e. pelvis , Major calyces, Minor calyces,
Collecting tubules, Ureter.
• URINARY BLADDER (except TRIGONE) is derived from Vesicourethral canal, cranial part of
urogenital sinus(endodermal).
• TRIGONE is derived from absorbed part of Wolffian duct/ mesonephric duct(mesodermal).
• Upper 2/3 or 3/4 of vagina is derived from paramesonephric (mullerian duct)- mesodermal.
• Lower l/3 or l/4 of vagina is derived from urogenital sinus-endodermal.
• Differentiation of genital ridge into female or male gonads (ovary & testes) occurs at 6-10 weeks.
• Germ cells in the OVARY are derived from yolk sac endoderm.
• Leyding cells, develop from mesoderm of the gonadal ridge and are located between sex cords.
• Cowden’s syndrome associated with GENITOURINARY SYSTEM.
• Malformations of genitourinary system of foetus are found to be m/c associated with single
umbilical artery.
• In newborns and infants, kidneys have a larger medullary and a smaller cortical volume than in
later life.
• Most common site of genitourinary tuberculosis is - KIDNEY.
• In Genitourinary TB, Sterile pyuria is consistent finding.
• Pipe stem ureter appearance is seen in patients with Genitourinary TB.
• Cystic fibrosis affects GENITOURINARY SYSTEM.
• Horse shoe kidney is the most common congenital renal anomaly.
• Congenital anomalies : Renal agenesis (unilateral/ bilateral) failure of the ureteric bud to contact
the ipsilateral metanephric blastema.
• Associated anomalies -in females: Unicornuate uterus, Uterus didelphys, Mayer- Rokitansky-
Küster-Hauser(MRKH), Gartner duct cyst
In males: Seminal vesicle cysts, Absence of the Vas deferen, Cystic dysplasia of the rete testis
• Incomplete closure of urachus results in Urachal cyst, sinus, fistula.
103. DIAPHRAGM
• Structure passing along the aorta in the diaphragmatic opening is Thoracic duct & Azygous vein.
• Aortic hiatus contains Azygous vein & Thoracic duct.
• The opening in central tendon of diaphragm transmits IVC & Branches of right phrenic nerve.
• Oesophagus enters through muscular part of diaphragm.
• Anterior diaphragnatic hernia is through Foramen of morgagni.
104. IMPORTANT FACTS ABOUT OSTEOLOGY OF HEAD & NECK
• The skull forms the cranial end of the axial skeleton. It is composed of 22 bones of which 8 bones
are present in calvaria (brain case) and 14 bones in facial skeleton.
• Mandible is the only mobile bone in skull. It is the strongest bone of body.
• Cribriform plate is thinnest and is a part of ethmoid.
• Greater wing of sphenoid presents following foramina: Foramen rotundum, foramen ovale,
foramen spinosum, canaliculus innominatus, and emissary sphenoidal foramen (Foramen of
Vesalius).
• Optic canal (foramen) is enclosed by lesser wing of sphenoid and body of sphenoid.
• Arcuate eminence in petrous part of temporal bone is caused by superior semicircular canal.
• Cartilaginous part of auditory tube (Eustachian tube) lies inferior to spheno-petrosal synchondrosis.
• Clinically Sternberg’s canal is important as it is clinically associated with:Craniofacial angle is 130
degree.
1. Infection to sphenoid sinus or cranial fossa.

2. Congenital intrasphenoid meningocele (encephalocele).
3. Lateral sphenoidal sinus ‘spontaneous’ CSF leak.
• Dorello canal is an opening to cavernous sinus that transmits abducent nerve underneath the
superior petrosal sinus.
• Anterior fontanelle (bregma) is closed by 18 months and posterior fontanelle (lambda) by 2-6
months.
• Premature closure of foramen ovale results in Right ventricular hypertrophy.
• Maxillary bone does not articulate with Sphenoid.
105. PHARYNGEAL APPARATUS
• Pierre Robin sequence is caused by defect in development of first (1st) pharyngeal arch.
• Branchial cyst derived from 2nd branchial cleft (2nd pharyngeal cleft).
• First pharyngeal arch (mandibular arch) develops two prominences: smaller maxillary
prominence (forms maxilla, zygomatic bone, squamous temporal bone) and larger mandibular
prominence (forms mandible).
• Tympanic membrane derived from first pharyngeal membrane (which seperates 1st pharyngeal
groove from 1st pharyngeal pouch) represents all three layers of embryonic disc.
• Parafollicular 'C' cells develop from Ultimobranchial body.
• Tongue muscles originate from myoblast of occipital somites (occipital myotomes).
• Anterior 2/3 of tongue develops from 1st (lingual swelling) and tuberculum impar.
• Posterior 1/3 is developed from 3rd arch (cranial part of hypobronchial eminence).
106. PHARYNGEAL/ BRACHIAL ARCH DERIVATIVES
• Skeletal derivative of 2nd pharyngeal arch -
1. Reichert’s cartilage, stapes (except footplate)

2. Styloid process
3. Stylohyoid ligament
4. Smaller cornu of hyoid
5. Superior part of body of hyoid
• Pharyngeal muscles are derived from IV pharyngeal arch.

• Musculature of first pharyngeal arch is supplied by Mandibular division of Trigeminal Nerve (V3).
• Cartilage of IInd pharyngeal arch is known as Reichert’s cartilage.
• Reichert’s cartilage derivative is Stapes (except footplate).
• Footplate of stapes develops from Otic capsule.
• The stapes is embryologically derived from 2nd pharyngeal arch .
• IVth pharyngeal arch develops into epiglottis .
• Mandible is derived from Meckel's cartilage.
• Palatine tonsil develops from second pharyngeal pouch.
• Nerve of 6th arch- Recurrent laryngeal nerve (branch oh Vagus).
• Thymus develops from 3rd pharyngeal pouch.
107. DERIVATIVES OF ECTODERM
Derivatives of surface Ectoderm
1. Skin & appendages • Epidermis,

• hair
• nails
• sweat glands
• sebaceous glands.
2. Mucous membrane of • Oral cavity, nasal cavity, oaranasal sinuses

• lower part of anal canal, terminal part of urethra
• outer surface of labia minora, whole labia majora
• lower part of vagina.
3. Eye • Crystalline lens

• epithelium of cornea and conjunctiva, lacrimal gland.
4. Ear • Outer layer of tympanic membrane

• epithelial lining of membranous labyrinth.
5. Glands • Exocrine glands (sweat glands, sebaceous glands

• salivary glands, mammary glands, lacrimal glands).
6. Teeth • Enamel (Ameloblast).
7. Pharyngeal Clefts
Derivatives of Neuroectoderm
From NEURAL TUBE: From NEURAL CREST:
• CNS (brain, spinal cord), A) NEURAL DERIVATIVES
• Astrocytes • Sensory neurons of 5th, 7th, 8th, 9th. 10th cranial nerve ganglia
(trigeminal, geniculate, sphenopalatine, submandibular,
cochlear, vestibular, otic and vagal parasympathetic
ganglia).
• Oligodendrocytes • Sensory neurons of spinal dorsal root ganglia.
• Ependymal cells • Sympathetic chain ganglia and

plexus (celiac/preaortic/renal ganglia, enteric plexus in GIT,
I.e. Auerbachs and Meissner’s).
• Retina • Parasympathetic ganglia and plexus of GIT.
• Pineal gland • Schwann cells of peripheral nerves, satellite cells of all

ganglia.
• Neurohypophysis (posterior • Adrenal medulla, chromaffin cells, parafollicular C-cells of

pituitary) thyroid gland.
• All cranial and spinal motor • Melanocytes and melanoblasts.

nerves
• Glomus cells
B) MESENCHYMAL DERIVATIVES
• Dermal bones of skull: Frontal, parietal, temporal, nasal,

vomer, palatine, mandible, maxilla.
• Leptomeninges : arachnoid and pia mater (Duramater is

mesodermal).
• Dentine of teeth (odontoblasts)
• Eye : choroid, sclera, iris epithelium, pupillary

muscles (sphincter and dilator pupillae, ciliary muscles).
• Pharyngeal arch cartilages.
• Retinal pigmented epithelium

• Connective tissues of head including dermis, tendon,
ligaments.
• Bulbar and ronal ridges of heart.
108. DERIVATIVES OF MESODERM
DERIVATIVES OF MESODERM
• Mesoderm is divided into three parts:-
1) Paraxial mesoderm 2) Intermediate mesoderm 3) Lateral plate mesoderm
1. PARAXIAL MESODERM:
• It is organised into somites which in turn gives rise to:-
1. Sclerotomes: Forms axial skeleton including vertebrae, ribs and parts of neurocranium.
2. Myotomes: Form all voluntary (skeletal) muscles of head, trunk and limbs.
3. Dermatomes: Form dermis of skin, especially over dorsal regions.
2. INTERMEDIATE MESODERM:
It gives rise to major portion of urogenital system:-
1. Urinary organs: Kidney, ureters, trigone of bladder, posterior wall female urethra, posterior wall of
upper half of prostatic part of male urethra, inner glandular zone of prostate.
2. Reproductive organs: Gonads (testis and ovary), epididymis, ducts deferens, seminal vesicle,
ejaculatory duct, uterus, uterine tube and upper part of vagina.
3. LATERAL PLATE MESODERM:
• It forms:-
i) Somatopleuric mesoderm (parietal layer)
• All connective tissues including specialised connective tissue like bone, cartilage, adipose tissue.
• Dermis of skin over ventrolateral body wall and limbs.

• Superficial and deep fascia.
• Ligaments, tendons, aponeurosis.
• Parietal pleura, parietal peritoneum and tunica vaginalis of testis.
• Dura-mater.
• Lid muscles, extraocular muscles.
• Sclera, choroid, vitreous.
• Corneal stroma, iris and ciliary body (except epithelium).
ii) Splanchnopleuric mesoderm (visceral layer)
• Smooth muscle and connective tissue of respiratory tract, gut, blood vessels and heart.
• Adrenal cortex.
• Mesothelium (visceral layer) of pleural, peritoneal and pericardeal cavities.
• Mesenchyme surrounding pericardial coelom gives rise to myocardium and serous pericardium.
• Spleen and lymph nodes.
iii) Spetum transversum
• Diaphragm
• Fibrous pericardium
iv) Angiogenic mesoderm
• Endocardium of heart
• Endothelium of blood and lymphatic vessels.
• Microglia, tissue macrophage.
• Circulating blood vessels.
109. DERIVATIVES OF ENDODERM
DERIVATIVES OF ENDODERM
• The endoderm gives rise to:-
1) Lining epithelium of:
• Gastrointestinal tract including gall bladder, extrahepatic duct system and pancreatic duct.
• Pharyngotympanic tube (eustachian tube), middle ear, inner layer of tympanic membrane,
mastoid antrum and air cells.
• Respiratory tract including larynx, trachea, bronchi and lungs (alveoli).
• Genitourinary tract urinary bladdet except trigone (mesodermal), female urethra except part of
posterior wall (mesodermal), male urethra except posterior wall of prostatic urethra (mesodermal)

and except part of penile urethra lying the glans (ectodermal(, part of vagina, vestibule and inner
surface of labia minora.
2) Glandular tissue
• Endocrine glands, e.g. thyroid, parathyroids, islets of langerhans of pancreas.

• Exocrine glands such as liver, pancreas, glands in walls of GIT, prostate (except inner glandular
zone).
3) Reticular tissue
• Of Thymus and Tonsils.
110. GAMETOGENESIS- SPERMATOGENESIS
• Spermatogenesis takes place in Seminiferous tubule.

• Spermatogenesis is maintained by Testosterone, FSH, & LH.
• Spermatogenesis occurs at Temperature lower than core body temperature.
• Time taken for spermatogenesis is 61 days.
• Sperms acquire motility in Epididymis.
• Length of a mature human spermatozoon is 50- 60 microns.
• Capacitance of sperms takes place in Uterus.
• Sperm capacitation takes about 4-6 hrs.
• Mitochondria of a sperm is seen in Body of the sperm.
• Daily sperm production is 120 million per day.
• Velocity of sperms in female genital tract is 1- 3mm/day.
111. GAMETOGENESIS- OOGENESIS
• Primary oocyte is Maximum in number in 5 month fetus

• Primary oocyte ls in prophase arrest
• At birth, oocytes are in Resting phase between prophase and metaphase of 1st meiotic division of
developÂment
• Primary Oocyte remains in ovary in Prophase
• Primary oocyte is arrested at prophase till puberty
• Primary oocyte is hormonally induced to resume the first meiotic division during onset of puberty
• Secondary oocyte enters the second meiotic division just before ovulation and arrests at
metaphase
• Polar bodies are formed during Oogenesis
• Ovary Develops in genital ridge
• Sex cords are derived from coelomic epithelium
• At birth ovary contains 2 million folliclesCells which surround the oocyst in graafian follicle are
called Cumulus oophoricus
• After first meiotic division, the primary oocyte remains arrested in Diplotene stage
• In oogenesis, first meiotic division completes Before ovulation
• One primary oocyte forms 1ovum
112. THYROID GLAND
• The isthmus lies against the 2nd and 3rd tracheal rings at the level of C7.
• Ligament of Berry in thyroid fixes Cricoids cartilage.
• Lymphatic drainage of thyroid gland mainly from deep cervical lymph node.
• Inferior thyroid artery is a branch of Thyrocervical trunk.
• Inferior thyroid vein drains into Brachiocephalic vein.
• Middle thyroid vein drains into internal jugular vein.
• The Recurrent laryngeal nerve lies very close to the inferior thyroid artery near the base of the
thyroid lobe.
113. PARATHYROID GLANDS
• Number of parathyroid glands is-4.

• The superior parathyroids are also referred to as 'parathyroids IV' because they develop from the
fourth pharyngeal pouch.
• Inferior parathyroids are also referred to as 'parathyroids III' because they develop from the
endoderm of third pharyngeal pouch.
• Each parathyroid receives blood supply from inferior thyroid artery.
114. PITUITARY GLAND
• Anterior pituitary develops from Rathke's pouch.

• Posterior piyuitary develops from infundibulum.
• Herring bodies are seen in Neurohypophysis.
• Routes for venous drainage of neurohypophysis:
1. To adenohypophysis via long and short portal vessels.
2. Into dural venous sinuses via inferior hypophysael veins.

3. To hypothalamus via capillaries passing to median eminence.
115. SUBMANDIBULAR GLAND
• Lobes of submandibular gland are divided by Mylohyoid muscle.

• Preganglionic fibers to the submandibular gland arise from superior salivatory nucleus.
• Nerve which loop around submandibular duct is Lingual nerve.
• Structure not injured in submandibular gland excision is Inferior alveolar nerve.
• In Submandibular gland surgery the nerve leastlikely to be injured is Inferior alveolar nerve.
116. OLFACTORY (I) NERVE
OLFACTORY NERVE: Ist CRANIAL NERVE
• Special visceral afferent nerve that mediates sense of smell (olfaction).

• Pure sensory nerve.
• Olfactory nerve has following unique features:-
i) The primary olfactory neurons lie at the body surface in the epithelium lining the roof of nasal cavity
(olfactory epithelium).
ii) The primary olfactory neurons undergo continuous turnover being replaced from stem cells in the
olfactory epithelium.
iii) It is the only cranial nerve that projects directly to forebrain (telencephalon).
iv) The olfactory neurons enter the allocrotex directly without relaying through thalamus.
v) The olfactory pathway to highest cortical center is ipsilateral.
Termination- Glomerulus of the olfactory bulb.
117. VAGUS (X) NERVE
Special visceral (branchial • Arise in nucleus ambiguus and supplies :

efferent) • Muscles of larynx, pharynx (except stylopharyngeus)
• Soft palate (except tensor veli palatine)

General visceral efferent • Arise in dorsal nucleus of vagus and carry preganglionic
parasympathetic fibers.
• These are distributed to thoracic (heart, lung) and
abdominal (upto right 2/3 of transverse colon) viscera.
• About 75% of all parasympathetic nerve fibers are vagus
nerve.
General visceral afferent • Nucleus tractus solitarius (lower part) receives sensations
from pharynx,larynx, trachea, esophagus and thoracic and
abdominal viscera.
Special visceral afferent • Nucleus tractus solitarius (upper part) receives taste
sensation from posterior most part of tongue (vallecula)
and epiglottis through internal laryngeal nerve.
General somatic afferent • Distributed to skin of auricle, external meatus and tympanic
membrane and terminate in spinal nucleus of trigeminal.
118. ACCESSORY (XI) NERVE
ACCESSORY NERVE
• Cranial root supplies (through branches of vagus) the:
1. muscles of soft palate (except tensor veli palatini),

2. pharynx (except stylopharyngeus),
3. larynx & possibly the heart
• CRANIAL ROOT arises from medulla and leaves the cranial cavity through jugular foramen.
2. SPINAL ROOT also contains special visceral (branchial) efferent fibers which arise from the spinal
nucleus in the ventral horn of C1 to C5 spinal cord segments.
• Its fibers supply sternocleidomastoid and trapezius.

• SPINAL ROOT arises from spinal nucleus in ventral horn of C1 to C5.
• It pierces anterior border of sternocleidomastoid at the junction of upper 1/3 & lower 2/3 of the
muscle and supplies the muscle.

• Due to its superficial course nerve can be easily damaged in posterior triangle of neck by surgical
incision and drainage of abscess, stab wounds in neck, and surgical removal of cancerous lymph
node.
PHARYNGEAL PLEXUS
Pharyngeal plexus formed by-
i) Pharyngeal branch of vagus carrying fibers of cranial accessory nerve→ Motor supply for muscles of
pharynx (except stylopharyngeus) & soft palate (except tensor palati).
ii) Pharyngeal branches of glossopharyngeal nerve→ for sensory supply of mucosa of pharynx (except
nasopharynx above the level of opening of auditory tube).
iii) Pharyngeal branches of superior cervical sympathetic ganglion.
119. FACIAL NERVE INJURY
• Facial nerve palsy is seen in Malignant otitis externa.

• Facial nerve palsy is seen in the fracture Middle cranial fossa.
• Recurrent facial nerve palsy is a feature of Melkersson Rosenthal syndrome.
• Iatrogenic traumatic facial nerve palsy is most commonly caused during Mastoidectomy.
• In supranuclear lesion of facial nerve lower part of the opposite side of the face is paralyzed.
• A Swelling of the facial nerve within the facial canal resulting from compression of nerve due to an
inflammatory process in the temporal bone results in paralysis of stapedius muscle
• Iatrogenic traumatic facial nerve palsy is most commonly caused during Mastoidectomy
• A patient with a facial nerve paralysis suffers from inability to dampen loud noises due to
denervation of stapedius muscle
• Facial nerve palsy occurs in 20% of longitudinal temporal bone fractures and 50% of transverse
temporal bone fractures.
• While doing posterior tympanotomy through the facial recess there are chances of injury to
the Chorda tympani & Vertical descending part of facial nerve but not Facial nerve horizontal part.
• Facial nerve palsy is seen in Malignant otitis externa.
• Facial nerve palsy is seen in Chronic suppurative otitis media(CSOM).
• Lacrimation is affected when facial nerve injury is at Geniculate ganglion
• In oedma of facial nerve at the level of geniculate ganglion hyperacusis, loss of lacrimation and loss
of taste sensation in the anterior 2/3rd of the tongue are seen
• In Dryness of mouth with facial nerve injury site of lesion is at Chorda tympani Nerve
• Level of injury of facial nerve region below Stylomastoid foramen Loss of corneal reflex
• Most common nerve injured in face lift surgery is Frontal branch of facial nerve
120. VESTIBULOCOCHLEAR (VIII) CRANIAL NERVE

• Vestibular component (vestibular nerve)→ Equilibrium & balance
• Cochlear component (cochlear nerve)→ Hearing.
• Trapezoid body is involved in auditory pathway (lateral lemniscus system).
• Auditory transmission is via Lateral lemniscus.
• Auditory pathway passes through Medial geniculate body.
121. BONES OF THE FOREARM- ULNA
• Olecranon process of ulna helps in formation of Trochlear notch.

• Ossification center of upper end of ulna is united by 16 years.
• The treatment of choice of fracture of radius and ulna in a an adult is Only plates.
• Both ulnar fracture and head of radius is displaced anteriorly
• Superior radioulnar joint is Pivot joint.
122. BONES OF THE FOREARM- RADIUS
• Radial bone is major contributor to wrist joint.

• Extensor carpi radialis longus (ECRL) & extensor carpi radialis brevis (ECRB) lies lateral to distal
radial tubercle.
• Carpal bone which articulates with radius is Scaphoid
• Two carpal bones articulate with radius are Scaphoid and lunate.
• Fracture of distal end of radius may results in loss of function of Extensor Pollicis Longus tendon.
• If head of the radius is removed, it will result in Valgus deformity.
• The forcible separation of the head of the radius from the capitulum of the humerus is mainly
prevented by the Annular ligament.
123. BONES OF HAND- METACARPAL
• 1st carpometacarpal joint is Saddle.

• Normal metacarpal index is 5.4 to 7.9.
• Short 4th metacarpal is a feature of Pseudohypoparathyroidism.
• Proximal interphalangeal, distal interphalangeal & 1st carpometacarpal joint involvement and
sparing of wrist is a feature of Osteoarthritis.
• Bennett's fracture is fracture dislocation of base of 1st metacarpal.
• Webbing of neck, increased carrying angle, low posterior hair line and short fourth metacarpal are
characteristics of Turner syndrome.
• All the metacarpals in the hand have one epiphysis per bone which is in the head of the bone
except the thumb, where it is in the base.

124. BONES OF HAND- CARPAL
• 4th carpal bones (Lunate) are present at 4 yrs of age.

• Carpal bones articulate with radius are Scaphoid and lunate.
• Carpal bone which fracture commonly is Scaphoid.
• The commonly injured carpal bone next to scaphoid is Trapezium.
• Lunate carpal bone fracture causes median nerve involvement.
125. BRACHIAL PLEXUS
• Posterior cord of brachial plexus is formed by Dorsal divisions of upper, middle & lower trunks.
• Radial nerve is the largest branch of brachial plexus and is the continuation of posterior cord (root
value C5- C8, T1).
• Axillary nerve is a branch of Posterior cord of brachial plexus .
• Axillary nerve supplies teres minor & deltoid.
• Musculocutaneous nerve is injured at the lateral cord of brachial plexus, positive clinical findings
would be Sensory loss on the radial side of forearm.
• Brachial plexus is surrounded by fascia derived from prevertebral fascia
• It starts from above the fifth cervical vertebra to underneath the first thoracic vertebra(C5-T1).
• Cord of brachial plexus are named as per their relation with the axillary artery behind PECTORALIS
MINOR muscle.
• All the muscles of pectoral girdle are supplied by Brachial Plexus except trapezius muscle which is
supplied by CN1
126. ERB’S PARALYSIS
• Erb's point is at junction of C5,6.

• Policeman's tip hand deformity seen in Erb's palsy.
• In injury to upper trunk of the brachial plexus causes Pronation of forearm & Inability to initiate
abduction of shoulder.
127. MEDIAN NERVE
• Median nerve is also known as labourer's nerve

• Formed from the branches of medial and lateral cord of brachial plexus.
• Medial most structure in cubital fossa
• Deep to pronator teres heads
• Lateral to axillary artery in axilla
• Passing deep to flexor retinaculum at wrist
• seen in supracondylar # humerus
• Median nerve supplies nail beds(anesthesized in surgeries related to nail bed)
• Median nerve supplies Pronator teres of forearm
• Median nerve supplies Opponens pollicis muscle of hand
• Adductor pollicus will not be affected in median nerve palsy
• Interosseous nerve is the branch of median nerve
• Pointing Index seen in median nerve palsy
• Thenar muscle is wasted in median nerve palsy
• Median nerve injury is Most common in lunate bone dislocation among all carpel bones
• Median nerve injury at wrist is Tested by contraction of abductor pollicis brevis(pen test)
• Ape thumb deformity observed in median nerve injury
• Carpal Tunnel Syndrome seen in median nerve injury
• Median nerve injury results in inability to pronate arm
128. KLUMPKE’S PARALYSIS
• In Klumpke's palsy nerve roots involved: Mainly T1 & partly C8.

• Horner syndrome is due to T1 injury proximal to white ramus communicans to 1st thoracic
sympathetic ganglion.
129. CARPAL TUNNEL SYNDROME
• Nocturnal parasthesias of the thumb and the index and middle fingers with atrophy of the thenar
eminence & positive Tinel sign is suggestive of Carpal tunnel syndrome.
• Carpal tunnel syndrome is caused by Hypothyroidism, Pregnancy & Acromegaly.
• Median nerve involvement is present in Carpal tunnel syndrome.
• Carpal tunnel syndrome is associated with Acromegaly,Rheumatoid arthritis,Gout, Wrist
osteoarthritis,Diabetes Mellitus,Hypothyroidism, Myxedema & Pregnancy
• The carpal tunnel involves Median Nerve, Flexor pollicis longus & Flexor digitorum superficialis.
• Compression of a nerve within the carpal tunnel products inability to Oppose the thumb.
• Most sensitive test for carpal tunnel syndrome is Phalen's test.
130. BRACHIAL PLEXUS NERVE BLOCK
• Most commonly used approach of brachial plexus block is Supraclavicular.

• Exposure of left subclavian artery by supraclavicular approach does not require cutting of Scalenus
medius.

131. MEDIAN NERVE PALSY
• Injury or compression of median nerve at wrist (eg carpel tunnel syndrome) can be tested by
1. Pen test for loss of action of Abductor pollicis brevis
2. Ape thumb deformity (adducted posture of thumb)
3. Loss of opposition & abduction of thumb (d/ t wasting of thenar muscles)
4. Sensory loss - lateral 31/2 of digits & 2/3 palm (autonomous zone is tip of index & tniddle finger)
• Median nerve injury at wrist, is commonly tested by Contraction of abductor pollicis brevis
• Carpal tunnel syndrome is caused by the compression of the median nerve at wrist and is most
common type of nerve entrapment syndrome.
• In High median nerve palsy sensory loss in the thumb, index, middle & radial half of the ring fingers
& lateral 2/3 of the palm.
132. ULNAR NERVE
• Ulnar nerve is Also known as musician nerve

• Ulnar nerve Arises from C7,8 & T1 roots
• No branch of ulnar nerve in Arm.
• Ulnar nerve injury results in Clawing of fingers.
• Most common nerve used for monitoring during anaesthesia is ulnar nerve.
• Forms Martin-Gruber connections with Median nerve.
• Cervical rib if present it causes pressure on ulnar nerve.
• Deep branch: accompanies deep ulnar artery & supplies 3 muscles of hypothenar
eminence(abductor digitii minimi, flexor digitii minimi and opponens digitii minimi), medial two
lumbricals(3rd & 4th), eight interossei, adductor pollicis & wrist joint and occasionally deep head of
the flexor pollicis brevis.
• Also supplies skin over Hypothenar eminence
• Hypothenar muscles is supplied by deep branch of ulnar nerve
• The four dorsal interossei is supplied by deep branch of ulnar nerve
133. ULNAR NERVE INJURY
• High ulnar nerve palsy is caused by injury proximal to the elbow..

• Tardy ulnar nerve palsy is seen in Lateral condyle # humerus.
• Knuckle bender splint is used for Ulnar Nerve Palsy.
• Claw hand is caused by lesion involving Ulnar nerve.
• Cubital tunnel syndrome involves Ulnar nerve.
• In Hansen's disease, the nerve commonly affected at elbow is Ulnar nerve.
• Most common nerve injured in fracture of medial epicondyle of humerus is Ulnar nerve.
• Inability to adduct the thumb is due to the injury of Ulnar nerve.
• Froment test is positive in lesion of Ulnar nerve.
134. STOMACH
• Stomach is derived from Foregut.

• Cardiac orifice of stomach is located at level of T11 vertebra.
• Chief cells are most abundant in Fundus part of the stomach.
• Electrical pacemaker of stomach is situated in Fundus.
• Most important blood supply to stomach left gastric artery.
• Pain sensations from stomach are carried along sympathetic fibers.
• The veins of stomach drain into the portal, superior mesenteric & splenic veins.
135. RADIAL NERVE PALSY
• Lateral & posterior cutaneous nerves of arm and posterior cutaneous nerve of forearm are spared
in low radial nerve lesions.
• Most common complication of mid shaft humerus fracture is Radial nerve palsy.
• Wrist drop is seen with Radial nerve palsy.
136. AXILLARY NERVE
• Axillary nerve also known as Circumflex nerve.

• Axillary nerve is a branch of the posterior cord of brachial plexus with root value C5 & C6.
• The axillary nerve innervates the deltoid muscle.
• Damage to axillary nerve causes :
1. deltoid paralysis
2. teres minor paralysis
3. loss of rounded contour of shoulder
4. sensory loss in small patch of skin & on the outer surface of arm
5. There is loss of abduction from 15-90 degree due to paralysis of deltoid (first 15 degree of flexion is
not lost as it is caused by supraspinatus & overhead abduction is preserved as it is caused by
trapezius & serratus anterior).
137. MUSCULOCUTANEOUS NERVE
• Musculocutaneous nerve branch of lateral cord of brachial plexus with root value C5,6,7.
• Musculocutaneous nerve supplies Biceps brachii, corachobrachialis, and brachialis.
• Damage to musculocutaneous nerve results in:
i) Weakness of flexion of elbow due to paralysis of biceps & brachialis.
ii) Loss of supination of semifixed forearm due to paralysis of biceps.
iii) Sensory loss along the lateral (radial) border of forearm.
138. RADIAL ARTERY
• Radial artery is the terminal branch of brachial artery, arising in cubital fossa
• Radial artery is the only content of anatomical snuff box.
139. ULNAR ARTERY
• Ulnar artery is larger terminal branch of brachial artery.

• The deep palmar arch lies deep to the oblique head of adductor pollicis, long flexor tendon &
lumbrical muscles.
• Deep palmar arch is formed mainly by radial artery & partly by deep branch of ulnar artery.
• Posterior interosseous artery is a branch of common carotid artery which in turn is a branch of
ulnar artery.
140. NERVE SUPPLY OF MUSCLES OF UPPER LIMB
• Musculocutaneous nerve supplies coracobrachialis, biceps brachii, and the greater part of the
brachialis.
• Abductor pollicis brevis is supplied by Median nerve .
• Deltoid & teres minor muscles supplied by Axillary nerve (C5,6).
• In deltoid paralysis Axillary nerve is involved.
• Teres major muscles supplied by Lower subscapular nerve.
• Pectoralis major & minor muscles is supllied by Medial pectoral nerve.
141. MUSCLES OF PECTORAL REGION & AXILLA

• Serratus anterior causes protraction of scapula..
• Injury to the long thoracic nerve results in paralysis of the serratus anterior muscle.
• Pectoralos major is the most common muscle to be congenitally absent (in Poland syndrome).
• Winging of scapula is due to paralysis of Serratus anterior.
142. APPLIED ANATOMY OF MUSCLES OF UPPER LIMB
• Pectoralis major is the most common muscle to be congenitally absent (POLAND SYNDROME)
• Winging of scapula is caused most commonly by serratus anterior palsy.
• Dropped shoulder is caused by paralysis of trapezius.
• Palmar brevis is a remnant of panniculus carnosus.
• Third head of coracobrachialis is denoted as struther’s ligament.
• Rotator cuff consists of supraspinatus, infraspinatus, teres minor & subscapularis.
• Most commonly tendon damaged among rotators is supraspinatus.
143. ANTERIOR ABDOMINAL WALL
• Xiphoid process lies at the level of T9 vertebra.

• Xiphoid process fuses with sternum after 40 years
• Pubic symphysis lies at the level of coccyx.
• Highest point of iliac crest lies at L4 vertebra .
• Umbilicus lies b/w L3 and L4 vertebrae.
• The angle b/w the last rib & outer border of erector spinae is known as renal angle.
• The umbilicus is a watershed, above the level of umbilicus lymph flows upwards to drain
into axillary lymph nodes.
144. FEMUR BONE
• Femur is the longest & strongest bone of the body. It is proximal end, shaft & distal end.
• True Supracondylar fracture of femur is Type A.
• Main blood supply to the head and neck of femur comes from Medial circumflex femoral Artery.
• Lower end of femur is ossified from 1 ossification center.
• Distal end of femur is the growing end.
145. TIBIA BONE
• Tibia is the second largest bone (after femur).

• Length of tibia is 20% of height.
• Posterior dislocation of tibia on femur is prevented by Posterior cruciate ligament
• Action of tibialis anterior is Inversion of foot.
• Upper end of tibia is the growing end. The secondary center for upper end appears just before birth
& fuses with shaft at around 16-18 years.
• Tibia is the commonest site of osteomyelitis from direct contamination as well as from
hematogenous spread.
146. ANATOMY OF LUNGS
• Lungs develop from Foregut.

• Right lung is shorter, wider & heavier (625 gm) than left lung (565 gm).
• Surface marking of inferior surface of lung is 2 level above the reflection of inferior surface of
pleura i.e. 6th rib in midclavicular line, 8th rib in midmaxillary line, & 10th rib at lateral border of
errector spinae.
147. EXTRAPULMONARY & INTRAPULMONARY BRONCHUS
• Each lung has 10 bronchopulmonary segments

• In the lungs bronchial arteries supply the bronchopulmonary tree Till segmental bronchi.
148. FISSURES & LOBES OF LUNGS
• Bulging fissures in lungs is seen in Klebsiella pneumonia.

• Each lung has 10 bronchopulmonary segments.
• Right lung is divided into 3 lobes (upper, middle & lower) by two fissures, oblique & horizontal.
• The left lung is divided into two lobes (upper & lower) by the oblique fissures.
149. HILUM OF LUNG
• At hilum of lung Primary/Principal bronchus enters.

• Posterior relation of hilum of lung is Vagus nerve.
• he hilum of the right lung is arched by Azygous vein.
• Pulmonary artery is the uppermost structure in left lung hilum.

150. ARTERIAL SUPPLY & VENOUS DRAINAGE OF LUNG
• Bronchial arteries are branches of the descending thoracic aorta. They supply the bronchial wall as
for as the respiratory bronchioles.
151. CONDUCTING SYSTEM OF HEART
Crista terminalis divided the right atrium into smooth posterior part & rough anterior part.
Maximum velocity of conduction is seen in purkinje fiber.
AV node is situated in Koch's triangle.
Slowest conduction is in AV node.
The SA node is composed of a cluster of small fusiform cells in the sulcus/crista terminalis at the right
atrial–superior vena caval junction.
SA node acts as a pacemaker of the heart because of the fact that it Generates impulses at the highest
rate.
SA Node is supplied by nodal artery, a branch of RCA in 65% cases & a branch of circumflex branch of LCA
in 35% cases.
SA node is supplied by right vagus/parasympathetic (inhibitory) and right Sympathetic (excitatory) system
Purkinje fibres are modified cardiac muscle.
152. OESOPHAGUS
• 3rd constriction of the oesophagus is at the level of Where it pierces the diapharm.
• Barrett's oesophagus is Lower esophagus lined by columnar ephithelium.
• Ilnd constriction in oesophagus is seen at the Crossing of Aorta
• Oesophagus crosses the diaphragm at the level of T10.
• Arterial supply of cervical part is by inferior thyroid artery, thoracic part by azygous vein,
& abdominal part by left gastric artery & left inferior phrenic artery.
153. TRACHEA

• Level of trachea bifurcation in pediatic patient is T3.
• Cartilage in trachea Hyaline.
• Angle of tracheal bifurcation is increased in enlargement of Left atrium.
• Bifurcation of trachea is at Opposite the disc between the T4-T5 vertebrae.
• Bifurcation of trachea is at the level of lower border of T4.
• The Sensory supply of trachea is by vagus .
154. THORACIC DUCT
• Thoracic duct is also called as Pacquet duct .

• Length of thoracic duct is 45 cm (18 inches).
• Thoracic duct does not drains Right upper part of body.
• Thoracic duct receives lymph from both halves of the body below the diaphragm & the left half
above the diaphragm.
• Thoracic duct enters from abdomen to thorax at T12
• Thoracic duct opens into Left brachiocephalic vein.
• Thoracic duct is formed by Continuation of upper end of cisterna chyli.
• The thoracic duct crosses from the right to the left at the level of T5 vertebrae.
• Thoracic duct terminates into the left brachiocephalic vein at the junction of Internal jugular vein
and subclavian vein
155. AORTA
• Aorta with thoracic duct & azygous vein crosses through aortic hiatus of diaphragm.
• Brachiocephalic trunk, Left common carotid artery & Left subclavian artery are the direct branches
of arch of aorta.
• Tracheal bifurcation lies at the level of arch of aorta.
• Left common carotid artery arising from brachiocephalic trunk is the commonest variation in the
arteries arising from the arch of aorta.
• Celiac trunk, Superior mesenteric & Inferior mesenteric are the branches of anterior part
of abdominal aorta.
• Inferior phrenic, Middle Suprarenal, Renal are lateral branches of abdominal aorta.
• External iliac Artery make anastomosis with superior epigastric artery.
• Muscular component of dorsal aorta develops from Lateral plate mesoderm.
• Arch of aorta crosses the esophagus at 25 cm from the incisor teeth.
• Sequestrated Lung lobes are supplied by descending aorta.
• Arch of aorta develops from Left fourth aortic arch artery.
• Aortic arch ends at level of left 2nd costal cartilage.
• Arch of aorta begins and ends at which level T4.
• Aortic arch Lies behind manubrium sterni.
• Coarctation of the aorta is common in Turner's syndrome.
156. SUPERIOR VENA- CAVA
• Superior vena cava opens into right atrium at the level of T5.
• Left sided superior vena cava drains into coronary sinus.
• Azygous vein drains into Superior vena Cava.
• Superior vena cava enters the heart at the level of 3rd costal cartilage.
• Pierces paricardium at 2nd costal cartilage.
• Superior vena cava receive azygous vein behind sternal angle.
157. SUPRARENAL GLAND
SUPRARENAL (ADRENAL) GLAND
• Suprarenal (adrenal) glands are a pair of endocrine glands.

• Situated retroperitoneally in posterior abdominal wall on each side of vertebral column on upper
pole of coressponding kidney.
• Each gland measures 50 mm in height, 30 mm in breadth & 10 mm in thickness.
• Weight- 5 gm.
• Each suprarenal gland is divided into outer cortex & inner medulla.
RIGHT SUPRARENAL GLAND LEFT SUPRARENAL GLAND
Shape • Pyramidal • Semilunar
Parts & relations • Apex: Bare area of liver • Upper end: Close to spleen
• Base: Upper pole of right • Lower end: Presents hilum,
kidney left vein emerges from here
Anterior surface • Inferior vena cava • Cardiac end of

• Bare area of liver stomach, pancreas with
splenic artery
ARTERIAL SUPPLY: through suprarenal vein
1. Superior suprarenal artery (branch of inferior phrenic artery)

2. Middle suprarenal artery (branch of abdominal aorta)
3. Inferior suprarenal artery (branch of renal artery)

VENOUS DRAINAGE:
1. Right suprarenal (adrenal) vein drains into IVC

2. Left suprarenal vein drains into the left renal vein & then into IVC.
LYMPHATIC DRAINAGE:
• From suprarenal glands drain into lateral aortic (para-aortic) nodes.
158. URETER
SITES OF ANATOMICAL NARROWINGS/ CONSTRICTIONS
• The lumen of the ureter isn’t consistent throughout and presents 3 constrictions at these sites:
1. At the pelviureteric junction where the renal pelvis joins the upper end of ureter.
It’s the upper most constriction, seen roughly 5 cm far from the hilum of kidney.
2. At the pelvic brim where it crosses the common iliac artery.
3. At the uretero-vesical junction (i.e., where ureter enters into the bladder).
Relations of pelvic part of ureter are:
POSTERIOR RELATIONS LATERAL RELATIONS

• Internal iliac artery • Obturator fascia
• Internal iliac vein • Obturator vessels & nerve
• Lumbosacral trunk • Inferior vesical vein
• SI Joint • Middle rectal artery
Important relations of abdominal part:
RELATIONS RIGHT URETER LEFT URETER
ANTERIOR • Duodenum (3rd part) • Peritoneum

• Right colic artery • Gonadal artery
• Iliocolic vessels • Sigmoid miscolon
• Gonadal vessels
• Ileum (terminal part)

MEDIALLY • IVC • Inferior mesenteric vein
• Left gonadal vein
POSTERIOR : Ureter lies on psoas major, transverse process (tips), & Genitofemoral nerve
BLOOD SUPPLY:
UPPER PART • Supplied by renal artery.

• Also receives branches from gonadal or colic vessels.
MIDDLE PART • Receives branches from the Aorta.

• Also receives branches from gonadal or iliac vessels.
LOWER (PELVIC) PART • Supplied by branches from the vesical, middle rectal or uterine
vessels.
159. FUNCTIONAL AREAS OF CEREBRAL CORTEX
• Locus coeruleus is the most important source of noradrenergic innervation to the cerebral cortex.
• Broca's area is formed of two minor gyri, called pars opercularis and pars triangularis, that lie in the
posterior end of the inferior frontal gyrus. This area subserves expressive language function.
• Area 8 (the frontal eye field) is concerned with eye movements.
• Spongiform degeneration of cerebral cortex occurs in Creutzfeldt-Jakob disease
• Trunk has small representation in somatosensory area of cerebral cortex
160. CERVICAL VERTEBRAE
• Cervical vertebrae can be differentiated from thoracic vertebrae on the basis of Presence of
foramen transversarium.
• First cervical vertebra (atlas) is ring like bone having lateral mass.
• Second cervical vertebra (axis) is characterized by presence of odontoid process or dens.
• Seventh cervical vertebra is called as vertebra prominens because it has most prominent spinous
process.
• The hyoid bone is found at the level of third cervical vertebrae in adults.
• Primary vertebral curve is Thoracic.
• The anterior tubercle on transverse process of C6 vertebra is prominent & is called carotid tubercle
or chaissagnac’s tubercle.
• Chassaignac’s tubercle loes at the level of Erb's point.
161. IMPORTANT JOINTS OF VERTEBRAL COLUMN
• primary curvatures (concave forwards) → thoracic & sacral

• secondary curvatures (concavity backwards) → Cervical & lumbar.
• Craniovertebral joint os formed by: Occipital condyles, Atlas (C1), Axis (C2) vertebra.
• Movements permitted at atlanto-occipital joint are:
i) Flexion & extension (nodding of head)

ii) Lateral flexion (bending of neck)
• Movements permitted at atlanto-axial joints are side to side rotation of head (looking towards right
or left).
• Maximum flexion in thoracic vertebrae accurs at Lower Thoracic.
• Membrane tectoria is a continuation of posterior longitudinal ligament.
• Anterior atlanto-occipital ligament is considered as continuation of anterior longitudinal ligament
• Membrane tectoria is continuation of posterior longitudinal ligament.
• Transverse ligament forms the horizontal part of cruciform or cruciate ligament
162. SPLEEN
• Spleen is derived from Dorsal mesogastrium.

• Spleen projects into greater sac.
• The normal spleen weighs about 150 gm.
• B-cells are dispersed in which part of spleen White pulp.
• Billorth's cord are present in which part of spleen Red pulp.
• Most common location of accessory spleen is Hilum of spleen.
• The spleen contains about 2 % of the total blood volume.
• "Lardaceous spleen" is due to deposition of amyloid in Sinusoids of red pulp.
163. PANCREAS
• Posterior relation of neck of pancreas is Origin of portal vein.

• Annular pancreas is a congenital anamoly resulting from failure of normal clockwise rotation of the
ventral pancreas. The histology of pancreatic tissue is normal.

• Treatment of choice for annular pancreas is Duodenojejunostomy.
• Most common site for carcinoma of pancreas is Head.
• The posterior relations of the head of the pancreas include the common bile duct, inferior vena
cava and the right and left renal veins terminating into it.
• The first part of the duodenum is an anterior relation of the head of the pancreas.
• Tail of pancreas contains maximum number of Islet of Langerhans.
• Glucagonomas are usually large tumors at diagnosis. 50–80% occur in the pancreatic tail
164. POSTERIOR TRIANGLE OF NECK
• The omohyoid muscle is an important landmark in both the anterior and posterior triangles of the
neck.
• Base of the posterior triangle of neck is formed by superior surface of middle third of clavicle.
• Superficial incision on posterior triangle of neck leads to difficulty in shrugging of shoulder.
• Contents of Suboccipital triangle are:
1. 3rd part of vertebral artery

2. suboccipital nerve (dorsal ramus of C1)
3. Suboccipital venous plexus.
165. TONSILS (Palatine/ Faucial Tonsils)
• Tonsils are derived from 2nd branchial pouch.

• Tonsils reach their maximum size by 5 years.
• Main source of arterial supply to tonsil is tonsilar branch of facial artery.
• Glossopharyngeal and lesser palatine nerves supply palatine tonsil.
• Referred pain from tonsil to middle ear is due to Glossopharyngeal nerve.
166. WHITE MATTER OF CEREBRUM
• Largest commissural fibers are seen in Corpus callosum.

• Corpus callosum connect same areas of two cerebral hemispheres.
• Rostral end of the corpus callosum called Genu.
• Rostrum connect orbital surface of both hemispheres.
167. EXOCRINE GLANDS
• Halocrine secretion is seen in Sebaceous gland.

• Mammary gland is a modified sweat of apocrine variety.
• Sweat glands are lined by the simple coiled tubular epithelium.
168. DEVELOPMENT OF HEART
• Tubular heart is formed at the end of 3rd week.

• Septum secundum arises from Primitive atrium.
• The cardiac jelly formed around the heart tube during early development, contributes to the
formation of Endocardial cushion valves.
• Septum secundum grows caudally from the roof of atrium.
• Fossa ovalis and anulus ovalis lie on the atrial septum, which separates the right atrium from the
left atrium.
• Heart is completely developed at 10th week of intrauterine life.
Physiology
1. RENIN- ANGIOTENSIN SYSTEM
RENIN-ANGIOTENSIN SYSTEM
• Renin secreted by Juxta-Glomerular (JG) cells of afferent arterioles.

• Most powerful stimulus for renin release is reduced renal perfusion pressure.
• Increased NaCl in distal tubules decreases renin release.
• Renin releases in response to sympathetic discharge from JG cells.
• Renin acts on angiotensinogen secreted by liver, converting to angiotensin I.
• By splitting Leucine-Valin bond of angiotensinogen.
• Angiotensin I converted into Angiotensin II by ACE.
• ACE is found on surface of capillary endothelium of lung.
• Hence, angiotensin II is formed on lung capillary endothelium.
• Angiotensin I has no established function & is solely "Angiotensin II precursor".
• Most prominent action of angiotensin II is Vasoconstriction.
• Angiotensin II cause,
• Na2+ & water retention in kidney by increasing aldosterone & ADH secretion.
• Reduces both GFR & RBF, by constricting both afferent & efferent arterioles.
• Angiotensin II acts centrally by increasing thirst.
• Angiotensin III (hexapeptide) is breakdown product of angiotensin II has about 40% of angiotensin
II pressor activity & complete aldosterone stimulating activity.

2. ANION GAP
• High Anion Gap Acidosis is seen in Renal Tubular Acidosis, Diabetic Ketoacidosis, Lactic Acidosis, &
Methanol Poisoning
• Starvation, Ethylene glycol poisoning are causes of increased anion gap
• The anion gap is calculated as AG = Na+ – (Cl- + HCO3-)
• Urinary anion gap is an indication of excretion of NH4+
• Cholera & Diarrhoea is associated with normal anion gap metabolic acidosis
• Renal Tubular Acidosis is diagnosed using a positive urinary anion gap
• Anion gap is mostly due to protein
• Normal anion gap is 10-12 mEq/L
3. ATRIAL NATRIURETIC PEPTIDE
ATRIAL NATRIURETIC PEPTIDE
• ANP causing natriuresis (Increased Na+ excretion), by increasing GFR & reducing Na+ reabsorption
from distal tubule & collecting ducts.
• Cyclic GMP act on Atrial natriuretic peptide.
• Effects of ANP are physiologically antagonistic to angiotensin II, mainly acts on kidney & blood
vessels.
• Reduces secretion of renin, aldosterone & ADH, inhibit ADH-stimulated water reabsorption
across collecting ducts.
• ANP is "Powerful vasodilator" relaxes vascular smooth muscle in arterioles & venules, lowering BP.
4. SPERMATOGENESIS
SPERMATOGENESIS
• Process of spermatozoa formation (sperm) from primitive germ cells (spermatogonia).

• Result of stimulation by gonadotropins - testosteroneFormation of mature sperm from primitive
germ cells require average of 74 days
o Secreted from Leydig cells under influence of LH
STEPS:
• Initial phase:
o Spermatogonia 1° spermatocytes 2° spermatocytes
• Maturation phase:
o Spermatids spermatozoa (sperms)
• Release of sperms - Spermiation
Hormonal influence:
• Testosterone diffuses into tubules.

• Binds to Androgen Binding Protein (ABP)
• Secreted from Sertoli cells under FSH influence.
• Except for "Maturation phase" all other phases are testosterone independent
Step 1:
• Seminiferous tubules in testis - Starting point of process.

• Spermatogonia (primitive germ cells) divide & migrate centrally in seminiferous tubules
Step 2 - Maturation - Spermiogenesis:
• Maturation of spermatids to spermatozoa depends on testosterone

• Occurs in epididymis
• Exact location - Deep cytoplasmic folds of Sertoli cells
• Spermatids undergo morphological changes to form Sperm
• Motility develops at this stage.
• Sertoli cells provide nourishment to mature spermatozoa
Step 3 - Spermiation
• Process of release of mature spermatids from Sertoli cells after maturation.

• Human sperm remains fertile for 24-72 hrs in female genital tract after ejaculation.
TEMPERATURE & SPERMATOGENESIS:
• Spermatogenesis requires temperature considerably lower than core body temperature.

• Location [Testes/Scrotum] is specifically important to produce viable sperm
• Specifically 1°-8 °C lower than normal body temperature of 37 °C (98.6 °F).
HORMONES INVOLVED:
• FSH, LH, testosterone, estrogen, growth hormones, inhibin & activin.
Individual action:
1. FSH -
• Responsible for initiation of spermatogenesis.

o Binds with sertoli cells & spermatogonia
o Induces proliferation of spermatogonia.
• Stimulates sertoli cells
o Secretes androgen-binding protein.
2. LH -
• Stimulates Leydig cells to secrete testosterone.
3. Testosterone -
• Principle hormone - Directly stimulates and maintains spermatogenesis.

• Responsible for sequencing remaining stages of spermatogenesis (after initiation by FSH).
4. Estrogen -
• Formed from testosterone (by aromatase) in Sertoli cells.

• Essential for spermiogenesis.
5. Growth hormone -
• Promotes early division of spermatogonia.
6. Inhibin -
• 7. Activin - Important role in regulation of spermatogenesis
• Stimulates FSH secretion & stimulates spermatogenesis.
Metrics:
• Healthy human adult forms up to 120 million sperm each day from both of testis together.
• Formation of mature sperm from primitive germ cells require average of 74 days
5. PARATHROMONE
PARATHORMONE/PARATHYROID HORMONE/PTH
• Synthesized by principal/ chief cells of parathyroid gland.

• Increases bone remodelling.

REGULATION OF SECRETION:
• Mainly depend on Plasma Ca+2 concentration.
PTH secretion increased:
• Decreased serum Ca+2 concentration.

• Hyperphosphatemia.
PTH secretion decreased:
• Increased serum Ca+2 concentration.
RECEPTORS
• Type 1:
• PTH 1R (h-PTH/ Parathyroid Hormone-related Protein PTH-rP)
• Bone (osteoblast) & kidney
• 2nd messenger - cAMP (main), IP3 & calcium.
• Osteoclasts do not have any PTH receptors.
RELATIONSHIP BETWEEN CALCIUM & PTH:
PTH raises plasma Ca+2 in three ways.
• Mobilizes bone Ca+2

• By increasing bone resorption
• Increases gastrointestinal absorption of Ca+2 indirectly.
• By increasing renal synthesis of 1,25 dihydroxy D3 calcitriol.
• Increases Ca+2 reabsorption in distal tubules of kidney.
RELATIONSHIP BETWEEN PHOSPHATE & PTH:
• Decreases phosphate reabsorption from proximal tubules of kidney.
ACTIONS:
1. ON BONE:
• PTH increases bone resorption.

• PTH receptors are located on osteoblasts & not on osteoclasts.
Step 1: Initial & fast action:
• Increases bone formation by direct action on osteoblasts.

Step 2: Long-lasting action:
o Indirect action on osteoclasts

o Increases bone resorption
o Thus, osteoblasts required for bone-resorbing action of PTH on osteoclasts.
ON KIDNEY:
• Major regulating factor for calcium reabsorption.

• On Proximal convoluted tubule:
• "Phosphaturic effect" - Inhibits renal phosphate reabsorption
• On Distal convoluted tubule:
o Increases renal Ca2+ reabsorption
On intestine:
• Indirect increases Ca2+ absorption.
6. CHOLECYSTOKININ (CCK)
CHOLECYSTOKININ (CCK)/Cholecystokinin-Pancreozymin (CCK-PZ)
o Secreted by I cells in small intestine (Duodenum, jejunum & ileum).
Stimulus for secretion:
• Products of protein digestion i.e., amino acids & peptides.

• Presence of long chain fatty acids (>10 carbon atoms) in duodenum.
• Acts through group IIC hormonal mechanism
FUNCTIONS:
• Stimulates pancreatic acinar cell enzymes secretion.

• Causes contraction of gall bladder.
• Relaxation of sphincter of oddi.
• Secretion of enzyme-rich pancreatic juice.
• Potentiates action of secretin on pancreas.
• Inhibits gastric emptying.
• Increases motility of small intestine & colon.
• Increases enterokinase secretion.
• Produces satiety.
• Augments contraction of pyloric sphincter.
• Prevents reflux of duodenal contents into stomach.
7. BASAL GANGLIA
BASAL GANGLIA
• Scattered masses of gray matter

• Submerged in sub-cortical substance of cerebral hemisphere
• Part of extrapyramidal system, associated with motor activities.
COMPONENTS OF BASAL GANGLIA

1. Corpus striatum -
• Receives afferent inputs coming to basal ganglia.
Divided into 2 by internal capsule.
• Caudate nucleus
• Lenticular nucleus -
o Divided into 2 by,
o External medullary lamina - Vertical plate of white matter
• Sub-divisions:
o Putamen
o Globus pallidus - Principle output nuclei & efferents arise here.
2. Subthalamic nucleus
3. Substania Nigra -
• Principle output nuclei & efferents arise here
CONNECTIONS OF BASAL GANGLIA
1. Afferent connections:
• Stiratum(caudate & putamen)

• Receives afferents form cerebral cortex - Sensory, motor, association & limbic cortex
2. Efferent connections:
• Globus pallidus & Substania Nigra - Major efferents arise

• Pathway - Efferent (GABAergic)thalamusprefrontal cortexpremotor
cortexsupplementary motor areaPrimar motor cortex
• Discharges motor activities from 1º motor cortex region
• No direct connections between brainstem/spinal cord & basal ganglia.
3. Internuclear connections:
• Connection 1:
o Dopaminergic nigrostriatal projection from "Substantia Nigra Pars Compacta"
(SNPC) striatum (caudate nucleus & putamen)
o Corresponding GABAergic projection from stratium Substantia Nigra Pars Reticulata
(SNPR).
o Dopamine - Major neurotransmitter in Substantia nigra
• Connection 2:
o Inhibitory GABAergic projections from Striatum to both Globus Pallidus Inner Segment
(IS) & External Segment (ES).
• Connection 3:
o GABAergic projections from Globus pallidus ES Subthalamic nucleus & to Globus pallidus
lS
• Connection 4:
o Excitatory Glutamate-ergic projections from Subthalamic nucleus Globus pallidus IS & ES
NEUROTRANSMITTERS IN BASAL GANGLIA:
1. Dopaine -
• Neuromodulatory neurotransmitter
• Used by SNPC selectively modulate areas of stratium(caudate/putamen)
2. Glutamate
• Excitatory neurotransmitter
• From Subthalamic nucleus Stimulate ventrolateral thalamus1° localized motor cortex.
3. GABA -
• Inhibitory neurotransmitter
• Caudate/striatum
o Direct Inhibit GPIS
o Indirect Inhibit GPES
FUNCTIONS OF BASAL GANGLIA
1. In planning & programming of movement
2. In process of conversion of an abstract thought into voluntary action.
3. Putamen circuit - Complex motor activity & skilled movement.

4. For motor activity, final common pathway - Corticospinal tract
5. Part of extra-pyramidal system - Regulation of tone & posture.
6. Caudate nucleus - Major role in cognitive control of motor activity
DISORDERS OF BASAL GANGLIA:
• Nigrostriatal dopaminergic system, Intrastriatal cholinergic system & GABAergic system

o Characteristics motor abnormalities occur with dysfunction of these pathways.
1. Hyperkinetic:
• Chorea, athetosis & ballism.
2. Hypokinetic:
• Akinesia & Bradykinesia.
3. Parkinsonism:
• Degeneration of dopaminergic neurons in SNPC.

• Fibers to Putamen are severely affected.
• Both hypokinetic & hyperkinetic feature.
• Presence of Lewy bodies in substantia nigra, locus coeruleus, nucleus basalis, raphe & ventral
tegmental area.
4. Huntington chorea
• Stratium -Mainly caudate & areas of putamen.

• Selective loss of GABAergic & cholinergic neurons
5. Wilson's disease -
• Hepato-lenticular degeneration.
• Affects lenticular nuclei (pallidus & putamen)
• Features: Rigidity, dystonia, chorea, athetosis, dysarthria, & tremor
6. Ballism -
• Subthalamic nucleus
7. Athetosis -
• Globus Pallidus (mainly)

8. PHYSIOLOGY OF EXERCISE
• Body temperature increases during exercise.

• In isometric exercise following parameters are increased:
• Heart rate.
• Cardiac output.
• Mean arterial pressure.
• Patients with Ventricular Arrhythmia or Myocardial infarction should avoid Isometric exercises.
• Accentuated S3, S4 due to isometric exercise.
• Effects on murmur due to Isometric exercise:
• Diastolic murmur of Mitral stenosis becomes louder
• Diastolic murmur of aortic regurgitation, systolic murmur of mitral regurgitation and ventricular
septal defect increases.
• Systolic murmur of aortic stenosis & of hypertrophic obstructive cardiomyopathy diminishes.
• Cerebral blood flow does not change due to the effect of moderate exercise.
• During heavy exercise,
• Cardiac output (CO) increases up to fivefold.
• Pulmonary arterial pressure rises very little.
• This physiological ability of the pulmonary circulation is best explained by the increase in the
number of open capillaries.
• Venoconstriction with decreased blood flow is responsible for a decrease in splanchnic blood flow
during exercise.
• Amount of blood flow to skeletal muscles during exercise:
• 50 to 75 mL/min of blood per 100 g of muscle.
• During exercise increase in O2 delivery to muscles due to,
• Increased stroke volume.
• Increased extraction of oxygen from blood.
• Increased blood flow to muscles
• During exercise, there is increased coronary circulation.
• A right shift of Hb - O2 dissociation curve is seen in exercising muscle.
• Increase blood supply to muscle, increase stroke volume & increased O2 extraction is seen due to
exercise.
• Hyperventilation in beginning & Hyperkalemia in later stages is seen during severe exercise.
• Type of exercise done to increase the muscle strength is Isotonic.
• Isocapnic exercise is Breathing of increased volume of ventilation for long period.
• Factors responsible for blood supply increase in muscle during exercise:
o Local metabolite.
o Sympathetic stimulation.
o Cholinergic stimulation
9. OXYGEN DISSOCIATION CURVE

OXYGEN-HEMOGLOBIN DISSOCIATION CURVE
• Sigmoid shaped-
o "Due to phenomenon "Cooperative binding of Oxygen to hemoglobin".
• Hemoglobin is a tetramer
o Four O2 molecules binds 1 Hb molecule.
st
o 1 O2 molecule bonds with greatest difficulty.
o Increasing affinity to next O2 molecule
o Saturation increases steeply between PO2 15mm Hg & 40 mm Hg.
o Beyond PO2 60mm Hg, curve becomes almost flat.
• PO50 is PO2, at which 50% hemoglobin saturated.

o PO50 of normal adult hemoglobin - 26mm Hg (3.47 kpa).
I) CURVE SHIFTING TO RIGHT:
• PO50 higher
o Indicating decreased hemoglobin affinity for oxygen.
Conditions associated:
• Low pH/Increased H+ ion concentration/acidosis.

• Hypoxia/Reduced PO2.
• High PCO2.
• Increased body temperature.
• Increased 2,3 - BPG/DPG.
• Exercise.
• Within systemic capillaries.
II) CURVE SHIFTING TO LEFT:
• PO50 lower.
• Indicating increase in affinity of hemoglobin for oxygen.
• High pH/Decreased H+ ion concentration/alkalosis.

• Reduced PCO2.
• Reduced body temperature.
• Reduced 2,3 BPG/DPG.
• Fetal hemoglobin.
• CO poisoning.
BOHR EFFECT:

• Increase in partial pressure of carbon dioxide/Hypercarbia
o Curve shifts to right.
o Main effect of raised PCO2 mediated by increased hydrogen ion concentration.
+
o Deoxyhemoglobin binds H more actively.
• DPG is an optional by-product of the glycolytic pathway, present in RBC.
o Increased DPG concentration shifts curve to right.
o One molecule of DPG binds with one mole of deoxyhemoglobin.
o Binds with deoxygenated hemoglobin but not with oxygenated hemoglobin.
• Raised DPG concentration releases oxygen from oxyhemoglobin.
• Resulting in O2 delivery/unloading to tissues.
• Factors increasing DPG & effect on O2 - Hb curve:
o Hypoxia.
o High altitude.
o Exercise.
o Anemia.
o Chemical agents (inosine).
• Factors decreasing DPG & effect on O2 - Hb curve:
o Acidosis.
o Stored blood.
o Fetal hemoglobin (HbF).
• HbF has low affinity of DPG.

• In human blood, affinity of fetal Hb for 2'3-DPG is only about 40% that of adult hemoglobin.
• Fetal hemoglobin behaves if 2,3-DPG levels are low.
• Poor binding of DPG to fetal Hb.
o Important factor in facilitating transplacental transport of oxygen between mother & fetus.
• Exercise shifts curve to right in muscles & other tissues.
• Dissociation curve for myoglobin is "Hyperbola" in shape.
• Myoglobin binds with only one molecule of oxygen.
o Due to no phenomenon of cooperative binding.
• Myoglobin has much higher affinity for O2 than hemoglobin.
10. SPIROMETRY
• Spirometry measures Tidal volume, IRV, Vital capacity & FEV.

• Residual volume cannot be measured directly with a spirometer.
• ERV is measured by the device, Bellow's spirometer.
11. CEREBELLUM - DIVISIONS & FUNCTIONS
CEREBELLUM
Embryologically cerebellum is derived from Metancephalon
DIVISIONS:
Cerebellum is divided by,
1. Transverse fissures into three lobes:
• Anterior lobe
• Posterior lobe
• Flocculonodular (lateral flocculus & medial nodulus)
2. Two longitudinal fissures into 3 parts:
• Midline vermis
• Left cerebellar hemisphere
• Right cerebellar hemisphere
• Two hemispheres are joined by vermis.
ATTACHMENTS:
• Medulla -
o By three cerebellar peduncles
PARTS OF CEREBELLUM:
• External cerebellar cortex

• Deep cerebellar nuclei
1. Deep cerebellar nuclei:
• Four nuclei - From lateral to medial

o Dentate
o Emboliform
o Globose
o Fastigial
• Globose & Emboliform are sometimes lumped together
• Referred as "Interpositus nucleus"
2. External Cerebellar cortex:
• Five types of neurons

o Purkinje cells
o Granule cells
o Basket cells

o Stellate cells
o Golgi cells
3. Layers of cerebellar cortex:
• External molecular layer - Basket cells & stellate cells.

• Middle Purkinje cell layer - Purkinje cells
• Inner granular layer - Granular cells & Golgi cells
4. Input & output units:
Input afferent from:
• Climbing fibers -
o From inferior olivary nuclei only.
• Mossy fibers -
o From all other parts of body
Output efferent to:
• Axons of Purkinje cells are the only output from cerebellar cortex.
• Deep Nucleus - Ultimate & final efferent output of cerebellum.
FUNCTIONAL DIVISION OF CEREBELLUM:
• 3 parts,
o Vestibulocerebellum/ Flocculonodular lobe
o Spinocerebellum
o Cerebrocerebellum/ Neocerebellum
1. Vestibulocerebellum/Flocculonodular lobe:
Parts:
• Flocculus & Nodulus
Connections:
• Receives afferents -
o From vestibular apparatus
• Sends efferents -
o To Vestibular nuclei
• Direct connection to vestibular nuclei without involvement of deep nuclei
Functions:
Works with vestibular apparatus to,
• Modulate muscular activity to achieve postural equilibrium/balance.

• Vestibulo-ocular reflex - Coordinate movements of eyes with movements of head
2. Spinocerebellum:
Functions:
• Compares plans.
• Smoothens & coordinates ongoing movements
3. Cerebrocerebellum/ Neocerebellum:
• Large lateral portion of cerebellar hemisphere

• Newest from a phylogenetic point of view
• Hence, "Neocerebellum".
Functions:
• Interact with motor cortex in planning & programming movements
4. Corresponding neuronal circuits:
• Vestibulocerebellar output passes directly to brainstem.

o From cerebellar cortex to brainstem without involvement of deep cerebellar nuclei.
FUNCTIONS OF CEREBELLUM:
• Co-ordination of movements
• Regulation of tone, posture & equilibrium
• Smoothening & coordination of voluntary movements
• Coordination of eye movements
• Planning & initiation of movements.
• Learning of frequently performed voluntary movements.
• Timing & comparison:
o Cerebellum - Timing device.
o Times duration of agonistic muscle activity & latency of antagonistic activity.
o Ensures halting movement at correct point.
12. LIMBIC SYSTEM
LIMBIC SYSTEM
• The neuronal circuit controlling emotional behavior & drives motivations.
COMPONENTS
Described from outer to inner
• Limbic cortex/Subcortical area

• Hippocampal formation/Subcortical structure
• Hypothalamus
1. Limbic cortex/Subcortical area:
• Cingulate gyrus Parahippocampal gyrus

• Subcallosal gyrus
• Orbitofrontal cortex
• Uncus
2. Hippocampal formation/Subcortical structure:
• Surrounds hypothalamus
Parts:
• Septum
• Hippocampus
• Amygdala
• Para-olfactory area
• Anterior nucleus of thalamus
• Portion of basal ganglia
3. Hypothalamus
• Central element surrounded by subcortical structures

• Major part of limbic system
NEURONAL CONNECTIONS
• Has two-way link between brainstem & neocortex
Pathways:
1. Papex circuit:
• Inter-connected closed circuit formed by union of limbic system nuclei.

Components:
• Hippocampus
• Mamillary body
• Anterior thalamic nuclei
• Cingulate gyrus
2. Medial forebrain bundle:
• Major efferent connection of limbic system

• One of reward system component
Reward center:
• Ventromedial hypothalamic nuclei + medial forebrain bundle
3. Other connections:
• Subiculum
o Provides reciprocal connections bt limbic system & neocortex
• Amygdala:
• Linking unit:
o Along with hippocampus, amygdala is extensively connected with Association cortex area &
Hypothalamus.
o Thus, provides link between limbic system & neocortex.
• Window of limbic system:
o Has two-way connections with hypothalamus

o Receives inputs from limbic system & higher cortical association areas.
o Hence, "Window of Limbic system"
FUNCTIONS OF LIMBIC SYSTEM:

1. Development of emotions:
• Fundamental role of limbic system: Generation of emotions
Neurophysiology of emotions:
• Emotions originate in limbic system

• Limbic system adds feelings to sensory experiences
Components in emotional state:

• Central component:
o Limbic cortex - Central component of emotions & evaluation site.
• Peripheral component:
o Hypothalamus - Co-ordinates peripheral & autonomic component of emotions.
• Co-ordinating component:
o Amygdala - Pivotal role in co-ordinating pperipheral & central component
2. Autonomic responses:
• Limbic & hypothalamic projection on reticular formation
3. Fear, rage, & placidity:
• Fear
o Produced by Amygdala
• Rage
o Produced by stimulation of lateral hypothalamus
• Placidity
o Caused by bilateral destruction of amygdala
4. Punishment & reward:
• Punishment center:
o Lateral portion of posterior hypothalamus &

o Dorsal region of midbrain
• Reward/pleasure center:
o Medial forebrain bundle &

o Ventromedial nuclei of hypothalamus
6. Memory & Learning:
• Memory function localized to Hippocampus & Temporal limbic cortex.
ASSOCIATED CONDITIONS:
KLUVER-BUCY SYNDROME:
• Neuro-behavioural syndrome.

• Associated with bilateral lesions in anterior temporal horn or amygdala
Causes:
• In humans occurs due to destruction of amygdaloid body & inferior temporal cortex
o Commonly due to Herpes Simplex Encephalitis (HES)
Features:
• Visual agnosia.
• Emotional changes
o Loss of normal fear & anger responses - "Placidity".
• Hypersexuality
o Less pronounced.
13. HYPOTHALAMUS - DIVISIONS & FUNCTIONS
HYPOTHALAMUS - DIVISIONS & FUNCTION
REGULATION OF NEURONAL FUNCTIONS

1. Regulation of body temperature:
• Controlled by Preoptic nucleus

• Anterior hypothalamus - Respond to heat
• Posterior Hypothalamus - Respond to cold (Shivering center)
2. Regulation of circadian rhythms:
• Suprachiasmatic nucleus
3. Regulation of hunger & food intake:
• Feeding center
o Lateral hypothalamic nucleus
• Satiety center
o Ventromedial nucleus
4. Regulation of thirst:
• Lateral nucleus
• Supra-optic nucleus
5. Regulation of BP:
• Pressor effect
o Posterior & lateral nuclei.
• Depressor effect
o Preoptic nucleus
6. Regulation of sexual function:

Anterior hypothalamus:
• In males:
o Medial preoptic nucleus
• In females:
o Lateral preoptic nucleus
7.Osmoreceptor:
• Anterior hypothalamus
8. Response to smell:
• Posterior hypothalamus
9. Other centers/neuronal regulations under control of hypothalamus:
• Sleep center
o Preoptic (Ventrolateral)
• Wakefulness center
o Reticular Activating System (RAS) in brainstem & hypothalamus
• Reward center
o Lateral & ventromedial nuclei of hypothalamus
• Punishment center
o Periventricular nuclei (mainly)
REGULATION OF ENDOCRINAL FUNCTIONS:

1. Control of anterior pituitary:
• Arcuate nucleus
o Releases activator hormone somatostatin
o For Growth hormone secretion.
• Preoptic nucleus
o Releases activator hormone Gonadotrophin Releasing Hormone (GnRH)
o For FSH & LH secretion
• Paraventricular nucleus
o Releases activator hormone Corticotropin-releasing hormone (CRH)

o For ACTH secretion.
o Releases Thyrotropin-releasing hormone (TRH)
For thyroxine secretion
• Dorsal & posterior nucleus

o Releases activator hormone for Catecholamines secretion
2. Control of posterior pituitary:
• Supraoptic nuclei - ADH (majority).

• Paraventricular nucleus - Oxytocin (majority).
14. PHYSIOLOGY OF PITUITARY GLAND
PITUITARY GLAND:
• Adenohypophysis / Anterior lobe of pituitary

• Neurohypophysis / Posterior lobe of pituitary
Anatomical considerations:
• Lies in bony walled cavity - Sella turcica of sphenoid bone at base of skull
• Closely associated with hypothalamus.
Embryological facts:
• From Rathke's pouch-

o Adenohypophysis
• As downward outgrowth of infundibular process from diencephalon-

o Neurohypophysis
HORMONAL SECRETIONS
1. Secretions from anterior lobe/adenohypophysis -
2 major cell types
1 a) Chromophobes / Chromophobic cell:
• No hormones secreted
1 b) Chromophils / Chromophilic cell:
• Acidophils-

o Forms 50 % - 80% of total cells
o Somatotropes - Secrete growth hormone
o Lactotropes - Secrete prolactin
• Basophils-
o Forms 20% - 30 % of total cells
o Gonadotropes - Follicle Stimulating Hormone (FSH) & Leutinizing hormone (LH)
o Thyrotropes -Thyroid stimulating hormone (TSH) Thyrotropin
o Corticotrophs- Adrenocorticotropin hormone (ACTH) Corticotropin
2. Secretions from intermediate lobe -
• Melanocyte Stimulating Hormone (MSH)
Note:
• ACTH & MSH are derived from larger molecule named "Proopiomelanocortin"
3. Secretions from posterior lobe/neurohypophysis -
• Oxytocin -
o From secretory granules of axons of paraventricular nuclei
• Antidiuretic hormone (ADH)/vasopressin
o From secretory granules of axons of hypothalamic supraoptic nucleus
CONTROL OF PITUITARY SECRETIONS:
• Almost all secretions (either hormonal/nervous signal) - By Hypothalamus
Control for anterior pituitary secretions:
• Mainly controlled by Hypothalamic releasing/inhibitory hormones from hypothalamus.

• Releasing hormone are important in stimulating majority of anterior pituitary secretions.
• Except, Prolactin - Mainly under inhibitory control.
Releasing hormone & its corresponding secretion:

1. Thyrotropin Releasing Hormone (TRH)-
• For release of Thyrotropin (Thyroid Stimulating Hormone (TSH)
2. Corticotropin-Releasing Hormone (CRH) -
• For release of Corticotropin (Adreno-corticotrophin Hormone (ACTH)
3. Growth Hormone Releasing Hormone (GHRH) -

• For release of Growth hormone (GH)
4. Gonadotropin Releasing Hormone (GnRH) -
• For release of Gonadotrophins (FSH & LH)
5. Prolactin Inhibitory Hormone (PIH) -
• For inhibition of release of Prolactin

• PIH is dopamine
• Among all anterior pituitary secretions, Prolactin is mainly under the control of inhibitory hormone.
• Hence, damaged pituitary stalk results in reduction of all anterior pituitary secretions except
Prolactin.
• Prolactin levels increases.
CONDITIONS ASSOCIATED WITH PITUITARY GLANDS:

1. Tumors:
Pituitary adenomas:
• Most common sellar tumors in adults.

• Most common pituitary adenomas are prolactinomas.
• Most common cause of hyperpituitarism.
Classification:
1. Based on symptoms & functionality:
• Functional (secreting) tumors -

o Associated with hormone excess & their clinical manifestations
o Hormones secreted abnormally are growth hormone & Prolactin - most common
combination.
• Nonfunctional (non-secreting) tumors -

o Symptoms caused by neurological effects
Important tumor to note:

Prolactinoma:
• Most common functional tumor of pituitary adenomas

• Causing amenorrhea & galactorrhoea in women.
Other conditions associated:
2. Pituitary apoplexy:

• Acute intra-pituitary hemorrhagic vascular event causing substantial damage to pituitary.
• Cause: Acute hemorrhage into an adenoma
3. Diabetes mellitus:
• Caused by deficiency of insulin

• Pancreatic hormone not under pituitary control.
• Transection of pituitary stalk in no way affect glucose levels or lead to diabetes mellitus.
15. DISTURBANCES IN ACID-BASE BALANCES
DISTURBANCES IN ACID-BASE BALANCES
• Metabolic acidosis is due to decreased plasma HCO3- which results in decreased pH and acidosis.
• Also associated with increased renal ammoniogenesis, which increases amount of ammonia
available in the tubule for buffering augmented H+ secretion.
16. ABSORPTION OF IRON
ABSORPTION OF IRON
• Iron absorbed from upper small intestine mainly duodenum.

• Iron is absorbed in ferrous form.
• Excretion of iron occurs predominately via feces.
• Transferrin - Transport glycoprotein for iron.
• Ferritin - Major storage form.
o Storage of iron inside ferritin is in ferric form.
o Mainly stored in reticuloendothelial cells monocytes/macrophages of liver, spleen &
bone marrow.
• Factors decreasing iron absorption -

o By complexing (forming chelate) with iron -
Phytate, Phosphate, EDTA, Tetracycline & Milk.
o By opposing reduction of ferric to ferrous forms -
Antacids, alkalies & pancreatic secretions.
• Factors increasing iron absorption -
o By enhancing reduction of ferric to ferrous form -
o Ascorbic acid, HCl, gastric secretions & citric acid.
• Conservation of iron by Haptoglobin & Hemopexin.
17. GLUCOSE TRANSPORTERS
GLUCOSE TRANSPORTERS
Transport of glucose -
• Into cells - By "Facilitated diffusion".

• In intestine & kidney - By "Secondary active transport" with Na2+.
1. SODIUM-DEPENDENT GLUCOSE TRANSPORTERS (SGLT):
• Present in small intestine & kidneys

• Acts via secondary active transport.
• Coupled with the Na2+-K+-ATPase pump.
o Hence, referred "Na2+- Glucose Co-transport" mechanism.
TRANSPORTER LOCATION
SGLT - 1 Small intestine & renal tubules
SGLT - 2 Renal tubules
2. SODIUM-INDEPENDENT GLUCOSE TRANSPORTERS (GLUT):
• Acts via facilitated diffusion of glucose across the cell membrane.
TRANSPORTER LOCATION FUNCTION

GLUT - 1 • Placenta. • Basal glucose uptake.
• Brain.
• RBC.
GLUT - 2 • B cells of islets. • B-cell glucose sensor.
GLUT - 3 • Neurons. • Basal glucose uptake.

• High affinity for glucose.
GLUT - 4 • In Heart (cardiac • lnsulin-dependent Glucose Uptake.

muscle). • Reduced in fasting state, when the insulin
• Skeletal Muscle levels are low.
• Adipose Tiissue
GLUT - 5 • Jejunum. • Fructose transport.

• Sperm. • Hence "Fructose transporter".

GLUT - 8 • Blastocyst. • Insulin-responsive glucose transporter of
Blastocyst.
Inhibitors of glucose transporters:
• Phlorizin & Phloretin.

• Phlorizin - Phloretin 2β Glucoside.
18. PANCREATIC SECRETIONS
PANCREATIC SECRETIONS
• Daily pancreatic secretion - About 1.5 - 2.0 L.

• Exocrine pancreas secretes pancreatic juice.
• Digestive pancreatic enzymes include -
o Trypsin (Trypsinogen).
o Elastase (proelastase).
o Carboxypeptidase A & B (Procarboxypeptidase A & B).
o Colipase (Procolipase).
o Pancreatic lipase.
o Ribonuclease.
o Phospholipase A2 (pro-phospholipase).
REGULATION:
1. SECRETIN:
• Acts on pancreatic 'ducts'.

• Causing secretion of large-amount highly alkaline pancreatic juice.
• Rich in bicarbonates & poor in enzymes.
2. CCK:
• Acts on "Acinar cell".

• Causing zymogen granules release & also pancreatic juice rich in enzymes.
PREVENTION OF PANCREATIC SELF-DESTRUCTION:
• Pancreas secretes enzymes as "Enzymatically inert/inactive pro-enzyme".

• Thus, preventing self-digestion & efficiently utilize enzymes inside the duodenal lumen.

19. PRESSURE CURVES IN CVS
PRESSURE CURVES IN CVS
• Aortic elastic recoil property & arteriolar resistance maintains relatively high aortic pressure during
diastole.
• An incisura/dicrotic notch in an aortic pressure curve, corresponds to aortic valve closure.
• Strength/amplitude/volume of pulse depends on,

o Stroke volume - Volume of blood ejected out with each beat.
o Extent of arterial wall elasticity/compliance.
o In turn are pulse pressure determinants.
PRESSURE-VOLUME LOOP:
• Loop shifting left - Aortic stenosis.

• Loop shifting right - Mitral regurgitation & aortic regurgitation.
JUGULAR VENOUS PRESSURE (JVP):
• a wave - Due to right atrial systole.

• v-wave - During tricuspid valve closure.
20. HEART SOUND
First heart sound (S1):
• Due to closure of AV valves (mitral and tricuspid)

• Soft S1:
o Mitral stenosis (long-standing, calcified), mitral regurgitation
• Loud S1:
o Mitral stenosis (prolonged flow through AV valve), anemia, fever, thyrotoxicosis
Second heart sound (S2):
• Due to closure of semilunar valves (aortic, pulmonary)

• Wide split of S2:
o Atrial septal defect, mitral regurgitation, pulmonary stenosis
• Reverse splitting of S2:
o LBBB, hypertension, aortic stenosis
Fourth heart sounds (S4):

• Occurs during pre-systolic phase.
• Produced during second rapid filling phase (before S1)
21. RENAL REGULATION OF ACID-BASE BALANCE
RENAL REGULATION OF ACID-BASE BALANCE
• In Proximal Tubule - 80%-90% HCO-3 reabsorption.

• H+ is secreted into the tubular fluid by Na2+ - H+ exchanger.
• H2 CO3 dissociates into CO2 & H2O by carbonic anhydrase.
• Carbonic anhydrase:
o Present in brush border of PCT, thick ascending limb, early DCT, & brain.
o Maximum - In Erythrocytes; Absent - In plasma.
• In late distal tubule & collecting ducts, H+ ions are secreted by primary active
transport in "Intercalated (I) cells".
o This mechanism is important in maximally acidic urine.
+
• H concentrating ability can be increased as much as 900-fold in the collecting tubules.
o Decreases tubular fluid pH to about 4.5, which is lower pH limit achieved in normal kidney.
• Bicarbonate buffer - Most important buffer in proximal tubule.

• Ammonia buffers - Most important buffer indistal tubule.
• Ammonia & phosphate buffers are excreted, in exchange for HCO-3 absorption.
22. DIGESTION AND ABSORPTION OF PROTEIN
DIGESTION AND ABSORPTION OF PROTEIN
• Begins in stomach.
Enzyme involved:
• Pepsin - Inactive (zymogen) form - Pepsinogen.

• Pancreatic enzymes - Trypsinogen, Chymotrypsinogen, Proelastase, Procarboxypeptidase A & B.
1. Pepsin activity:
• Pepsin is a proteolytic enzyme.

• Secreted by chief cells of stomach in an inactive (zymogen) form i.e., pepsinogen.
• Acid in stomach lumen converts pepsinogen to active pepsin.
• Pepsin breaks food protein into smaller units called peptides

2. Pancreatic enzymes:
• Pancreatic enzymes are secreted in an inactive form (Zymogen).
• Inactive forms include

o Trypsinogen
o Chymotrypsinogen
o Proelastase
o Pro-carboxypeptidase A & Procarboxypeptidase B.
Enzyme activation:
• Trypsinogen is initially activated by enterokinase (enteropeptidase)

• Enterokinase an enzyme present in brush border of small intestinal epithelial cells.
• Conversion of inactive trypsinogen into active trypsin requires removal of an N-terminal
peptide by enteropeptidase (enterokinase)
Chemical characteristics of enzymes:
• Trypsin, chymotrypsin, & elastase - Endopeptidases

• Carboxypeptidases (A & B) - Exopeptidases
Final step for protein digestion:
• Significantly assisted by surface enzymes of small intestine.

• Major proteolytic brush border enzymes are dipeptidase & aminopeptidase
ABSORPTION OF AMINO ACIDS:
• Sodium-dependent co-transport.
Note on enzymes involved:
1. Peptidases (Proteases)
1a). Endopeptidases (Endoproteinases)
• Pepsin, Trypsin, Chymotrypsin & Elastase.
1b). Exopeptidases(Exoproteinases)
• Aminopeptidases & Carboxypeptidases(A & B).

23. DIGESTION AND ABSORPTION OF FATS
DIGESTION AND ABSORPTION OF FATS
• Digestion begins in Duodenum
Enzymes involved:
1. Pancreatic juice
• Pancreatic lipase - Most important for fat digestion

• Digests triglycerides (Triacylglycerols) into free fatty acids & 2-monoglycerides (2-
monoacylglycerols).
• Pancreatic lipase hydrolyzes 1- & 3-bonds of triglycerides.
2. Bile salts
1. Properties of bile salts:
• Detergent action of bile salts (Lowering surface tension).

• Due to amphipathic property of bile salts.
• Due to presence of polar & non-polar ends
1a) Dual functionality of amphipathic property of bile salts:
• Helps in digestion & absorption of fats and micelle formation

• Conversely, bile salts inactivate lipase.
1b) Functions of bile salts in fat digestion:
• Bile salts help in digestion by emulsification of fat in small intestine.

• Detergent action of bile salts is necessary for both emulsification & micelles formation.
Absorption of digested fat:
• After fat digestion, fatty acids & monoglycerides are absorbed in small intestine (especially
jejunum)
Short-chain fatty acids (SCFAs):
• Produced by bacterial action in colon.

• Reabsorbed back in colon
Emulsification and micellar formation:

1. Emulsification of fat:
• Emulsification increases surface to volume ratio of the lipid droplets facilitating lipases action.
• Hence, emulsification facilitates action of lipases & mainly helps in digestion of ingested fats.
• Bile salts help in fat emulsification in small intestine
o Due to detergent action of bile salts.
2. Micellar formation:
• Micellar formation solubilizes digested fats & facilitates absorption into enterocytes.
o I.e., Helps in absorption of digested fats
• Bile salts have the property of forming micelles.
• Each micelle contains detergents (Bile salts) & absorbable fats.
24. DIGESTION AND ABSORPTION OF CARBOHYDRATE
DIGESTION AND ABSORPTION OF CARBOHYDRATE
• Starch - Polysaccharide composed of glucose units linked by 1, 4 - alpha linkage & 1, 6 branching
point.
• Enzymes involved:
o Salivary amylase (Ptyalin).
o Pancreatic amylase.
-
o Both activated by Cl
• Optimal pH is 6-7. (vs acidic in stomach).
Mechanism of starch hydrolysis:
• Amylase attacks only internal, 1-4 α glucose-glucose bonds.

• Spares 1-6 linkages & terminal 1-4 α linkages.
• End products:
o Maltose
o Maltotriose
o Alpha limit dextrins
Digestion in Intestine:
• Digestion of starch derivatives (disaccharides),

• Enzymes (oligosaccharides) present in brush border of small intestinal epithelial cells.
Enzymes involved:
1. Maltase (c-glucosidase):
• Breaks 1:4 linkages in maltose & maltotriose
2. Isomaltase (α -limit dextrinase)
• Only enzyme that attacks 1:6 α linkages

• Sucrose-isomaltase:
o Sucrase α -limit dextrinase.
o Bifunctional enzyme that catalyzes hydrolysis of sucrose & isomaltose (α -limit dextrin).
3. Sucrase:
• Present in brush border of intestinal epithelium

• Hydrolyses Sucrose into Fructose & Glucose
4. Lactase (β-glucosidase):
• Hydrolyses Lactose into Galactose
ABSORPTION OF DIGESTED CARBOHYDRATES:
1. End products of carbohydrate digestion -
• Glucose, Galactose & Fructose needs absorption.
2. Absorption mainly in:
• Small intestine, especially in proximal part of jejunum.
3. Mechanism:
• Rapid absorption - Seen with monosaccharides specially hexoses (glucose, fructose, galactose).
3a) Absorption of Glucose & galactose:
• By secondary active transport (cotransport) with Na2+.

• Absorbed from lumen against concentration gradient
• Carrier protein:
o Cotransporter SGLT-1.
• Transportation by GLUT-2 located in basolateral membrane.
3b) Absorption of Fructose:
• By facilitated diffusion
• Absorbed along concentration gradient
• Carrier protein- GLUT-2.

• Fructose is transported from enterocytes out into interstitium by GLUT-2.
3c) Absorption of Pentose sugars:
• Pentose sugars {D-xylose & D-arabinose}:

o By simple diffusion in proximal small intestine (jejunum).
25. STRETCH REFLEX
STRETCH REFLEX/ MYOTACTIC REFLEX
• Stretch receptor within a muscle - "Muscle Spindles".

o Detects increasing muscle length due to stretching.
• Stimulus - Passive stretch.
• "Monosynaptic reflex".
o Lowest most level of integration of stretch reflex is spinal cord.
• Reflex mechanism involves α-motor neurons in spinal cord.
o In turn, supply extrafusal fibers.
• Main functions: Mainly maintaining muscle tone & making muscles respond to stretch & release.
ROLE OF GAMMA(y) -MOTOR NEURON:
• Stretch reflex arc involves only alpha motor neurons.

• y-motor neuron (Ay-fibers) alter spindle sensitivity to stretch.
o Activation causes intrafusal fiber contraction
Factors increasing y-motor neuron discharge:
• Stimulation of skin.
• Anxiety.
• Jendrassik's maneuver.
26. INSULIN - METABOLIC ACTIONS
INSULIN - METABOLIC ACTIONS:
EFFECTS ON CARBOHYDRATE METABOLISM:
• Increased Glycogenesis.
• Increased glycolysis
o By inducing phosphofructokinase & pyruvate kinase enzymes.

• Inhibition of gluconeogenesis.
o By inactivating pyruvate carboxylase, PEP carboxykinase, fructose 1, 6 - bisphosphatase,
glucose - 6 - phosphates.
Glucose uptake:
• In Muscle and Adipose tissue:

o “Insulin-facilitated diffusion”
o By increasing GLUT-4 on cell membrane
o Transport occurs against concentration gradient.
• In Liver:
o Insulin-Independent glucose entry.
o Induction of glucokinase - “Glucose trapping”
EFFECTS ON LIPID METABOLISM
• Induces Lipogenesis by enzyme acetyl CoA carboxylase.

• Increases triglyceride synthesis by inducing lipoprotein lipase.
• Reduces lipolysis by inhibting hormone-sensitive lipase.
• Reduces ketogenesis (“Anti-lipolytic action”)
EFFECTS ON PROTEIN METABOLISM
• Stimulates anabolism -
o Increasing the rate of synthesis of mRNA
• Inhibits catabolism -
o Increases active transport of amino acids into tissues.
EFFECTS ON ELECTROLYTES
• Causes Hypokalemia
EFFECTS OF INSULIN ON VARIOUS TISSUE:
• On Adipose Tissue:
o Increased glucose entry converted to triglycerides.
o Increased fatty acid synthesis.
o Increased lipogenesis.
o Increased glycerol phosphate synthesis.
o Activation of lipoprotein lipase.
o Increased clearance of VLDL & chylomicron.
o Inhibition of lipolysis.
o Inhibition of hormone-sensitive lipase
• On Muscle:
o Increased glucose entry.
o Increased K+ uptake
• On Liver:
o Decreased ketogenesis.
o Increased protein synthesis.
o Increased lipid synthesis.
o Decreased glucose output.
o By ↓ing gluconeogenesis & ↑ing glycolysis.
o Increased glycogen synthesis.
o Inhibits glycogenolysis.
27. ELECTRO-ENCEPHALOGRAM (EEG)
EEG (Berger's rhythm)
Types Of Rhythms (Important in sleep-wake cycle) - Bilaterally Symmetrical
• Alpha
• Beta
• Theta
• Delta
Alpha Wave
• Occur when at rest & eyes closed with active/wandering mind

• Associated with decreased level of attention (relaxed/subconscious thinking)
• Origin - Most evident on parietal & occipital region
• Regular Rhythm
• Frequency 8-13 Hz; Amplitude - 50-100 V)
Beta Wave
• Occurs during Focused attention

• At full alert & awake (maximum concentration/conscious thinking)
• Irregular rhythm
• Frequency: 13-30 Hz high frequency & low voltage activity compared to alpha waves.
• Most evident on parietal & frontal regions.
• ALPHA BLOCK
o Replacement of beta rhythm for alpha rhythm is called Arousal / Alerting response / Alpha
block.
o Phenomenon occurs during any form of sensory stimulation or mental concentration such
as solving arithmetic problems.

Theta Rhythm
• Also seen during transition state from wakefulness to sleep. Similar to Stage 1 of REM.
• Frequency: 4 - 7 Hz
• Occur normally in parietal & temporal in children,
o In adults during EMOTIONAL STRESS, particularly during disappointment & frustration.
o Brain disorders like degenerative brain conditions.
Delta Rhythm
• Collectively referred to as SLOW WAVES

• In deep sleep (NREM stage 3 & 4) & in state of no thinking
o Fully relaxed.
• Delta waves are abnormal in awake adult.
• Frequency: 3-5 Hz(lowest); but has largest amplitude and voltage (2 to 4 times > than others).
Farady Cage
• EEG cabins completely shielded by a continuous sheet of copper wire mesh to avoid picking up of
noise from external electromagnetic disturbances
• This shielding is Faraday cage.
Special Pattern Observed in EEG
• Burst suppression EEG pattern

• Seen in acute cerebral insults like Hypoxic ischemic encephalopathy/ Anoxic Encephalopathy
• Phenobarbital administration to lower ICP in traumatic brain injury
• Severe hypothermia.
• Creutzfeldt Jakob disease presents with periodic sharp BIPHASIC wave complexes with frequency
about 1/second.
• Delta waveforms are seen in metabolic encephalopathy.
• TRIPHASIC slow symmetric and high-voltage wave (2 – 5 /second) pattern is characteristic but non-
specific of Hepatic encephalopathy.
• Absence Seizures shows bursts of bilaterally synchronous & symmetric 3 Hz spike & dome, slow
wave activity in EEG.
28. ANTI-DIURETIC HORMONE (ADH) / VASOPRESSIN
ANTI-DIURETIC HORMONE (ADH) / VASOPRESSIN
SYNTHESIS:
• In Hypothalamus
• Supra-optic nucleus
• Along with binding protein Neurophysin-I
• Stored in Pituicytes
RECEPTORS:
RECEPTOR TYPE SITE OF ACTION

V1 Blood vessels
Vaso-constriction
V2 Kidney
V2 receptors are more Blood vessel -
sensitive Increased water permeability
to ADH than V1 Vaso-dilatation Release of vWf & Factor VIII
Regulation of secretion:
• By Osmoregulators
• Circum-ventricular organs, primarily from
o Organum Vasculosum of Lateral Terminalis (OVLT)
o Antero-lateral wall in 3rd ventricle
Stimulating factors:
• Hyperosmolarity
• Decreased ECF volume
• Drugs - Carbamazepine, Morphine
Inhibiting factors:
• Hypo-osmolarity (Decreased osmolarity)

• Increased ECF
• Alcohol
Principle physiological effects:
Effects on Kidney:
• Retention of water:
o Increase permeability & water absorption
Effects on Blood vessel:
• Constrict blood vessel - Hence, "VASOPRESSIN"
Disorders with increased ADH:
• Syndrome of inappropriate ADH secretion

• Effective circulating volume depletion
• Heart failure
SYNDROME OF INAPPROPRIATE ADH SECRETION (SIADH):
• Increased & inappropriate vasopressin release,
Characteristics:
• Excessive fluid retention (Water intoxication)

• Hyperosmolar urine
• Clinical Euvolemia
o Absence of signs of hypervolemia (edema)
• Hyponatremia
o due to impaired urinary dilution
• Increased sodium excretion
o High urinary sodium
• Absence of signs of hypovolemia
o orthostatic hypotension, tachycardia & dehydration
Causes:
• Ectopic production from carcinomas

o Mainly Small cell carcinoma of Lung
• Drugs potentiating ADH effects

o Vincristine
Investigations:
• Water loading test
Treatment:
• Demeclocycline & Lithium

Central Diabetes insipidus:
• Characteristics features:
o Large volumes of dilute urine formation
o Resulting in severe dehydration in unconscious patients
Treatment:
• Desmopressin
Nephrogenic diabetes insipidus:
• Renal tubule resistance/ Hyposensitivity

• Irresponsive to ADH action
Causes:
• Failure of forming hyper-osmotic counter-current mechanism

• Drugs - Furosemide, Lithium & Tetracyclin
Difference central & nephrogenic types:
• By administrating synthetic analog of ADH
29. PULMONARY COMPLIANCE
PULMONARY COMPLIANCE
• Lung compliance (CL) - Measure of the elastic properties (Distensibility/stretchability) of lung

• Total compliance of both lungs in normal human adult
.
o 0 2 L/cm (200ml/cm) water
• Compliance of respiratory system (combined lung & thorax),

o Exactly half of compliance of lung alone - 110 ml/cm H20.
Volume-pressure curve (Vp curve):
• High compliance lungs:

o Curve shifting upward & left with steep slopes.
o Emphysema
• Low complaint lungs:

o Curve shifting downward & right.

o Pulmonary congestion & interstitial pulmonary fibrosis.
Variations in compliance:
• Increased compliance:
o Emphysema (COPD)
o Old age
• Decreased compliance:
o Pulmonary interstitial fibrosis
o Pulmonary congestion
o Reduced surfactant (Pre-mature infants)
Factors affecting compliance:
• Surface tension:
• More surface tension = Less compliance
Variations in static compliance:
• Increased static compliance:

o Emphysema
o Due to destruction of elastic tissues in alveolar walls
• Decreased static compliance:

o ARDS
• Emphysema (COPD) -
o Increased pulmonary compliance
o Pressure-volume curve is shifted upward & to left.
Relationship bt. Surfactant & pulmonary compliance:
• Secreted by type-II pneumocytes of the alveolar epithelium

• Main surface tension lowering phospholipid in surfactant,
o Dipalmitoyl-phosphatidylcholine (DPPC) (dipalmitoyl-lecithin)
Mechanism of action:
• Breaking water molecule inside alveoli and its surface tension subsequently
Functions:
• Acts on alveoli
• Alveolar stabilization
• Reduction in alveolar surface tension.
• Increases lung compliance
Effects of surfactant deficiency:
• Decreased compliance
• Hyaline membrane formation
Important metrics:
• Total compliance of both lungs together in the normal adult human - 200 ml/cm water (0.2 L/cm)
30. NEUROTRANSMITTERS - FUNCTIONS & MECHANISM OF ACTION IN CNS
NEUROTRANSMITTERS
Classification:
1. Based on chemical nature:
• Class I - Acetylcholine
• Class II - Amines:
o Norepinephrine
o Epinephrine
• Class III - Amino Acids
o Glutamate
o Glycine
o GABA
o Aspartate
2. Based on molecular size of neurotransmitter:
a. Small molecular transmitters:
• Acetylcholine
• Serotonin
• Glutamate
• Glycine
• GABA
• Aspartate
• Nitric oxide
b. Large molecule transmitters:

• Neuropeptides:
o Substance P
o Encephalin
o Beta-endorphins
4. Classification based on mode of action:
• Excitatory:
o Glutamate - Cheif excitatory neurotransmitter in brain & spinal cord
o Aspartate - Cheif excitatory neurotransmitter in cortical pyramidal cells
• Inhibitory:
o Gamma-AminoButyric Acid (GABA)
Major inhibitory neurotransmitter of CNS
Exerts indirect inhibition
o Glycine - Direct inhibition.
5. Classification based on receptors:
Inotropic:
• Glutamate: AMPA, Kainate, & NMDA

• GABA: GABA a type
• Acetylcholine: Nicotinic (N m and N n)
• Serotonin: 5HT3
Functions:
• G-protein coupled receptors

• Acting through second messenger
Characteristics of neurotransmitters:
1. Acetylcholine: Excitatory action
2. Nor-epinephrine:
Origin:
• Secreted by terminals of neurons

• With cell bodies in brainstem & hypothalamus.
• Specific location: Locus cerulus
3. Dopamine, Glycine, & GABA: Inhibitory action

4. Glutamate: Excitatory action
5. Serotonin:
• Inhibitory of pain pathways

• Actions on higher regions of nervous system
• Controls mood of a person and induce sleep.
6. Nitric oxide:
• Neither produced from neuronal calls nor stored in vesicles.
7. Neuropeptide transmitters:
• Synthesized in ribosome-golgi apparatus in neuronal cell body

• Stored in nerve terminals
• Mostly act as hormone (eg:- ADH, Oxytocin)
Substance P:
• Dorsal horn of spinal cord, hypothalamus & from nigrostrial pathway of basal ganglia.
Opioid peptides:
• Encephalin, endorphins & dynorphin

• Important role as central inhibitor of pain signals.
31. SECOND MESSENGER
SECOND MESSENGERS:
• Common second messengers:

o Cyclic Adenosine 3' 5'- Monophosphate (cAMP)
o Cyclic Guanosine Monophosphate (cGMP)
o Diacylglycerol (DAG)
o Calcium ions (Via Calmodulin)
o Inositol Triphosphate (IP3)
o Gaseous molecules - Nitric oxide (NO), Carbon-mono-oxide (CO) & Hydrogen Sulphite (H2S)
CLASSIFICATION:
• Group I hormones:

o Directly binds to intracellular receptors.
• Group II hormones:
o Acts on cell membrane receptors.
o Hormone/ligand is 1st messenger effecting on 2nd messenger
MECHANISM OF ACTION:
1. Intracellular receptors:
• Act by stimulation of transcription.
2. Secondary messengers of membrane receptors:
• Act by post-translational modification.

• Most predominant - "Phosphorylation".
Cellular phosphorylation by,
1. Protein kinases -
• Enzymes catalyzing phosphorylation of tyrosine or serine or threonine residues in proteins.

• 2nd messengers act on protein kinases stimulating protein phosphorylation.
2. Phosphatases I-
• Enzymes removing phosphates from protein.
CALMODULIN:
• Calcium-dependent regulatory protein is calmodulin.

• Marked conformational change allows calmodulin to activate enzymes & ion channels.
Important enzymes & proteins regulated:
• Adenylyl cyclase.
• Ca2+ dependent protein kinase.
• Ca2+-Mg2+ ATPase.
• Phosphodiesterase.
• Ion channels.
• Nitric acid synthase.
• Phosphorylase kinase.

32. RESTING MEMBRANE POTENTIAL
RESTING MEMBRANE POTENTIAL
• RMP is principally due to K+ concentration/chemical difference in ECF & ICF.

• In neurons, RMP is usually about -70 mV.
o Value close to K+ equilibrium potential.
-
o Exactly same as Cl equilibrium potential.
o Due to negligible effect of other ions diffusing through membrane.
• Values of equilibrium potential/isoelectric potential/Nernst potential:
2+
o Na - (+60 mV).
+
o K - (-90mV).
-
o Cl - (-70 mV)
CALCULATION OF RMP
• RMP magnitude calculated from Nernst equation/"Nernst potential/Equilibrium

potential/Diffusion potential of K+.
Effect of Na2+ & Cl- on RMP:
• Each ion derives membrane potential on its own Nernst potential.

o Referred as "Equilibrium potential of membrane".
o Calculated by Goldman's equation
FACTORS IN GENESIS OF RMP:
1. Difference between ICF & ECF potassium concentration -
• Important factor influencing RMP genesis.
1a) If increased ECF K+ concentration:
• Depolarization occurs.
• Mechainsm:
+
o Decreases K movement to ECF.
o Decreases RMP magnitude.
o Increases positivity/decreases negativity (depolarization).
2+
o Opens voltage-gated Na channels.
1b) If decreased ECF K+ concentration:
• Hyperpolarization occurs.
o Increases RMP magnitude.
o Decreases positivity/increases negativity of membrane (hyperpolarization)

2. Poor sodium membrane permeability:
• Sodium-potassium pump:
2+
o Pumps 3Na out of cell & 2K+ into cell.
RMP FOR VARIOUS EXCITABLE TISSUES:
• Neuron: -70 mV
• Ventricle (cardiac muscle) : -90 mV
• Smooth muscle: -30 to -50 mV
• Hair cells baseline membrane potential: - 60mV
33. ACTION POTENTIAL
ACTION POTENTIAL (AP)
4 phases:
1) Resting stage:
• At rest, membrane is "Polarized".

• (This stage is not a part of action potential).
2) Depolarization phase:
• There is "Voltage-gated Na2+ channels" opening.

o Causing sodium influx.
• "Firing level/Threshold point":
o -70 mV to -55 mV
o Partially opened voltage-gated Na2+ channels.
o This AP portion also called "Pre-Potential"/"Foot of AP".
2a) Depolarization:
o At threshold level -55 mV:

Complete opening of voltage-gated Na2+ channels.
3. Repolarization phase:
o Closure of voltage-gated Na+channels.

o Opening of voltage-gated K+channels.
• Causing efflux of K+ out of cell.

4) After depolarization:
• Slower phase of repolarization.
5) After-hyperpolarization :
• Increased K+ ions leak out.

• Causing brief period of voltage fall below -70 mV.
o Ie., "Hyperpolarization".
1. Channels involved in RMP:
• K+ - "Leak" channels.
2. Channels involved in AP:
• Voltage-gated Na2+ channels:

o During Depolarization
• Voltage-gated K+ channels:
o During Repolarization
FEATURES OF ACTION POTENTIAL:

1. Self-propagation:
• AP is propagated without decrement.

• Nerve impulse conduction is rapid yet, much slower than electricity.
2. All or none phenomenon:

3. "Threshold Stimulus" is "Minimum stimulus strength for triggering AP.
4. "Absolute Refractory Period" -
• Period where any stimulus strength fails to produce response.

o Because only about one-third response completes from onset of depolarization until early
repolarization.
• Only sufficiently high stimulus can elicit a response.
5. Relative Refractory Period:
• Period between later part of repolarization till onset of after depolarization.

o Where once initiated, AP does not depolarize membrane below firing level.
• There is increased RMP magnitude.
o RMP changes from - 70 mV to - 85mV.
o Results in less excitable membrane.

34. NERVE CONDUCTION
NERVE CONDUCTION
Point of impulse origination:
• In a motor neuron, axon hillock & initial segment of axon have lowest excitation threshold.
• Because they have a much higher density of voltage-gated sodium channels.
• Axon hillock of body & initial segment of axon Generator area (Nerve impulse is generated).
• Schwann cells are found both in myelinated & non-myelinated nerve fibers of peripheral nervous
system.
o ln myelinated nerves Schwann cells provide structural support & form myelin sheath.
o Schwann cells are derived from neuroectoderm
CONDUCTION PROCESS:
• Experimentally, an axon can conduct impulse in either direction.

• In Natural situation, impulses are conducted in one direction only (in an intact body)
o I.e. From synaptic junction or receptors along axons to their termination.
o Such conduction is called "Orthodromic conduction".
"Antidromic conduction":
• Conduction in opposite direction (i.e., opposite to physiological direction).
Direction of flow in nerve fiber:
• In nerve fibers, action potential propagation is unidirectional (orthodromic)

• I.e., In natural situation, impulses travel only orthodomically.
Reason for unidirectional flow:
o Conduction is unidirectional at synapses or in NM junction

o Because, transmission across synapses & NM function is unidirectional
o Inturn due to presence of neurotransmitters at terminal end of axon (Presynaptic terminal)
FACTORS AFFECTING NERVE CONDUCTION:
Propagation of action potential (nerve conduction) is favored by,
• Low axoplasmic resistance (Ri).

• High membrane resistance (Rm).
• Low membrane capacitance (Cm).
• Thick (large) nerve Linear relation with conduction.
• Myelination of nerve.
1. Effect of myelination on conduction of AP:
• The rate of propagation of nerve impulse is faster in a myelinated nerve fiber than in unmyelinated
nerve fiber.
Main purpose of myelin sheath:
• Is to increase in speed at which impulses propagate along myelinated fiber.

• In myelinated fibers, they jump from one node of Ranvier to next node.
• So propagation is much faster.
• This type of conduction of nerve impulse in myelinated nerves is called "Saltatory conduction" or
"Propagation by Saltation".
• Myelination of nerve decreases membrane capacitance.
o Allows depolarization to occur very fast.

o So, myelination increase speed of action potential propagation.
2. Membrane capacitance:
• Measure of quantity of charge that must be moved across a unit area of membrane to produce a
unit change in membrane potential.
• If membrane has low capacitance Number of ions (charge) crossing membrane is less.
o Hence, faster AP conduction.
35. NERVE FIBER - CLASSIFICATION
NERVE FIBER - CLASSIFICATION
ERLANGER & GASSER CLASSIFICATION:
• A & B type fibers are myelinated.

• Only C fibers are nonmyelinated.
FEATURES OF FIBERS:

Classification Characteristics of Function High susceptibility
Erlanger & fibers to
Gasser
A alpha Myelination - • Proprioception. Pressure
Heavily myelinated
& thick • Motor supply to
skeletal muscle
Conduction - 70- (extrafusal to muscle spindle)
120 (maximum
velocity)
A beta Diameter - 4-13 Kinesthesia Pressure
A delta Diameter - 1-5 "Fast"/"Epicritic"/"First" pain Pressure
B fiber Diameter - 1-3 Preganglionic autonomic fibers Hypoxia
C fiber Myelination - • Pain - Local anesthetics

Unmyelinated oSlow pain
("Protopathic/Second
Conduction - 0.2-2 pain)
(minimum) • Temperature
• Pressure
• Postganglionic autonomic
fibers.
• Local anesthesia, hypoxia & pressure can block the conduction of nerve impulses.
• Most susceptible fibers to pressure - "A" fibers.

o Especially, Aα type
• Hypoxia:
o Most susceptible - "B" fibers.
o Least susceptible - "C" fibers.
• Local anesthesia:
o Most susceptible - "C" fibers.
o Least susceptible - "A" fibers.
SUMMARY:
1. For Pressure: A>B>C
2. For Hypoxia: B>A>C
3. For Local anesthesia: C>B>A
36. SPINAL REFLEX & PROPERTIES
SPINAL REFLEX & PROPERTIES
• Reflex - Involuntary response to stimulus.
• Mediated through a chain of neurons passing through CNS.
• Sensory impulse is automatically converted into a motor effect through CNS involvement.
COMPONENTS OF REFLEX ARC:
1. Receptor organ
2. An afferent neuron
3. Interneurons (Internuncial neuron):
• An interneuron can be excitatory or inhibitory.

• Interneuron is not involved in monosynaptic reflex (e.g., stretch reflex)
4. An efferent neuron
5. Effector organ
TYPES OF REFLEXES:
1. Based on number of synaptic junctions involved:
• Reflexes may be divided into 3 types:

o Monosynaptic, Bisynaptic & Polysynaptic.
1a) Monosynaptic:
• Only example of monosynaptic reflex in body is "Stretch reflex" like knee-jerk & ankle jerk.
1b) Bisynaptic:
• Eg: Golgi-tendon organ reflex (Inverse Stretch Reflex).
1c) Polysynaptic:
• Eg: Flexor reflex ("Withdrawal reflex) & Crossed Extensor reflex.

2. Based on sensory signal pathway:
• Suprasegmental reflex, Local segmental reflex & Intersegmental reflex.
2a) Spinal reflexes
• Local segmental reflex & intersegmental reflex are mediated entirely by spinal cord, without any
participation of brain.
• These are referred as "Spinal reflex".
• Bell-Magendie Law:
o Principle wherein spinal cord dorsal roots are sensory & ventral roots are motor.
PROPERTIES OF SPINAL REFLEX:
1. Delay
2. Subliminal fringe
3. Summation:
• Types: Temporal & Spatial summation
3a) Temporal summation -
• Application of two subthreshold stimuli maybe sufficiently quickly, one by another.
3b) Spatial summation -
• Two subthreshold stimuli together at different places
4. Adaptation:
• Habituation & Sensitization:
o Habituation - Repeated application of non-injurious stimuli may show decreased intensity of

response in withdrawal reflex.
o Sensitization - Repeated application of injurious stimuli may show intensification of
response.
5. Fatigue:
• Fatigue of synptic transmission can cause fatigue of stretch reflex, if the muscle spindle k stimulated
repetitively.

6. Occlusion.
7. Recruitment & after discharge.
8. Irradiation.
37. NEPHRON
NEPHRON
• Approximately 1 -1 .3 million nephrons in each kidney.

• Total length of nephron - 45-65 mm.
• Glomerulus composed of loops of capillaries which arise from afferent arterioles.
• PCT - About 15 mm long & located in cortex.
• Distal convoluted tubule (DCT) - About 5 mm long.
• Collecting ducts - 20 mm long passing through renal cortex & medulla.
• Epithelium in collecting ducts - Principal cells (P cells) & Intercalated cells (I cells)
• P cells - Involved in Na+ reabsorption & ADH stimulated water absorption.
• I cells - Concerned with acid (H+) secretion & HCO3- transport.
• Juxtamedullary nephron - Remaining 15% with glomerulus deep in cortex at cortico-
medullary junction.
• Long loop of Henle reachs deep into medulla up to papilla.
• Efferent arteriole of juxtamedullary nephrons drains into Vasa recta along with peritubular
capillaries.
38. INTERACTION BETWEEN CO2 & O2 TRANSPORT
INTERACTION BETWEEN CO2 & O2 TRANSPORT
O2 tissue delivery depends
• Amount of O2 entering lungs

• Adequacy of pulmonary gas exchange
• O2 carrying capacity of blood
• Blood flow to tissue
Inturn,
• Blood flow to tissue depends:

o Degree of constriction of tissue vascular bed
o Cardiac output

• Amount of O2 in blood determined:
o Amount of dissolved O2
o Amount of hemoglobin in blood
o Affinity of hemoglobin for O2
TRANSPORT OF OXYGEN (O2)
1. Oxygen trap:
• Oxygen diffuses into blood & combines with hemoglobin.

• Hemoglobin lays trap for carrying large amounts of oxygen in blood.
2. Oxygen transport:
• Orygen traped by hemoglobin in alveoli travels in blood in 2 forms -

o In dissolved form in plasma
o In association with hemoglobin (as Oxyhemoglobin)
2a) Dissolved form:
• Amount of O2 transported in dissolved form -

o 1.5 - 3% (0.3 ml/100 ml) of total amount transported
• With higher PO2, unlimited O2 carried in dissolved form
o Concentration of dissolved O2 is directly proportional to PO2
2b) As oxyhemoglobin:
• Bulk of oxygen (97%) in blood is normally transported as Oxyhemoglobin
Oxyhemoglobin content:
• Hemoglobin concentration in normal blood is about 15g/dl (15 g/100ml).

• Each gram of hemoglobin normally carries 1.34 ml of O2
o Hence,1 dl (100ml) of blood contains 20.1 ml (1.34 ml x 15) of oxyhemoglobin.
• Hemoglobin in systemic arterial blood is only 97% saturated.
o Hence, Arterial blood contains a total of about 19.8 ml of O2/dl
At rest:
• Tissues remove about 4.6 ml of O2 each deciliter of blood passing through them.
• Hence, 230 ml (by 5 liters of blood) of O2 per minute is transported from blood to tissue, at rest.
3. Oxygen transfer:
• Diffusion of O2 from capillaries to tissue - Along pressure gradient.

• PO2:
o At arterial end of capillaries - about 95 mm Hg
o At tissues - about 40 mm Hg.
TRANSPORT OF CARBON DIOXIDE (CO2):

1. CO2 transfer:
• Driving force is partial pressure gradient.

• PCO2 -
• In tissues - 46 mm Hg
• At arterial end of capillaries - 40 mm Hg.
• Hence, CO2 diffuses from tissues to capillaries
2. CO2 transport in blood:
• As bicarbonate
Metrics:
• 100 ml (1 dl) of blood takes away 4 ml of CO2.

• Hence, 5L of blood transports 200 ml of CO2 from the tissues each minute
2a) As plasma bicarbonate
• 7O% of CO2 transport - Major mechanism of CO2 transport.

• Enzyme carbonic anhydrase catalyzes reaction generating HCO3- ions in RBC
• Chloride shift/Hamburger phenomenon:
• Movement of chloride ions into RBC.
• HCO3- ions generated diffuse out into plasma in exchange for Cl- ions.
• Hematocrit value:
• For venous blood is normally 3% > arterial blood.
• Carbhemoglobin is major carbamino compound in blood.
Haldane effect:
• Binding of O2 reduces affinity of hemoglobin to CO2.Deoxyhemoglobin binds more H+ ions than

oxyhemoglobin and forms carbamino compounds more readily.
• Hence, venous blood carries more CO2 than arterial blood facilitating tissue CO2 uptake &release
into lungs.
3. Expulsion of CO2:
• CO2 is removed from pulmonary capillaries by diffusion.

• PCO2 -
• Venous blood - 45 mm Hg
• Alveolar air - 40 mm Hg.
• CO2 diffuses along pressure gradient from alveolar capillaries into alveoli.
• 200 ml of CO2 per minute at rest is transported from tissues to lungs & excreted.
39. PRODUCTION & REGULATION OF BILE
PRODUCTION OF BILE:
Introduction:
• Bile salts - Mainly, taurcocholates & glycocholates)

• Bile pigments - bilirubin & biliverdin
• Glucuronides of bile pigments, bilirubin & biliverdin - "Golden yellow color".
Synthesis:
• Small amount of bile is continuously synthesized in the liver.

• About 500 ml of bile is secreted per day (20.8 mL/hr) by liver.
Components:
1. Bile acids:
• Primary bile acids synthesized from cholesterol in liver.

• Important acids - Cholic acid & chenodeoxycholic acids.
• Rate limiting enzyme- 7α - hydroxylase (cholesterol 7α - hydroxylase).
2. Bile salts:
• Are sodium & potassium salts of bile acids, conjugated to amino acids, glycine or taurine.
REGULATION:
Stimulating factors:
• Bile production increased by vagus nerve stimulation & by hormone secretin.
Cholerectics:
• Substances increasing hepatic bile secretion.

• Most important cholerectics - Bile salts themselves.
• Others - Secretin
Cholagogues:

• Substances causing gallbladder contraction secreting bile.
• Most important cholagogue - Cholecystokinin (CCK).
• Fatty acids & amino acids in duodenum stimulates CCK release.
40. CEREBELLUM - NEURONAL CIRCUIT & DISORDERS
CEREBELLUM - NEURONAL CIRCUIT & DISORDER
Neruonal circuit:
• Input & output unit
INPUT NEURONAL TRACT:
1. Input afferent from:
• CLIMBING FIBERS-
o From inferior olivary nuclei only
o Establish excitatory synapses with Purkinje cells
MOSSY FIBERS-
• From all other parts of body

• Steps:
• Establish excitatory synapse with granule cells in granular cell layer
• Granular cells are only excitatory (stimulatory) cells in cerebellar cortex.
• Parallel fibers indirectly activate Purkinje cells
PARALLEL FIBERS:
• Axon of granule cells from Parallel fibers
Actions:
1. Indirectly activate Purkinje cells
2. Stimulate three types of interneurons,
• Stellate & basket cells in molecular layer - Inhibit Purkinje cells.

• Golgi cells in granular layer - inhibit granular cells
OVERALL EFFECTS ON INPUT:
• Climbing fibers - Exert strong excitatory effect on single Purkinje cell

• Mossy fibers - Exert weak excitatory effect on multiple Purkinje cells via granular cells.
TRACTS & CORRESPONDING INPUTS:
1. Dorsal spinocerebellar tract -
• Ipsilateral proprioceptive impulses from leg & trunk
2. Olivocerebellar tract -
• Proprioceptive impulses from all over body relayed through inferior olive
3. Cuneocerebellar tract -
• Ipsilateral proprioceptive impulses from arms & neck
4. Tectocerebellar tract -
• Visual & auditory impulses via superior & inferior colliculi
OUTPUT NEURONAL TRACT:
Output efferent to:
• Axons of Purkinje cells are the only output from cerebellar cortex.
• Deep Nucleus - Ultimate & final efferent ouput of cerebellum
1. Output of cerebellar cortex
• By axons of Purkinje cells

• Projected towards deep cerebellar nuclei
2. Output of deep cerebellar nuclei:
• Overall excitatory to brain stem & thalamus
Reason:
• As deep nuclei receive combined inhibitory & excitatory

PURKINJE CELL CONNECTIONS:
• Purkinje cells - Only output cells of cerebellar cortex

• Inhibitory to deep cerebellar nuclei
Direct connections for Purkinje cells:
• Afferent -
o With Basket & stellate cells
o Climbing & Parallel fibers
• Efferent -
o Deep cerebellar nuclei
CONCLUSION ON OUTPUT TRACT:
• Output of cerebellar cortex is always inhibitory (via Purkinje cells)

• Output of deep cerebellar nuclei is excitatory
• Hence overall effect from cerebellum is excitatory
DISORDERS OF CEREBRELLUM:
Clinical features,
• No paralysis/sensory deficit but incoordination is prominent in all voluntary muscles

• Two major disorders:
o Lateral cerebellar lesion
o Midline cerebellar lesion
LATERAL CEREBELLAR LESION:
• Also referred as "Cerebellar hemisphere lesion"
Features of Lateral Cerebellar lesion:
1. Dysmetria:
• Inability to control range of motion

• "Past pointing"- Failure to gauge exact degree of muscle contraction required.
2. Asynergia & Ataxia:
• Incoordination & muscles don't act in synergism

• Ataxia means lack of coordination between voluntary muscles
• Limb ataxia - Common.

3. Intention tremor
• There is no tremor at rest

• On attempting/ intending to do some motor activity produces tremors
• Hence,"Intentional Tremors"
4. Dysdiadochokinesia
• Also referred "Adiadochokinesia"

• Inability to perform rapid alternating movements
5. Dysarthria
• Defect in speech
• Scanning speech - Breaking every word & articulating separately
• Due to incoordination of muscles of vocalization
6. Rebound phenomenon
• Failure/inability to control movement on sudden release of opposing forceful restrain.

• Associated with hypotonia & Pendular tendon jerk
MIDLINE CEREBELLAR LESION:

Features:
• Truncal ataxia –
• Inability to sit unsupported.
• Gait ataxia –
• Wide based gait
• Drunken gait
• Imbalance - Falling in any direction
OTHER CONDITIONS ASSOCIATED:

1. Von Hippel-Landau disease:
• Vascular tumors (hemangioblastomas) of retina, cerebellum, and/or medulla.
2. Medulloblastoma:
• In children - As midline swelling arising from cerebellum

• In Adults - As lateral swelling
41. SURFACTANT
SURFACTANT
• Soap like substance secreted by type-II pneumocytes of alveolar epithelium
Embryological factors of surfactant:
• Surfactant synthesis occurs in 24 - 28th week of gestation

• Amniotic fluid appearance in 28 - 32nd week.
• Pre-term conditions - Deduction in 28th week.
• Mature levels of surfactant after 35th week.
Composition:
• Surface-active lipoprotein complex (phospho-lipo-protein)

• Main surface tension lowering phospholipid in surfactant
o Dipalmitoyl-phosphatidylcholine (DPPC) (dipalmitoyl-lecithin
• Breaking water molecule inside alveoli

• Surfactant breaks surface tensional force of water molecules.
Functions:
• Acts on alveoli
• Reduces surface tension of fluid-lined alveoli
• Increases lung compliance
Special physiological effects:
• Reduction in alveolar surface tension.

• Alveolar stabilization:
o Is a property of alveoli to reduce the natural tendency of smaller alveoli to collapse into
larger ones.
Effects of surfactant deficiency:
• Decreased compliance.
• Hyaline membrane formation.
Conditions associated with surfactant:
1. Acute Infant Respiratory Distress Syndrome (IRDS)
• Also referred “Hyaline membrane Disease” (HMD).

• In premature infants.
• Glucocorticoids accelerate surfactant production in premature lungs.
• Cause:
o Due to Immature functional surfactant system
o Insufficient production of surfactant dipalmitoyl lecithin
• Treatment:
o Corticosteroid administration to pregnant women.
o Promote accelerated fetal lung maturation.
o Production of surfactant.
2. Cigarette smoking:
• Decreased surfactant
42. NEOCORTEX - ORGANIZATION & FUNCTIONS
NEOCORTEX - ORGANIZATION & FUNCTIONS
• Non-limbic portion of cerebral hemisphere.

• Phylogenetically referred as neocortex - One type of cerebral cortex division.
• Forms major part (almost 90%) of cerebral cortex
• Comprised of the most superficial areas of brain.
CELLS IN CEREBRAL CORTEX:

Cortical cells:
• Majority are pyramidal cells

• Pyramidal cells - "Sine qua non" for cerebral cortex
• Axons of pyramidal cells leave the cortex
• Forms descending tract (e.g. Corticospinal, Corticobulbar etc).
LAYERS OF CEREBRAL CORTEX:
Composed of 6 layers -
• Layer/Lamina I - "Molecular layer".

• Layer/Lamina II - "External granule cell layer"
• Layer/Lamina III - "External pyramidal cell layer"
• Layer/Lamina IV - "Internal granule cell layer"
• Contains predominately granule cells & nerve fibers
• Specific sensory input through thalamocortical fibers terminate primarily in cortical layer IV on
stellate (granule cells)
• Layer/Lamina V - "Internal pyramidal cell layer"
• Contains large pyramidal cells.
• Descending tracts, i.e. projection fibers from cortex (corticospinal tract, corticobulbar tract) are the
axons of these pyramidal cells of Layer V
• Layer/Lamina VI - "Multiform layer"
FUNCTIONAL DIVISION OF CEREBRAL CORTEX:
• Primary cortical area

• Association area
Other functions:
• First center activated to initiate skilled movements is "Neocortex".
43. HYPOTHALAMUS - NEURONAL FUNCTIONS
HYPOTHALAMUS - NEURONAL FUNCTIONS
• Functions of hypothalamus included both endocrine & neuronal regulations of activities.
Neuronal functions:
1. Regulation of body temperature:
• Hypothalamic control of body temperature:

o Controlled by Pre-optic nucleus
• Heat regulation:
o By anterior hypothalamus
• Response to coldness:
o By posterior Hypothalamus (Shivering center)
2. Regulation of circadian rhythms:
• Suprachiasmatic nucleus in hypothalamus - "Biological clock"/ "Endogenous clock".

• Afferents from "Retinohypothalamic fibers & lateral geniculate nuclei".
3. Regulation of hunger & food intake:
• Feeding center
o Lateral hypothalamic nucleus

• Satiety center
o Ventromedial nucleus
Mechanism involved:
• Direct neuronal signaling to hypothalamus

o Signal for stimulating regulation of feeding activity is from 'Glucose'
o Glucosensitive neurons located in satiety center (Ventromedial nucleus)
4. Regulation of thirst:
• Thirst center/drinking center:

o Lateral nucleus
o Supra-optic nucleus
Inputs received from:
• Osmoreceptors
o Present in anterior hypothalamus
• Baroreceptors:
o Subfornical organ & Organ Vasculosum of Lamina Terminalis (OVLT)
5. Regulation of BP:
• Pressor effect
o By Posterior & lateral nuclei
• Depressor effect
o By Preoptic nucleus
6. Regulation of sexual function:
• By Anterior hypothalamus
• In males:
o Medial preoptic nucleus
• In females:
o Lateral preoptic nucleus
7. Response to smell:
• By Posterior hypothalamus
8. Other centers/neuronal regulations under control of hypothalamus:
• Sleep center
By Preoptic (Ventrolateral)
o
• Wakefulness center
o By Reticular Activating System (RAS) in brainstem & hypothalamus
• Reward center
o By Lateral & ventromedial nuclei of hypothalamus
• Punishment center
o Periventricular nuclei (mainly)
44. VENTILATION-PERFUSION RATIO (V/Q RATIO)
VENTILATION - PERFUSION RATIO (V/Q ratio)
V/Q ratio:
• Pulmonary perfusion (Q) -

o 5.0 L/min
• Alveolar ventilation (V) -

o 4.2 L/min
• Overall Ventilation-Perfusion (V/Q) ratio value - 0.8
Interpretations of V/Q ratio values:
• Value is 0.8
o "Ventilation-Perfusion matching"
• If V/Q is > 0.8 -

o Means more ventilation than perfusion.
• If V/Q is < 0.8 -

o "V/Q mismatch"
Factors causing variations in V/Q ratio:

1. Position of lung
2. Gravity:
• Main reason for V/Q ratio differences between base & apex of lung
Effect of gravity on variations bt. basal & apical V/Q ratio:
• Base is more perfused than apex.

• Effects on apex:
o Due to gravity, apical alveoli are both underventilated & under-perfused
o Hence, V/Q is maximum at apex
• Effects on base of lung:

o Basal alveoli are both overventilated & over-perfused.
o Hence, V/Q is minimum at base of lung.
• Values:
• V/Q at apex
o About 3.0 (maximum)
• V/Q at base of lung

o About 0.6 (minimum)
COMPARISON Bt. PO2 & PCO2 conc. IN BASE & APEX:
• PO2 & PCO2 concentrations in well-perfused basal alveoli -

o Low PO2 & high PCO2
o Approximately same as PO2 & PCO2 levels in pulmonary artery
• PO2 & PCO2 concentrations in poorly perfused apical alveoli -

o High PO2 & low PCO2
o Approximately same as PO2 & PCO2 levels in inspired air.
Reason for varied PO2 & PCO2 levels:
• Ventilation-perfusion mismatch.
45. COMPOSITION OF ALVEOLAR AIR
COMPOSITION OF ALVEOLAR AIR
Factors causing difference:
• Constant gaseous exchange process

• Humidification:
• Partial/slow replacement with atmospheric air:
Gaseous concentration & its partial pressure in alveoli:

1. Oxygen:
• Partial pressure of O2 in inspired air (Pi O2)

o 158 mm Hg

• Partial pressure of O2 in alveolar air (PA O2)
o 100 mm Hg
o Calculated by "Alveolar gas equation".
• Partial pressure of O2 in expired air (PE O2).
o 116 mm Hg
2. Carbon-di-oxide:
• Partial pressure of CO2 in inspired air (Pi CO2)

o 0.3 mm Hg
• Partial pressure of CO2 in alveolar blood (PA CO2)
o 40 mm Hg
• Partial pressure of CO2 in expired air (PE CO2)
o 32 mm Hg.
46. MEASUREMENT OF RENAL BLOOD FLOW
MEASUREMENT OF RENAL BLOOD FLOW
Renal Plasma & Blood flow:
• Total renal blood flow (RBF) is approximately 1.1 - 1.3 Lit/min

o i.e., 22-25% of cardiac output
Measurement of RPF & RBF:
• PAH clearance used as a measure for calculating renal plasma flow.
IMPORTANT METRICS:
1. Measure of Effective Renal Plasma Flow (ERPF):
• Is through PAH clearance

• In normal adult is about 625 ml/minute
2. Extraction ratio of PAH - 0.9
3. Actual RPF - 10 % more than ERPF.
• 690 ml/minute.

47. GLOMERULAR FILTRATION RATE (GFR) & FACTORS AFFECTING
GLOMERULAR FILTRATION RATE (GFR)
Filtration barrier/surface:
• Glomerular membrane.
• Basement membrane acts as "Functional barrier"
• Performs selectivity & filtration function of glomerular membrane.
• Filtration done by, hydrated channels approx. 6 nm wide
Factors influencing:
• Membrane charge:
• Membrane glycoproteins are strongly negatively charged.
• Hence, filtration surface is impermeable to negatively substances.
• e.g., like plasma proteins, albumin.
• Clinical implication:
• Albuminuria is such a sensitive indicator of glomerular disease
• Size of filtration channels:
o About 7 nm
Metrics:
• Resting glomerular filtration rate is about 125 ml/min

• About one-fifth (20%) of plasma passing through kidney is filtered.
• Filtration fraction - 0.2
DETERMINANTS OF GFR:
1. Net effective filtration pressure:
• 10 mm/Hg
Factors promoting filtration:
• Hydrostatic pressure in glomerular capillaries - 60mm Hg.

• Most important determinant of GFR
• Nil/Zero Bowman's capsule colloid osmotic pressure
Factors opposing filtration:

• Hydrostatic pressure in Bowman's capsule (PB) - 18mm Hg
• Glomerular capillary colloid osmotic/oncotic pressure (∏G) - 32 mm Hg
Formula for GRF:
• GFR = Kf * net filtration pressure

• Normal resting glomerular filtration rate - Approx. 125 ml/min
EFFECTS ON GRF:
1. Effect of Hydrostatic pressure on GRF:
• Increased glomerular capillary hydrostatic pressure Increases GFR

• Glomerular hydrostatic pressure inturn determined by,
o Arterial pressure, Afferent & Efferent arteriolar resistance
1 a) Arterial pressure on GFR:
• ↓ed arterial pressure/Hypotension ↓ed GFR

1 b) Afferent arteriolar resistance on GFR:
• ↑ed afferent arteriole resistance(constriction) ↓ed GFR

• ↓ed afferent arteriole resistance(dilation) ↑es GFR
1 c) Efferent arteriolar resistance on GFR:
• Increased efferent arteriole resistance (Constriction) has biphasic effect on GFR

• Moderate constriction slight ↑es GFR.
• ↓ed efferent arteriole resistance(dilation) ↓es GFR.
2. Effect of glomerular capillary colloid osmotic/oncotic pressure on GFR:
• ↑ed colloid osmotic pressure ↓es GFR.

• ↓ed colloid osmotic pressure ↑es GFR.
o Eg: Hypoproteinemia.
3. Effect of renal blood flow on GFR:
• ↑ed renal blood flow ↑es GFR

4. Effect of mesangial cells & Kf on GFR:

• ↓ed Glomerular capillary filtration coefficient (Kf) ↓es GFR
• Kf altered by mesangial cells
es
o Contraction of mesangial cells ↓ Kf & GFR
Caused by endothelin, angiotensin II, vasopressin, PGF2 & Histamine.
es
o Relaxation of mesangial cells ↑ Kf & GFR
Caused by ANP, Dopamine, PGE2 & cAMP
5. Other factor affecting GFR:
• ↑ed Bowman's capsule hydrostatic pressure ↑ed tubular hydrostatic pressure (result of
es
obstruction) inturn results in ↓ GFR
48. REGULATION OF RENAL BLOOD FLOW
REGULATION OF RENAL BLOOD FLOW:

RENAL AUTOREGULATION:
Type I - Myogenic autoregulation:
• Maintains renal blood flow as well as GRF.

o Produced by direct contractile response to smooth muscle stretch of afferent arteriole.
Type II - Tubuloglomerular feedback–mediated renal vasoconstriction
RENAL VASODILATION:
• Prostaglandins & bradykinins

o PGE1 & PGE2 mainly.
49. GLOMERULAR FILTRATION RATE (GFR) - MEASUREMENT
GFR - MEASUREMENT
GFR estimation usually done by,
1. Clearance test:
Criteria for selection:
• Substances should pass freely through glomerular membrane.

• Should neither reabsorbed/nor secreted by tubular activity.
1a) Inulin clearance test:
• Most accurate measure for GFR estimation.
• Properties qualifying inulin:

• Small molecular size.
o Hence, free passage through glomerular membrane.
• Neither secreted/nor synthesized/nor metabolized/ & non-toxic.
• Inulin clearance = 126 ml/min (Equal to GRF).
1b) Other clearance tests:
• Creatinine clearance:
o Less accurate method since gets secreted in renal tubules.
o Yet, more convenient to determine creatinine clearance
o Is a metabolic product with constant levels.
o Hence, used as "Index of GFR".
2. Radiological methods:
• Tc99 In-labeled DTPA scan

• DTPA (Diethylenetriaminepenta acetic acid)
• Excretory rate measures GFR.
• Uses of DTPA Scan:
o Useful for evaluation of renal perfusion & functionality of each kidney
1. Substance filterability:
a) Free filterability:
• Filterability value = 1
o Means freely filtrable through glomerular membrane barrier.
o Eg., Water, sodium, bicarbonate, inulin, Creatinine
b) Partial filterability:
• Filterability value = 0.75

o Implies only 75% substance is filtered.
o Partially filtered.
o Eg: Myoglobin
c) Substance not filtered:

• Plasma proteins not filtered.
• Eg., Albumin, Hemoglobin (since are bound inside RBC).
o Yet, significant amounts of FREE hemoglobin gets excreted.
2. Interpretation of afferent & efferent arteriole concentration:
• Equal afferent & efferent concentrations:

o Implies substance unfiltered by glomerulus.
• Lower efferent arteriole concentration:
o Implies partial filtration by glomerulus.
• Completely absent efferent concentration:
o Positive for concentration in afferent arteriole.
o Implies complete filtration by glomerulus.
50. REGULATION OF GFR
REGULATION OF GLOMERULAR FILTRATION RATE
• GFR & renal blood flow are usually autoregulated by,

• Tubuloglomerular feedback
• Myogenic feedback,
1. Tubuloglomerular feedback:
• Usually refers, Afferent arteriole feedback mechanism.
1a) Afferent arteriolar feedback mechanism:
• Transmitter involved - Adenosine causing Ca2+ channel opening.
1b) Efferent arteriolar feedback mechanism:
• Activates renin-angiotensin system generating angiotensin II efferent arteriole constriction

↑ed GFR.
• Feedback depends on juxtaglomerular apparatus & its specialized cells.
• Macula densa - Specialized epithelium of distal tubule in close contact with afferent arteriole
• Autoregulation feedback mechanism utilizes Na+ - Cl- concentration at macula densa under control
of renal arteriolar resistance.
2. Myogenic autoregulation:
• Arteriole stretching opens "stretch-sensitive Ca2+ channels on arteriolar smooth muscle cells.
• Results in Ca2+ influx causing constriction.
51. GALL BLADDER - FUNCTIONS
FUNCTIONS OF GALLBLADDER
1. Storage & concentration of bile
• Storage of Bile.
• Concentration of Bile
o Increases 5 to 10 times
2. Alteration of Bile pH:
• Bile pH decreases from 8 – 8.6 to 7 – 7.6.

• Less alkaline.
3. Secretion of Mucin
4. Maintenance of biliary system pressure
52. MECHANISM OF RENAL TRANSPORT OF SODIUM & GLUCOSE
MECHANISM OF RENAL TRANSPORT OF SODIUM & GLUCOSE
1. RENAL SODIUM TRANSPORT:
RENAL PART MECHANISM BEHIND SODIUM TRANSPORT

2+ +
Proximal Convoluted • Driven by Na -K ATPase located on basolateral membrane
2+
Tubule (PCT) o 60-70% filtered Na reabsorbed.
2+ +
• Na entry coupled to H secretion, via NHE3 antiporter.
• Highly permeable to water & relatively permeable to solutes like

sodium, chloride & urea.
Descending Thin Limb • Hence, no sodium resorption.
(DTL)
Thick Ascending Limb • 30% filtered Na2+reabsorbed.

(TAL) • Via Na2+- K+-2Cl- symporter/co-transporter (NKCC).
• Transports one Na2+& K+ & 2 Cl- ions.

• Apical membrane contains Na+- Cl- symporter/Co-transporter (NCC).
• Approx. 7% filtered Na2+ reabsorbed.
Distal Convoluted
Tubule (DCT)
Collecting Tubule (CT) • Via apical sodium channels (ENaC)-P cell.
• Aldosterone - Important for Na2+ & water resorption.
2. RENAL GLUCOSE TRANSPORT:
• Glucose reabsorption by 2º active transport.

• Complete reabsorption in proximal tubules.
• Occurs by sodium-glucose cotransporter - 1 (SGLT-1) in brush border(luminal membrane)
Factors influencing resorption:
1. Transport maximum for glucose (TmG)-
• 375 mg/min in males

• 300 mg/min in females
2. Actual value of renal threshold.
• In arterial blood - 200mg/dl.

• "Glucose threshold value" in blood to activate urinary excretion.
• When glucose filtered load - 250mg/min urinary glucose is mildly positive.
SPLAY EFFECT:
• Deviation in renal threshold from calculated predicted value

• Overall Tm for kidneys (375 mg/min) is reached, all nephrons reached their maximal capacity for
glucose reabsorption.
53. PERISTALSIS
PERISTALSIS
• Stimulus for peristalsis - Distention of gut

• Local stretch reflex.
Activation:
1. Neuronal activation factors:

• Requires an active myenteric plexus.
• Local stretch by chyme releases serotonin, which activates myenteric plexus.
• Activated neurons secreting Nitric Oxide (NO), VIP & ATP, producing relaxation ahead of stimulus.
o VIP, NO & ATP → Producing relaxation ahead of stimulus
o Acetylcholine & substance P → Causing smooth muscle contraction.
2. Hormonal activation factors:
• Gastrin, Cholecystokinin, insulin, motilin & serotonin enhance intestinal motility.

• Secretin & glucagon inhibit small intestinal motility.
• Can be increased/decreased by autonomic input to gut.

• Yet occurrence independent of extrinsic innervation
Peristaltic rush -
• Occurs when intestine is obstructed
54. RESPIRATORY RESPONSE TO EXERCISES
RESPIRATORY RESPONSE TO EXERCISES
• A 25-fold increased oxygen consumption as well as carbon dioxide production during exercise.
• Pulmonary ventilation increases abruptly with onset of exercise.
• Abrupt increase due to psychic stimuli & afferent impulses from proprioceptors in muscles,
tendons, and joints.
• During moderate exercise, increased pulmonary ventilation due to increased respiratory depth.
• During strenuous exercise, increased pulmonary ventilation due to increased respiratory rate.
• In severe & sustained exercise, lactic acid accumulates in blood & pH of blood may drop as low as
7.2.
• During this period arterial PCO, may drop significantly.
• Exercise increases body temperature.
• Arterial pH & HCO decrease with severe exercise.
• Strenuous exercise causes hyperkalemia
• Oxygen-hemoglobin dissociation curve is shifted to right.
• Increased O2 extraction by tissues
• Lactic acid accumulation causes muscle soreness.
55. DIGESTION IN STOMACH - MOTILITY & GASTRIC EMPTYING

DIGESTION IN STOMACH (MOTILITY & GASTRIC EMPTYING)
Proximal stomach - Storage unit:
• Proximal stomach serves primarily the function of storage (receptive area).
Distal stomach:
• Pacemaker location -
o Along the greater curvature of an upper part of distal stomach (middle third of body)
o Generates BER of 3 to 4/min
Gastric contraction:
Inter-digestive phase:
Migratory Motor Complexes (MMC/Inter-digestive myoelectric complexes)
• Gastric antrum shows bursts of propulsive (peristalitic) muscular activity every 90 minutes.
• MMCs are initiated by motilin
• Purpose of MMC is to clear stomach & small intestine of luminal contents in preparation for next
meal.
• Activity is conducted along entire length of small intestine, from stomach to distal ileum at a rate
of about 5 cm per minute
• On reaching terminal ileum, a new wave begins in stomach.
Factors affecting gastric emptying rate:
1. Increasing factors:
• Type of food ingested.

• Emptying is slowest after fat-rich meal.
• Distension of stomach.
• Triggers long (vagally mediated) & short (intrinsic neural plexus mediated) reflexes
• Leads to strong peristaltic waves Increasing gastric emptying.
• Gastrin
2. Decreasing factors:
• Duodenal distension.
• Duodenal hyperosmolarity (Hyperosmolar chyme).
• Presence of acid, fats, & end products of fat digestion.
• Done by release of several intestinal hormones like secretin, cholecystokinin, VIP, & GIP.

56. MINERALOCORTICOIDS - FUNCTIONS & REGULATION
MINERALOCORTICOIDS - FUNCTIONS & REGULATION
Adrenal cortex:
• Essential for life

• Zona glomerulosa - Outermost layer & site of mineralocorticoid synthesis.
Mineralocorticoid hormone:
Aldosterone -
• Chief mineralocorticoid.
• Acts primarily on kidney.
1. Action on sodium:
• Increases sodium reabsorption in distal convoluted tubules & collecting ducts.

• Occurs in exchange for K+ & H+
2. Potassium hemostasis:
• Aldosterone is a major controller of K+ homeostasis.

• K+ & H+ excretion is increased.
Mineralocorticoid (aldosterone) receptors:
• Expressed at high levels in renal distal tubules & cortical collecting ducts.
• Also in brain (hippocampus), myocardium, peripheral vasculature, brown adipose tissue, salivary
gland & colon.
REGULATION:
• Stimulated by hyperkalemia, angiotensin-II, ACT, and hyponatremia, in reducing order of efficacy.

• Stimulation in response to hyperkalemia -
o Most important renal regulation of body potassium balance.
• In response to angiotensin II -
o Through renin-angiotensin system.
• In response to ACTH -
o Results in diurnal variation of aldosterone secretion.
57. GLUCOCORTICOIDS - FUNCTIONS & REGULATION

GLUCOCORTICOIDS - FUNCTIONS & REGULATION
• Adrenal cortex is essential for life.
Glucocorticoids:
• Secreted by Zona fasciculata - Middle layer

• Referred as "Glucocorticoid" widespread effect on glucose (and protein) metabolism.
• Highly essential hormone for life.
• Chief natural glucocorticoids - Cortisol
• All corticosteroid hormones act on intracellular cytoplasmic receptors
Functions:
• Primary role - Help body cope with acute or chronic stress.

o To execute "Fight" / "Flight" response
Effects:
1. Carbohydrate metabolism -
• Corticosteroids promote gluconeogenesis & glycogenesis in liver.

• Reduce peripheral utilization of glucose in most tissues except "Brain & Heart".
• Facilitating action:Combined result,
o Presence of cortisol - Glucagon & adrenaline is more effective in producing muscle
glycogenolysis.
2. Protein metabolism -
• Cortisol has both catabolic (in muscles) & anabolic (in liver) effects.
• In muscle -
o Cortisol inhibits protein synthesis
o Enhances protein breakdown (proteolysis)
• In Liver -
o Cortisol has an anabolic effect
o Increases synthesis of enzymes involved in hepatic proteins production
Overall effect -
• Anti-anabolic (catabolism).
o Hence, excess cortisol (Cushing syndrome) causes negative nitrogen balance

3. Fat metabolism -
• Cortisol promotes lipolysis

• FFA level is increased due to lipolysis.
4. Effect on blood cells -
• Reduces no. of circulating lymphocytes, eosinophils & basophils.
5. Anti-growth effects -
6. Leads to osteoporosis & delayed wound healing.
3. Actions during inflammatory process -
• Corticosteroids induce production of lipocortins

• Results phospholipase A2 inhibition.
58. CALCITROPIC HORMONES
CALCITROPIC HORMONE
VITAMIN D/CHOLECALCIFEROL
Synthesis process:
• Keratinocytes of stratum corneum of epidermis of skin contain 7-dehydrocholesterol converted to

Vitamin D3
Step 1:
Action of sunlight (UV light)
7-dehydrocholesterol Converted to Vitamin D3 (Cholecalciferol)
Step 2:
Enzyme hydrolase
Vitamin D3(Cholecalciferol)Calcidiol(Calcifediol/25-hydroxycholecalciferol/25 hydroxyvitamin D3)

In liver
• Calcidiol - Major circulating form of vitamin D3.

Step 3:
Hydroxylation
Calcidiol Calcitriol (1-25 dihydroxy-cholecalciferol/1-25 dihydroxy vitamin D3)
In Kidney
• Final hydroxylation in kidney is rate limiting step

• Calcitriol is active form of vitamin D3
Important points:
• Vitamin D is considered as "Hormonal vitamin".

• On high levels of Ca2+
• Little calcitriol is produced
• Relatively inactive metabolite 24, 25 di-hydroxycholecalciferol produced.
• Osteoclasts do not have any calcitriol receptor.
Lab tests:
• Measurement of blood levels of 25 dihydroxy vitamin D / Calcifediol

• Accurate information on Vitamin D status.
PARATHORMONE/PARATHYROID HORMONE/PTH:
• Osteoclasts do not have any PTH receptor.
RELATIONSHIP BETWEEN CALCIUM & PTH:
• PTH raises plasma Ca2+ in three ways.
1. Mobilizes bone Ca2+
• By increasing bone resorption
2. Increases gastrointestinal absorption of Ca2+ indirectly.
• Activating 1- alpha-hydroxylase, resulting in calcitriol formation.
3. Increases Ca2+ reabsorption in distal tubules of kidney
4. Increasing renal synthesis of 1,25 dihydroxy D3 (Calcitriol) in proximal tubules.
CALCITONIN:

• Produced by Parafollicular 'C' cell of thyroid (Major source)
Regulation:
• Rise in plasma Ca2+ Increases calcitonin release

• Fall in plasma Ca2+ Decreases calcitonin release
Major physiological actions:
1. Decreases calcium levels by,
Action on Bone:
• Inhibits bone resorption

• By direct action on osteoclasts
• Osteoclasts have receptors for calcitonin
59. MENSTRUAL CYCLE
MENSTRUAL CYCLE
• Four cycles are involved in menstrual cycle:

o Ovarian cycle.
o Uterine/Endometrial/Menstrual cycle
o Cervical cycle
o Vaginal cycle
• Length of typical menstrual cycle - Approx. 28 days.

• Menstrual cycle is counted from 1st day menstruation/menstural bleeding.
• Ovulation occurs appox. on 14th day.
• Length of post-ovulatory period appox. 14 days.
• Interval between ovulation & end of cycle is essentially constant at 14 days, irrespective
of cycle length.
• First 14 days - Follicular development; Hence referred as "Follicular phase".
• Changes of "Preovulatory/follicular phase" are due to physiological effects of estrogen.
• Also referred "Estrogenic phase".
• Inside graffian follicle, ovum is surrounded by granulosa cells.
• Granulosa cells contain FSH receptors, secretes estrogen & inhibin
• Ovarian granulosa cells are "Primary source of circulating estrogen"
• Theca interna cells are essential for estrogen production.
• Since they secrete androgen aromatizing to estrogen.
• Early growth of follicles influenced by FSH action.
• FSH stimulates granulosa cells secreting estrogen.
• LH indirectly influences estrogen secretion.
• By stimulating theca interna cells to increase androgen synthesis, which in-turn are taken up by
granulosa cells & converted to estrogen by aromatase.
• Just before ovulation –
• FSH secretion gradually declines
• Plasma estrogen concentration reaches critical level
• Midcycle LH surge is responsible for ovulation.
• Onset of LH surge is fairly precise indicator of ovulation.
• Post-ovulatory phase also referred as "Luteal phase".
• Because LH initiates luteinization process.
• Luteal cells synthesise & secrete both progesterone, estrogen & inhibin.
• Concentration of both progesterone & estrogen peak in mid-luteal phase (20-22 days of cycle).
• Luteal/post-ovulatory phase is also called Progestational phase.
• Since progesterone secreted in greater amounts.
• Progesterone is associated with a 0.5°C rise in basal body temperature
• Occurs immediately after ovulation.
• If ovum is not fertilized, Corpus luteum starts degenerating due to decline in LH levels.
• Since LH required for corpus luteum maintenance.
• Happens around day 24 of cycle.
• (About 10 days after ovulation).
• Human Ovum remains fertile for 12-24 hours after ovulation.
• On fertilization, Corpus luteum is maintained under influence of HCG secreted from placenta.
• Placental HCG continues to secrete estrogen & progesterone till third month of pregnancy.
• Progesterone inhibits LH.
• Inhibin inhibit FSH.
• Estrogen, whose secretion stimulated by both LH & FSH
• But in-turn estrogen inhibits both LH & FSH
• During uterine cycle, Progesterone is more important & responsible for secretory changes.
• Progesterone peaks on 21st day.
• Mammals other than primates do not menstruate & their sexual cycle referred as"Estrous cycle".
60. LACTATION
LACTATION
• Estrogen influences mammary duct proliferation & growth.

• Progesterone influences lobuloalveolar system development.
• Lactogenesis is milk synthesis & secretion from breast alveoli influenced by prolactin.
• Galactokinesis influenced by Oxytocin.
• Oxytocin stimulates myoepithelial cells contraction in mammary alveoli & lactiferous ducts.
• Oxytocin is released on nipple stimulation during sucking.
• Galactopoiesis is process of lactation maintainence influenced by prolactin.

61. OVARIAN HORMONES
OVARIAN HORMONES
ESTROGEN:
• Primarily secreted by granulosa cells of ovarian follicles, corpus luteum & placenta.
• Estradiol - Major estrogen secreted by ovary.
Receptors:
• Two ERs designated ER-α & ER-β.

• ER-β receptor present in Ovaries.
Major physiological actions of estrogen:
1. Metabolic effects:
• Maintain bone mass by reducing bone resorption.

• Decrease LDL while increasing HDL & triglycerides
PROGESTERONE:
• 21 carbon steroid.
Major physiological actions:
1. In Uterus
• Progesterone withdrawal (Lack of progesterone support) causes mucosal shedding &

bleeding during menstruation.
2. On Body temperature:
• Causes a slight (0.5°c) rise in body temperature.
3. On Metabolism
• Raises LDL
• Lowers HDL
4. On Pituitary

• Inhibits LH secretion by feedback inhibition - "Anovulatory action"
OTHER OVARIAN HORMONES:
1. Inhibin:
• Secreted by granulosa cells & corpus luteum in ovary & Sertoli cells in males.
• Inhibits FSH secretion in feedback manner.
62. NEUROENDOCRINE RESPONSE TO STRESS
NEUROENDOCRINE RESPONSE TO STRESS
• Sudden exposure to any type of stress initially produces sympathetic alarm reaction.
• Eg: Seen typically in patients undergoing major abdominal surgery - "Surgical Stress"
EVENTS:
1a) Leads to increased hormonal secretion -
• ACTH
• Glucocorticoid - Cortisol
• Growth hormone
• Adrenal medullary catecholamines (epinephrine)
• Thyroxine
• Antidiuretic hormone
1b) Decreased hormonal secretion seen with -
• Pituitary gonadotropin (LH, FSH).
2. Sympathetic reaction:
2b) On Pancreas:
• Increased pancreatic sympathetic discharge depressing insulin secretion.

• Promotes glucagon secretion.
3. Renal reaction to stress:
• Activation of Renin-angiotensin system

• Increases secretion of renin, angiotensin II & aldosterone.

METABOLIC EFFECTS DURING STRESS
1. On protein metabolism:
• Most important metabolic change in stress.

• Causes "Catabolism".
• Loss of lean body mass (mainly muscle proteins).
• Due to Cortisol.
2. On Carbohydrate metabolism:
• Causes Hyperglycemia due to,

o Suppression of insulin secretion.
• Coupled with increased secretion of hormones like -
o Glucagon.
o Growth hormone.
o Glucocorticoids (cortisol).
o Catecholamines (epinephrine & norepinephrine).
63. GASTROINTESTINAL HORMONES
GASTROINTESTINAL HORMONES
1. Gastrin family:
• Gastrin
• Cholecystokinin (CCK)
2. Secretin family:
• Secretin
• Glucagon
• Vasoactive Intestinal Polypeptide (VIP).
• Gastric Inhibitory Polypeptide (GIP).
3. Other:
• Motilin
1. GASTRIN
• Polypeptide.
• Produced mainly by,
• G cells of gastric mucosa in stomach antrum.
• lso present in Pituitary gland, Brain & Nerves and in Fetal pancreatic islets.
Forms:
• G -17 - Principal form of gastrin causing gastric acid secretion.
1. Increasing gastrin secretion:
• Presence of protein digestion products in stomach

• Especially tryptophan & phenylalanine
• Gastric distension.
• Vagal stimulation.
2. Inhibiting gastric secretion:
• Acid in stomach inhibits gastrin secretion.

• Mechanism:
o Partly by direct action on G cells.
o Partly by somatostatin release inhibiting gastrin release.
• Other hormones inhibiting gastrin secretion include,
o Secretin.
o VIP.
o Glucagon.
o Calcitonin.
Major Physiological actions:
• Stimulation of gastric acid & pepsin secretion.

• Stimulation of gastric motility
2. CHOLECYSTOKININ (CCK)/ "Cholecystokinin-Pancreozymin"(CCK-PZ)
• Secreted by cells in upper intestinal mucosa

• I cells in small intestine (Duodenum, jejunum & ileum).
Stimulus for secretion:
• Products of protein digestion i.e., amino acids & peptides

• Presence of long chain fatty acids (>10 carbon atoms) in duodenum
• Acts through group IIC hormonal mechanism
Functions:
• Stimulates pancreatic acinar cell enzymes secretion.
• Causes contraction of gall bladder.
• Relaxation of sphincter of oddi.
• Secretion of enzyme-rich pancreatic juice.
• Potentiates action of secretin on pancreas.
• Inhibits gastric emptying
• Increases motility of small intestine & colon.
• Increases enterokinase secretion
• Produces satiety
• Augments contraction of pyloric sphincter.
o Prevents reflux of duodenal contents into stomach.
3. SECRETIN:
• Secreted by "S" cells located in duodenum & jejunum.

• Most important stimulus - Presence of acid in duodenum.
• Also by protein digestion products contact with duodenal & jejunal mucosa.
Functions:
• Stimulates secretion of watery, alkaline (bicarbonate-rich) "Pancreatic fluid".

• "Poor" in enzymes.
• Potentiates CCK action on pancreas.
• Increases hepatic secretion of bile.
• Decreases gastric acid secretion.
• Increases tone of pyloric sphincter.
• Decreases rate of gastric emptying.
• Inhibits gastrin secretion.
64. SYNTHESIS OF THYROID HORMONE
SYNTHESIS OF THYROID HORMONE
• Both T4 & T3 are iodine derivatives of thyronine.

• Thyronine - condensation product of two molecules of amino acid tyrosine.
PRODUCTION STEPS:
• Iodide uptake via "Secondary active transport"- Na2+: I- symporter in folllicular cells.
• Trapping is TSH stimulated.
• Na2+: I- symporter also found in,
• Salivary glands.
• Mammary glands.
• Placenta.
• Oxidation, iodination, coupling & thyroglobulin proteolysis are TSH stimulated.
• Thyroid hormones are stored in thyroid follicles for 2-3 month.
• Wolff- Chaikoff Effect: Excess iodide inhibits its self-transport in thyroid cells, results in
reduced T4 / T3 synthesis.
65. GASTROINTESTINAL MOTILITY
GASTROINTESTINAL MOTILITY
• BER initiated by Pacemaker cells called "Interstitial cells of Cajal".

• Threshold for action potential is -50 mV.
• Rate of BER:
o About 4/min in stomach.
o About 12/min in duodenum.
o About 8/min - distal ileum (falls down).
o In Colon - Rate rises from about 2/min at Cecum about 6 min at Sigmoid colon
Pacemaker cells -
• Interstitial cells of Cajal.

• Are absent in esophagus & proximal stomach.
• In distal stomach & small intestine - Located in outer circular muscle layer near myenteric plexus.
1. MOTILITY IN STOMACH:
• Gastric contraction.
• Gastric emptying.
2. MOTILITY IN SMALL INTESTINE:
• Propulsive movement (Peristalsis).

• Mixing movement/Segmentation.
3. MOTILITY IN LARGE INTESTINE:
• Propulsive movements.
• Mixing movements / Haustrations
Reflexes involved:
1. Gastrocolic & Duodenum reflex:

• Facilitates appearance of mass movements after a meal.
• Ex., For gastrocolic reflex –
• Seen in early infancy.
• Where defecation often follows a meal.
• Maximum post-prandial motility seen in proximal part of descending colon.
2. Defecation reflex / Rectoanal inhibitory reflex:
• Initiated by distension of rectum with feces.

• Leads to propulsive wave extending from descending colon through sigmoid colon to rectum.
• Also referred"Rectoanal inhibitory reflex".
Transit time:
• From sigmoid colon to anus, slower transport & quarter of test meal residue retained in rectum
upto 3 days.
• Food residue spends more than 20 hrs in colon before lost in feces
66. DIGESTION IN SMALL INTESTINE - MOTILITY, SECRETION & CONTROL
DIGESTION IN SMALL INTESTINE - MOTILITY, SECRETION & CONTROL
Propulsive movement:
• Referred as "Peristalsis".
• Stimulus - Distention of gut
Activation:
1. Neuronal activation factors:
• Requires an active myenteric plexus.

• Local stretch by chyme releases serotonin, which activates myenteric plexus.
• VIP, NO & ATP → Producing relaxation ahead of stimulus
• Acetylcholine & substance P → Causing smooth muscle contraction.
2. Hormonal activation factors:
• Gastrin, Cholecystokinin, insulin, motilin & serotonin enhance intestinal motility.
3. Hormonal inhibiting factors:
• Secretin & glucagon inhibit small intestinal motility.

• Can be increased/decreased by autonomic input to gut.

• Occurrence is independent of extrinsic innervation.
Peristaltic rush -
• Very intense peristaltic wave.

• Not seen in normal individuals.
• Occurs on intestinal obstruction.
2. MIXING MOVEMENTS:
• Also referred "Segmentation".
REFLEXES INVOLVED:
1. Gastroileal reflex:
• Increased secretory & motor activity of the stomach.

• Occurring normally after a meal,
o Increases motility of ileum.
o Mediated by gastrin.
2. Ileogastric reflex & Intestointestinal reflex.
67. DIGESTION IN LARGE INTESTINE - MOTILITY & REFLEXES
DIGESTION IN LARGE INTESTINE - MOTILITY & REFLEXES
1. Mixing movement/Haustrations:
• Resulting in a division of large intestine into very distinct segments called "Haustra".
• Hence "Haustration".
2. Propulsive movement/Mass movement/Mass peristalsis/Mass contraction"
• Modified peristalsis type.
REFLEXES:
1. Ex., For gastrocolic reflex -

• Seen in early infancy.
• Where defecation often follows a meal.
• Maximum post-prandial motility seen in proximal part of descending colon.
2. Defecation reflex:
• Initiated by distension of rectum with feces.

• Leads to propulsive wave extending from descending colon through sigmoid colon to rectum
• Urge to defecate is first felt when rectal pressure increases to about 18 mm/Hg.
• On reaching 55 mm/Hg rectal pressure -
o "Rectoanal inhibitory reflex" - Internal sphincter relaxes reflexly.
Transit time:
• From sigmoid colon to anus, slower transport & quarter of test meal residue retained in rectum for
upto 3 days.
• Food residue spends more than 20 hrs in colon before lost in feces.
68. THYROID HORMONE - METABOLISM, TRANSPORT & REGULATION.
THYROID HORMONE - METABOLISM, TRANSPORT & REGULATION
• T4 & T3 - Iodine derivatives of thyronine.

• Thyronine - Condensation product of two molecules of amino acid tyrosine.
Properties:
• T4 - "Prohormone of T3".
• Most T4 secreted by thyroid is converted to T3 in liver, kidney & pituitary, by action of enzyme 5'-
deiodinase.
• T3 -"Principal Thyroid Hormone".
• Half-life of T4 - 6 days.
• T4 - Major circulating hormone.
• Half-life of T3 - 1 day.
• T3 - More avidly bound to nuclear receptor than T4.
• T3 - More potent & acts faster.
• Hence, T3 - Active hormone.
• T4 - Mainly a transport form & functions as "Prohormone of T3".
• Only 20% circulating T3.
TRANSPORT:
Thyroxine-binding globulin-
• Major thyroid hormone binding protein.
• Level increase in pregnancy & by drugs estrogens, methadone, heroin, tranquilizers & clofibrate.
• Level decreased by glucocorticoid, androgen, danazol, asparaginase (Cancer
chemotherapy) & nephrotic syndrome.
METABOLISM:
• Transport across target cells affected by number of transport proteins -

• Includes monocarboxylate transporter 8 (MTC 8) & organic anion
transporter polypeptide 1C1(OATPIC1) in brain.
• Metabolized in liver
o By deiodination, deamination & finally conjugation with glucuronic acid.
REGULATION:
• Thyroid activity is TSH controlled.

• Thyroid secretion is regulated in "Classical Negative Feedback" mechanism.
69. THYROID HORMONE - FUNCTIONS
THYROID HORMONE - FUNCTIONS
• Three forms of thyroid hormone receptor - TR - α1, TR - β1 & TR - β2.

• Fourth isotypes TR- α2 is unable to bind thyroid hormone.
TR - β1 - Predominantly expressed in brain, liver & kidney.
FUNCTIONS:
• Thyroid hormones enhance oxygen consumption & hence, BMR.

• On Carbohydrate metabolism: Net effect - Hyperglycemia & depletion of glycogen.
• On Fat metabolism - Stimulates both lipogenesis & lipolysis.
• On Protein metabolism - Has an anabolic effect, yet large doses has catabolic effect.
• Net effect: Increases both protein synthesis & protein degradation.
• On Cardiovascular system:
• Increases heart rate, cardiac contractility, stroke volume & cardiac output.
• Reduces diastolic BP.
• Due to vasodilatation in several vascular beds.
• Decreased peripheral vascular resistance.
• Effects are partly mediated by potentiation of effects of catecholamines.
• Role in temperature adaptation:
o Associated with cold adaptation.
o Increased thyroxine release

70. INSULIN - RECEPTORS AND REGULATION OF SECRETION
INSULIN - RECEPTORS AND REGULATION OF SECRETION
Insulin:
• Two-chain polypeptide hormone, with 51 amino acids.

• Structure:
• 2 chains - A-chain - 21 amino acids; B-chain - 30 amino acids.
• Half-life: About 5 mins.
Synthesis:
• Synthesized as larger preprohormone (Pre-proinsulin)

• Converted to "Prohormone" (Proinsulin).
• Proinsulin structure - Made up A & B chain, connected by C-peptide/chain.
• Normally, 90% - 97% insulin from B cells,
• Along with equimolar amounts of C-peptide.
RECEPTORS:
• Combination of four subunits.

• 2 Beta subunits -
• Gets attached locally to tyrosine kinase.
• Hence, insulin receptor is an example of enzyme-linked receptor.
• Insulin belongs to group IID hormone.
REGULATION:
1. Plasma glucose concentration:
• Increased plasma glucose concentration stimulate insulin release.

• Glucose entry is "Insulin-independent" via GLUT-2.
• Glucose metabolized to pyruvate.
• Ca2+ influx causes insulin efflux from secretory granules (secretion).
FACTORS INFLUENCING:
1. Stimulating factor:
• Glucose - Relationship between glucose concentration & insulin secretion is "SIGMOIDAL"

• Intestinal hormones -
o GIP.

o Gastrin.
o Secretin.
o CCK
• GLP -1.
• Parasympathetic stimulation - via acetylcholine.
• Endocrine hormones - Growth hormone, Glucagon & Glucocorticoids.
2. Inhibiting factors:
• α-adrenergic stimulation.
• K+ depletion
LATEST RESEARCH POINTS:
• GLP-1 (7-36):
o Glucagon-like polypeptide 1 (7-36)

o GLP-1 - More potent insulinotropic hormone.
71. SODIUM-POTASSIUM PUMP
SODIUM-POTASSIUM PUMP/Na+- K+ ATPase/Na+- K+ pump
• Most important pump for primary active transport in body.

• An Electrogenic pump.
• Na+- K+ pump extrudes –
• 3 Na+out from cell
• Pumps 2 K+ into cell
• Coupling ratio of Na+- K+ pump is 3:2.
• Both Na+ & K+ are transported against concentration gradient.
• Na+- K+ pump uses energy by hydrolyzing ATP; this pump contain ATPase activity
• Na+- K+ pump - Carrier protein – Heterodimer
• Na+- K+ transport occurs through α-subunits.
• Intracellular portion of α-subunit has,
• Three Na+ binding/receptor sites for Na+.
• An ATP binding site.
• A phosphorylating site.
• ATPase activity.
• Extracellular portion has,
• Two K+ binding/receptor sites for K+.
• An Ouabain binding site.
• β-subunit has three extracellular glycosylation site.

• Na+ - K+ pump contributes only 4 millivolts to total resting membrane potential of 90 volts which
is almost negligible.
• Active transport of Na+ & K+- One of major energy-using process in body.
72. CARDIAC MUSCLE CONTRACTIONS
CARDIAC MUSCLE CONTRACTIONS
• Cardiac muscle contraction are initiated by Ca2+.

• Increased cytoplasmic/sarcoplasmic Ca2+ cause contraction.
• AP generation causes Ca2+ influx within cardiac cell via L-type of Ca2+ channels in sarcolemma.
• Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum to sarcoplasm via
ryanodine receptors.
• Phospholamban is the regulatory protein present in cardiac muscles.
• Normally sarcoplasmic reticulum calcium pump/SR Ca2+- ATPase/SRCA, transports Ca2+ into SR
lumen causing muscle relaxation.
• Phosphorylation of phospholamban is activated by β-adrenergic stimulation with help of
protein kinase 'A'.
• On phospholamban phosphorylation, its inhibitory effect on SRCA is relieved.
• This causes increased Ca2+ uptake into sarcoplasmic reticulum from sarcoplasm of cardiac muscles.
• Also produces positive chronotropic effect - Increased heart rate.
• Phospholamban is called "Critical Repressor of Myocardial Contractility".
• Because of positive inotropic effect.
• Type of calcium channels in skeletal, smooth & cardiac muscles - L-type channels.
73. SKELETAL MUSCLE CONTRACTIONS - CHARACTERISTICS
SKELETAL MUSCLE CONTRACTIONS -CHARACTERISTICS
• Characteristics of skeletal muscle contractions include:

o All or none law.
o Stimulus-response relationship.
o Frequency of stimulus.
o Motor unit recruitment.
o Starling's Law.
o Isometric contractions
o Muscle Tone.
o Denervation hypersensitivity.
• Motor unit obey all or none law.

• Unit of activation - Nerve fiber.
• Unit of contraction - Motor unit.
• 3-6 fibers in a motor unit
o Seen with muscles for fine graded & precise movement
o Eg: Fingers & eye.
• Contractile response depends on strength of stimulus.

• With increasing stimulus strength Number of contracting motor units increase.
• Larger number of motor units contracting Stronger muscle contraction.
• Strength of contraction is increased by increasing frequency of stimulation.
• This, in turn increases frequency of activation of motor units.
• Tetanus is due to summation of twitches.
• On stimulating muscle in rapid succession, there is progressive sarcoplasmic Ca2+ accumulation.
• Tetanic tension is reached when sarcoplasmic Ca2+ levels reach their maximum.
• Tetanic tension is about four times the twitch tension.
• Larger motor units recruited on insufficient power generation.
• "Henneman principle"/ "Size principle":
o Order of recruitment from smaller to larger motor unit.
o This increases contraction strength
• According to Starlings law, there is an optimal length at which force generated by a muscle
is maximal.
• Isotonic contraction: Contraction in which there is change of length at constant tension.
• Isometric contraction: Contraction in which there is constant length with increased tension.
• Hence, generates more force of contraction/tension.
• Muscle strength is best increased by isotonic exercise.
• Exercises one does in the gym are isotonic exercises as muscle length changes in each step but not
tension.
• Tonus involves γ-motor neuron activity leading to muscular contraction.
• Fine irregular contraction of individual fiber appears, referred as "Fibrillation".
• Fasiculations - Jerky, visible contractions of muscle group.
• Type II motor units:
o Type IIa/"Fast-Fatigue Resistant" (FR) units.
o Type IIb/"Fast-Fatigable" units.
Factors increasing force of muscle contraction include:
• Increased number of motor units.

• Increasing frequency of stimulus (Tetanic stimulus)
• Larger motor unit recruitment (Henneman principle)
74. MUSCLE SPINDLES
MUSCLE SPINDLE
• Are "Stretch receptor" located within muscle.

• 'Intrafusal fibers' - Specialized muscle fibers seen within spindle .
TYPES OF INTRAFUSAL FIBERS:
1. Nuclear bag fibers -
o 2 per spindle.
• Nuclear bag fiber 1 -

o With low level of myosin ATPase activity.
• Nuclear bag fiber 2 -

o With high level of myosin ATPase activity.
2. Nuclear chain fibers:
• Are thinner & shorter.

• Four or more fibers per spindle (more than nuclear bag fibers).
DIVISIONS OF INTRAFUSAL FIBERS:
• Central/equatorial region:
o Does not contain contractile protein.
o Hence, non-contractile portion of muscle spindle.
o Are more sensitive to stretch & acts as "Stretch receptors".
• Peripheral region:
o Contain contractile proteins.
o Hence, contractile part of muscle spindle.
• Greater concentration of spindles found in -

o Lumbrical muscles of hand.
o Suboccipital muscles.
o Extraocular muscles.
• Two types of sensory/afferent innervation of muscle spindle:
• Annulospiral/primary endings:
o Found wound around central region of both nuclear bag & nuclear chain fiber.
o Are "Aα" / "Ia" fibers.
• Flower-spray/secondary endings:
o Innervates peripheral parts/ends of nuclear chain fiber.
o Are "Aβ" / "II" fibers.

• Motor innervation/efferent of muscle spindle:
o Innervates peripheral parts of both nuclear bag & nuclear chain fibers.
o Mainly by "Aγ" type.
Also referred "γ-motor neurons"/"Fusimotor neuron" /"Small motor nerve system
of Lekcell efferents".
Because of their characteristic smaller size.
• γ1/dynamic γ-fibers:
o Innervates nuclear bag fiber.
o Their terminals are called 'Plate ending'.
• γ2/static γ-fibers:
o Innervates nuclear chain fibers.
o Their endings are called 'Trail ending'.
75. SENSORY RECEPTORS
SENSORY RECEPTORS
TYPES OF SENSORY RECEPTORS:
• Exteroreceptors.
• Proprioceptor
• Interoceptors/Visceroreceptors.
EXTERORECEPTORS:
1. General exteroreceptors:
1a) Cutaneous mechanoreceptors -
• Superficial
o Detect touch.
o Slowly adapting Merkel's disk.
o Rapidly adapting Meissner's corpuscle.
• Deep
o Detect deep touch, pressure, & Vibration.
o Slowly adapting Ruffini's end organ.
o Rapidly adapting Pacinian corpuscle.
1b) Thermoreceptors:

• Warmth receptors & Cold receptors.
1c) Nociceptor / Pain receptors:
• Thermal nociceptors.
2. Special Exteroreceptors:
• Chemoreceptors: Gustatory receptors (taste buds) & olfactory receptors.
INTEROCEPTORS / VISCERORECEPTORS:
TYPES:
• General interoceptors:
o Chemoreceptors - Osmoreceptors.
o Glucoreceptors.
76. FEATURES OF SENSORY RECEPTORS
FEATURES OF SENSORY RECEPTORS
Features include,
• Generator potential/Receptor potential.

• Adaptation.
• Coding of intensity of stimulus (Intensity discrimination).
• Sensory unit & receptor field.
• Law of projection (Sensory projection).
• Muller's law of specific nerve energies.
• Proprioceptive sensations.
1. ADAPTATION:
• When steady stimulus is applied to a receptor Frequency of action potential generated declines
gradually.
• This gradual decline in receptor response referred as "Adaptation".
Based on development of speed of adaptation, sensory receptors are divided into -
1a. Tonic receptors:
Subtypes:

• Adapt slowly (slow adaptation): Proprioceptors, Merkel's disc & Ruffini's end organ.
• Non-adapting receptors: Nociceptors (pain receptors), vestibular receptors & muscle spindle.
1b. Phasic receptors:
• Receptors showing fast adaptation.

o E.g. Meissner & Pacinian corpuscles.
2. CODING OF INTENSITY OF STIMULUS /INTENSITY DISCRIMINATION:
2a. Frequency coding:
• At level of an individual receptor frequency of action potential generated is proportional to

magnitude of generator potential
o In turn, magnitude of generator potential is dependent on intensity of stimulus.
• Hence,
o If intensity of stimulus increased Increases amplitude of generator potential.
o In turn, Increases firing rate of sensory neuron (frequency of action potentials generated).
2b) Population coding:
• As intensity of stimulus increases Number of receptors stimulated increases

• I.e. sensory recruitment.
• Note: Magnitude of sensation felt is proportional to log of stimulus intensity.
o Referred as "Weber-Fechner law".
3. SENSORY UNIT AND RECEPTOR FIELD:
3a. Sensory unit:
• Dendritic ends of a single neuron are connected to several superficial sensory receptors.
o Such neuron, with all its peripheral terminals & their attached receptors, referred as
"Sensory unit".
3b. Receptor field:
• Receptors detecting sensations from larger surface area is referred as "Receptor area"
Summary:

• Sensory unit (a sensory neuron with its connected superficial receptors) detects touch from an
area.
• Receptor field detects sensations greater than from area detected by a single receptor.
3c. Two point discrimination:
• Is "Minimum distance between two points that can be perceived as a separate point stimulation.
• Measure of tactile acuity or sensory acuity.
• Surface area of receptor field:

• Smaller the receptor field More acute will be power of two-point discrimination.
• I.e., Greater sensory (tactile) acuity.
• Stimulation points on the back must be separated by at least 65 mm before being distinguished as
separate
• Conversely, on fingertips, two stimuli are recognized with a minimum separation distance of 2 mm.
3d. Lateral inhibition:
• Responsible for localization of stimulus site & two-point discrimination.
3e. Receptor field overlapping:
o Greatest overlap seen with pain receptors.

o Relatively less receptos field overlaps with tactile receptors.
Variations in sensation loss:
• On cutting a spinal nerve, variations occur with sensation loss.

• In Tactile sensation:
• Area of tactile loss is greater than pain.
• Because lost tactile receptor area has less overlapping fibers from adjacent receptor areas.
• Resulting in loss of tactile sensation in more area.
• W.r.t temperature:
• Receptor area of thermoreceptors does not show any overlap.
o Hence, area of temperature loss will be maximum.
4. LAW OF PROJECTION/SENSORY PROJECTION:
• Typical example is "Phantom limb".
5. PROPRIOCEPTIVE SENSATIONS:

o I.e. Sense of position for tendon & muscle and Sense of equilibrium.
Types of proprioceptive sensations:
• Static & Kinesthesia.

• Kinesthesia - Sense of degree of movement.
Receptors & nerve involved:
• Receptors for sense of position - Chiefly located in joint capsules & ligaments around joint.
• Most important receptors - Ruffini's end organs
• ensations are carried by thick myelinated nerve fibers
• I.e. Group I (Aα) - All proprioception
• Group II (Aβ) for kinesthesia to Dorsal columns of spinal cord.
• Ultimately, conscious proprioceptive sensations reach somatic sensory cortex.
77. GENERAL EXTERORECEPTORS
GENERAL EXTERORECEPTORS
• Provide information about external environment, like touch, pressure, temperature, light, sound,
taste, & smell.
TYPES OF GENERAL EXTERORECEPTORS:
• Cutaneous mechanoreceptors, Thermoreceptors & Nociceptors.
SUBTYPES:
1a) Cutaneous mechanoreceptors/Tactile/Touch receptors -
• Superficial & deep receptors.
1b) Thermoreceptors/temperature receptors:
• Warmth receptors & Cold receptors.
1c) Nociceptor/Pain receptors:
• Thermal nociceptors, Mechanical nociceptors, Polymodal nociceptors & Silent nociceptors.
TYPES OF SENSATIONS RELATED TO EXTERORECEPTORS:
• Epicritic sensations & Protopathic sensations.

• Protopathic sensations:
o Involve pain & temperature sense.
o Mediated by receptors with free nerve endings.
CUTANEOUS MECHANORECEPTORS/TACTILE/TOUCH RECEPTORS:
1a. Superficial receptors:
• Present in epidermis or papillary layer of dermis.

• In glabrous (nonhairy) skin, receptors are,
o Merkel's disc (slowly adapting).
o Meissner's corpuscle (rapidly adapting).
1b. Deep receptors:
• Includes Ruffini's end organ (slowly adapting) & Pacinian corpuscle (Rapidly adapting).
Receptors and its adaptability:
1. Slowly adapting:
• Ruffini's end organ -

o Meant to detect sustained pressure.
o Useless for vibrations.
2. Rapidly adapting:
• Pacinian corpuscle -
o Useful to detect vibrations.
• Meissner's corpuscle -
o Detect surface texture.
Receptors & sensation detected:

1. Superficial sensations:
• By Meissner's corpuscle (detect surface texture i.e. rough or smooth)
2. Deep sensations:
• Pressure (Deep touch) - Detected by Rufini organ.

• Vibrations - Detected by Pacinian corpuscle.
SUMMARY:
1. Superficial cutaneous receptors:
• Merkel's disk -
o Slowly adapting & detect two-point discrimination.
• Meissner's corpuscle -
o Rapidly adapting & detect surface texture.
2. Deep cutaneous receptors:
• Ruffini's end organ -

o Slowly adapting & detect sustained pressure/deep touch.
• Pacinian corpuscle -
o Rapidly adapting & detect vibrations.
PAIN RECEPTORS/NOCICEPTORS:
• These are receptors with free nerve endings.

• Thermal nociceptors important subtype.
TEMPERATURE RECEPTORS/THERMOCEPTORS:
• Cold & warmth receptors.
NERVE FIBERS FOR PAIN & TEMPERATURE:
• Pain and temperature are carried by Aδ (type III) & C (type IV) sensory neurons.
• For temperature:
o C (Type IV) neuron - Both cold & warmth.
78. THERMO-REGULATORY MECHANISM
THERMO-REGULATORY MECHANISM
• Temperature of body is determined by "Thermostat".

• Thermoregulatory center - In preoptic area of hypothalamus.
• Anterior hypothalamus responds to heat
• Posterior hypothalamus respond to cold (shivering center)
• Hypothalamic thermostat setpoint - 37°C.
THERMOREGULATORY EFFECTOR MECHANISMS:
1. Mechanisms activated by cold / Mechanism of heat gain:

1a. Increased head production:
• Shivering.
• Increased catecholamines secretion.
• Increased thyroxine secretion.
1b. Decreased heat loss:
• Cutaneous vasoconstriction.
• Piloerection -
o Important for animals with fur or feathers but not for human
2. Mechanism activated by heat/Mechanism of heat loss:
2a. Increased heat loss:
• Sweating
• Cutaneous vasodilation (Earliest response).
• Earliest response to heat stress - Cutaneous vasodilatation
NON-SHIVERING THERMOGENESIS/CHEMICAL THERMOGENESIS:
• Important in young mammals & in adults of small species.

• In human nonshivering thermogenesis seen only in neonates & young infant.
• Due to brown fat & underdeveloped shifting mechanism in neonates.
• Adults do not have brown fat -
o Hence, chemical thermogenesis is not important.
1. Brown fat:
• Amount of chemical thermogenesis is proportional to amount of brown fat in tissues.

• Brown fat is important in infants.
• Found in interscapular region, subscapular region, axilla, between shoulder blades, around
neck, behind sternum, around heart, kidney, adrenal glands & around thoracoabdominal great
vessels.
• Brown fat contains large number of special mitochondria.
o Where uncoupled oxidation occurs due to uncoupler protein (UCP-1).
o These cells have sympathetic innervation, especially β3 receptors.
2. Thyroxine - Promotes chemical thermogenesis.
Events:

• Involves heat production by organ systems including liver, abdominal visceral organs, skeletal
muscles & brown fat.
• Cellular mechanisms:
o Under catecholamines control (e.g. norepinephrine).
SWEATING:
• Unique nerve supply to sweat glands - Sympathetic yet cholinergic.
HEAT ACCLIMATIZATION:
• An acclimatized individual acquires an enhanced capacity to sweat.

• I.e. Maximum sweat output is increased.
• Shows decrease in temperature threshold for sweating.
• Decreased sweat salt (NaCl) concentration.
• Due to adaptive increase in aldosterone secretion.
• Aldosterone acts mainly on kidney Decreased salt secretion in urine.
• Renal & splanchnic (liver, GIT, pancreas & spleen) vasoconstriction decreased blood flow.
ZONE OF THERMAL NEUTRALITY / THERMONEUTRAL ZONE:
• Narrow range of ambient temperature (25°-27°C).

• Normal body temperature maintained by physical mechanisms only.
o Without involvement of any regulating mechanisms.
79. INVERSE STRETCH REFLEX
INVERSE STRETCH/GOLGI TENDON/NEGATIVE STRETCH REFLEX
• Initiated by Golgi tendon organ located in muscle tendon.

• Golgi tendon organ consists of net-like (ramified) collection of knobby nerve endings among
tendon fascicles.
• About 3-25 muscle fiber per Golgi tendon organ.
• Two fiber types - High threshold & low threshold type.
Functions:
• Acts as "Stretch receptor".

• Acts as "Muscle tension-detector.
• Golgi tendon organ reflex is a protective reflex.
• By providing "Negative feedback" preventing muscle fiber damage.
• Golgi tendon reflex referred as "Autogenic inhibition reflex".
• As it produces "Autogenic Inhibition".
• Activation of Golgi tendon reflex results in muscle relaxation.
• Provide both static & dynamic responses.
• Both muscle tension & rate of change in tension.
• Golgi tendon stimulated by passive stretch & active muscle contraction.
• Golgi tendon organ innervated by Aα sensory/afferent fibers (type Ib sensory).
DIFFERENCE BETWEEN FUNCTIONS OF MUSCLE SPINDLE & GOLGI TENDON ORGAN:
• Muscle spindle - Detects muscle length.

• Golgi tendon organ - Detect muscle tension.
80. SKELETAL MUSCLE CONTRACTION & RELAXATION -MECHANISM
SKELETAL MUSCLE CONTRACTION & RELAXATION -MECHANISM
• Basic contractile unit of muscle - Sarcomere.

• Four muscle proteins are Actin, Myosin, Tropomyosin, & Troponin.
• Myosin are thick filament protein.
• Myosin-II - Specific type in skeletal muscle.
• More concentrated in H-zone (Central part of A-band).
• Acts as an ATPase.
• Actin are major protein with thin filaments.
• Slides over myosin during contraction.
• Absent in H-zone.
• Tropomyosin is thin filament protein.
• Covers active myosin binding sites on actin.
• Troponin is thin filamented Ca2+ binding protein.
• Titin connects Z-lines to M-lines.
• Act as framework holding myosin & actin filaments in place.
• Cytoplasmic/sarcoplasmic Ca2+ levels regulate muscular contraction & relaxation mechanisms.
• Increased sarcoplasmic Ca2+ concentration results in Ca2+ binding to troponin-C.
o Troponin - Ca2+complex further induces changes in Troponin-I & Troponin-T for muscle
contraction.
Important events in muscle contraction:
Discharge in motor neuron (Aα motor neuron).
↓
Release of acetylcholine at NM junction from presynaptic vesicles.

↓
Binding of acetylcholine to nicotinic (Nm) Ach receptors.
↓
Interaction of Di-Hydropyridine (DHPR) & Ryanodine (RyR) receptor in terminal cisterns of sarcoplasmic
reticulum.
↓
Ca2+ ion release from sarcoplasmic terminal cisterns through Ryanodine receptor.
↓
Increased sarcoplasmic Ca2+ concentration.
↓
Binds with troponin C & Ca2+.
↓
Lateral movement of tropomyosin with uncovering of active sites of actin.
↓
Cross-linkage of myosin with actin & Muscle contracts.
• Changes in muscle fibers during contraction:
o Z lines come closer Shortens sarcomere.

o H-band disappears.
o I bandwidth decreases.
Summary:
• First event during muscle contraction is troponin C binding to Ca2+.

o In turn, triggers tropomyosin sliding away from active sites of actin.
o Myosin cross-links with actin contracting muscle.
MECHANISM OF MUSCLE RELAXATION:

Ca2+ Pumped back into terminal cisterns of sarcoplasmic reticulum by SRCA
↓
Results in very high Ca2+ concentration in terminal cisterns & very low in sarcoplasm.
↓
Release of Ca2+ from Troponin.
↓
Tropomyosin covering active sites of actin.
↓
Cessation of interaction between myosin & actin with resultant muscle relaxation.
• ATP provides energy for power stroke of myosin head.

• Dissociates myosin head from actin filament.
• Only under low Ca2+ sarcoplasmic concentration.
• Pumps out sarcoplasmic Ca2+ into terminal cisterns of sarcoplasmic reticulum, causing muscle
relaxation.
• ATP depletion results in,
o Rigor mortis - Muscle rigidity after death.
o Muscle fatigue during severe exercise resulting in a contracted state.
81. SKELETAL MUSCLE PHYSIOLOGY - STRUCTURE & TYPES OF MUSCLE FIBERS
SKELETAL MUSCLE PHYSIOLOGY - STRUCTURE & TYPES OF MUSCLE FIBERS
• Skeletal muscle constitutes nearly 40% of total body mass.

• "Sarcolemma" - Cell membrane surrounding each muscle cell/fiber.
• Myofibril consists series of interlocking actin & myosin myofilaments.
• Presence of well-developed cross striation - Characteristics of skeletal muscle fiber.
• Sarcomere -
o Portion of myofibril between two Z lines.
o Basic contractile unit of muscle
• Two types of sarcomeric filaments -

o Thin filament (made up of actin)
o Thick filament (made up of myosin).
• H Zone -
o Comparatively lighter zone in middle of A band.
Due to non-overlapping of actin over myosin filament in central portion.
o Absence of actin filament.
o Disappears on muscle contraction.
Changes in muscle during contraction:
• Two Z-lines come closer

• H-Band disappears.
• I bandwidth decreased.
SARCOLEMMA:
Has two protein types:
• Integral/Transmembrane proteins -
o Dystroglycan.
o Sarcoglycans (SG).
• Peripheral/surface proteins:
• Dystrophin.
• Sarcotubular T-system contains "Transverse tubules"
• Infoldings of cell membrane/sarcolemma.
• Allows penetration of electrical membrane discharge to inner core of muscle cell.
• Sarcoplasmic reticulum contains high calcium concentration.
• Is concerned with sarcomeric calcium transport.
• "Triad" - Central longitudinal part with two cisterns at both ends.
• Terminal cistern is where maximum calcium is stored. Hence, "Storehouse of calcium ions".
• Foot processes are mainly of Dihydropyridine receptors (DHPR).
• Ryanodine receptors function as calcium channels.
o Gene mutation on Ryanodine receptor encoding causes malignant hyperthermia.
o Due to excessive uncontrolled calcuim release.
• Characteristics of:
o Type I/red fibers
o Type II/white fibers.
Parameters/Characteristics Type I muscle fiber Type II muscle fiber
Difference according to fiber • Red - • White -

type o Due • Have few mitochondria.
to ↑ed myoglobin &
mitochondrial
content.

Subtypes - Nil - Type IIA & Type IIB
• Oxidative & glycolytic - IIA.

• Glycolytic - IIB.
• Type II fibers usually refer
Type IIB fibers.
Other names 1. "Slow-twitch" fibers: • "Fast-twitch" fibers

o Due to bigger
• Due to small fiber length & diameter
diameter. & ↑ed myosin &
• Maintain relatively sustained actin filaments.
contraction.
• "Fast fatigable units"/Type
IIb
•
o Late recruitment
threshold
Glycolytic Low High

capacity & glycogen content
Sarcoplasmic reticulum Normal Extensive
Blood supply High Normal
Myosin ATPase activity Low High
Type of muscle • Red muscles - • White/pale muscles -
• Seen in, • Seen in hand muscles &
o Back muscles. extraocular muscles.
o Gluteus muscles
o Calf muscles.
82. PROCESS OF SYNAPTIC INHIBITION
PROCESS OF SYNAPTIC INHIBITION

• Post-synaptic/direct inhibition occurs due to inhibitory neurotransmitter release (GABA or
glycine).
• Typically seen in stretch reflex.
• Also referred as "Reciprocal inhibition" due to inhibitory interneuron/golgi tendon bottle neuron
in spinal cord, releasing glycine.
• Strychnine can antagonize direct type of inhibitions.
• In pre-synaptic/indirect inhibtiion, post-synaptic neuron is indirectly inhibited by, axo-axonic
transmission of another synapse, proximal to inhibited postsynaptic neuron.
• This results in decreased excitatory neurotransmitter release (glutamate)
• Postsynaptic neuron has been indirectly inhibited because it may develop smaller EPSP in response
to excitatory neuron activity.
• Picrotoxin inhibits presynaptic inhibition, whereas local anesthetics do not effect it.
• Renshaw cells are activated by collateral from post-synaptic neuron itself, rather than inhibition
from presynaptic neuron.
• Feed-Forward inhibition seen in cerebellum.
83. DEVELOPMENT OF POSTSYNAPTIC POTENTIAL
DEVELOPMENT OF POSTSYNAPTIC POTENTIAL
EXCITATORY POSTSYNAPTIC POTENTIAL (EPSP):
Steps:
Neurotransmitter-receptor binding on postsynaptic membrane triggers ligand-

gated Na2+ channels opening.
↓
Causes Na2+ influx & postsynaptic membrane depolarization.
↓
Increases post-synaptic neuron excitability.
Hence, "Excitatory Post-Synaptic Potential (EPSP).
Characteristics:
• Graded in nature.
• Not follows all or none law.
• Magnitude depends upon stimulus intensity.
• Stimulus here is amount of neurotransmitter released.
• Not-self propagated.
• Travels with decrement.
• May or may not be followed by an effect
INHIBITORY POSTSYNAPTIC POTENTIAL (IPSP):
Steps:
Neurotransmitter-receptor binding on postsynaptic membrane triggers ligand-gated Cl- channels opening.
↓
Causes Cl- influx & postsynaptic membrane hyperpolarization.
Also, opens ligand-gated K+ channels.
↓
Reduces post-synaptic neuron excitability.
↓
Hence, "Inhibitory Post-Synaptic Potential (IPSP).
FAST & SLOW POSTSYNAPTIC POTENTIAL:
• Slow EPSP/Slow IPSP are particularly important in autonomic-sympathetic ganglia & is very
complex.
• Fast EPSP is primary event in postsynaptic ganglionic receptor.

o Rapid depolarization mediated by acetylcholine acting on nicotinic-acetylcholine
receptors on post-synaptic ganglionic neuron.
o Due to ligand-gated Na2+ channel opening.
• Slow EPSP occurs after 1 second latency.

o Mediated by acetylcholine acting on muscarinic (M) receptors.
o Due to temporary closure of some K+ channels.
• Slow IPSP -
o Mainly due to dopaminergic & adrenergic receptors
stimulation by catecholamines products (dopamine & norepinephrine).
o Mediated by acetylcholine action on M2 muscarinic receptors.

o Due to K+ channels opening.
• Two types of summation/synaptic integration:

o Spatial summation
o Temporal summation.
• Action potential mainly generated in axon hillock & its initial segment.
o Because of their maximum concentration of voltage-gated Na+ channels
o Also are site of lowest threshold
84. EXCITATION-CONTRACTION COUPLING
EXCITATION-CONTRACTION COUPLING
• Skeletal muscle fiber is innervated by Aα motor neuron.

• Stimulated Aα motor neuron releases acetylcholine from presynaptic vesicle.
• Acetylcholine binds to specific receptors (Nm-nicotinic) on motor-end plate (post-
synaptic membrane).
• Ca2+ diffusion into sarcoplasm induces further events for muscle contraction.
• Excitation-contraction coupling mediated by calcium ions.
• Smooth muscles have no T-tubules.
• Phospholipase C breaks down Phosphatidyl-Inositol bisphosphonate (PIP2) into
inositol triphosphate (IP3) & Diacylglycerol (DAG).
• IP3 receptor interaction causes calcium release from sarcoplasmic reticulum.
• IP3 receptors exist on sarcoplasmic reticulum.
• During electromechanical coupling, sarcolemma depolarization causes opening of voltage-gated (L-
Type) Ca2+ channels releasing calcium from ECF into sarcoplasm.
o This Ca2+ stimulates further Ca2+ release from sarcoplasmic reticulum.
o Referred as "Ca2+- Induced Ca2+ Release" (CICR).
85. CYANOSIS
CYANOSIS
• Presence of at least 5 gm% (4-5 gm/dl) of deoxyhemoglobin in capillary blood is essential to

produce cyanosis.
• Common sites - Lips, nail beds, earlobes, cheeks, & mucous membranes of oral cavity.
• Central cyanosis:
o Due to generalized disorder of oxygenation of blood due to decreased arterial PO2.
o Hence, any cause of hypoxic hypoxia can cause central cyanosis.

• Peripheral cyanosis:
o Due to blood stagnation leading to greater extraction of oxygen in peripheral areas like nail
beds, nose tip & earlobes.
o Any cause of stagnant hypoxia (CHF, shock) & cutaneous vasoconstriction can cause
peripheral cyanosis.
• In Hypoxic Hypoxia:
o Cyanosis is seen - Yet, only in severe hypoxia.
o Note: Cyanosis appears at saturation <85%.
o Thus, cyanosis considered as "Late sign of hypoxia in trauma patients".
• In Anemic hypoxia:
o No cyanosis observed.
o Because in case of severe anemia causing hypoxia, there will not be enough deoxygenated
hemoglobin to produce cyanosis.
o In CO poisoning, CO-Hb color - cherry red.
o No cyanosis is seen in CO poisoning.
• In Stagnant hypoxia:
o Cyanosis is seen.
• In Histotoxic hypoxia/"Cyanide poisoning":

o Cyanosis is not seen.
• Uncommon causes of cyanosis due to,

o Sulphaemoglobin & Methaemoglobin.
• Required levels to produce cyanosis:
o Methaemoglobin concentration of ≥ 1.5 gm/dl.
o Sulphaemoglobin concentration of ≥ 0.5 gm/dl.
86. CARBON MONOXIDE POISONING
CARBON MONOXIDE POISONING
• Small amounts of CO is formed in body functions as "Gaseous Transmitter Vasodilator" (along with
NO & H2S).
EFFECTS OF CARBON MONOXIDE POISONING:

1. CO poisoning causes anemic hypoxia -
• Because Hb amount carrying O2 is reduced but total Hb amount of blood is unaffected by CO.
2. COHb cannot take up O2 -

• Liberates CO very slowly Shifting dissociation curve of remaining HbO2 to left.
3. Affinity of Hb to CO is 200-250 times its affinity to O2.

4. Even though O2 content of blood is greatly reduced in CO poisoning, PO2 of blood may be normal.
5. First organ affected - Brain
6. Death results when 70-80% circulating Hb is converted to COHb.
7. CO is toxic to cytochromes in tissue, (Yet at 1000 times of lethal dose)
• Hence, "Tissue toxicity" plays no role in clinical CO poisoning.
TREATMENT:
1. Most commonly available treatment for CO poisoning - 100% oxygen.
MORE BENEFICIAL METHODS:
1. Administration of mixture of 95% oxygen & 5% carbon dioxide is beneficial.
• Because carbon dioxide stimulates respiration.
2. Hyperbaric oxygen - Oxygen administered at high pressure (up to 2000 mmHg) - More beneficial.
87. RESPIRATORY REFLEXES
RESPIRATORY REFLEXES
1. HERING-BREUER INFLATION REFLEX:
• Limits tidal volume.

• Prevents lung hyperinflation.
2. "J-REFLEX" ("J-RECEPTORS"):
• "J" refers to "Juxtacapillary"

o Juxtaposition to pulmonary capillaries in alveolar interstitium.
Major stimulating factor:
• Increased pulmonary capillary pressure.

o During exercise, especially at high altitude.
3. HEAD'S PARADOXICAL REFLEX:

• Lung inflation further induces inflation.
4. AFFERENT FROM PROPRIOCEPTORS:
• Impulses from muscles & joints Stimulate inspiratory neurons,

o Hence, increased pulmonary ventilation during exercise.
88. CHEMICAL REGULATION OF RESPIRATION
CHEMICAL REGULATION OF RESPIRATION
• Response to changes in PO2 (hypoxia) -

• Mediated entirely by peripheral chemoreceptors.
• Central chemoreceptors are located in chemosensitive area on ventral surface of medulla.
• Primary stimulus for central chemoreceptors -
• Increased hydrogen (H+) ion concentration.
• Physiological stimulus -
• Increased PCO2.
• H+ directly stimulates central chemoreceptors in CSF & brain interstitial tissue.
• Resultant of changed arterial PCO2 (PaCO2).
• Central chemoreceptors not stimulated by hypoxia.
• Peripheral chemoreceptors are located in connective tissue associated with vessel wall, at
bifurcation of common carotid, & on arch of aorta.
• "Glomus cells" are characteristics cellular content of both the chemoreceptors.
• Type I glomus cells -
• Contain High dopamine content.
• Afferent neurons from carotid & aortic bodies pass close to glossopharyngeal & vagus
nerve respectively.
• Blood flow to peripheral chemoreceptors, on per unit mass basis, is "Highest" to any tissue in body
• Most potent natural stimulus for peripheral chemoreceptors,
• Low arterial PO2 (Hypoxic hypoxia) less than 60mm Hg.
• Also O2 saturation - 89%.
• Other stimuli for peripheral chemoreceptors include,
o High arterial PCO2
o Increased arterial hydrogen ion concentration ("Acidosis"/"low pH").
89. NEURAL MECHANISM OF BREATHING REGULATION
NEURAL MECHANISM OF BREATHING REGULATION
VENTRAL RESPIRATORY GROUP (VRG):

Ventral VRG neurons :
• Mostly "Expiratory (E) neurons".

o Since expiration is generally a passive process, E neurons are silent mostly.
PRE-BOTZINGER COMPLEX:
• Located in ventrolateral medulla.

• Neurons are responsible for "Respiratory Rhythm Generation".
• Contains "Pacemaker cells".
90. HYPOXIA
HYPOXIA
HYPOXIC HYPOXIA:
• Most common type of hypoxia.

• Fall in arterial blood PO2 & Low O2 content.
• Seen in hypoventilation - E.g., In Restrictive lung diseases, COPD etc.,

• In High Altitude.
• Right to left shunt (e.g., Cyanotic CHD or AV malformation).
ANEMIC HYPOXIA:
• O2 content of blood is lower despite normal PO2.

• Due to low oxygen saturation of hemoglobin.
• As PO2, is normal, respiration is not stimulated by anemic hypoxia.
• Because peripheral chemoreceptors are sensitive only to PO2.
• Seen in "Carbon monoxide poisoning"
o Hypoxia produced by CO poisoning also called "Anemic hypoxia".
STAGNANT HYPOXIA/HYPOPERFUSION HYPOXIA:
• Due to sluggish blood flow.

• E.g., As in CHF or Circulatory shock.
• Both arterial blood PO2 & oxygen content is normal.
• Blood stays in capillaries for longer time than normal due to sluggish blood flow, because of greater
O2 extraction.
• Hence, cyanosis is a prominent feature.
• Arterio-venous O2 difference (A-V O2 difference) is maximum in stagnant hypoxia.
HISTOTOXIC HYPOXIA:
• Best example is "Cyanide poisoning".

• This inhibits cytochrome oxidase
• Also, A-V O2 difference markedly reduced & it may be zero.
HYPOXEMIA:
• Arterial PO2 < 80 mm Hg.

• It does not consider hemoglobin.
• Most common cause of hypoxia.
CAUSES:
• Decreased PO2 of inspired air (Decreased FiO2).

• Low barometric pressure such as in high altitude & causes of elevated PCO2.
• Any cause of hypoventilation will cause hypoxemia if PCO2 rises high enough.
91. ALTITUDE PHYSIOLOGY
ALTITUDE PHYSIOLOGY
• PO2 is low at high altitudes.

• PO2 of inspired air (PiO2) is low.
• Earliest response to fall in PO2 – Hyperventilation
• Acute mountain sickness is characterized by hypoxia-like symptoms Tachycardia.
• High altitude pulmonary edema causes raise pulmonary capillary hydrostatic pressure.
• During acclimatization, Hyperventilation is most fundamental response to hypoxia.
• Low arterial PO2 (hypoxemia) stimulates carotid body peripheral chemoreceptors Causing
hyperventilation.
• Leading to "Arterial PCO2 fall" & "Respiratory alkalosis (increased pH).
• Respiratory alkalosis compensated by increased renal excretion of bicarbonate.
• Thus blood carbonic acid/bicarbonate ratio & pH maintained at normal level.
• Peripheral chemoreceptors are not affected by pH.
• "Increase in sensitivity of respiratory chemoreceptor mechanisms to hypoxia & CO2.
• Eventual effect is "Increased minute volume", as a result of increased tidal volume.
• Acclimatization increases DPG.
• Causing "Rightward" shift of oxygen-Hb dissociation curve.
• Resulting in increased tissue O2 delivery.
• Hypoxia stimulating erythropoiesis Increased RBC count & hemoglobin concentration.
• Hence, absolute polycythemia with increased red cell mass.
• Other compensatory mechanisms - Increases renal alkali (HCO3-) excretion.
• Exercise performed at high altitude hastens acclimatization process.
• Increasing duration of exercise increases work capacity.
• Work capacity at high altitude can be increased by,
• Increasing duration of exercise.
• Also by reducing/maintaining workload at an optimum level corresponding to maximum rate
of oxygen uptake.
• All available oxygen can be utilized.
• Chronic mountain sickness/Monge's disease can lead to right ventricular failure (cor pulmonale).
92. PHYSIOLOGY OF DEEP SEA DIVING
PHYSIOLOGY OF DEEP SEA DIVING
• Because at higher atmospheric pressure, nitrogen dissolved in body fluid & even more easily
dissolves in fatty substances in neuronal membrane & produces necrosis.
CAISSON'S DISEASE/DECOMPRESSION SICKNESS/DIVER'S PARALYSIS/DYSBARISM/BENDS:
• A particular form of gas embolism.

• Occurs with individuals exposed to sudden lowering of atmospheric pressure.
Eg:
• Rapid ascent of scuba & deep sea divers.

• Individuals in unpressurized aircraft in rapid ascent (e.g., in Pilots).
93. DEAD SPACE
DEAD SPACE
• Volume of anatomical dead space - 150 ml.

• In a normal adult, the anatomical dead space is approximately 2.2 cc/kg.
• Normal Dead Space (Vd) - Tidal volume (Vt) ratio is 0.30 (150:500).
• I.e., Equivalent to 1/3rd of tidal volume.
• Increased anatomical dead space:
o Seen during inspiration.
o Halothane.
o Atropine.
o During neck flexion.

• Decreased anatomical dead space associated with endotracheal intubation.
• In healthy individuals, anatomical dead space & physiological dead space are identical.
• Increased physiological dead space seen with lung diseases.
• Anatomical dead space measured by Single-breath N2 method.
• Physiological dead space calculated by using "Bohr's Equation".
• Dead space reduces volume of air reaching alveoli participating in gas exchange.
• Normal alveolar ventilation = (500 - 150) x 12 = 4200 ml/minute.
• Increased alveolar ventilation results in decreased alveolar PCO2 & increased alveolar PO2
94. RESPIRATORY PRESSURE
RESPIRATORY PRESSURE
Muller's maneuver:
• During "Forceful Inspiratory Effort" against a closed glottis producing intrapulmonary pressure as
low as -80 mm Hg.
INTRAPLEURAL/PLUERAL PRESSURE:
• Intrapleural pressure always negative.

• During quiet breathing, Intrapleural pressure fluctuates between -3.8 mm Hg (-5.0 cm water) to -
6.0 mm Hg (-8.0 cm water)
• Intrapleural pressure is negative during quiet expiration (-3.0 mm Hg).
o More negative (-6.00 mm Hg) during normal inspiration.
o Becomes positive only on forceful expiration.
REASON FOR NEGATIVE PLEURAL PRESSURE:
• Pleural pressure is more negative during inspiration & less negative during expiration.
• Yet, always negative during quiet breathing.
• 2 major reasons for negativity:
o Because both thoracic cage & lungs are elastic structures & both tend to recoil but in
opposite direction.
o Lymphatic drainage of pleura.
TRANSPULMONARY/TRANSMURAL PRESSURE ACROSS LUNGS:
• Difference between alveolar pressure (intra-alveolar pressure) & pleural pressure (intrapleural
pressure).
• Is a measure of "Elastic recoil pressure".
• More expanded at end of inspiration:
• Hence, Transpulmonary pressure = 0 - (- 8.0) = + 8 cm H2O.
• Less expanded at end of expiration:
• Hence, Transpulmonary pressure = 0 - (- 5.0) = 5cm H2O.
• Airway dynamic compression causes expiratory flow limitation.
o I.e., Beyond a limit increased expiratory efforts do not produce further increase in flow.
95. BLOOD PRESSURE
BLOOD PRESSURE
• SI unit for measuring blood pressure - Kilopascals (kPa).

• Basic unit for pressure is newton per square meter & is called Pascal (Pa).
• BP in mm Hg = BP in kPa x 7.5 or 1 mm Hg= 0.133 kPa.
• Cardiac waves recorded from brachial artery of a young adult in sitting or supine position.
• Pulse pressure is difference between systolic & diastolic pressure.
• Mean BP - (2 DBP +SBP)/3 (Or)
• Mean BP - DBP + 1/3 Pulse pressure.
• Normally, mean BP is about 93 mm Hg I.e.,(2 x 80 + 120)/3.
• Arterial blood pressure is product of cardiac output & total peripheral vascular resistance (TPR).
• Changes in cardiac output (or stroke volume) affect mainly systolic pressure.
• Changes in peripheral resistance affect mainly diastolic pressure.
• Maintenance of fairly high pressure during diastole (80 mm Hg) is achieved by aortic elasticity & its
immediate branches (Windkesselvessels) and arteriolar resistance.
REGULATION OF BLOOD PRESSURE:
1. SHORT TERM REGULATION:
• Antidiuretic hormone (ADH): Increases water reabsorption in kidney.

• Angiotensin II: Causes vasoconstriction.
o Yet, Aldosterone II associated with short-term regulation.
96. MEASUREMENT OF BLOOD PRESSURE
MEASUREMENT OF BLOOD PRESSURE
INDIRECT METHOD (USING SPHYGMOMANOMETER):
• Cuff is rapidly inflated until pressure is well above expected systolic BP so that brachial artery is
occluded.
• Blood pressure measured by an auscultatory method using sphygmomanometer tends to be higher
than true intra-arterial pressure measured by arterial cannulation.
o Because some cuff pressure gets dissipated between the cuff and artery in soft tissue.
IDEAL METHODOLOGY:
• While measuring BP, patient should be in resting position (seating or lying down).
• Patient's arm with attached cuff shows be at heart level.
• Cuff should be applied to upper arm.
• Cuff should encircle at least 80% of arm.
o I.e. Cuff length of bladder should be at least 80% arm circumference.
o Cuff width should be at least 40% of the circumference.
TYPES OF METHODOLOGY:
1. PALPATORY METHOD:
• Diastolic point cannot be identified by this method.
3. AUSCULTATORY METHOD:
• Method uses stethoscope, placed over brachial artery in cubital fossa.

• "Korotkoff's sounds" appear at systolic pressure & disappear at diastolic pressure.
o Sounds are attributed to turbulence.
o Caused by partial arterial occlusion.
• According to Americal Heart Association, Korotkoff's sound occurs in five phases:
o Onset of phase I Korotkoff's sound corresponds to systolic pressure.
o Disappearance of sounds (phase V) corresponds to diastolic pressure.
AUSCULTATORY GAP:
• Falsely low recording of systolic BP may occur.
CONDITIONS INCREASING BP:
1. Size of inflatable cuff:
• Width of cuff should be 40% of circumference/1.2 times diameter of extreme.

• Length of inflatable cuff should be 80% of arm circumference.
• Ie., Length-to-width ratio of 2:1.
• Pseudohypertension:
o With usage of too narrow a cuff.
o In obese patients.
o Seen with thick calcified arteries.
E.g., in elderly, atherosclerosis, diabetes & Monkenberg's sclerosis.
BP AT VARIOUS PORTIONS OF CVS:

• Right ventricle - 25/0 mm Hg (Systolic/diastolic).
• Left ventricle - 120/0 mm Hg.
• Left atrium (Pulmonary Capillary Wedge Pressure) - 5 mm Hg (4-10 mm Hg).
97. NEURAL REGULATION OF CVS
NEURAL REGULATION OF CVS
• Vasomotor Center (VMC) & Cardiovagal/Cardio-Inhibitory Center act together to maintain BP.
• "Pressor area" of VMC, located in Rostral Ventrolateral Medulla (RVLM).
• Under resting conditions, neurons of VMC pressor area have an inherent tonic discharge in
vasomotor nerve supplying blood vessels.
• Vasomotor center (VMC) receives afferent fibers from cerebral cortex, both directly &
via hypothalamus (cortico-hypothalamic pathways.
• Receptors for baroreceptor reflex process is located in the adventitia of carotid artery & aorta,
at specialized locations called "Sinuses".
• Baroreceptors are highly sensitive to any change in mean blood pressure.
o Respond to BP changes between 70 mm Hg & 150 mm Hg.
EFFECTS OF BARORECEPTOR REFLEX:
1. ON INCREASED BP:
Increased BP Stimulates Baroreceptors & their afferents (through sinoaortic nerves).
In turn, stimulate nucleus of tractus solitarius (NTS).
Inhibits VMC pressor area. i.e., Rostral Ventrolateral Medulla (RVLM) Decreased sympathetic outflow.
Hence, decrease vasomotor tone & vasodilation.
Vasodilation reduces BP helping hemostasis.

Activated NTS also stimulates nucleus ambiguous (cardioinhibitory center) of medulla.
Increases parasympathetic (vagal) output through vagus Decreases heart rate, cardiac output, & BP
eventually.
2. ON DECREASED BP:
Decreased BP (Eg: While changing posture from lying down to standing.
Central venous pressure & venous return decrease.
Causes fall in stroke volume & systolic BP.
Eventually increases heart rate, stroke volume & BP ultimately.
• Valsalva's maneuver is activated by "Carotid massage".

• This reflex increase in vagal discharge to AV node is of therapeutic value in controlling
supraventricular tachycardia.
• At rest, arterial baroreceptors are stimulated during systolic upstroke of pressure pulse wave.
• Regulation of BP in severe hypotension:
• Ie., below 70mm Hg
• By chemoreceptor reflex.
• Regulation of BP below 40mm Hg.
• By CNS ischemic response.
• Regulation of BP between 70-150 mm Hg:
• By Baroreceptor mechanism.
• Bilateral section of sinus & aortic nerves,
• In normal and mild hypotensive animals causes,
• Elevation of BP & heart rate.
• In severe hypotensive animals,
• Further fall in BP.
• Proximal clamping of common carotid causes
• Increased blood pressure, heart rate, & respiratory rate.
• Bilateral clamping of carotid arteries causes,
o Decreased BP, heart rate & respiratory rate.

98. CHEMICAL REGULATION OF CVS
CHEMICAL REGULATION OF CVS
1. VASOCONSTRICTORS:
• Noradrenaline.
• Adrenaline.
• ADH (Vasopressin).
• Angiotensin II.
• Endothelins.
• PGF2.
• Thromboxane A2.
2. VASODILATORS:
• Kinins (Bradykinin, lysyl-bradykinin).

• PGE2.
• PGI2 (prostacyclin).
• VIP.
• ANP.
• Nitric oxide (NO).
I. NITRIC OXIDE (NO):
• Also called "Endothelium-Derived Relaxing Factor (EDRF):

o Because the most important physiological source of NO is "Endothelial cells".
• Formed from amino acid arginine.

o By enzymatic action of NO synthase.
• Acts through group IIB hormonal mechanisms.

o I.e., Via cGMP as second messenger.
• Reacts with superoxide produces peroxynitrite (ONOO-).

o Which decomposes to form highly reactive OH radical.
• NO synthase -
• Complex cytosolic enzyme.
• Employs five redox cofactors -
o NADPH.
o FAD.
o FMN.
o Heme.
o Tetrahydrobiopterin.

• NOS-1 & NOS-3 are activated by Ca2+
II. ENDOTHELIN (ET):
• Primarily secreted by paracrine regular.

• Produces,
o Vasoconstriction.
o Broncho-constriction.
o Cardiac stimulation (ionotropic action).
o Release of aldosterone & ANP.
o Decreases GFR.
9. CARDIOPULMONARY REFLEXES
CARDIOPULMONARY REFLEXES
• Atrial stretch receptors also referred as "Low-pressure" receptors –

• Especially type B receptors.
• Functions along with pulmonary arterial receptors.
• Minimize arterial pressure change in response to blood volume change.
• Receptors with large myelinated efferent fibers include,
• Atriocaval receptors:
• Located in right atrium, at entrance of SVC & IVC.
• Pulmonary venoatrial receptors:
• Located in left atrium, at entrance of pulmonary artery.
• "Bain-bridge reflex" - Atrial reflex control of heart rate.
• Ventricular stretch receptors are stimulated by injection Serotonine, Veratibine/Nicotine into left
coronary artery.
• Produces apnea, bradycardia & hypotension.
• This is referred as "Bezold-Jarisch reflex" / "Coronary chemoreflex".
• Pulmonary artery baroreceptors are "Low-pressure receptors" (similar to atrial low-pressure
receptors).
• Important role in minimizing arterial pressure changes in response to blood volume change.
o (Along with atrial stretch receptors).
100. CARDIAC OUTPUT

CARDIAC OUTPUT
• Average CO in adults - 5 liters/min.

• Cardiac index:
• Cardiac output per minute per square meter of body surface area.
• Ie., Cardiac output / Body surface area.
• Average cardiac index is about 3.2 /min/m3.
• Stoke volume - Amount of blood pumped out by left ventricle in each stroke/every heart rate.
• Ejection fraction –
• Stroke volume / End-diastolic ventricular volume.
• Normally around 60%.
• Cardiac reserve in healthy adult - 300-400%.
MEASUREMENT OF CARDIAC OUTPUT:
1. Fick principle method:
• Cardiac output - Oxygen consumption (uptake) per minute / Arteriovenous oxygen difference.
2. Dye (Indicator) Dilution method:
• Based on "Stewart-hamilton" principle.

• Cardiac output - Amount of dye injected /(Average concentration of dye * circulation time).
3. Thermodilution method:
• Also based on Stewart - Hamilton principle.
4. Combining doppler techniques with echocardiography.
5. Most recent advance noninvasive method -Electrical impedance cardiograph technology.
PRELOAD:
• Increased preload
• Results in higher end-diastolic volume.
• Conditions associated with ↑ed Stroke volume:
• Increased total blood volume.
• Increased venous tone.
• Increased negative intrathoracic pressure.
• (e.g. inspiration).
ed
• Conditions associated with ↓ Stroke volume:
• Sitting or standing.
• Increased ventricular contractile strength Increased stroke volume.

• By increasing sympathetic discharge.
• Afterload is defined by mean arterial pressure.
INCREASED CO:
o Anxiety & excitement (50-100%).

o Eating (30%).
o Exercise (up to 700%)
o High environmental temperature.
o Pregnancy (40%).
DECREASED CO:
o Sitting or standing from lying position (20% -30%).

o Rapid arrhythmias.
101. PRINCIPLES OF BLOOD FLOW
PRINCIPLES OF BLOOD FLOW
1. OHM'S LAW:
• According to Ohm's law,

o Blood flow (Q) - Pressure gradient(ΔP) / Resistance(R).
• In exchange Ohm's law for flow of electric current.
o Flow of current (i) - Electromotive force (E) / Electrical resistance (R).
2. POISEUILLE'S LAW/HAGEN-POISEILLE'S LAW:
• Poiseuille's equation states,

o Q = P1 - P2 * { (Π r4) / (8 η L)};
o Q - Flow rate.
• If everything else remains constant,
o Blood flow is directly proportional to 4th power of radius.
o Resistance to blood flow is inversely proportional to 4th power of radius.
• Arterioles are chief site of vascular resistance.
3. FLOW CHARACTERISTICS (LAMINAR vs TURBULENT FLOW):
• "Critical velocity" -
o Limit beyond which flow velocity exceeds resulting in turbulent flow instead laminar.
o Most important determinant of blood flow turbulence.

• Velocity is inversely proportional to total cross-sectional area.
o Thus, smaller vessels have laminar flow.
o Due to low velocity & large total cross-sectional area.
• Reynold's number(R):
o Determines if tubular blood flow is laminar/turbulent.
• Calculated by R=SDV/η.
o S - Fluid density.
o D - Tube diameter.
o V - Fluid velocity.
o η - Fluid viscosity.
• If R exceeds 2000 - Turbulent flow.
Factors favoring turbulence (increasing R):
• Increased blood density (S).

• Increased vessel diameter (D).
• Increased blood velocity (V).
4. BLOOD FLOW & VELOCITY:
• Constant flow (Q) -

o Blood flow velocity is inversely related to vessels area/square of vessel radius.
o As area =2Πr2.
o where r is radius.
5. Axial Streaming:
• At high flow rate/high shear rate,

o RBCs occupy tube's central axis.
o Also moves along blood vessel long axis with maximum velocity.
• Plasma skimming:
o Results in,
o "Hematocrit of capillary blood is about 25% lower than the whole-body hematocrit".
o "Hematocrit changes having relatively lower effect on peripheral resistance unless
changes are large".
• Fahreus - Lindqvist effect:

• At low flow rate:
o Increased interaction time between RBCs & adjacent lamina,
o Results in erythrocyte adherence increasing blood viscosity.
o Causes "Rouleaux formation" -
RBC sticking together forming chains of several cells.
• Effect of increased viscosity:

o Decreased plasma skimming.
o Rouleaux formation.
o Increased capillary RBC count.
6. LAW OF LAPLACE:
• States that tension (T) in wall of a cylinder is equal to product of transmural pressure (P) & radius (r)
divided by wall thickness (w).
o I.e., T = Pr/w.
7. Perfusion pressure:
• Pressure difference between arterial & venous pressure.

• Hence, blood flow through an organ is directly proportional to perfusion pressure & inversely
proportional to resistance.
102. ERYTHROCYTES
ERYTHROCYTES (RED BLOOD CELLS)
ERYTHROPOIESIS:
• In early fetal life (up to 10 weeks) - Occurs in yolk sac.

o By third month of intrauterine life - Moves to liver (major) & spleen.
o Later in bone marrow.
• At 20 years -
o Only in flat bones of axial skeleton (Eg., Skull, vertebrae, ribs, sternum & pelvis).
RBC LIFE SPAN:
• Neonatal - 60-90 days.

• Fetal - 80 days (2/3rd of adult RBC lifespan).
CHANGES IN RBC ON MATURATION:
• Reduction in cell size.

• Hemoglobin appears at intermediate normoblast stage.
• Mitosis is most active & occurs up to intermediate normoblast stage.
HEMOGLOBIN:
• Hb molecule - An assembly of four globular protein.

• Also has nonprotein part (heme).
• Each Hb molecule contains four heme units.
o 2 pairs of globin.
o Ie., 4 polypeptide chains.
• Minor hemoglobin (HbA2) -
o 2 identical α-chains.
o 2 identical δ-chains.
• Adult blood -
o About 96% HbA (α2 β2).
o 3-3.5% HbA2 (α2 δ2).
o Small amount of fetal Hb HbF (α2 γ2).
• Fetal Hb binds to 2-3 DPG less avidly than adult Hb.
• Fetal Hb - Resistant to alkali denaturation.
o Alkali denaturation test (ADT) - Done to identify fetal Hb.
RBC DESTRUCTION:
• RBC removed daily from circulation by macrophages.

o Mainly from spleen (major), liver & bone marrow.
o Inside macrophage, heme of hemoglobin is degraded to bilirubin.
• Certain metalloproteins (like zinc-or tin-porphyrins) -
o Used in jaundice.
o Helps decrease bilirubin production by inhibiting enzyme heme oxygenase.
103. CARDIAC CONDUCTION
CARDIAC CONDUCTION
• SA node - Located in superolateral wall of right atrium, at SVC junction with right atrium.
• Conduction system entirely made up of modified cardiac muscles.
• Fastest conduction - Purkinje system.
• Conduction velocity - 4 (Maximum).
• Slowest conduction - AV node & SA node.
• Conduction velocity in AV & SA node - 0.05 (Minimum).
• SA node discharges impulses at fastest rate.
o Thus, rate at which SA node fires, determines heart rate.
o Hence, SA node is "Normal pacemaker of Heart".
o I.e., Determines pace of heart.
• AV node has next highest automaticity after SA node.

• Sequence of ventricular myocardial depolarization:
o In ventricles, endocardial surface depolarizes before epicardial surface.
o Depolarization starts at left side of interventricular septum.
o Proceeds from endocardial to epicardial surface.

• Sequence of ventricular repolarization:
o Epicardial surface repolarizes first.
o I.e., Repolarization spreads from epicardium to endocardium.
• AV conduction speed nodal is only 0.05 min/sec so that impulses take 0.1- 0.13 sec to travel across
AV node.
o This 0.1 - 0.13 sec delay called "AV nodal delay".
o Due to fewer gap junctions Leading to impaired conduction.
• Action potential in non-automatic fiber (Cardiac muscles - Atria & Ventricles):

o Normal RMP in myocardial fibers is about -90mV.
o AP in myocardial fibers has 5 phases - Phases (0-4).
• Phase 2 -
o Plateau phase.
o Due to opening of "Voltage-gated slow Ca2+channels.
o Also referred as "Calcium-Sodium Channels" - Causing calcium influx.
• Action potential in automatic fibers (SA node and AV node):

• Pacemaker Potential/Prepotential:
o Slow & gradual depolarization between two action potentials (between one AP termination
& beginning of other).
o Starts due to opening of "Funny" (F) channels.
o Referred so because - Of activation by hyperpolarization & can pass both Na2+ & K+.
o Yet, dominant effect - Na2+ influx.
o Later part of prepotential is due to opening of 'T' type calcium channels.
• Repolarization - Opening of K+ channels resulting in K+ efflux.

o Repolarizing potassium efflux declines steadily during pacemaker potential.
o K+ efflux decline makes an indirect contribution to pacemaker potential.
EFFECT OF ANS ON CARDIAC CONDUCTION:
• Parasympathetic innervation -
o Right vagus is distributed primarily to SA node & left vagus mainly to AV node.
1. Parasympathetic (vagal) stimulation:
• Negative chronotropic effect - Decreased heart rate.

• Vagal stimulation cause decrease in slope (flattening) of prepotential (pacemaker potential).
2. Sympathetic stimulation:
• Positive chronotropic effect - Increased heart rate.

o Sympathetic stimulation increases slope of phase 4 prepotential (pacemaker potential).

• Positive inotropic effect -
o Increased contractility.
• Positive dromotropic effect -
o Increased conduction velocity in conductive tissue.
• Decreased in refractory period of all cardiac cell types.
104. COAGULATION SYSTEM
COAGULATION SYSTEM
COAGULATION FACTORS/CLOTTING FACTORS:
FACTOR NO. COAGULATION FACTOR
Factor I Fibrinogen.
Factor II Prothrombin.
Factor III Thromboplastin/Tissue factor.
Factor IV Calcium ions.
Factor V Labile Factor.
Factor VI Earlier referred as "Accelerin". Now dropped.
Factor VII Stable factor/Earlier referred as "Pre-Accelerin".
Factor VIII Anti-hemophilic globulin.
Factor IX Christmas Factor.
Factor X Stuart-Prower Factor.
Factor XI Plasma Thromboplastin Antecedent (PTA).

Factor XII Hageman factor.
Factor XIII Fibrin Stabilizing Factor/Laki Lorand factor.
HMWK High Molecular Weight Kininogen.
Pre - K Pre-Kallikrein.
Ka Kallikrein.
PPL Platelet Phospholipids.
HALF-LIFE OF CLOTTING FACTORS:
FACTOR HALF-LIFE IN HRS.
Prothrombin 60 hrs
Factor VIII/Anti-hemophilic globulin. 8-12 hrs.
COAGULATION PATHWAYS:
1. INTRINSIC PATHWAY:
• Largely an "In Vitro" pathway.

• Initiation of intrinsic coagulation pathway occurs when factor XII (Hageman factor/Contact factor) is
exposed to negatively charged surface.
• Factor XIIa hydrolyzes Pre-kallikrein to Kallikrein.
2. EXTRINSIC PATHWAY:
• Activated by Factor III/Tissue factor/Thromboplastin at site of tissue injury.

• First step in extrinsic pathway -
o Activation of factor VII (Pre-accelerin) by tissue factor (factor III).
3. COMMON PATHWAY:
• Common step in both intrinsic & extrinsic pathway -

• Activation of Factor X.
• Prothrombinase complex –
• Converts inactive prothrombin to active thrombin
• Includes platelet phospholipid, factor V, factor X & factor IV (Calcium ions).
• Prothrombin converts fibrinogen to fibrin.
• Factor XIII - "Fibrin stabilizing factor".
IMPORTANT POINTS ON COAGULATION PATHWAYS:
1. Factors involved in intrinsic system -
• XIII, XII, XI, IX, VIII, X, V, IV (Ca2+), Prothrombin & fibrinogen.
2. Vitamin K dependent factors -
• Factor II, VII, IX, & X.
3. Von Willebrand factor (vWF) -
• Mainly synthesized in endothelium.
4. Plasmin breaks down fibrin.
REGULATION OF CLOTTING PROCESS:
1. α2 - Macroglobulin -
• Contributes most of remaining anti-thrombin activity.
2. Heparin cofactor II -
• Minor inhibitor of prothrombin under physiological conditions.
3. Protein "C" & "S" -
• Are Vitamin K dependent proteins.

• Inactivates Factor V & VIII.
105. HEMOSTASIS
HEMOSTASIS
• Thrombin converts fibrinogen to fibrin.

• Clot retraction occurs due to contraction of platelets.
• Vascular endothelium is smooth, coated with a layer of glycocalyx (mucopolysaccharide).
o Prevents intrinsic system activation.
o Repelling clotting factors & platelets.
o Hence, preventing blood clotting within vessels.
Anti-coagulant property of endothelium:
• All endothelial cells produce thrombomodulin except cerebral circulation.

o Results in proteolytic cleavage of factor V & VIII.
• After endothelial injuryplatelets contacts subendothelial ECM (especially collagen).
• Platelet secretes "Thromboxane A2 & Serotonin" Results in vasoconstriction.
• Platelet contraction cause clot retraction.
o Occurs due to contractile proteins like thrombosthenin, actin & myosin.
• Factors promoting platelet aggregation:
o TXA2.
o Serotonin.
o Immune complex.
o Thrombin.
• Factors inhibiting platelet aggregation:

o PGI2.
o Bradykinin
106. CARDIAC CYCLE
CARDIAC CYCLE
• Isovolumetric contraction:
o Closure of AV valves - Marks 1st Heartbeat.
• Causes bulging into atrium.
o Resulting in small, sharp rise in atrial pressure.
o Referred as "C" wave on Jugular Venous Pulse (JVP).
• Both AV & semilunar valves are closed.
o Thus no volume change.
o Hence, "Isovolumetric" contraction.
• Isovolumetric contraction ends with opening of semilunar (aortic & pulmonary) valves.
• Ventricular ejection:
o Begins with semilunar valve opening.
o Sharp fall in atrial pressure.
o Represents "X-decent" in JVP.

• Protodiastole:
o Closure of semilunar valves.
o Produces "2nd heart sound".
• Iso-volumetric relaxation:
o Phase is period between semilunar valve closure & AV valve opening.
o Ends with AV valve opening.
o Coronary blood flow is maximum during this period.
• Rapid ventricular filling:

o Represents Y-descent in JVP.
• Last rapid filling phase

o Associated with sharp rise atrial pressure rise.
o Producing "a"-wave in JVP.
• Each cardiac cycle lasts about for 0.8 seconds.

o Atrial systole - 0.1 sec.
o Atrial diastole - 0.7 sec.
• Heart rate decreases diastolic duration than systolic duration.
• Electromechanical systole (QS2):

o Time interval between onset of QRS complex (ventricular activation) to aortic valve closure
(S2 heart sound).
o Calculated by ECG & phonocardiogram.
o Carotid pulse is not required.
• Left ventricular ejection time (LVET):

o Requires only carotid pulse recording.
• Pre-ejection systole (PEP):

o All 3 recordings of ECG, phonocardiogram & carotid pulse required.
107. PLASMA PROTEINS
PLASMA PROTEINS
FUNCTIONS:
1.Osmotic pressure:
• Albumin - Most important contribution.

Reasons:
• Increased total albumin concentration.

• Smaller molecular weight .
2. Defense mechanism:
• Includes "Immunoglobulins" & complement system proteins.
3. Carrier proteins:
• Acts a carrier of metals, hormones, lipid & drugs.
• Albumin -
o Transport of FFA.
• Pre-albumin -
o Thyroxine transport & Vitamin A.
• Haptoglobin -
o Binds to hemoglobin.
• Ceruloplasmin -
o Binds to copper.
• β-lipoproteins -
o Transport of triglyceride & cholesterol (I.e., Chylomicrons).
• Transferrin -
o Iron transport.
108. HORMONES INFLUENCING RENAL ACTIVITY
HORMONES INFLUENCING RENAL ACTIVITY
1. ANTIDIURETIC HORMONE (ADH):
• Increases water reabsorption.

• By increasing water permeability in late DCT & on cortical and medullary collecting ducts.
• More pronounced effect in medullary collecting duct.
o Because of maximum urinary concentration occurrence.
2. ALDOSTERONE:

• Actions localized to distal tubular & collecting ducts.
• Stimulates basolateral Na2+ - K+ ATPase.
• Major regulator of Na2+ & water balance -"Thirst - ADH" mechanism.
3. Atrial Natriuretic Peptide (ANP):
• Causes natriuresis.
• Due to increased GFR, by relaxing glomerular mesangial cells.
• Decreases Na2+ reabsorption from distal tubule & collecting duct.
• Relaxes arteriolar & venular smooth muscle lowering BP.
4. PARATHORMONE/PARATHYROID HORMONE/PTH:
Actions on kidney:
• Major regulating factor for calcium reabsorption.

• Production of 1,25-dihydroxycholecalciferol (Calcitriol).
• On Proximal convoluted tubule:
• "Phosphaturic effect" - Inhibits renal phosphate reabsorption.
• On Distal convoluted tubule:
o Increases renal Ca2+ reabsorption.
109. GROWTH HORMONE
GROWTH HORMONE
• Effect on skeletal growth mediated by "Somatomedins"/"Insulin-like Growth Factors" (IGF)

• GH, through somatomedin (IGF-1), stimulates proliferation of chondrocytes & osteocytes, resulting
in increased chondroitin sulfate deposition in cartilage.
• Growth hormone excess in adulthood results in acromegaly.
• Anti-insulin effects due to the direct effect of GH include decreased peripheral utilization of
glucose, increased gluconeogenesis & hyperglycemia.
• Insulin-like effects due to somatomedins(IGF) include "Anti-lipolytic" activity.
• GH is secreted in a pulsatile fashion.
• Large bursts of secretions occur at night during the onset of deep sleep.
• Stimuli increasing GH secretion - Exercise, hypoglycemia, fasting & stress.
• Stimuli decreasing GH secretion - REM sleep, Somatostatin & Cortisol.
• GH deficiency leads to "delayed fusion of epiphysis" - Ie., Proportionate dwarfism.
• Short stature, secondary to growth hormone deficiency is associated with "Normal body
proportion".

110. SPINAL CORD INJURY
SPINAL CORD INJURY
1. Central cord syndrome - Sacral sparing.
2. Brown - Sequard syndrome -
• Ipsilateral sensory loss –

• Fine touch, Proprioception (Joint position & body position sense) & Vibration.
• Due to ipsilateral dorsal column involvement.
• Ipsilateral motor deficit –
• Due to ipsilateral corticospinal tract (Pyramidal tract) involvement.
• Upper motor neuron paralysis.
• Contralateral sensory loss –
• Pain & temperature.
• Due to contralateral spinothalamic tract involvement.
• Unilateral segmental sign.
3. Anterior cord syndrome -
• Caused by compression of anterior spinal artery.

• Complete motor function loss, pain & temperature sensation below level of injury.
• Preservation of vibration, proprioception & fine touch.
o Due to spared posterior (dorsal) column.
111. PAIN AND ANALGESIA
PAIN AND ANALGESIA
• Idiopathic/unspecified pain - Purely psychological in nature; Hence, "Psychogenic pain".

• Brain is the most conspicuous part of body which has no pain receptors at all.
• Pain receptors (Nociceptors) - Free nerve endings.
• Pain receptors absent in Brain.
• Fast pain/Epicritic pain/First pain - Carried by thin myelinated Aδ (Type-III) fibers with
conduction velocity - 12-30 m/s.
• Slow pain/Protopathic pain/Second pain - Carried by unmyelinated C (Type IV) fibers.
• Neurotransmitter released by C fibers - Mainly substance P.
• Slow pain receptor sensitive to chemicals - Histamine, serotonin, substance P & acetylcholine.
• Serotonin - Most potent allogenic substance.
• Hyperalgesia - Exaggerated response to noxious (painful) stimulus.
• Allodynia - Pain sensation in response to non-noxious (non-painful) stimuli.
• Repetitive stimuli Cause tissue damage.
• Thus increasing nociceptors sensitivity Producing primary hyperalgesia.
• A viscus does not have any other sensation (e.g. touch, temperature etc) except pain.
• Visceral pain is poorly localized due to sparse distribution of nociceptors.
Stimuli for visceral pain -
o Excessive distension of a hollow viscus.

o Stretching of connective tissue surrounding viscus.
o Eg. Mesentery stretching in violent intestinal contraction.
• Visceral pain sensation carried by - Type C afferents.
o In sympathetic system - From thoracic & abdominal viscera.

o In parasympathetic system - From pelvic viscera.
o Important pain producing viscera - Heart & Stomach
o Completely insensitive viscera - Liver parenchyma.
o Intracranial structures sensitive to pain - Duramater around venous sinuses & vessels,
o Intracranial structures insensitive to pain - Brain parenchyma, pia meter & pial veins.
112. G-PROTEIN COUPLED RECEPTORS
G-PROTEIN COUPLED RECEPTORS
• G-protein has seven transmembrane segments.

• (I.e.7 α-helical) membrane spanning.
• Hormone binding site - Extracellular domain.
• G protein activation results in exchange of GDP by GTP on α-subunit.
• α-subunit dissociates from other two subunits.
• α-subunit inactivates itself by converting its bound GTP to GDP, with help of GTPase activity.
• Active G protein may either be effector activator/inactivator, because of different α-subunits (Gα -
subunits).
• Gαs (Gs alpha) Stimulates adenylyl cyclase & ↑es cAMP.
• Activation of AC results in increased synthesis & intracellular accumulation of cAMP.
• cAMP acts through "cAMP-dependent Protein Kinase'A' phosphorylates.
o Examples:
o Corticotropin-releasing hormone (CRH).
o FSH.
o LH.
o ACTH (corticotropin).
o Catecholamines (α2, β2).
o Glucagon.
o Dopamine (D1 & D2).
o Histamine (H2).
• Phospholipase activation by stimulatory G protein hydrolyzes "Membrane Phospholipid
Phosphatidylinositol 4, 5-Bisphosphates (PIP2), in turn, generating second messenger "Inositol I, 4,
5 triphosphate" (IP3) & "Diacylglycerol" (DAG).
• Ca2+ acts as "Third messenger".
• Protein kinase-C phosphorylates various intracellular proteins.
o Examples of IP-DAG system:
o Cholecystokinin.
o Catecholamines (some actions via α1 receptors).
o Histamine - H1.
• Examples of channel regulation:

2+
o Increased Ca -β1 adrenergic.
+
o Increased K -Adrenergic - α2.
113. STAGES OF SLEEP
STAGES OF SLEEP
• Non-REM sleep also referred as "N-REM/Slow sleep/S-sleep/Synchronized sleep/Orthodox sleep.

• Stage 1 N-REM sleep - There is disappearance of alpha activity & appearance of beat activity.
• Stage 2 - Sleep spindles & "K" complexes.
• Stage 3 & 4 - Deep sleep stages - Characterized by slow delta waves.
• REM - Presence of "Rapid Eye Movements".
• REM also referred as "Paradoxical sleep" - Because of paradoxical elevation of brain
activity, metabolism & physiological activity.
• High-amplitude slow waves seen in stage 3,4 of REM sleep is replaced by rapid low voltage activity
(beta wave).
• Features of REM sleep in EEG recording - Beta-wave, reappearance of alpha wave & ponto- genital-
occipital spike, dreaming, generalized muscular atony & increased pulse rate & BP.
• REM sleep - 20-30% of total sleep.
• N-REM Sleep - 60-70% of total sleep.
o Stage 2 - 40-50%.
• Events during NREM sleep include,
o Deep sleep/Slow wave sleep disorder - Occur during stage 3 & 4 of N-REM.
o Somnambulism - Night walking.
o Sleep terror/Night terrors - Pavor nocturnus.
o Bruxism - Teeth grinding.
• Events during REM sleep include,
o Nocturnal Penile Tumescence - Normal phenomenon.

o Nightmares/Dream anxiety disorder.
o Narcolepsy presents,
Cataplexy.
Hypnagogic hallucination - Hallucination just before falling asleep.
FEATURE/SIGN UPPER MOTOR NEURON LOWER MOTOR NEURON PARALYSIS

PARALYSIS
Paralysis Present - Spastic paralysis Present - Flaccid paralysis
Muscle tone Increased - SPASTICITY. Leading to "Hypotonia/flaccidity" muscle

tone.
With "Clasp-Knife rigidity".
Deep tendon Exaggerated - Hyperreflexia. Absent/Reduced
reflexes
(Areflexia/Hyporeflexia).
Superficial reflexes Absent - Only if specific neuron supplying muscle is
affected.
Abdominal & cremasteric.
Babinski sign Positive - Extensor plantar Absent -
response.
Plantar reflex flexor.
Indicates corticospinal
tract involvement.
115. REGULATION OF FEEDING BEHAVIOR
REGULATION OF FEEDING BEHAVIOR
• Feeding center in "Lateral hypothalamus".

• Satiety center in "Ventromedial nucleus" of hypothalamus.
• Signal for regulation food intake comes from glucose.
• Glucosensitive neurons are located in the ventromedial nucleus (satiety center).
LEPTIN:
• Acts on hypothalamus to reduce food intake.
• Increases lipolysis.
• Inhibits Agouti-related peptide (AgRP) secretion.
• Plasma leptin levels are proportional to amount of body fat; Hence, higher in women & obese
individuals.
• Levels increased in obesity.
• Levels decreased in testosterone (androgen), exercise & starvation.
NEUROPEPTIDES:
• Neuropeptides inhibiting food intake - α-Melanocyte Stimulating Hormone (α - MSH).

• Neuropeptides increasing food intake - Neuropeptide Y (NPY), Agouti-related peptide (AgRP) &
melanin-concentrating hormone (MCH).
• Neuropeptide Y - Polypeptide with 36 aminoacid residue.
• Produced in hpothalamus.
• Level increases during starvation.
• Decreases thermogenesis & melanocorticotropin activity.
• Orexins - Synthesized in lateral hypothalamus.
• Ghrelin is released from stomach.
o Increases hunger.
o Stimulates GH secretion.
116. BLOOD BRAIN BARRIER
BLOOD-BRAIN BARRIER
ANATOMICAL BASIS:
• Endothelial cells are joined by 'Tight-Junction', reducing capillary permeability.

• Capillaries are surrounded by glial cell foot process (especially astrocytes).
PERMEABILITY OF BBB:
• Highly permeable - Water, CO2, O2, Lipid-soluble substances (alcohol & most anesthetics).
• Totally impermeable - Plasma proteins.
STRUCTURES OUTSIDE BBB:
• Circum-ventricular organs.
• Posterior pituitary (neurohypophysis)
• Area postrema
• Organ Vasculusum of Lamina Terminalis (OVLT).
• Subfornical organs (SFO).
117. CEREBROSPINAL FLUID
CEREBROSPINAL FLUID
• CSF major source - Choroidal plexus.

• Other sources of CSF are ependymal cells of the ventricles & brain itself, via perivascular spaces.
• CSF pressure is regulated by "Rate of CSF absorption" by arachnoid villi.
• CSF Total volume in an adult - 125 - 150 ml.
• Rate of CSF formation - 500-550 ml/day.
• CSF production per minute - 0.3 - 0.35 ml/minute.
• Each of CSF constituents is actively transported.
• CSF circualtes from lateral ventricle into 3rd ventricle and ultimately into subarachnoid space.
• CSF is absorbed from subarachnoid space by arachnoid villi (arachnoid granulation tissue)
into Subdural venous sinuses.
• CSF is partly absorbed by lymphatics around cranial nerves I, II, VII, VIII.
• CSF does not pass through Epidural space.
• CSF Pressure - Measured through a lumbar puncture.
• CSF is obtained from space between Arachnoid & pia mater.
• About 150 mm of water/CSF in supine (horizontal).
• Range - 65-200 mm water/CSF (5-15 mm Hg).
• CSF pressure is regulated by rate of CSF absorption by arachnoid villi.
• Decreased CSF volume results in severe headache in case of continuous leak after lumbar puncture.
• Process of CSF absorption stops, below pressure of 68 mm H2O.
• Choroid epithelium secretes sodium ions by active transport.
• Osmolarity & sodium ion concentration of CSF - "Same" as that of plasma.
• CSF Glucose & K+ ion concentration is lower than plasma.
• CSF H+ ion concentration is slightly higher than plasma.
• Ie., pH is slightly low.
• CSF Cl- ion concentration is higher than plasma.
• β - 2 transferrin is found only in CSF; Hence, "Specific CSF marker".
• CSF Specific gravity - 1.007
COMPOSITION OF VARIOUS SUBSTANCES IN PLASMA & CSF:
PARAMETER IN CSF IN PLASMA RATIO

Sodium (Na2+) 147.0 150.0 0.98
Magnesium (Mg2+) 2.2 1.6 1.39
Calcuim (Ca2+) 2.3 4.7 0.49
Chloride (Cl-) 113.0 99.0 1.14
Bicarbonate (HCO-3) 25.1 24.8 1.01

pH 7.33 7.40
Glucose 64.0 100.0 0.64
• CSF glucose level is 2/3 of plasma glucose.

• CSF is stored at 4º C.
118. SPEECH
SPEECH
• Areas involved - Broca's area & Wernicke's area.

• Wernicke's area - Located in posterior end of superior temporal gyrus.
• Wernicke's area is concerned with comprehension.
• Broca's area - Located in inferior frontal gyrus.
• Center for motor part of speech.
• Sentence is formulated in Broca's area.
• Lesions of the Broca's area produce an inability to express oneself by spoken speech called "Motor
aphasia"/"Nonfluent aphasia".
• Inability to express the idea by spoken speech usually occurs.
• Ie., Motor aphasia refers to defect in Verbal expression
• Conduction aphasia is caused due to a lesion in arcuate fasciculus.
• Conduction Aphasia is a 'Fluent' Aphasia with preserved comprehension & impaired repetition.
• Repetition is impaired in both Broca's & Wernicke's aphasias.
119. GUSTATION
GUSTATION
• Fungiform papillae - Numerous near tip & margins of tongue.

• Circumvallate (Vallate) papillae - V-shaped region near base of tongue.
• Foliate papillae - Confined to tongue's back edge.
• Filiform papillae - No taste buds.
• Edges of tongue are more sensitive to sour taste.
• Anterior half of the tongue is more sensitive to salty taste.
• Tip of tongue - Most sensitive to sweet.
• Back of tongue - Sensitive to bitter.
• Bitter taste receptors are G protein-coupled receptors.
• Salty-tasting substances depolarize taste cells by activating amiloride-sensitive Na2+ channels.
• Umami taste acts through glutamate taste receptors with release of neuronal glutamic acid.
• Taste fibers from anterior two third of tongue are carried by Facial nerve via Chorda tympani.
• Taste sensations from posterior 1/3rd of tongue are carried by Glossopharyngeal Nerve.
120. RESPIRATORY FAILURE
RESPIRATORY FAILURE
• Type I respiratory failure due to perfusion or diffusion failure disorders.

o Main causes of type I failure - Parenchymal diseases (V/Q mismatch) & right to left shunt.
o Increased alveolar-arterial O2 gradient (PA- PaO2).
• Type II respiratory failure due to Alveolar Hypoventilation - Ventilatory failure.

o Main causes of type II failure - Bulbar poliomyelitis, Poliomyelitis, Kyphoscoliosis &
in alveolar edema.
o Normal alveolar-arterial O2 gradient (PA- PaO2).
o Due to Hypoxia" (decreasd PO2) & "Hypercarbia/hypercapnia" (Increased PCO2 due to
CO2 retention).
121. OLFACTION
OLFACTION
• Olfactory receptors are "Neurons" themselves.

• Main receptor part - "Projecting cilia" into nasal mucosa, acting as dendrites of neruon/receptor
cell.
• “Peri-glomerular cells” - Are "Granulare type".
• Pathway to neocortex involves a relay in olfactory tubercle to thalamus then & finally orbitofrontal
cortex.
122. TRANSPORT MAXIMUM
TRANSPORT MAXIMUM
• Transport maximum is "Maximum limit allowed for transportation (either absorption/secretion) for
actively transported substances".
• Transport maximum for glucose is 375 mg/min.
• If plasma glucose concentration rises > 200 mg/dl, increases filtered load 250 mg/min & is "Renal
Glucose Threshold point".

• Reason for difference between glucose threshold & Tm levels - Because Glucose Tm is not same for
all nephrons.
• Overall Tm for kidneys - About 375 mg/min.
• Filtered glucose load above 375 mg/min, Glucose excreted completely.
• Substances with Tm -
• Glucose, phosphate, Sulfate, Amino acids, Urate, Lactate, Plasma proteins, Creatinine & Para-
aminohippuric acid.
• Substances without Tm -
o Water, urea & Sodium ions.
123. MEMORY
MEMORY
• Episodic memory Impairment causes “Amnestic syndrome”.

• Implicit memory otherwise termed as "Non-declarative memory".
• Implicit memory concerns with the memory of procedures without being able to actively remember
it.
• Striatum (part of basal ganglia) responsible for procedure memory.
• Patients with impaired short-term memory cause "Antegrade amnesia" -
o Are unable to learn any new material because they are unable to transfer it to long-term
memory.
• Short-term memory lasts only as long as person continues to think.
• Patients with impaired long-term memory cause "Retrograde amnesia" for the already stored
memory of the past.
• True long-term memory is due to actual structural changes/physical restructuring/spatial synaptic
organization.
o Most important change - Increased number of transmitter vesicle release.
o Structural changes are produced by DNA stimulation of protein replication.
• Medial temporal lobe is the area of brain responsible for consolidation - Mainly "Hippocampus".
• Consolidation is "Processing of short-term into long-term memory".
• Lesion in hippocampus leads to ”Antegrade amnesia” - Causing inability to consolidate recent
events into long-term memory.
• After consolidation long-term memory is stored in the neocortex.
124. LEARNING
LEARNING
• Features of non-associative learning - Habituation & sensitization.

• Associative learning depends on repeatedly observing association between two phenomena.
• Typical example of classical conditioning - Pavlov's experiment.
• Unconditioned stimulus (food) + Conditioned stimulus (Bell) Unconditioned response (salivation).
• Features of operant conditioning - Reinforcement & Punishment.
• Number of neurons & their connectivity often change significantly during learning.
125. THALAMUS
THALAMUS
• Acts as "Sensory Relay Station" for all sensory pathways, includes Gustatory & Olfactory
tracts reaching cortex.
• Concerned with conscious interpretation of crude touch, pain & temperature.
• Every thalamic nuclei sends output to different cortical areas.
• Motor thalamic nuclei relay & process messages from basal ganglia & cerebellum to motor &
premotor cortex.
o Mainly by Ventral anterior nuclei.
• Specific sensory nuclei receives all sensory afferents from ascending pathways projecting to
somato-sensory cortex.
o Mainly by Ventro-posterior nuclei.
126. SALIVA
SALIVA
• Salivary pH is 6.5 - 7.
• Saliva contains salivary amylase or tylin.
• Lingual lipase is secreted by Ebner's glands on dorsum of tongue.
• Saliva is secreted is around 1-1.5 L/day.
• Predominant ions in saliva in HCO3- & K+.
127. HORMONAL CHANGES AT PUBERTY
HORMONAL CHANGES AT PUBERTY
• Puberty is triggered by release of gonadotropins (FSH & LH).

• Puberty triggers estrogen & progesterone production in women & testosterone in men.
• Testosterone is responsible for the development of pubic hair, accelerated bone growth, body odor
and acne during puberty
• Estrogen is major hormone responsible for female pubertal development.
• Estrogen promotes bone maturation & epiphyseal plates closure in long bones.
• Progesterone causes proliferation of acini in mammary glands and converts watery cervical
secretion to viscid and scanty.
• Leptin facilitates the release of Gonadotropin-Releasing hormone (GnRH), thereby helping in
pubertal onset by this permissive action.
• Other hormones involved in puberty are thyroxine & growth hormone.
128. SEMEN
SEMEN
• Each ml of semen normally contains about 100 million/mL.

• Sperm counts belows 20 million considered minimal count & sterile by WHO.
• Human sperm move at a speed of approximately 3mm/min.
• Semen pH - 7.35 – 7.50
• Seminal vesical secretions contributes 60% of total volume, contains Fructose & Protaglandins.
• Prostatic secretions contribute Zinc to semen.
129. REABSORPTION & SECRETION OF PROXIMAL TUBULE
REABSORPTION & SECRETION OF PROXIMAL TUBULE
• GFR & its volume is reduced to 1/3rd (About 60-70% reabsorbed) in proximal tubule.
• Fluid out of proximal tubule is isotonic with GR & plasma.
• Primary active step for sodium reabsorption in proximal tubule involves Na+-K+-ATPase at baso-
lateral membrane.
• About 60-70% of water reabsorbed in proximal tubules because of osmosis through aquaporin-1
channel.
• Passive water reabsorption is coupled mainly to sodium reabsorption.
• Glucose is absorbed completely (100%) in proximal tubule by Na2+-Glucose cotransporter-1 (SGLT -
1) in luminal membrane & by glucose transporter GLUT-1 in basolateral membrane.
• Amino acids are completely reabsorbed in proximal tubules.
• H+ ions secreted into tubular fluid is mainly by Na2+-H+ exchanger.
• Phosphate reabsorption occurs along with sodium co-transport.
• Maximum (90%) bicarbonate absorption in proximal tubules is coupled with H+ ions secretion
by Na2+-H+ exchanger.
• About 40-50% of urea reabsorbed.
• Glucose, amino acids, & bicarbonate are reabsorbed along with Na+ in early portion of proximal
tubule.
130. RENAL TRANSPORT OF POTASSIUM, CALCIUM & UREA
RENAL TRANSPORT OF POTASSIUM, CALCIUM & UREA
1. Potassium transport:
• K+ both reabsorbed & secreted by renal tubules.

• About 2/3rd filtered K+ reabsorbed in proximal tubules.
• In Distal tubule & collecting ducts, K+ is both reabsorbed & secreted.
• Acidosis decreases K+ excretion, by decreasing its secretion.
• On High potassium diet, K+ secretion increases , accounting about 60-65% of excreted K+.
2. Calcium transport:
• Normally 99% filtered calcium reabsorbed in kidney.

• Maximum calcium reabsorbed (65%) filtered calcium reabsorbed in proximal tubules.
• In Henle loop, calcium is only reabsorbed in thick ascending limb.
• Parathormone is primary controller for calcium reabsorption.
• Increased plasma phosphate causes calcium secretion by,
o Increasing its reabsorption & decreasing its excretion
• Decreased plasma phosphate causes calcium secretion by,
o Decreasing its reabsorption & increasing its excretion .
3. Urea transport:
• Urea is secreted into thin descending limb of Henle loop.
131. RE-ABSORPTION & SECRETION IN DISTAL TUBULE
RE-ABSORPTION & SECRETION IN DISTAL TUBULE
• Over-all impact of reabsorption in early distal tubule is to dilute urine by removing solutes.
• Late segment of distal tubule is functionally similar to cortical collecting duct.
• Principal (P) cells reabsorb sodium & water from lumen & secrete potassium into lumen.
• Intercalated (I) cells reabsorb potassium & secrete hydrogen into lumen.
• Cl- is reabsorbed into late distal tubule.

132. GASTRIC ACID SECRETION - MECHANISM & PHASES
GASTRIC ACID SECRETION - MECHANISM & PHASES
• H+ secreted by proton pump (H+-K+-ATPase) into gastric lumen in exchange for K+ ion.
• Sight/smell/even thought of food stimulate acid secretion in cephalic phase.
• Cephalic phase is mediated by Parasympathetic system activation via vagus.
• Cephalic phase accounts for 20% of acid secretion.
• Gastric phase is stimulated hormonally due to gastrin.
• Stretching of stomach wall during gastric phase is mainly due to gastric distension.
• Gastric phase accounts for 72-80% acid secretion.
• Local GI hormones released inhibiting gastric acid secretion & motility are secretin, CCK, VIP &
Somatostatin.
• Presence of food plays a lmajor role in inhibiting duodenal acid secretion.
133. REABSORPTION & SECRETION IN LOOP OF HENLE
REABSORPTION & SECRETION IN LOOP OF HENLE
• Only water is reabsorbed from thin descending limb of Henle loop due to its high permeability to
water.
• Tubular fluid in thin descending limb is hypertonic.
• Thick ascending limb is totally impermeable to water.
• Tubular fluid in thick ascending limb is hypotonic.
• In thick ascending limbcarrier pump Na-K-2Cl transporter, transports one Na, one K & two Cl.
134. GASTRIC ACID SECRETION - REGULATION & OUTPUT
GASTRIC ACID SECRETION - REGULATION & OUTPUT
• Parietal/Oxyntic cells secrete Hydrochloric acid (HCl) & Intrinsic factor of castle.
• Chief/Zymogen/Peptic cells secretes pepsinogen.
• Delta (D) cells secrete Somatostatin.
• Pylorus contains "mucus-secreting pylorus gland".
• In human - 2.5 L (105ml/hr) gastric juice secreted daily.
• Important cationic constituents in acid - Na2+, K+, & Mg2+.
• Main activators of acid secretion are mainly Histamine (H2 receptors), Acetylcholine (M3 receptor)
& Gastrin.
• Vagal (Parasympathetic) stimulation increases acid secretion through acetylcholine.
• Proton Pump/H+ inhibitors act by blocking H+ receptors.
• Inhibitors of acid secretion are Somatostatin, Secretin, Cholecystokinin (CCK), GIP & VIP.
• Best established inhibitor of acid secretion is "Low pH" (Acid itself).
• Normal BAO - < 10 (2 - 5) mmol/hr.
• Maximal Acid Output (MAO)/Total Acid Output values reflect total parietal cell population in the
stomach, hence referred “Parietal cell mass".
135. REABSORPTION & SECRETION IN COLLECTING DUCTS
REABSORPTION & SECRETION IN COLLECTING DUCTS
• Cortical collecting duct is functionally similar to late segment of distal tubule.

• Principal (P) cells reabsorb sodium & water from lumen & secrete potassium into lumen.
• Intercalated (I) cells reabsorb potassium & secrete hydrogen into lumen.
• Cl- is reabsorbed into cortical collecting duct.
136. PHYSIOLOGY OF MOTOR CORTEX
PHYSIOLOGY OF MOTOR CORTEX:
• Premotor area corresponds to Brodmann's Area 6.

• Cortical representation of the body in the cerebrum is Vertical.
• The most important area involved in planning & organizing complex sequential skilled
movements is "Supplementary motor area".
137. REGULATION OF THIRST
REGULATION OF THIRST
• Angiotensin II causes stimulation of thirst during volumetric thirst.

• ADH is responsible for thirst mechanism during dehydration.
• Osmoreceptors are present in anterior hypothalamus.
• Osmoreceptors are sensitive to intracellular dehydration and are insensitive to solutes like glucose
& urea.
138. REGULATION OF POSTURE
REGULATION OF POSTURE
• In decorticate rigidity, rigidity is less pronounced than decerebrate rigidity.
• Reflex absent in decorticate animal Long loop stretch reflex.
• Decorticate rigidity is not seen as a manifestation of uncal herniation.
• Decorticate child shows in acute brain injury, subthalamic, CT & frontal lobe lesion and shows
flexion of arm & extension of lower limb.
139. ASSOCIATION AREAS
ASSOCIATION AREAS
• Premotor area corresponds to Area 6.

• Brodmann's area 17 corresponds to visual cortex.
• Processing of tactile stimulation occurs in Brodmann's area 1,2,3.
• Neurophysiological defects present in right lobe involvement are Visuospatial defect, Anosognosia
& Dysgraphia.
• Senseless, fluent speech indicates damage to the categorical hemisphere.
140. CELLULAR ELEMENTS OF CNS
CELLULAR ELEMENTS OF CNS
• Macroglia are derived from Neuroectoderm.

• Macroglia subtypes -
o Astrocytes
o Oligodendrocytes
o Ependymal cells.
• Astrocytes subtypes -
o Protoplasmic astrocytes - Found in Grey matter
o Fibrous astrocytes - Found in White matter.
• Important function of astrocyte
o Prevents neurons from excitotoxicity by converting excess ammonia & glutamate into
glutamine via glutamine synthase.
o Limits protein filtration across cerebral capillaries, mainly by foot processes of astrocytes.
• Oligodendrocytes:
o Responsible for nerve myelination in CNS.
• Microglia:
o Phagocytic in function.
o Mesodermal in origin & derived from circulating monocytes.

141. RETICULAR FORMATION
RETICULAR FORMATION
• Reticular Activating System (RAS) causes arousal from sleep producing "δ-block" where EEG
pattern changes from high voltage slow δ-wave to high-frequency low voltage β-wave activity.
142. LUNG VOLUMES & CAPACITY
LUNG VOLUMES & CAPACITY
• Tidal Volume (TV) - Volume of air that moves in or out of the lung with each normal breath.
• Residual volume (RV) - Volume of air remaining in lungs after maximal expiration.
• Expiratory reserve volume (ERV) - 1200 ml
• Inspiratory capacity (IC) calculated by sum of tidal volume & inspiratory reserve volume IC = TV
+ IRV.
• Functional residual capacity (FRC) - Volume of air in lungs after expiration.
o Calculated by FRC - ERV + RV.
o About 2400 ml
• Total Lung Capacity is about 5900 ml. Depends on lung compliance.
• Vital capacity (VC) is about 4700 ml.
• Fraction of FVC breathed out in 1st second - Forced Expiratory Volume 1 (FEV1).
143. SYMPATHETIC Vs. PARASYMPATHETIC NERVOUS SYSTEM
SYMPATHETIC Vs. PARASYMPATHETIC NERVOUS SYSTEM
PARAMETERS SYMPATHETIC NERVOUS SYSTEM PARASYMPATHETIC NERVOUS

SYSTEM
ORIGIN Pre-ganglionic neurons from "Dorso- Pre-ganglionic neurons
lumbar (T1 to L2)". from Cranio-sacral (lll, VII, IX, X,
S2-S4).
Post-ganglionic via muscarinic &

nicotinic receptors.
GANGLIA Away from organ Close to organ

GANGLIONIC FIBERS Post-ganglionic fibers are longer Post-ganglionic fibers are shorter
PRE: POST-GANGLIONIC 1:20 to 1:100 1:1 to 1:2

FIBER RATIO
TRANSMITTER Pre-ganglionic transmitter - Pre- & post-ganglionic

INVOLVED - Acetylcholine transmitter - Acetylcholine
Majorly Acetylcholine Post-ganglionic transmitter - Nor-

adrenaline
RECEPTORS INVOLVED • Muscarinic - All
postganglionic sites.
• α2 receptors - Pancreatic beta
cells. • Nicotinic - Found at
ganglia, skeletal muscle,
• β1-receptors - Heart & JG cells. adrenal medulla & CNS.
• β2-receptors - Bronchi, blood

vessels, uterus, liver, GIT,
urinary tract, & eye.
• β3-receptors - Adipose tissue
IMPORTANT PHYSIOLOGICAL ACTIONS OF SYMPATHETIC SYSTEM:
MUSCARINIC RECEPTOR Heart • Mainly due to M2 receptors

EFFECTS • Decreased heart rate (negative
chronotropic)
• Decreased conduction (negative
dromotropic)
Blood vessels • Due to M3 receptors
Respiratory system • Broncho-constriction.
Glands • Increased sweating, lacrimation &

salivation.

Eyes • Miosis.
GIT • HCl secretion in stomach.

• Increased intestinal secretions.
• Increased peristaltic movements.
Urinary bladder • Stimulates detrusor.
Male reproductive • Erection of penis.

system
PHYSIOLOGICAL ACTIONS OF PARA-SYMPATHETIC NERVOUS SYSTEM:
ORGAN PHYSIOLOGICAL EFFECTS
Heart • Mainly due to β1 receptors.
Actions:
• Increased heart rate (Positive chronotropic)

• Increased force of conduction (Positive ionotropic)
• Increased conduction velocity (Positive dromotropic)
Blood vessels Actions:
• Vasoconstriction - Due to α1 receptor.

o Predominate in skin.
• Vasodilation - Due to β2 receptor.

o Predominate in coronary blood vessels.
Respiratory system • Broncho-dilation - Due to β2 receptor agonists (Exogenous drugs).
Glands • Increased sweating - Due to cholinergic sympathetic receptors (M3)
Eyes • Mydriasis.

Metabolic • Due to β3 action:
o Lipolysis
• Due to α2 action:
o Decreased insulin release from pancreas.
Renal system • Urinary system:

o Relaxation of detrusor - Due to β2 action.
144. MOLECULAR MOTORS & MARKERS
MOLECULAR MOTORS:
• Are proteins produce force for inter-cellular movements.
IMPORTANT CYTOSKELETAL MOLECULAR MOTORS:
• Kinesin
• Dynein
• Dynamin
• Myosin
IMPORTANT CELLULAR MARKERS:
ORGANELLE MARKERS
Mitochondria ATP synthase, Creatine kinase, Glutamate dehydrogenase
Plasma membrane 5' -Nucleotidase, Adenyl cyclase, Na+K+ATP'ase
Lysosome Acid phosphatase
Golgi apparatus Galactosyl transferase, Golgi mannosidase II, Sialyl transferase.
Peroxisome Catalase
Cytosol Lactate dehydrogenase
145. CYTOSKELETON

CYTOSKELETON
MICROTUBULES:
• Hollow fine tubules made of protein "Tubulin".
Properties of microtubules:
• Polar.
• Dynamic instability.
• Microtubule assembly utilizes GTP energy.
Functions:
• Determines cell shape by providing structural support.

• Necessary for formation & function of mitotic spindle.
INTERMEDIATE FILAMENTS:
• Very stable
• Important components included,
o Lamins.
o Keratins.
o Desmin - Used diagnostically in pathologic cases to indicate disorders of muscle origin.
o Neurofilaments.
MICROFILAMENTS:
• Made of 2 F-actin (filamentous actin).

• Useful in muscular contraction.
• Microfilaments are abundant in Lamellipodia.
146. IMPORTANT FACTORS & FEATURES OF SMOOTH MUSCLE CONTRACTION
SMOOTH MUSCLE CONTRACTION - IMPORTANT FACTORS & FEATURES
IMPORTANT FEATURES OF SMOOTH MUSCLE CONTRACTION

1. Slow cycling of cross-bridges:
• Hence, smooth muscle contraction is slow & sustained.
2. Low energy is required to sustain smooth muscle contraction.

3. Maximum contraction force is greater in smooth muscle.
4. "Latch mechanism":
• Mechanism facilitates prolonged holding of smooth muscle contraction with minimal energy
expenditure.
• Due to low/nil cross-bridge cycling rate.
5. Plasticity:
• Smooth muscle usually defies the usual length-tension relationship valid for skeletal muscle.
6. Percentage of shortening.
IMPORTANT FACTORS AFFECTING SMOOTH MUSCLE CONTRACTION

1. Stretch
Stretch of visceral smooth muscle leads to,
• Spike potential development

• Contraction.
• Increased tension, even in absence of nervous innervation.
2. Neural control
3. Local factors:
• Local factors causing smooth muscle relaxation in arterioles & pre-capillary sphincters include,
o Lack of oxygen.
o Excess of carbon dioxide.
o Lower pH
4. Hormones
147. COMPONENTS OF BODY FLUIDS
COMPONENTS OF BODY FLUIDS
Total Body Water (TBW)
(60% of body weight) - 42 liters

Intracellular fluid(ICF) Extracellular fluid
(ECF)
40% 33% Total body water & 20% body weight - 14 litres
body weight (28 litres) Interstitial fluid Plasma

15% of body 5% of body
weight (3.5 liters)
weight (10.5 -15 liters)
• An adult weighing 70 Kg contains 42 liters of water.
• In early fetal life, TBW is 90% reduced to 75-80% at birth Reducing further to 60% by end of one
year.
COMPOSITION OF ECF & ICF:
• ECF:
o Most abundant cation-Na+ (142 meq/l)
o Most abundant anion- Cl- (103 meq/l)
o Bicarbonate concentration HCO3 (28 meq/l)
• ICF:
o Most abundant cation - K+ (150 meq/l) & Mg2+ (58 meq/l)
o Most abundant anion - Phosphates (75 meq/l) > Proteins (40 meq/l).
o pH - Slightly alkaline in nature.
MEASUREMENT OF BODY FLUID COMPARTMENTS
VOLUME MEASUREMENT
TBW By Heavy water (Deuterium oxide)

ECF • By inulin (most accurate), Sucrose, radioactive sodium.
PLASMA VOLUME(PV) • By using Evans blue (T1824), Serum albumin labeled with
radioactive Iodine
RED CELL VOLUME • By RBCs tagged with radioactive Chromium -51.
148. INTERCELLULAR JUNCTIONS
INTERCELLULAR JUNCTIONS
1. Tight junctions/Zona Occludens:
• Seal adjacent epithelial cells tightly beneath their apical surface.

• Are formed by - Occludins, Junctional Adhesion Molecules(JAMs), & Claudins
• Seen in epithelial cells of intestinal mucosa, renal tubules, & choroid plexus
Functions:

• Prevent passage of molecules & ions through space between cells.
2. Gap junctions/Nexus/Hemichannels/connexons:
• Are intercellular connections typically seen in cardiac & smooth muscles.

• Each unit is a connexon, made of 6 transmembrane proteins called connexins.
• Space narrows from 25nm-3nm
• Permit free passage of ions, glucose and amino acids between the cells without cell membrane
passage
• Permit membrane potential to pass from cell to cell. – “Conduct ionic current”.
• CHARCOT -MARIE TOOTH DISEASE:
o Due to mutation in gene for connexins coding
3. Desmosomes:
• Mainly comprised of intermediate filaments.
4. Hemi-desmosomes:
• Attach epithelial cells to connective tissue (basal lamina).
149. OSMOSIS
OSMOSIS
• Osmosis is the passive transfer of solvent, especially water, across the membrane.
o Also, there is diffusion of solvent towards an area of higher solute concentration.
OSMOTIC PRESSURE:
• Van’t Hoff law is used for calculating osmotic pressure of a solution.
Contributors:
Plasma Protein Concentration Contribution to osmostiv
Albumin 3.5 - 5g% 80%
• Plasma proteins have lower molar mass (weight) & high plasma molar concentration (number).
o Hence, contribute greatly to plasma osmotic pressure.
• Albumin with low molecular weight contributes more.
IMPORTANT & RELATED FACTORS:

OSMOLE:
• 1 osmotically active molecule (1 osmole) of a substance exerts osmotic pressure equal to 22.4
atmospheres.
• Major contributor to body fluid (ECF) osmolarity is Na+.
Types:
• Ineffective osmoles - Eg: Glucose & urea.

• Effective osmoles - Eg: Sodium & chloride ions.
o Causes “tonicity & osmosis of water”.
“Osmolarity":
• The osmolar concentration of a solution in osmole/ liter.

• Normal serum osmolality is about 290mOsm/Kg.
• ECF osmolarity is measured by osmometer.
• Mannitol infusion increases osmolarity.
SOLVENT DRAG/BULK TRANSPORT:
• Refers to influence exerted by, allowing solvent through membrane on simultaneous solute
movement through membrane.
150. NEURONAL TRANSPORT
NEURONAL/AXOPLASMIC TRANSPORT
Types:
FAST AXOPLASMIC TRANSPORT:
1. Fast antegrade transport:
• Occurs along microtubules & driven by kinesin.
2. Fast retrograde transport:
• This also occurs along microtubules & driven by dynein.
SLOW AXOPLASMIC TRANSPORT:
• Carries protein subunits of neurofilament.

151. NERVE INJURIES
NERVE INJURIES
Classification:
Based on Seddon's classification,
Nerve injury type Injury Axonal Degeneration Recovery Prognosis

damage
NEUROPRAXIA Temporary injury. No. Axon No Complete Best
preserved. recovery
Physiologicalconduction
lockwithout anatomic
disruption.
AXONOTMESIS Disrupted axons & Yes. Yes. Spontaneous Good

myelin.
Intact endoneurium
NEUROTMESIS Complete anatomical Yes Yes No possible Bad

section of nerve recovery
PATHOLOGICAL CHANGES AFTER NERVE INJURY:
• Not seen in neuropraxia – Due to no anatomical disruption.
NERVE DEGENERATION:
1. Wallerian/Secondary degeneration:
• Secondary degeneration occurring distal to site nerve injury site (within 24hrs)
• Axon degeneration followed by myelin degeneration.
2. Retrograde/primary degeneration:
• Chromatolysis (Breakdown of Nissl granules)

• Disappearance of golgi apparatus & neurofibrils.

NERVE REGENERATION:
1. Distal to injury:
• Rate of axon recovery - 1 mm/day.

• Shows “Positive Tinel’s sign” - Absent in neuropraxia.
• “Motor march” – Seen only in axonotmesis.
Biochemistry
1. HMP Shunt
The pentose phosphate pathway is an alternative route for the metabolism of glucose. The two major
functions of this pathway are:
• The formation of NADPH for synthesis of fatty acids and steroids, and maintaining reduced
glutathione for antioxidant activity.
• The synthesis of ribose for nucleotide and nucleic acid formation.
Three molecules of glucose 6-phosphate give rise to three molecules of CO2 and three 5-carbon sugars
• Two Phases
o Oxidative – Non Reversible
o Non Oxidative -Reversible
o No ATP is produced or consumed in HMP Shunt
o Rate Limiting Step glucose-6-phosphate is oxidized to 6-phosphogluconolactone by glucose-
6-phosphatase.
Difference Between Glycolysis and HMP Shunt
• Oxidation utilizes NADP rather than NAD,

• Co2 is not produced in Glycolysis
• No ATP is generated in HMP Shunt
• Both are Cystolic Cycles
• Mg2+ ions are required for both glycolysis (for the phosphorylation of glucose by glucokinase) and
the pentose phosphate pathway (for the functioning of transketolase and several other enzymes).
• In order to maintain a red cell membrane structure, erythrocytes utilize the pentose phosphate
pathway for the generation of large amounts of NADPH.
Occurs in Liver , Testis and Lactating Mammary Gland
2. Glutathione

• Glutathione Serves as a vehicle for the transport of amino acids into some cells
• Glutathione is a tripeptide
• Glutathione conjugates xenobiotics
• Glutathione is co-factor of various enzymes
• Glutathione scavenges free radicals and superoxide ions
• Glutathione peroxidase contains Selenium
• Glutathione reductase contains FAD
• Selenium is found in the active site of glutathione peroxidase for its function
• Cysteine in glutathione act as reducing agent
• Glutathione helps in membrane transport
• Glutathione consist of glutamate, cysteine and glycine
4. GLUT
• Glucose transporter in myocyte stimulated by insulin is GLUT 4

• After an overnight fasting, levels of glucose transporters are reduced in Adipocytes, Cardiac muscle
& skeletal muscle
• Insulin stimulated glucose uptake into fat and muscle cells is mediated by GLUT 4.
• GLUT 4 glucose transporter is present in the skeletal muscle and adipose tissue
• GLUT 2 glucose transporter present in beta cells
• Major site for expression of GLUT5 sperm
• Insulin resistance down-regulates GLUT-4
• Glucose diffusion in RBC by GLUT I
• Insulin secretion is decreased by Somatostatin
5. Gluconeogenesis
• During gluconeogenesis reducing equivalents from mitochondria to cytosol are transported

by Malate
• Lactate and alanine can both serve as substrates causing hyperglycemia in diabetes
• Aldolase is the glycolytic enzyme used in gluconeogenesis
• Muscle cannot take part in gluconeogenesis due to absence of Glucose 6 phosphatase
• Hormone that stimulates gluconeogenesis is Epinephrine
• Gluconeogenesis is important in maintaining blood glucose during the normal overnight fast
• The synthesis of glucose from pyruvate by gluconeogenesis Requires the participation of biotin
• Fructose-1,6-bisphosphatase and pyruvate carboxylase pairs of enzymes is required for the process
of gluconeogenesis
• Alanine released from muscles is an important substrate for gluconeogenesis
• During prolonged starvation, the rate of gluconeogenesis depends on Increased alanine levels in
liver
• Major contribution towards gluconeogenesis is by alanine
• Lactate, pyruvate, glucogenic amino acids, propianate and glycerol are the precursors of
gluconeogenesis
• In well fed state gluconeogenesis in liver is inhibited by ADP level
• Gluconeogenesis in Fasting state is indicated by Pyruvate Carboxylase activation by Acetyl CoA
• After 50 gm of glucose is feed orally Decreased gluconeogenesis
• Phosphohexose isomerase, Aldolase,Phosphotriose isomerase,Glyceraldehyde 3-phosphate
dehydrogenase,Phosphoglycerate kinase,Phosphoglycerate mutase,Enolase are the common
enzymes of gluconeogenesis & glycolysis
• Tyrosine enters gluconeogenesis by forming Fumarate substrate
6. Urea Cycle
• Urea cycle linked to kreb's cycle by Fumarate

• Sources of the nitrogen in urea cycle are Aspartate and ammonia
• Urea cycle occurs in Liver
• Inherited hyperammonemia in Krebs-Henseleit urea cycle is a result of deficiency of N-acetyl
glutamate synthetase
• Ornithine transcarbamylase deficiency of the Krebs-Henseleit urea cycle is X-linked dominant in
inheritance
• Number of ATP required for synthesis of 1 mole of urea is 3
• Enzymes for urea synthesis are present in Both Cytoplasm & Mitochondrial matrix
• N acetylglutamate serve as allosteric actor of Carbamoyl phosphate synthetase I
• Carbamoyl phosphate synthetase I is the rate limiting enzyme in urea synthesis
• Urea is produced by the enzyme Arginase
• Urea is mainly formed in liver and to small extent in Brain
• First 2 steps of urea cycle occurs in mitochondria
• Aspartate converted to fumarate in urea cycle
• Ornithine-citrulline transporter aminoacids
• The urea in the brain is derived from Glutamine
• Amino acid involved in urea synthesis is Aspartic acid
• In argininosuccinase deficiency, Arginine should be supplemented to continue the urea cycle
• 1st Carbon to urea comes from CO2
• Carbamoyl phosphate synthase - 1 acts in urea cycle
7. Purine Salvage Pathway
• The purines salvage pathway is for Hypoxanthine and Adenine

• First purine nucleotide, which is synthesized in purine biosynthesis is IMP
• Salvage pathway of purine biosynthesis is important for RBCs
• PRPP glutamyl amidotransferase is increased to increase purine synthesis in Liver
• Salvage pathway of purine nucleotide synthesis are used by Brain, RBC,Leukocytes
8. Vitamin A
• Vitamin A is present in milk, egg yolk, fish , liver, fruit and vegetables
• Vitamin A promotes maintenance of epithelial tissue
• Vitamin A is stored mainly as retinol esters in Liver
• Vitamin A consist of Retinol, retinal and retinoic acid
• During the dark phase of visual cycle 11-cis-Retinaldehyde combines with opsin to make Rhodopsin
• Anti infective vitamin is vitamin A
• Daily dose of vitamin A in a 6-12 months old child is 300 microgram
• The highest concentrations of Vitamin A is seen in Cod liver oil
• Vitamin 'A' requirment for a Pregnant woman is 800 mg/d.
• Dose of vitamin A prophylaxis given in age group 16 years 200000 iu
• Absorption of vitamin A can be enhanced by giving the child a diet rich in Fat
• Highest vitamin A content is seen in Green leafy vegetables
• First dose of vitamin A should be given at 9 months
• Vitamin A prophylaxis is given to children every 6 months
9. Vitamin A Deficiency
• Vitamin A prophylaxis to a child is Specific protection

• Vitamin A intoxication causes injury to Lysosomes
• Bitot spots in 10 month children should be given 3 dose of 1 lakh units IM on day 0, 1 and 14
• Under national programme for prevention of nutritional blindness, a child in the age group of 6-11
months is given a mega dose of vitamin A equal to 1,00,000 IU
• Extra ocular manifestations of vitamin A deficiency include anorexia, growth retardation and
follicular hyperkeratosis.
• Vitamin A deficiency is characterized by Bitot's spot,Xerophthalmia , Night blindness, Corneal
xerosis, Keratomalacia and corneal ulcers.
• A child with dry skin and scaling is suspected of having vitamin A deficiency shows early
features Nyctalopia
• Growth retardation is common in vit. A deficiency
• Frequent infections can occur in vit. A deficiency
• Hydrocephalus is infrequent in vit. A deficiency
• The earliest clinical sign of Vitamin A deficiency is Conjunctival xerosis
• Most common cause of blindness in children in India is Vitamin A deficiency
• Abnormalities of bone metabolism is associated with excess of Vitamin A deficiency
• Vitamin A is teratogenic
• 1st symptom of vitamin A deficiency is Night blindness
• Xerosis/ Xerophthalmia is due to deficiency of Vitamin A
• 3 doses of vitamin A are required to treat deficiency
• Follicular hyperkeratosis is related to deficiency of vitamin A
10. FISH(Fluorescent in situ hybridization)

• Gene mapping,Study of 3D chromosome organization in interphase nuclei ,Monitoring the success
of bone marrow transplantation ,etc are the applications of FISH.
11. Glucokinase
• Glucokinase enzyme plays an important role in regulating blood glucose levels after feeding.
• Glucokinase is not inhibited by Glucose-6-phosphate.
• Insulin increases the activity of Glucokinase.
• The rate-limiting enzyme in Glycolysis is Glucokinase.
• Insulin acts on Glucokinase enzyme in glycoysis.
12. Tay-Sachs disease
• The substance which accumulates in Tay Sach’s disease is Ganglioside.

• Deficiency of enzyme Hexosaminidase-A causes Tay Sach’s disease.
• Cherry red spot at macula may be seen in Tay Sach’s disease.
13. Maple Syrup Urine Disease
• An inherited deficiency of branched chain a keto acid dehydrogenase result in Maple syrup urine
disease.
• In maple syrup disease, the amino acids excreted in urine are Valine, Leucine ,Leucine.
• Decarboxylation of valine, leucine and isolucine is defective in Maple syrup urine disease.
• Enzyme deficient in maple syrup urine disease is α-ketoacid dehydrogenase.
• In maple syrup urine disease FeCI3 test with urine gives blue color.
14. Cholesterol Biosynthesis
• Rate limiting step in cholesterol synthesis is HMG CoA reductase.

• Lovastatin acts by inhibiting which enzyme Hydroxymethylglutaryl-CoA reductase(HMG CoA
reductase).
• HMG-Co-A Synthase enzyme is common to the synthesis of cholesterol and ketone bodies.
• Cholesterol is synthesized from Acetyl Co-A.
• Mineral required for cholesterol biosynthesis is Mg.
15. Malate Shuttle

• Glycolysis is associated with the malate shuttle
16. Vitamin C
• Vitamin C is also called as antiscorbutic factor.

• Maximum amount of Vitamin C is found in adrenal cortex.
• Most animals synthesize vitamin C from glucose by uronic acid pathway.
• Humans and higher primates cannot synthesize due to absence of Gluconolactone Oxidase.
• RDA- 90mg/d for males and 75mg/d for females.
Biochemical Functions of Ascorbic Acid-
• Ascorbic acid functions as a reducing agent and scavenger of free radicals.

• In collagen synthesis- post-translational modification by hydroxylation of proline and lysine residues
converting them into hydroxyproline and hydroxylysine.
• Synthesis of norepinephrine.
• Tyrosine metabolism
• Bone formation
• Vitamin C as respiratory catalyst.
17. Collagen
• Collagen of Type II is found in hyaline cartilage .

• Collagen is not found in fibroblasts.
• Complete wound strength in terms of collagen recovery is never regained .
• Type IV of collagen is predominant in basement membrane.
• Vitamin C is required in proper synthesis of collagen.
• Type I is the predominant collagen type in bone .
• Hydroxylation of peptidyl prolyl residues in collagen require Ascorbate , α ketoglutarate , Oxygen , Fe2+
,Dioxygenases.
• The collagen triple helix structure is not found free in Cytoplasm.
• Osteogenesis imperfecta is a group of diseases characterized by genetic mutations which lead to Shortened
a1(I) collagen chains.
• Collagen is Triple helix structure.
• Intracellular events occuring in fibroblast during synthesis of collagen : Formation of triple helix.
• The 40 nm gap in between the tropocollagen molecule in collagen which serve as the site of bone formation
is occupied by Calcium.
• Type of collagen forming basement membrane of kidney is type IV.
• Articular cartilage is made up of type II collagen.
• Maximum collagen in wound healing is seen at end of second week.
• Highest concentration of hydroxy proline is seen in Collagen.
• Keloid scar is made up of dense Collagen.

• Tensile strength of wound after laparoscopic cholecystectomy in a 30 years old woman depends upon
extensive crosslinking of tropocollagen.
• Type of collagen present in cornea is Type I.
• Strength of wound after 2 months is governed by Collagen cross linking.
• Major protein of bone is Collagen type I.
• Sequence of amino acid in collagen is Gly-X-Y.
• Vitreous humor contains type II of collagen.
• Components of collagen : Glycine, lysine, proline.
18. Trace element:Iodine
• The best indicator for monitoring the impact of Iodine Deficiency Disorders Control Programme
is Neonatal hypothyroidism.
• The Iodine content in iodized salt at production point should be 30 ppm.
• The recommended content of Iodine in salt at the consumer level is 15 ppm.
• Iodine deficient population in the world is 20 million.
• Endemic cretinism is seen when Iodine uptake is below 20 micro gram/day of daily intake .
• The impact and efficiency of an iodine control program can be determined by Neonatal thyroxine
levels.
• Highest concentration of iodine is found in lobsters and oysters.
• Iodized salt in iodine deficiency control programme is a type of primary prevention.
• Total body iodine is about 50mg.
• Richest source of iodine is sea food.
• The RDA of iodine for adults is 150 microgram.
• Fortification of salt is a component of Iodine deficiency control programme .
• Efficiency of the goiter control program can be assessed by Neonatal thyroxine levels.
• As per the World Health Organisation guidelines, iodine deficiency disorders are endemic in a
community if the prevalence of goiter in school age children in more than 5%.
• Hypothyroidism in sub-himlayan region/India is due to deficiency of Iodine.
• Neonatal Hypothyroidism is the best indicator of environmental iodine deficiency .
19. Trace element : Iron
• Bone marrow iron is increased in Thalassemia; Anemia in chronic disease.

• The normal total iron binding capacity is 30-35 mg/litre.
• The blood indices which reflects iron deficiency more accurately is MCHC.
• Raised iron content is not found in testis in Hemochromatosis
• Antidotes for acute iron poisoning :Desferioxamine.
• Iron is absorbed actively in the Duodenum.
• The iron preparation that can be given intravenously is Iron Dextran.
• The formula for parenteral iron therapy? 4.4 body weight (kg) Hb deficit (g/dl).
• Vitamin C increases absorption of oral iron.
• Oral iron chelating agent(s) is/are Deferiprone, Deferasirox.
• Iron supplementation in a healthy term breast fed baby should be started at the age of 6 months.
• Serum ferritin depletes first in a case of iron deficiency anemia .
• Decreased irritability is the first change of improvement noted after iron therapy is initiated.
• The earliest indicator of response after starting iron in a 6-year-old girl with iron deficiency is
Increase reticulocyte count.
• Milk is not a good dietary source of iron.
• Highest amount of iron is seen in red meat.
• Iron absorption from intestine is regulated by mucosal block in the intestinal cells according to iron
requirement.
• Iron requirement in pregnancy is 35 mg.
• Daily iron requirement in healthy Indian male is 17 mg.
• Best test to detect iron deficiency in community is Serum Ferritin.
• Tablets supplied by Govt. of India contains 100 mg elemental iron + 500 g Folic Acid.
• Among the pulses,Soya bean has the highest content of iron .
• Poor man's iron source is Jaggery.
• Elemental iron supplementation in Iron deficiency anemia is 100 - 150 mg .
• Most useful method of estimating total iron content of blood is ferritin.
• Iron is transported bound to Transferrin.
• Active absorption of iron decreases following gastrectomy.
• Iron binding protein is Transferrin.
• Haemaochromatosis is defined as Syndrome caused by systemic iron overload.
• Iron deficiency anemia is seen in Chronic blood loss , Achlorhydria , Extensive surgical removal of
the proximal small bowel.
• Iron Deficiency anemia is commonly caused by Ankylostoma Duodenale.
• Milk decreases the absorption of iron into the body.
• Iron is absorbed in ferrous form.
• Iron is stored in ferritin form.
• Hypochromic Microcytic pattern in peripheral smear is seen in iron deficiency anemia.
• Iron Dextran binds to transferrin and can be given IM or IV.
• Hepcidin inhibits transfer of iron into enterocytes.
• Ferritin biosynthesis is regulated by serum level of Iron.
• Mentzer index more than 13 suggests a diagnosis of Iron deficiency anemia.
• Bone marrow iron is decreased earlier than serum iron in Iron deficiency anemia.
• Indications of Intravenous Iron administration : Iron malabsorption , Inability to Tolerate oral Iron ,
Patients on Erythropoietin Therapy.
• Iron dextran is associated with highest risk of Anaphylaxis
20. Trace element:Zinc
• A highest level of zinc is found in Prostate.

• Daily requirement of zinc in humans is 9.4 mg/day.
• Dose of zinc used in acrodermatitis enteropathica is 2-3 mg/kg body weight.
• Zinc is an essential component of several enzymes like carbonic anhydrase, alcohol dehydrogenase,
alkaline phosphatase, carboxypeptidase and superoxide dismutase.
• Acrodermatitis enteropathica is an autosomal recessive disorder of zinc absorption.
• Advantages of Zinc therapy for Wilson disease are as follows: Produces negative copper balance
,Blocks intestinal absorption of copper , Induces hepatic metallothionein synthesis.
• Micronutrient associated with rash and diarrhea is Zinc.
• Dose of zinc recommended for 9 month old during acute diarrhoea is 20 mg daily.
• Zinc has a role in regulation of binding of proteins to DNA.
• Zinc is absolutely required for normal spermatogenesis, fetal growth, and embryonic development.
• Daily requirement of Zinc for adult men is 9.4mg/d and for women is 6.8mg/d.
• Paneth cells contain Zinc.
• Metal fume fever is common in chronic poisoning with Zinc.
• Zinc poisoning is likely in a person presenting with rigors and chills and a clinical picture resembling
malaria.
• Hypogonadism (sexual infantilism, loss of libido), poor weight gain (growth retardation) ,taste
alteration,decreased immunity, hepatosplenomegly, hypochromic microcytic anemia, loss of
hair,Dermatitis, Diarrhea,poor wound healing are seen in zinc deficiency.
• Zinc supplement given in 12 month baby is 3.5-5 mg/day.
• RDA of zinc in a child is 6-8 mg /day.
21. Trace element : Copper
• Copper sulphate poisoning manifests with Acute hemolysis.

• Copper containing enzymes are Superoxide dismutase , Cytochrome oxidase ,Tyrosinase.
• Increased copper excretion in urine is seen in Primary sclerosing cholangitis , Wilson's disease ,
Primary biliary cirrhosis.
• Copper is mainly transported by Ceruloplasmin.
• Purple lining over gums is seen in chronic poisoning of Copper.
• The average fatal period of copper poisoning is 1-3 days.
• The probable diagnosis in a person found dead with bluish green frothy discharge at the angle of
mouth and nostrils is Copper poisoning.
• Copper sulfate poison is not dialyzable.
• Diseases related to copper metabolism :- Wilson's disease , Menkes kinky hair syndrome ,Indian
childhood cirrhosis.
• Copper deficiency leads to normocytic hypochromic anemia.
• The most toxic intraocular foreign body is a particle of Copper.
• Chalcosis is deposition of Copper.
• Death in copper sulphate poisoning occurs due to Renal failure.
• Antidote for copper poisoning is Potassium ferrocyanide.
• Chelating agent for copper, mercury, lead which is given by oral route is Penicillamine.
• Copper sulfate acts both as poison and antidote.
• Copper binding protein is Ceruloplasmin.
• Menke's disease" is a disease of Impaired copper transport.
22. Trace element : Fluorine
• The clinical manifestations of Fluorosis are fluoride deposition in bones,teeth,Genu Valgum.

• Defluoridation is done by Nalgonda technique.
• Fluoride, used in the collection of blood samples for glucose estimation, inhibits the enzyme
Enolase.
• Maximum permitted level of fluoride in drinking water is 1 meq/L.
• "Maidon Teeth" is due to Fluoride .
• The primary mechanism of action of fluoride on topical application is as follows: Conversion of
hydroxyapatite to fluorapatite by replacing the OH- ions.
• In a case of suspected poisoning, the preservative used for vitreous during autopsy is Fluoride.
• Confirmed case of fluorosis is defined by presence of fluoride in urine more than 1 mg/L.
• Permissible level of fluoride in drinking water as per WHO is 1.5 mg/litre.
• Mottled enamel will be the earliest manifestation of fluorosis in a child.
• Excessive levels of Fluoride may have produced the defect in an 8 month old female child
presenting with her first four teeth showing several discrete, discolored, circumferential bands that
show very little enamel.
• In a PHC, Potassium oxalate + sodium fluoride anticoagulant is used to sent the blood sample for
blood glucose estimation .
• Sodium fluoride may be used for preservation of Alcohol.
• Double edged sword is Fluorine.
• Recommended level of fluoride to be present in water to prevent caries is 0.5-0.8 mg/L..
• Fluoride helps in Dentition.
• Dental fluorosis occurs if fluoride level is more than 1-5 mg/dl.
23. Trace element :Selenium
• Selenium sulfide is indicated for treating Tinea Versicolor.

• Sunflower seeds are good source of B complex vitamins,Vitamin E ,Selenium.
• Biological antioxidants which act against the free radicals formed inside the body are Selenium,
Uric acid ,vitamin E, Ascorbic acid,Ubiquinone and carotenes .
• Selenium act as a cofactor for enzyme Glutathione peroxidase.
• Selenium deficiency causes cardiomyopathy.
• Keshan disease is caused due to deficiency of Selenium.
• Hypothyroidism in Himalayan region is associated with Iodine Deficiency and Selenium deficiency.
24. NIACIN
• Nicotinamide is preferred over Niacin because Flushing is seen with niacin
• A 54-year-old man has a total cholesterol of 272 and LDL level of 210. His therapy is initiated with
dietary modification and an exercise regimen, but he is unresponsive and so is prescribed nicotinic
acid (Niacin) develops facial flushing
• Consumption of maize may aggravate Pellagra because Some strains of maize contains excess of
Leucine which interferes in the conversion of Tryptophan into Niacin
• Pigmented rash of sun-exposed areas, bright red tongue, diarrhea, apathy, memory loss and
disorientation are symptoms of niacin deficiency
• Development of pellagra like skin lesion in carcinoid syndrome is due to Inadequate conversion of
Tryptophan to Niacin
• Niacin is synthesised from Tryptophan
• About 60 mg of tryptophan is required to result in I mg of niacin.
• Diarrhea, Dementia & Dermatitis are seen in niacin deficiency
25. Proline
• Metabolism of proline takes place in Mitochondria

• The amino acid residue having an iminoside chain is proline
• A mutation is most likely to alter the three-dimensional conformation of a protein if It places proline in the
middle of a α-helix
• Amino acid, that destabilizes alpha-helix is proline
• Vit C, O2 , Dioxygenases,Fe2+ and α–ketoglutrate are elements required for hydroxylation of proline in
collagen synthesis
• Glutamate is precursor of proline
• Purely glucogenic amino acid is proline
26. Histidine
• Haemoglobin synthesis starts with Histidine

• Histidine is a polar amino acids
• Aminoacids with its PKR value within physiological range is Histidine
• FIGLU is a metabolite of Histidine
• Histidine is most responsible for the buffering capacity of hemoglobin and other proteins
• Amino acid with dissociation constant closest to physiological pH
• The amino acid which on decarboxylation gives rise to a product with potent vasodilator properties
is Histidine
• Histidine is is heterocyclic in structure
• Histidine is a semiessential basic amino acid
• Maximum influence of local milieu on ionization is on Histidine
• Histidine can protonate & deprotonate at neutral pH
• Amino acids with extra NH; (amino group) in strucuture

27. Carnitine
• Amino acid used in Carnitine synthesis is Lysine

• The substance essential for transfer of fatty acids across mitochondrial membrane is Carnitine
• Carnitine is synthesised from Methionine
• Carnitine is involved in transport of long chain acyl-CoA in mitochondria
• Hepatotoxicity caused by valproate can be prevented by Carnitine
• Carnitine palmitoyl transferase I is present in outer mitochondrial membrane & Carnitine palmitoyl
trasferase II in inner mitochondrial membrane
28. Hartnup Ds
• Massive aminoaciduria without a corresponding increase in plasma amino acid level is characteristic
of Hartnup disease
• Metabolism of Tryptophan amino acid is at fault in Hartnup's disease
• Hartnup disease is related to Pellagra symptoms
29. Niemann–Pick disease
• A severely retarded infant is noted to have hepatosplenomegaly and a cherry-red spot in the
macula is diagnosed to have Niemann-Pick disease
• A 2 year old retarded child is evaluated by a metabolic specialist. The child's history is significant for
failure to thrive and progressive neurologic deterioration, including deafness and blindness.
Physical examination is remarkable for hepatosplenomegaly, as well as a cherry-red spot on
funduscopic examination. These symptoms are consistent with a diagnosis of Niemann-Pick disease
• Examination of the fundus shows Cherry red spot in Niemann-Pick disease
• Accumulation of sphingomyelin in phagocytic cells is feature of Niemann-Pick disease
• Foam cells seen in Niemann-Pick disease
• Deficiency of sphingomyelinease causes Niemann-Pick disease
• Niemann-Pick disease is autosomal recessive
30. Bile Pigment
• Any of several colored compounds derived from porphyrin(myoglobin and heamoglobin)

• That are found in bile; principally bilirubin and biliverdin.
• Bilirubin is hydrophobic and potentially toxic compound.
• Daily production is 4 mg/kg of bilirubin,deriving mainly (70-80%) from hemoglobin
• Also from ineffective erythropoiesis and from various other heme proteins such
as cytochrome and myoglobin.
• Bilirubin is metabolised like xenobiotics.
• I gm of Hemoglobin yields 35mg of bilirubin
• Bilirubin has affinity for elastin, therefore jaundice is most easily seen in the sclera.
• Iron –porphyrin (heme) group of heamoglobin is degraded, mainly in the reticuloendothelial cells of
the liver, spleen, and bone marrow.
• Bilirubin is lipophilic and hydrophobic i.e solubility in water is less hence circulating in plasma by
covalently binding with albumin.
• Bilirubin is taken up across the sinusoidal membrane of hepatocytes by a carrier-mediated
mechanism
• Where it is bound to ligand
• In liver unconjugated bilirubin is metabolized to bilirubin diglucuronide
• This conjugation process occur in endoplasmic reticulum UDP-glucuronosyl transferase.
• UDP-glucuronate (a product of uronic acid pathway) is a donar of glucuronate residue for
conjugation
• Conjugation increase the solubility of whole molecule hence making it polar,able to cross cell
membrane
• Delete the toxicity of bilirubin(unconjugated bilirubin toxic to neuron).
• Stone formation is related to the deconjugation of bilirubin diglucuronide by bacterial beta
glucuronidase.
• Conjugated bilirubin is directed toward the canalicular membrane, and it is transported into the bile
canaliculus by an adenosine triphosphate (ATP)-dependent pum
• Conjugated bilirubin in plasma undergoes renal elimination .
• Urobilinogen is oxidized by intestinal bacteria to the brown Stercobilinogen which provide color to
stool.
• Normal urine does not contain bilirubin because normal blood contains bilirubin in the
uncongugated form which is not allowed to filter through the glomerulus
• Conjugated bilirubin is water soluble and filterable at the glomurulus, but not presaent in blood
normally and hence does not filter to appear in the urine.
31. Krebs Cycle
Krebs Cycle/Citric acid cycle (CAC)/Tricarboxylic (TCA) Cycle
• Amphibolic pathway (anabolic and catabolic).

• Takes place in the Mitochondrial matrix.(Erythrocytes (RBC) lack mitochondria)
VITAMINS ESSENTIAL FOR CYCLE (4)
• Riboflavin
• Thiamine is co-enzyme for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase.
• Niacin
• Pantothenic acid

STEPS
STEP 0(links glycolysis to the Krebs cycle)
Reactants Enzyme Products
Pyruvate(3C) + CoA(1C) + NAD+ Pyruvate dehydrogenase Acetyl CoA(2C) + CO2 + NADH +

H+
STEP 1
Acetyl CoA (2C) + Oxaloacetate (4C) + H20 Citrate synthase Citrate (6C) + CoA + H
• Citrate is converted into Cis aconitate, after losing a molecul of H20.

• Fluoroacetate can be converted to fluorocitrate, which is an inhibitor of aconitase
• Isocitrate not be added or removed by other metabolic pathways.
STEP 3
Isocitrate (6C) + NAD+ Isocitrate dehydrogenase α-Ketoglutarate (5C) + CO2 + NADH
STEP 4
α-Ketoglutarate (5C) + NAD+ + CoA α-Ketoglutarate dehydrogenase complex Succinyl CoA (4C) + CO2 + NADH
• The decarboxylation of an alpha-ketoacid

• Hyper ammonaemia inhibit TCA cycle by depleting a-keto glutarate.
STEP 5
Succinyl CoA (4C) + Pi + GDP + H20 Succinyl CoA synthase/Succinate thiokinase Succinate (4C) + GTP + CoA

• The substrate phosphorylation of GDP to GTP is coupled by the breakdown of the thioester bond in
the molecule of succinyl CoA which powers it.
• Only reaction in the citric acid cycle that directly yields a high-energy phosphate bond.
• Valine, Isoleucine and MethionineQ produce succinyl COA
STEP 6
Succinate (4C) + FAD Succinnate dehydrogenase Fumerate (4C) + FADH2
• Succinnate dehydrogenase is iron-sulphur protein imbedded in the inner membrane of

the mitochondria
• Inhibited by malic acid.
STEP 7
Fumerate (4C) + H20 Fumerase L- Malate (4C)
STEP 8
L-Malate (4C) + NAD+ Malate dehydrogenase Oxaloacetate (4C) + NAD + H+
Products
o The cycle produces three moles of NADH and one mole of FADH2 per mole of acetyl CoA oxidized
to CO2 and H2O
o NADH is produced and CO2 is liberated at 3 steps :
o Conversion of isocitrate to a-ketoglutarate by isocitrate dehydrogenase
o Conversion of a-ketoglutarate to succinyl CoA by oc-ketoglutarate dehydrogenase
o Conversion of L-malate to oxaloacetate by malate dehydrogenase.
INTERMIDIATE PRODUCTS
• Pyruvate, malonate and nitric acid
In vivo control of citric acid cycle is effected by ATP

CONTROL PIONTS
1. Pyruvate dehydrogenase
• Inhibited by high levels of: ATP, acetyl CoA and NADH
2. Isocitrate dehydrogenase(allosteric inhibitor)
• Inhibited by high levels of: ATP and NADH
3. α-Ketoglutarate dehydrogenase
• Inhibited by high levels of: ATP, succinyl CoA and NADH, arsinate
ANABOLIC PROPERTIES
• α-Ketoglutarate glutamate, other amino acids and purines

• Oxaloacetate(Unaltered final product of TCA cycle) aspartate, other amino acids, purines and
pyrimidines
32. Ketone Bodies
• Three water-soluble compounds produced by the liver from fatty acids.

• Result of intense gluconeogenesis during fasting, carbohydrate restrictive diets, , prolonged
intense exercise, alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus.
• Acetone is responsible for the characteristic "fruity" odor of the breath of persons in ketoacidosis
• Two of the three are used as a vital source of energy in the heart and brain when glucose low.
• The concentration of ketone bodies in blood is maintained around 1 mg/dl.
• Their excretion in urine is very low and undetectable by routine urine tests (Rothera's test)
• Diabetic Ketoacidosis is associated with serum glucose levels between 250-300 mg/dl'
33. Classification of Amino Acid
• Amino acids having an asymmetric carbon atom exhibit optical activity.

• Glycine is the simplest amino acid and has no asymmetric carbon atom and shows no optical
activity
• Aliphatic Side Chains : Glycine, Alanine, Valine, Leucine, Isoleucine
• Side Chains Containing Hydroxyl (OH) Groups :Serine, Threonine, Tyrosine
• Side Chains Containing Sulphur Atoms :Cysteine, Cystine, Methionine

• Side Chains Containing Acidic Groups or their amides : Aspartic acid, Asparagine, Glutamic acid,
Glutamine
• Side Chains Containing Basic Groups : Arginine, Lysine, Histidine
• Containing Aromatic Rings : Phenylalanine, Tyrosine, Tryptophan(photochromosity seen in this
group.)
• Imino acids or heterocyclic amino acids : - One of the 20 amino acids, proline is an imino (-NH) acid
not an amino (-NH2) acid, as are other 19.
• Cell membrane has its hydrophobic ends in the centre of membrane while its hydrophilic ends lie
on the outer surface of membrane.
• Hydrophobhic or Non polar aminoacid are present in transmembrane region.
• Hydrophillic or polar amino acids are present on outer surface of membrane.
• Sulfur containing Aminoacid: Cysteine alone.
• Simple amino acid: Alanine alone
• Sulfur containing amino acid: Methionine alone
• Aromatic Amino acids except Histidine .
• All branched chain amino acids: Leucine(most non polar),Isoleucine and Valine
• Imino acid: Proline
• Eight of these amino acids are essential (or indispensable) and cannot be produced by the body.
• Leucine, Isoleucine, Lysine, Threonine, Methionine, Phenylalanine, Valine, Tryptophan
• Nonessential- Asparagine, Alanine, Arginine, Aspartic acid, Cysteine, Glutamic acid, Glutamine,
Proline ,Glycine, Tyrosine, Serine
• Semi-essential- Histidine and Arginine
• Ketogenic :Leucine, Lysine
• Glucogenic:Valine, Cysteine, Serine,Alanine, Histidine,Threonine, Arginine, Glycine, Glutamate,
Proline/Hydroxy proline
• Both Glucogenic & Ketogenic :Isoleucine, Tyrosine ,Tryptophan , Phenylalanine
AMINO ACID CLASSIFICATION SPECIAL PRODUCTS

Isoleucine Ketogenic+Glucogenic/Essntl/Aliphatic
Valine Glucogenic/Essntl/Aliphatic(neutral)
Leucine Ketogenic/ Essntl/Aliphatic(neutral)
Lysine Ketogenic/ Essntl/Basic Carnitine
Methionine Glucogenic/Essntl/Sulphur(neutral) Creatine, epinephrine,

poiyamines
Phenyl alanine Ketogenic+Glucogenic/Essntl/aromatic(neutral)
Threonine Glucogenic/Essntl/Aliphatic(neutral)
Tryptophan Ketogenic+Glucogenic/ Essntl/aromatic(neutral) NAP, NADP, serotonin,

melatonin
Alanine Glucogenic/Non-Essntl/Aliphatic(neutral) Coenzyme-A

Glycine Glucogenic/ Non-Essntl/ Aliphatic(neutral) Creatine, glutathione, heme,
purines, conjugated bite
acids
Serine Glucogenic/Non-Essntl/ Aliphatic(neutral) Phosphatidyt serine,
sphingomyelins, choline
Cystiene Glucogenic/Non-Essntl/Sulphur(neutral) Glutathione, taurine, co

enzyme-A, active sulfate
Tyrosine Ketogenic+Glucogenic/ Non-Essntl/Aromatic(neutral) Thyroxine, epinephrine, nor

epinephrine, dopamine,
melanin
Valine Glucogenic/Non-Essntl/Aliphatic(neutral)
Proline Glucogenic/Non-Essntl/Heterocyclic
Glutamate Glucogenic/Non-Essntl/Acidic GABA, glutathione, gamma-
carboxy glutamate
Asparagine Glucogenic/Non-Essntl/acidic
Glutamine Glucogenic/Non-Essntl/acidic Purines, pyrimidines, amino
sugars
Arginine Glucogenic/Semi-essntl/basic Creatine , nitric oxide
Histidine Glucogenic/Semi-essntl/Imidazole ring Histamine
34. Antioxidant
ANTIOXIDANT
• Molecule that prevent oxidation of other molecule.
NATURAL AND SYNTHETIC ANTIOXIDANT

Antioxidant Source
Vitamin C Citrus Fruits
Vitamin E Vegetable Oil
Polyphenolic (resveratol and Flavoniod) Fruits, Red wine, Tea,Choclate, Orgeno, Coffe, Olive
oil,Soy

Careteniods (lycopene carotene, lutien) Fruits Vegetable egg
Synthetic Propylgallate, Butylated Hydroxyanisole, Butylated
Hydroxytoulene, Tertiarbutylhydroquinone.
CLASSIFICATION OF ANTIOXIDANTS
1. ANTIOXIDANT ENZYMES
1. Catalase
2. Glutathione peroxidase(selenium imp.component)
3. Glutathione reductase
4. Super oxide dismutase(both Cu -Zn and Mn)
2. METAL BINDING PROTIENS
1. Ceruloplasmin
2. Ferritin
3. Lactoferrin
4. Metallotheinein
5. Transferrin
6. Hemoglobib
7. Myoglobin
3. Bilirubin
4. Caroteniod
5. Beta Carotene
6. Alpha carotene
7. Lutien
8. Lycopene
9. Zeaxanthin
10. Vitamins A,C,E,D
11. Uric acids
12. Thiols
13. Other-Copper, Selenium,Zinc,Alpha lipoic acid,Glutathione
MECHANISM OF ACTION
• Vit. E prevents peroxidation of membrane phosphor lipids

• Vit.C reactivate oxygen and scavenges free radicals
• Super oxide dismutase reduces superoxide.
• Catalase and glutathione convert hydrogen peroxide.
35. Chemistry of Carbohydrates
1. General Formula for Carbohydrates-

a) Cn(H2O)n-1
b) Cn(H2O)n
c) Both of above
d) None of the above
Answer- Cn(H2O)n
Explaination- The general formula for carbohydrates is Cn(H2O)n where n= no of carbon atoms.
2. Glycogen is the main source of energy for human beings. What is the percentage of that-
a) 70-90% of total energy
b) 25-35% of total energy
c) 10-20% of total energy
d) 45-65% of total enegy
Answer- 45-65% of the total energy
Explanation- Primary source of energy for human beings is Carbohydrates as Glycogen which is around 45-
65% of total energy.
3. In a starving state in which form does body have energy?
a) Glucose
b) Fructose
c) Galactose
d) Mannose
Answer- Glucose
Explaination- Glucose is the main metabolic fuel for mature erythrocytes in a starving state.
4. Reducing sugar except-
a) Glucose

b) Sucrose
c) Fructose
d) Mannose
Answer- Sucrose
Explanation- Sucrose is a non reducing sugar.
5. Which of the following is not an aldose?
a) Glucose
b) Mannose
c) Fructose
d) Galactose
Answer- Fructose
Explanation-
Triose Glyceraldehyde
Tetrose Erythrose
Pentose Ribose, Xylose, Arabinose
Hexose Glucose, Galactose, Mannose
Heptose
6. Lactose is a constituent of-
a) Maltose
b) Mannose
c) Fructose
d) Galactose
Answer- Galactose
Explanation- Galactose is a constituent of Lactose(milk sugar) synthesized in the mammary gland for
synthesis of lactose.
7. Glucose detection can be done by all except-
a) Glucose oxidase
b) Ferric Chloride test
c) Dextrostix
d) Folin-Wu method
Answer- Ferric Chloride test
Explanation- Ferric Chloride test is the test done in Alkaptonuria and
Phenyl Ketonuria.
8. Which of the following are enantiomers-
a) D-Galactose and L-Glucose
b) D-Galactose and I-Glucose
c) D-Mannose and L-Mannose
d) D-mannose and I-Mannose
Answer- D-Mannose and L-Mannose
Explanation- examples of enantiomers-
• D Glucose and L Glucose

• D Fructose and L Fructose
• D Mannose and L Mannose
• D Glyceraldehyde and L Glyceraldehyde
9. Cellulose is-
a) Complex Lipoprotein
b) Starch Polysaccharide
c) Nonstarch Polysaccharide

d) Complex Lipoprotein
Answer- Nonstarch polysaccharide
Explanation- Foods contain a wide variety of other polysacdnarides that are collectively known as
nonstarch polysaccharides. They are not digested by human enzymes/ and are the major components of
dietary fiber.
Examples are cellulose from plant cell walls (a glucose polymer) and inulin, the storage carbohydrate in
some plants (a fructose Polymer)'
10. Mucopolysaccharide that doesn’t contains Uronic acid residue is-
a) Heparan Sulfate
b) Heparin
c) Chondritin sulphate
d) Keratan sulphate
Answer- keratin sulphate
Explanation-
GAG with no Uronic Acid- Keratan Sulfate
GAG with no Sulfate group- Hyaluronic Acid
GAG not covalently linked to protein- Hyaluronic Acid.
36. Classification Of Carbohydrates
Major source of energy for human beings is carbohydrates, as Glycogen (45-65%)
Glucose is dextrorotatory hence called as Dextrose.
The only metabolic fuel for mature erythrocytes in fed and starving state is glucose.
Galactose is the constituent of lactose (milk sugar) and part of glycosaminoglycan in proteoglycans
glycolipids.

Fructose is present in honey, seminal fluid.
Glycosaminoglycan with no uronic acid is Keratan sulphate.
General formula- Cn (H2O)n (for monosaccharide)
If ring structure formed by cyclization is six sided called as pyranose ring (pyran) (seen in glucose)
Dihydroxyacetone (no asymmetric carbon atom)
Mannose is an epimer of glucose
37. Mucopolysaccharidoses
1. Lysosomal enzymes needed to be degrade into glycosaminoglycan results in Intralysosomal

accumulation of glycosaminoglycan.
2. impaired degradation of Heparan sulfate associated with Mental deterioration.
3. Muccpolysaccharidoses with no corneal clouding is Hunter's disease and Sanfilippo disease.
4. All muccopolysaccharidoses are autosomal recessive except Hunter disease.
38. Derived Sugars
1. Derived Sugars include- Acid sugars, Sugar alcohols, Deoxy sugars, Amino sugars, Glycosides, Furfural
derivatives.
2. The immediate precursor of Glucosamine is Fructose 6 phosphate.
39. Isomerism
1. Monosaccharide with no Asymmetric Carbon atom- Dihydroxyacetone.
2. Aldose sugar is converted to ketose and vice versa by enzyme isomerase.
3. Glucose and mannose are C2 epimers and glucose & galactose are C4 epimers.

4. Maltose is a reducing disacharide.
5. Lactose is a reducing dissacharide.
6. Sucrose is a non-reducing sugar.
7. Benedict's quantitative reagent detects any reducing sugar.
8. Fehling solution contains CuSO4 and Ruchelle salt .
9. Glucose oxidase method is used for glucose.
10. Perioxidase and oxidase enzymes are used for estimation of glucose.
40. Digestion & Absorption of Carbohydrates
1. Widely distributed Glucose transporter - GLUT-1
2. Most abundant Glucose transporter in RBC- GLUT-1
3. Major Glucose transporter of Placenta - GLUT-1
4. Insulin dependent Glucose transporters- GLUT-4, GLUT-8, GLUT-12
41. Glycolysis Cycle
1. Principal route for Carbohydrate metabolism is glycolysis.
2. Only pathway which can operate ananerobically and aerobically.
3. Mature Erythrocytes which lack mitochondria are completely dependent on glucose for metabolic fuel.
4. Glucokinase is induced by Insulin following a meal.
5. Fructose 6 phosphate to Fructose 1,6 bisphophate is the major regulatory step in glycolysis and is a
committed step also.
6. Irreversible steps of glycolysis are- Hexokinase, Phosphofructokinase, Pyruvate kinase.

42. Glycogenesis
1. Glycogen phosphorylase is a cardiac biomarker.
2. Enzyme common to glycogenesis and glycogenolysis is Phophoglucomutase.
43. Rapoport- Leubering Cycle
Rapoport Leubering cycle occurs in erythrocytes
2, 3 –bisphosphoglycerate combines with hemoglobin & reduces affinity towards oxygen.
2,3 BPG shifts the oxygen Dissociation curve to right due to reduced affinity towards oxygen
No ATP is generated (only one molecule generated through glycolysis in RBC utilized)
Under hypoxic conditions, 2, 3- BPG increases in RBCs
Cancer cells switching to glycolysis even in the presence of adequate O2 for oxidative phosphorylation c/d Warburg
effect
44. Cori's Cycle
1. In Glucose- alanine cycle, amino acid increased in blood during starvation is Alanine.
45. Gluconeogenesis
1. Sites for gluconeogensis is liver and kidney.
2. Organelle is Cytoplasm and mitochondria
3. Enzymes common for glycolysis and gluconeogenesis.
4. Pyruvate carboxylase is repressed by Insulin.
5. Acetyl CoA as an allosteric activator of Pyruvate Carboxylase.
6. After 12-18hour of fasting, liver glycogen is completed depleted.

46. Glycogenolysis
1. Iso enzymes of Glycogen Phosphorylase is present in Muscle, Liver and Brain.
2. Glycogen phosphorylase BB is a cardiac Biomarker.
3. PLP is the coenzyme of Glycogen phosphorylase.
47. Glycogen Storage Disease
1. Most common GSD in adolescent and adults- Type V GSD (McArdles Disease)
2. Liver GSD disorder causes fasting hypoglycemia and hepatomegary

3. GSDs associated with liver cirrhosis- Type lll, Type lV, Type lX GSDs
4. GSD associated with renal dysfunction- Type I GSD
5. Liver GSD with myopathy- Type lll GSD and Type lV GSD
6. Liver GSD with neurological (brain and anterior horn cells) involvement - Type II GSD
48. Citric Acid Cycle
1. There is no net generation oxaloacetate or cycle intermittents.
2. First product of the cycle is citrate.
3. Two irreversible steps are-
i) oxaloacetate to citrate catalyzed by citrate (synthase)
ii) alpha ketoglutarate to succinyl CoA.
4. NADH is produced and CO2 is liberated.
5. GTP is produced by substrate level phosphorylation by succinate thiokinase.
6. 4 dehydrogenases are used in Kreb's cycle.
7. Isolucine, Methionine, Valine enter by conversion into succinyl CoA.
8. Tyrosine, phenylalanine enter conversion into fumarate.
9. Pyruvate Carboxylase reaction is the classical example of the anaplerotic reaction.

49. Properties of Amino Acids
1. Amino acids not coded by genetic code are all derived amino acids.
2. The charge of carboxyl group and amino group at physiological pH (pH= 7.4)
3. Carboxyl group is negative & amino acid group is positive.
4. Aromatic amino acids absorbs UV light.
5. Most polar amino acid is Arginine.
6. Most abundant amino acid in the body present is Alanine.
50. Metabolism of Amino Acid
1. GDH is a mitochondrial matrix enzyme.

2. GDH catalyzes reversible oxidative deamination.
3. α-ketoglutarate is the keto acid which accept the amino group of α-amino acids and produces other
α amino acid ie. Glutamate.
4. Deamination (removal of –NH2 group)
5. Glutamine is a nontoxic major transport form of ammonia
6. Transport of ammonia from skeletal muscle as Alanine.
7. Sources of Urea-
NH2 from ammonia
CO CO2
NH2 from aspartate
51. Metabolism of Aromatic Amino Acids
1. Specialized Products from Tyrosine-
a) Melanin
b)Catecholamines
c) Thyroxine
2. Epinephrine and norepinephrine is catabolized by Catechol O Methyl then by Monoamino Oxidase.

3. The major end product of epinephrine and norepinephrine is Vanillyl Mandelic Acid.
4. Diagnosis of Phenylketonuria is by Guthries test.
52. TRYPTOPHAN
• Specialized products from tryptophan are- Niacin, Seratonin, Melatonin

• 60 mg Tryptophan is converted to 1 mg of Niacin.
• Pellagra Like Symptoms in Hartnup's Disorder-
• Decreased absorption of Tryptophan from intestine.
• Decreased availability of Trp for NAD' pathway leading to Niacin deficiency.
53. PHENYLKETONURIA
1. The children have a mousey or musty odour of phenylacetic acid.
2. Brain is the main organ affected by hyperphenylalaninemia.
3.Due to the deficiency of enzyme phenylalanine hydroxylase.
4. Phenylketonuria is the most common metabolic disorder in amino acid metabolism.
5. Increased excretion of phenylalanine in urine gives the urine a mousy odour.
6. The classical PKU child is mentally retarded with low IQ.
7. Accumulation of phenylalanine inhibits tyrosinase and impairs melanin formation resulting

in hypopigmentation.
54. ALKAPTONURIA
1. Belongs to Gerrads Terad ( Alkaptonuria, Albinism, Pentosuria, Cystinuria)
2. No mental retardation is seen in alkaptonuria
55. TYROSINEMIA

1. Tyrosinemia has cabbage like smell due to succinylacetone.
56. Albinism
1. OCA-2 tyrosinase is the most common type of albinism
2. Most common cause is due to deficiency of enzyme tyrosinase leading to defective synthesis of melanin.
3. Color of iris is pink.
4. Syndromes associated with Oculocutaneous syndrome-
a) Prader willi and Angelman syndrome
b) Hermansky- Pudlak syndrome
c) Chediak- Higashi syndrome
57. Metabolism of Sulphur containing Amino Acids
1. Cysteine and cystenine are synthesized from 2 amino acids, methionine and serine.
2. Methionine acts as a methyl donor in transmethylation reaction.
3. Cystine is formed by formation of disulfide bond between two cystein molecules.
58. HOMOCYSTINURIA
1. High homocysteine is a risk of factor for coronary atherosclerosis.
2. Osteoporosis, fracture and neuropsychiatric problems seen in homocysteine.
59. Metabolism of Simple Amino Acids
1. Glycine is optically inactive amino acid.

2. Vitamins involved in the conversion of Serine to Glycine are PLP and Folic acid.
3. When Serine is converted to Glycine, the β carbon atom of Serine is donated to THFA.

4. Glycine do not contribute to Pyrimidine ring.
5. Cystenine is synthesized from methionine and serine.
6. Serine is synthesized from 3- phosphoglycerate and also from glycine.
7. Selenocysteine is considered as 21st standard amino acid.
60. Metabolic Disorder of Glycine
1. Sarcosine is N-Methyl Glycine.
2. Betaine is Trimethyl Glycine.
61. Metabolism of Branched Amino Acid
1. All branched amino acids are essential.
2.
Gene Component Maple Syrup Urine Disease

E1α Branched Chain α Ketoacid Type I A MSUD
decarboxylase
E1β Branched Chain α ketoacid Type I B MSUD

Decarboxylase
E2 Dihydrolipoyl Transacylase Type II MSUD

(contains lipomide)
E3 Dihydrolipomide Dehydrogenase Type III MSUD
3. Ketoacids are detected by Dinitrophenylhydrazine (DNPH) test.
4. Odour of Sweaty Feet is present in Isovaleric Aciduria.
62. Metabolism of Basic & Acidic Amino Acid
1. Bacterial Putrefaction (Decarboxylation) of Lysine forms Cadaverine.

2. Histone Proteins are Lysine rich.
3. Arginine splits to Omithine and Urea.
4. Amino group of all Amino Acids are concentrated as Glutamatea by transamination.
5. Amino Acids enter TCA cycle at different level-
a) To Succinyl CoA
- Valine
- Isoleucine
- Methionine
- Threonine
b) To Fumarate
- Tyrosine
- Phenylalanine
- Aspartate.
c) To Oxaloacetate
Asparugine to Aspartate, which is transaminated to Oxaloacetate.
63. Classification of Proteins
1. Most of the structural proteins are fibrous proteins. E.g.- collagen, elastin and keratin
2. Simple proteins include- albumin and globulin
3. Primary derived proteins are formed without breakage of peptide bonds.
4. Secondary derived proteins are formed with successive breakage of peptide bonds.
64. Structure of Protein

1. Weak non-covalent- hydrogen, hydrophobic, electrostatic, Van der Waals.
2. Tertiary structure is maintained by weak con- covalent interactions.
3. Glycine tends to disrupt to α-helix.
4. Proline is never found in α-helix.
5. Each hydrogen bond has nitrogen to oxygen distance 2.80 A.
6. Primary structure by covalent ‘peptide bond’.
7. Oxidoreductase with Rossmann Fold
- Lactate dehydrogenase
- Alcohol dehydrogenase
65. NUCLEOTIDES
1. DNA labelling is done by using P- 32

2. Carbon-I of pentose sugar with nitrogen-9 of the purine base or nitrogen-I of pyrimidine base.
3. Nucleic acids are polymers of nucleotides joined by 3’-5’ phosphodiester bond.
4. - Nucleotides – Nucleoside + phosphoryl groups
5. Double helix is the structure of DNA.
6. Purine bases present in RNA and DNA are adenine (A) and guainine (G)
7. Cytosine (C)- present in both DNA and RNA
8. Thymine (T)- present in DNA
9. Uracil (U)- Present in RNA
10. Nucleosides – Nitrogenous base + pentose sugar by covalent N- glycosidic bond.
11. No. Of strands in DNA are 2.
12. No. Of strands in RNA is 1.
66. STRUCTURE OF DNA
1. Uracil (Pyrimindine) is not found in DNA.

2. Alternating phosphate and deoxyribose units form the backbone structure of DNA while purine and
pyrimidine bases are stacked inside.
3. All the purine and pyrimidine bases present on one strand of molecule take part in hydrogen
bonding with complementary bases on opposite strand.
4. Alternating phosphate and deoxyribose sugar unit form the backbone structure of DNA strand.
5. Bacterial DNA Gyrases is a subset of Topoisomerases type ll
6. The simplest form of labelling DNA is by 5'- 3' end labelling.
7. Negative strands of DNA direction is 31 ----> 51
8. DNA is located in nucleus and is also present in mitochondria.
9. Width of double helix is 20 A0 and length is 34 A0 .
67. STRUCTURE OF RNA
1. mRNA contains a poly A tail.

2. Poly-A tail made up of several adenylate residues which stabilize mRNA by preventing attack of 3'-
exonuclease.
3. tRNA may be modified and known as modified or unusual bases.
4. Modified base is altered purine or pyrimidine.
5. Acceptor arm in tRNA has CCA tail is added during post-transcriptional modification.
6. rRNA is synthesized in nucleolus.
7. Specific Nucleaees lnvolved in the Post Transcriptional modification of miRNA and siRNA is- Drosha-
DGCR8 Nucleases
68. METABOLISM OF PURINE
1. First Nucleotide formed in Purine Synthesis-lnosine Mono Phosphate (lMP)
2. Liver is the major site of nucleotide biosynthesis.
3. Tissues which cannot synthesis purine nucleotides by de nevo pathway are- brain, erythrocytes and
leuckocytes.
69. GOUT- PURINE METABOLISM DISORDER
1. Glucose-6- phosphate deficiency (Van Gierke’s disease)- generates large amout of ribose -5-
phosphate.
2. Gout is caused due to overproduction of uric acid.
3. The typical characteristic of Gout is Tophi deposits, hyperuricemia, acute gouty arthritis.
4. The most common joint affected by gout is the Knee joint.
5. Lead poisoning leads to gout.

70. LESCH- NYHAN SYNDROME
• It is a sex linked disorder. (X Linked Recessive Disorder)

• The structural gene of HGPRT is located on X-chromosome.
• There is a complete deficiancy of HGPRT
• Self mutilation is one of the characteristic feature of the syndrome.
• Allopurinol is used in the treatment.
71. SEVERE COMBINED IMMUNODEFICIENCY (SCID)
1. There is a decrease in T and B cells.

2. Adenosine accumulation is seen in SCID.
3. DNA synthesis decreases.
4. X Linked Pattren of Inheritance is most common
72. Different Types of DNA
1. A, B, C, D and E DNAs are right handed double helix

2. Z- DNA is a left handed double helix DNA
3. B- DNA is the most common form.
4. B- DNA describes the Watson and Crick model of DNA
5. Z- DNA is longer and thinner than B- DNA.
6. Z- DNA has phosphodiester bond
7. Z- DNA has alternate G-C sequences
8. Four stranded has high guanine content.
9. Hoogsteenpairs seen in triple stranded and four stranded DNA.
73. DENATURATION OF DNA
1. Hydrogen bond is broken in denaturation.

2. Disruption of hydrogen bond can be due to increase in temperature or change in pH
3. Phosphodiester bond is intact in denaturation.
4. Loss of helical structure of DNA is denaturation.
5. Primary structure is not altered by denaturation.
6. Formamide is effectively used in recombinant DNA.
7. Increase in salt concentration increases DNA duplex stability.

74. ORGANIZATION OF DNA IN THE CELL
1. Chromatin is unfolded and uncondensed.

2. Chromatin and chromosome are made up of DNA and non-histone proteins.
3. At the physiological pH, DNA is negatively charged because of phosphate group.
4. DNA molecule is an amphipathic.
75. HISTONES
• Total number of chromosome in humans is 46 (23 pairs).

• The number of base pairs in haploid set of chromosome is 3.0 x 1O9 (3 billion bp)
• Percentage of exons in human genome is approximately 1.14% (1.5-2%)
• The number of protein coding genes in human genome is 20,687.
• The genes account for 10-15% of DNA.
• Euchromatin is transcriptionally active and heterochromatin is transcriptionally inactive.
• For euchromatin, chromatin is less densely packed.
• For heterochromatin, chromatin is densely packed.
76. DE NOVO SYNTHESIS
1. Sites where de novo synthesis do not take place:
• Brain
• Erythrocytes
• Polymorphonuclearleukocytes
• Bone marrow.
1. Nucleotides are the products of De Novo synthesis.

2. PRPP amidotransferase catalyzes the committed step.
77. SALVAGE PATHWAY OF PURINE NUCLEOTIDES
• Two main enzymes of salvage pathway are-
i) Adenine phosphoribosyl transferase
ii) Hypoxanthine Guanine phosphoribosyl Transferase (HGPRTase)
• Hypoxanthine to IMP by Hypoxanthine Guanine phosphoribosyl Transferase (HGPRTase)

• Adenine to AMP by Adenine phosphoribosyl transferase
• The end product of all purine metabolism is uric acid.
78. Degradation of Purine Nucleotides
1. Human catabolise purines (adenine and guanine) to uric acid.

2. First metabolic product of purines is xanthine.
3. In non primate mammals, uric acid is converted to water soluble allantion by enzyme uricase.
4. The end product of purine catablism is uric acid, which is excreted.
79. Metabolism of Pyrimidine
1. Precursors for de novo synthesis of pyrimidine are.
i) Glutamins provides N3
ii) Aspartic acid furnishes C4, C5, C6, and N1
iii) CO2 provides C2
2. Aspartate transcarbamoylase catalyzes a coomitted step in pyrimidine synthesis.
3. Pyrimidines are degraded to amino acids, namely β- alanine and β- aminoisobutyrate which are then
metabolized.
80. Degradation of Pyrimidine Nucleotides
1. The end products of pyrimidine catabolism are highly water soluble. E.g. CO2, NH3, β-
aminoisobutyrate, beta alanine.
2. Pseudouridine is excreted unchanged as it cannot be catabolized in human.
3. Humans have no enzyme that can catabolise pseudouridine derived from degradation of t-RNA.
4. There is no energy generated in pyrimidine catabolism.
5. The end products of pyrimidine catabolism is CO2 and H2O.
81. OROTIC ACIDURIA- Pyrimidine disorder
1.Synthetic nucleotide used in the treatment of AIDS- Zidovudine.

2. The bifunctional enzymes deficient in orotic aciduria are
> orotate phosphoribosyl transferase
> Orotic acid decarboxylase (orotidylate decarboxylase)
3.Type II orortic aciduria is caused due to deficiency of Orotic acid decarboxylase (orotidylate
decarboxylase)
4. 6-Azauridine (after its conversion into 6-azauridylate) also cause orotic aciduria and orotinuria by
inhibiting orotidylate decarboxylase.
5. orotate phosphoribosyl transferase and Orotic acid decarboxylase (orotidylate

decarboxylase) together called as UMP Synthase.
82. ANTIMETABOLITES
• Synthetic nucleotide used in the treatment of AIDS- Zidovudine.

• Synthetic nucleotide used in the treatment of Gout-Allopurinol
• Synthetic nucleotide used to suppress immunologic rejection during organ transplantation-
Azathioprine.
• Allopurinol is a powerful inhibitor of xanthine oxidase.
83. Regulation of Gene Expression
1. Genome of humans contains 30,000 to 40,000 of genes.

2. Gene is expressed in terms of synthesis of protein.
3. Transcription is the primary site of regulation in both prokaryotes and eukaryotes.
4. Regulation of transcription usually embedded in the non-coding region of genome.
5. Cis-acting factors influence expression of genes only on the same chromosome.
6. Trans-acting factors influence expression of genes on other chromosomes.
7. Structural genes (code for protein) are present in the code region.
84. OPERON CONCEPT
1. Regulation of transcription usually embedded in the non-coding region of genome.

2. Operator, segment of DNA regulates structural genes of operon and repressor binds to this site to block
transcription.
3. 3 structural genes- Z, Y and A.
4. Promoter site- CAP site
5. In glucose situation, lac operon is repressed.
6. CAP site is a positive regulator.
85. Codons & Genetic code
1. Information for synthesis of protein is contained in the mRNA.

2. Thymine is not involved in codons.
3. 64 (43) possible codon sequences.
4. tRNA acts as the adapter molecule between the codon and specific amino acid.
5. UUU is the codon for phenylalanine.
6. Degeneracy of the codon lies in the 3rd base.
7. Amino acid with maximum number codons are Serine, Arginine, Leucine.
8. Monocistronic- e.g. eukaryotic mRNA
9. Polycistronic- e.g. Prokaryotic mRNA
86. STEPS OF PROTEIN SYNTHESIS (Translation)
1. Translation occurs in ribosomes.

2. mRNA is translated from its 5’ end to its 3’- end (51 à 31 )
3. AAS is identified by DHU arm and is considered as proofreading mechanism of translation.
4. Aminoacyl synthase implements genetic code by acting as molecular dictionaries.
5. Two initiation factors(eIF3 & eIF-1A) binds to 40S subunit of eukaryotic ribosome (80S).
6. AUG serves as initiation codon for protein synthesis and codes for methionine
7. Shine- Dalgarno sequence located -6 to -10bp from AUG codon. (purine rich).
8. 3 sites on 80S Ribosome-
i)A site- new aminoacyl tRNA binds
ii) P site- growing peptidyl chain present
iii) E site- deacylated tRNA present.
1. 2 ATPs are required for activation of amino acid.

2. There is no tRNA for hydroxyproline and hydroxylysine.
87. INHIBITORS OF PROTEIN SYNTHESIS
1. Streptomycin is an irreversible and bactericidal.

2. Aminoglycosides drugs include gentamicin, amikacin, neomycin, streptomycin.
3. Tetracycline drugs include doxycycline, minocycline.
4. Mechanism of action of tetracycline is binds to 30S ribosome subunit.
5. Aminoglycosides is bactericidal.
6. Chloramphenicol is administered orally and IV.
88. ENZYMES
1. Ribozymes RNA molecule with catalytic activity.

2. Holoenzyme= apoenzyme + non protein apart.
3. Co- substrates- In a group transfer reaction coenzyme acts either a donar or acceptor. Most
common mechanism of coenzymes.
4. Enzymes are proteins or polypeptide (building blocks).
5. Non protein part- coenzyme, cofactor, prosthetic
6. Non protein- chemical components are organic molecules(coenzyme)
89. COENZYMES
1. Co- substrates- In a group transfer reaction coenzyme acts either a donar or acceptor. Most
common mechanism of coenzymes.
2. Non protein- chemical components are organic molecules(coenzyme)
3. Classification of coenzymes-For transfer of hydrogen- Lippoic acid
4. Zinc- carbonic anhydrase, Alcohol dehydrogenase
5. Metalloenzymes (Cofactors)-
Metal Metalloenzymes
Copper (Cu+2/Cu+) Cytochrome oxidase, Lysyl oxidase, ceruloplasmin
Iron (Fe+2/Fe+) Xanthine oxidase
Zinc (Zn+2) Carbonic anhydrase, alkaline phosphatase, alcohol dehydrogenase,
carboxypeptidase, glutamate dehrdogenase, lactate dehdrogenase,
superoxide dismutase
Magnesium (Mg+2) Phosphatases, kinase, glutathione synthase
Selenium Glutathione peroxidise
Molybdenum Xanthine oxidase, sulphite oxidase
6.
Vitamin Coenzyme Function Entity transferred

as Coenyme
Riboflavin (Vit B2) FAD, FMN Oxidation & Hydrogen atoms
reduction reaction
Niacin NAD+, NADH+ Oxidation & Hydride ion
reduction rxn Coenzyme for
pyruvate
dehydrogenase-
NADPH
7. Coenzyme for Glucose-6 phosphate dehydrogenase- NADP
8. Coenzyme for malate dehydrogenase- NAD+
9. Coenzyme for pyruvate dehydrogenase- NADPH
90. CLASSIFICATION OF ENZYMES
1. According to International Union of Biochemistry, enzymes classified into 6 classes called

as enzyme code (EC)
2. A/c to IUB classification, Fourth digit- individual enzymes
3. Class I enzyme (EC-1)- Oxidoreductases- oxidation- reduction reaction.
4. Ligases- binding two compunds together from source of energy ATP.
5. Oxireductases- Hydroperoxidases- Peroxidases, catalases.
6. Hydrolases make use of water cleave a single molecule into two molecules.
91. MECHANISM OF ENZYME ACTION
1. Also called as Enzyme- Substrate Complex Theory.

2. Enzyme (E) combines with its substrate (s) to form enzyme- substrate complex to form product (P).
3. Vo =Vmax (S) /Km + (S)
4. Km- michaelis menten constant
5. The reaction takes place in active site.
6. Fischer’s template theory is the lock and key model.

92. ENZYME INHIBITION
1. Reversible Inhibition- binds through non-covalent bonds and activity of enzyme is restored.
2. Competitive inhibitor- Km increased, Vmax unchanged.
3. Competitive inhibitor- Succinate dehydrogenase by melanate.
4. Non competitive inhibitor- Km unchanged, Vmax decrease, mostly irreversible.
5. Non competitive inhibitor- E.g.- Cyanide by Cytochrome C Oxidase.
6. Suicidal Inhibitor- Allopurinol inhibit Xanthine oxidase.
93. REGULATION OF ENZYME
• Allosteric modulation example-
Enzyme Pathway Stimulator Inhibitor

Phosphofructokinase Glycolysis Fructose-2,6- Citrate
biphosphate
• The most common covalent modification is the addition or removal of a phosphate group.
• Irreversible covalent modification- partial proteolysis/ zymogen activation
• Methods of Reversible covalent modifications-
a) Phosphorylation/ dephosphorylation (most common)
Enzyme Active Inactive
Glycogen Synthase Dephosphorylated Phosphorylated
Pyruvate dehydrogenase Dephosphorylated Phosphorylated
HMG- CoA- reductase Dephosphorylated Phosphorylated
HMG- Co reductase kinase Phosphorylated Dephosphorylated
• Protein kinase mostly add phosphoryl group to a serine, threonine or tyrosine.

• Specific activity- number of enzyme units per milligram of protein.
• Catalase has the highest turnover number and hence is the fastest active enzyme.

94. ISOENZYMES
1. Isoenzymes differ from each other structurally, electrophoretically and immunologically.

2. Isoenzymes possess quaternary structure and are made up of two or three different subunit
(mutimeric).
3. Functional plasma enzymes- specific function in the plasma.- E.g. Coagulation factors (thrombin),
lipoprotein lipase, clotting factors.
4. Non functional enzymes- E.g. alkaline phosphatase, acid phosphatase, gamma glutamyl
transpeptidase, LDH, Creatine kinase.
5. LDH has five isoenzymes.
Name of the isoenzyme Tissue location
LDH-1 Heart muscle
LDH-2 RBC
LDH-3 Brain
LDH-4 Liver and skeletal muscle
LDH-5 Liver and skeletal muscle
6. In MI, LDH1 is raised more than LDH2.
7. Creatine Kinase (CK)- Three isoenzymes.
CK-1 Brain
CK-2 Heart
8. ALP found in liver, bone, kidney, intestinal mucosa and placenta.
9. Serine Proteases- serine residue at the active site(serine, histidine, aspirate).
10. Serine proteases- E.g.- Trypsin, chymotrypsin, elastase (Catalytic triad).
11. Serine proteases activated in intestine by proteolytic activation.
12. Most important carboxyl proteases is Pepsin.
95. ENZYME MARKERS

1. SERINE PROTEASES-
• Trypsin cleave basic amino acid.

• Chymotrypsin cleave hydrophobic amino acid.
• Elastase cleave alanine, glycine.
2. BI-BI Reactions-
E.g. – Aminotransferases and Serine Proteases.
3. ENZYMES AS MARKERS OF ORGANELLE AND MEMBRANES-
• Endoplasmic reticulum- Glucose- 6- phosphatase

• Golgi Complex- Galactosyl Transferase
• Plasma- 5’-Nucleotiddase, Adenylyl cyclase
1. Perioxidase enzyme is used in estimating- Glucose, Cholesterol.
4. ENZYMES IN OTHER BODY FLUIDS-
• Lactate dehydogenase in CSF, pleural fluid- malignant tumour but no confirm.

• Adenosine deaminase in pleural fluid- tuberculous pleural effusion
• Amylase in urine- pancreatitis
5. Biomarkers of Acute Kidney Injury-
• Kidney Injury Molecule-1 (KlM-1)

• Neutrophil Gelatin associated Lipocalin (NGAL)
• IL-18
• Alanine Amino Peptidase
• Alkaline Phosphatase
• γ Glutamyltranspeptidase
96. Lipids
• The building blocks of most lipids are fatty acid.

• Cholesterol and terpens lack fatty acid.
• Compound or complex lipids- include phospholipids, glycolipids (Glycosphingolipids) , lipoprotein.
97. FATTY ACIDS
1. Monounsaturated (Monoenoic) fatty acids-single double bond. Cn H2n-1 COOH

2. Monoenoic fatty acids contain double bond at 9th position.
3.
No. of C atoms and number & Family Common Name Occurence

position of double bonds
Trienoic acids 18:3, 6, 9, 12 ω6 γ-Linolenic Oil of evening primrose, borage oil,

linseed oil
18:3, 9, 12, 15 ω3 α-Linolenic Linseed oil

Tetraenoic acids 20:4, 5, 8, 11, ω6 Arachidonic acid Found in animal fats
14
Hexaenoic acids ω3 Cervonic Fish oil, phospholipids in brain,
Breast milk
Monoenoic acid 18:1, 9 ω9 Oleic High in olive oil
4. Short chain length- less than 6 carbon atoms chain
5.
ω-3 fatty acids ω-6 Fatty acids ω- 9 fatty acids
Alpha linolenic acids Linolenic acids Oleic acids
Clupandonic acid Gamma linolenic acid Nervonic acid
Cervonic acid Arachidonic acid Elaidic acid
98. ESSENTIAL FATTY ACIDS
• Polyunsaturated fatty acids (PUFA) are 3 fatty acids- linoleic acid, linolenic acid and arachidonic
acid are called essential fatty acids.
• Fatty acids requires but not synthesized fatty acids in humans.
• Human cannot synthesize linoleic acid and linolenic acid.
• Linoleic acid is the most important essential fatty acids.
• Linoleic acid in decreasing order-
• Safflower oil > cornoil > sunflower oil> Soyabean oil
• Arachidonic acid has maximum carbon atoms (20).
• Linolenic acid- (3 double bonds)- C17 H29COOH

Functions of Essential Fatty Acids-
• Arachidonic acid a 20 carbon polyunsaturated fatty acid.

• Arachidonic acid is an essential precursor of eicosanoids (prostaglandins)
• EFAs are required to maintain structural integrity by maintaining cell membrane structure.
• Docosa hexaenoic acid (DHA: ω-3)- derived linolenic acids. (brain and retina during neonatal period)
• Docosa hexaenoic acid (DHA: ω-3)- supplied by breast milk.
99. ISOMERISM IN FATTY ACIDS
• Cis- trans isomerism occurs in unsaturated fatty acids.

• Double bonds in naturally occuring vegetable unsaturated long-chain fatty acids are nearly all in the
cis configuration.
• Trans fattyacids are formed during the hydrogenation.
• Trans fatty acids are in deep fried foods.
• Trans fatty acid is increased in vegetable oil refining, hydrogenation and food frying.
• Saturated fatty acid-
• Carbon chain length of 14- myristic (increases cholesterol)
• Carbon chain length of 16- palmitic
• Carbon chain length of 18- Stearic acid
• Fatty acid present in human milk is Docosa Hexaenoic Acid (Cervonic Acid).
• Least source of PUFA ls Coconut oil
• Richest source of medium chain fatty acid is Coconut oil
100. TRIACYLGLYCEROL
• Also called as triglycerides or neutral fat.

• It is a trihydric alcohol.
• Triglycerides are the main storage form of energy and fat.
• They are stored in adipose tissues.
101. PHOSPHOLIPIDS
1.Glycerophospholipids (phosphoglycerides)- that contains glycerol as alcohol. They are-
a) Phosphatidylcholine (lecithin)
• Most abundant phospholipids in cell membrane.

• Dipalmitoyl lecithin in lungs
• Insufficient production of Dipalmitoyl lecithin- acute pulmonary distress syndrome in premature
infants.
b) Phosphatidylethanolamine (Cephalin)- contains ethanolamine.
c) Plasmogens- platelet activating factor
d) Cardiolipin (Diphosphatidylglycerol) - is a major lipid of inner mitochondrial membrane.
• It has antigenic properties (only humans).

• Deficiency causes- Barth syndrome.
102. GLYCOLIPIDS
• Glycosphingolipid = Sphingosine + long chain fatty acid + sugars

• Glycolipids are synthesized in endoplasmic reticulum.
• Glycosphingolipids are 4 types-
1. Cerebrosides- ( ceramide + monosaccharides)
• Cerebroside= sphingoside + long chain fatty acid + glucose

• Monosaccharides used is mostly glucose (glucocerebroside) or galactose (galactocerebroside).
• Clinical Aspect-
1. Krabbe’s disease caused by deficiency of enzyme of ?- galactosidase.
- Galactocerebroside accumulates in brain.
2. Gaucher’s disease caused by deficiency of ?- glucosidase (glucocerebrosidase)
- Glucocerebroside (glucosylceramide) is accumulated in brain.
2. Sulfatides- cerebroside + sulphate
3. Globosides- ceramide + oligosaccharide
4. Gangliosides
• ceramide + oligosaccharide chain (glucose+galactose) + N- acetylneuromic acid (NANA)

• Gangliosides= Sphingosine+ long chain fatty acid + oligosaccharide chain (glucose or galactose)+
NANA
• Tay- Sach’s Disease- caused due to deficiency of hexosaminidase (alpha subunit) .
103. SPHINGOPHOSPHOLIPIDS

• Contains sphingosine as alcohol (no glycerol)
• Most important sphingophospholipid is sphingomyelin.
• Ceramide= sphingosine + long chain fatty acid.
• Sphingomyelin = Ceramide + Phosphoryl group + Nitrogenous base
• Phosphorylcholine= phosphoric acid + Choline.
• Sphingomyelin is one of the principal structural lipids of membrane in nervous tissue.
• Role in signalling and apoptosis.
• Sphingolipids are present in nerve cells and brain cells.
• Sphingomyelinase Deficiency causes- Niemann- Pick disease (accumulation of sphingomyelinase in
brain, liver and spleen)
104. GAUCHER'S DISEASE
• It is an autosomal recessive trait.

• It is the common lysosomal storage disorder.
• Type I Gaucher’s disease (most common)
• Deficiency of lysosomal hydrolase, acid β- glucosidase (β- glucocerebrosidase)
• Bone marrow examination- The pathologic hallmark of Gaucher disease is the Gaucher
cell particularly in the bone marrow.
• Treatment- Enzyme Replacement Therapy (ERT)
105. BIOMEMBRANES
• Membranes consist of lipid, proteins and carbohydrates.

• Membranes are non covalent.
• Major lipid in mammalian membranes are- phospholipids, glycosphingolipids and sterol
(cholesterol).
• Fluid Mosaic Model of Biomembranes- proposed by Singer and Nicolson.
• This model is likened to integral membrane protein 'icebergs' floating in a sea of predominantly
fluid phospholipid molecules.
106. Metabolism of Triacylglycerol
• Triacylglycerol contains one molecule of glycerol and 3 molecules of fatty acid.

• Occurs in liver, adipose tissue, intestinal mucosal cells.
• Organelle- endoplasmic reticulum.
• 3 steps-
1. Fatty acid to acyl CoA by Acyl CoA synthase (thiokinase)

2. Glycerol to glycerol-3-phosphate (formed from glucose-3- phosphate dehydrogenase in adipose
tissue) by glucose kinase.
3. Phosphatidate undergoes hydrolytic dephosphorylation which is esterified to form triacylglycerol.
• In adipose tissues- insulin enhances triacylglycerol synthesis.

• In Diabetes, glycerol-3-phosphate is hampered leading to decrease triglyceride synthesis.
• Triglyceride is the major lipid for adipose tissues.
• Triacylglycerol hydrolysis (lipolysis)-
• Triacylglycerol (stored fat) is degraded.
• Enzyme- hormone sensitive lipase.
• Lipolysis refers to hydrolysis of triacylglycerol in adipose tissues.
Regulation of lipolysis-
• Hormone sensitive lipase activated by-
1. Epinephrine
2. Catecholamines
3. Thyroid hormones
4. Growth hormone
5. ACTH
6. Glucocorticoids
• Hormone sensitive lipase inactivated by-
1. Insulin
2. Prostaglandin
107. De Novo Fatty Acid Synthesis
• De Novo fatty acid synthesis is cholesterol synthesis.

• It is synthesized in cytosol.
• It occurs in liver, lactating mammary gland, kidney, brain, lungs and adipose tissues.
• Cofactors required are- NADPH, Mn+2 , Biotin and HCO3- .
• The basic bulding block is acetyl CoA of fatty acid synthesis.
• Glucose is the primary substrate for lipogenesis and acetyl CoA.
• Citrate cleaves into acetyl CoA and oxaloacetate in cytosol by ATP Citrate lyase.
• Production of Malonyl CoA is the initial and rate limiting step catalysed by Acetyl CoA carboxylase.
• Malonyl CoA is a 3- carbon compound is an activated form in the cycle. (committed step)
• Acetyl CoA carboxylase requires B complex vitamin Biotin.
• Fatty acid synthase is a multienzyme complex made of 6 enzymes and acyl carrier protein (ACP).
• ACP contains vitamin Panthotenic acid.
• 6 enzymes are-
a) E1- acyl transacylase
b) E2- malonyl transacylase
c) E4- ketoacyl reductase
d) E5- hydratase
e) E6- Enoyl reductase
f) E7- Thioesterase
• Priming reactions- (total 4 carbon atoms are incorporated)

• Malonyl transacylase catalyzes to phosphopantetheine – SH group of ACP to form acetyl- malonyl
enzyme.
• Condensation by 3 ketoacyl synthase- malonyl moiety liberates CO2 molecule forming ketoacyl
enzyme.
• Reduction by 3- ketoacyl reductase- NADPH serves as a reductant (electron donor).
108. Oxidation of Fatty Acids
• It is the pathway for catabolism of fatty acids.

• β oxidation mainly occurs in mitochondrial matrix.
• Most common type of fatty acid oxidation.
• Organ sites- liver, adipose tissue, muscle
• Cell organeele- mitochondria
• Two carbon at a time are cleaved at the carboxyl end of activated fatty acid generates Acetyl CoA.
• Fatty acids must first be converted to an active intermediate before they can be catabolised.
• Two high energy phosphate bonds are required for activation.
• Long chain fatty acids penetrate the Inner Mitochondrial Membrane as Carnitine.
• It is synthesized from Lysine and methionine in liver and kidney.
• Acylcarnitine is able to penetrate the inner membrane.
• In fed state, Increased Insulin/Glucagon ratio.
• Malonyl CoA is an inhibitor of Carnitine Palmitoyl Transferase (CPT-I).
• In fasting state, decreased Insulin/Glucagon ratio.
109. Regulation of fatty acid synthesis

• The rate limiting step is Acetyl CoA carboxylase.
• Short Term Regulation-
a) Allosteric regulation- allosteric activation of Acetyl CoA Carboxylase by Citrate
b) Covalent modification- Acetyl CoA Carboxylase is active in dephosphorylated state.
Activation of acetyl CoA Carboxylase Inactivation of acetyl CoA carboxylase
Citrate Acyl CoA
Insulin Glucagon, Epinephrine
Dephosphorylation Phosphorylation
• Elongation of Fatty Acid- It occurs in endoplasmic reticulum.

• Synthesis of Unsaturated Fatty Acid-
Occurs in endoplasmic reticulum.
By enzyme Fatty Acyl CoA Desaturase.
110. Different types of Fatty Oxidation
• Oxidation of Very Long Chain Fatty Acid- It takes place in Peroxisomes till Octanoyl CoA.
• Oxidation in peroxisome produces Acetyl CoA and H2O2
• Oxidation of Unsaturated Fatty Acid- It occurs in mitochondria
• The energy yield by oxidation of Unsaturated Fatty Acid is 1.5 ATP less per double bond.
• Odd chain fatty acids are also Beta-oxidized normally but the last step produces a 3-carbon
propionyl.
• Alpha- oxidation of fatty acids- It occurs in endoplasmic reticulum and mitochondria.
111. Ketone Bodies
• Ketone bodies refers to three compounds acetoacetate, β- hydroxybutyrate, acetone.

• Ketone bodies produced in liver from acetyl CoA.
• Ketogenesis occurs when there is a high rate of fatty acid oxidation in liver which provides excessive
acetyl CoA.
• Acetoacetyl CoA is the starting material from Beta oxidation.
• HMG CoA Synthase is the rate limiting step.
• HMG- CoA serves as the immediate precursor for acetoacetate.
• Acetoacetate is the primary ketone body.
• Ketone bodies serve as fuel for extrahepatic tissues.
• Utilization of Ketone Bodies with the exception of Liver and RBCs.
• Acetoacetate and β-hydroxybutyrate are used in preference to glucose as energy source by certain
tissues, e.g. heart, muscle and renal cortex.
• Brain also switches to using predominatly acetoacetate in starvation.
• In extrahepatic tissues, acetoacetate is activated to acetoacetyl-CoA by succinyl-CoA-acetoacetate
CoA transferase or Thiophorase.
(First step in ketone body utilization)
• Factors that inhibit lipolysis also ketogenesis.

• Ketogenic Hormone- Glucagon, glucocorticoids, growth hormone.
• Anti-Ketogenic hormone- Insulin
Test for Ketone Bodies in Urine-
• Gerhardt’s Ferric Chloride- Acetoacetate

• Rothera’s Nitroprusside Test- Acetoacetate and Acetone
112. Metabolism of Chylomicron
• Chylomicrons transport the dietry lipid from intestine to liver.

• Function of chylomicrons is to transport exogenous triglyceride to adipose tissue (for storage).
• Step I- Formation of Nascent Chylomicron
• Step II- Formation of Mature Chylomicron- by receiving apo C-II and apo E from HDL.
• Step III- Formation of Remanant Chylomicron- Apo C-II activates Lipoprotein Lipase
• Step IV- Uptake of Remnant Chylomicron-
• Chylomicron remnant is taken up by the liver.
• Uptake is mediated by apo E via two apo E dependent recptors, LDL receptor and LDL receptor
related protein-I (LRP-I).
113. Metabolism of VLDL
• VLDL is synthesized in liver contains high triglyceride, cholestryl ester, cholesterol, phospholipid
and Apo B-100.
• IDL is taken up in the liver by apo E Receptor present in the liver.
• Apo C- II activates Lipoprotein lipase
• apo B-100 acts as ligand for LDL receptors
• LDL elevated serum concentration of LDL causes excessive deposition of cholesterol in peripheral
tissues and enhance atherosclerosis therefore it predisposes to MI.
• LDL is metabolized by LDL receptor.
• LDL is a bad cholesterol considered as a marker for cardiovascular disease called as lethally
dangerous lipoprotein (LDL).
• LDL receptor present in hepatic and extrahepatic tissues.
114. Fatty Liver
• Fatty liver is the excessive accumulation of fat i.e. triacylglycerol in the liver (25- 30%)
• Triglycerides is stored in the adipose tissue.
• Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder.
• Causes- Overproduction of triacylglycerols and Raised levels of plasma free fatty acids- (VLDL
synthesis impaired)
• Lack of lipotropic factors (choline, betaine, methionine, lecithine and inositol, vitamin B12, Vitamin
E)
• Lipotropic Factors- which prevents the accumulation of fat (triglycerides) in liver.
115. CHOLESTEROL SYNTHESIS
• Cholesterol is the major sterol in humans.

• Major sites- Liver, adrenal cortex, testis, ovaries and intestine.
• Cell organelle- endoplasmic reticulum and cytoplasm
• First material is Acetyl CoA.
• Acetyl- CoA condenses with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)
• Then HMG-CoA is converted to mevalonate by HMG-CoA reductase, (the key regulatory enzyme of
cholesterol synthesis)
116. Metabolism of HDL
• Nascent HDL is synthesized and secreted from intestine and liver.

• Nascent HDL contain phospholipids, cholesterol and Apo A.
• Lecithin cholesterol Acyl Transferase (LCAT) esterified by cholesterol.
• Apo- A- I activates LCAT.
• Cholesterol is transported to liver in 2 ways-

1. Indirect pathway- Cholestryl ester is transferred from HDL to VLDL and chylomicrons by cholestryl
ester transfer protein (CETP)à Liver
2. Direct pathway- HDL cholesterol by liver via scavenger receptors.
• HDL particles are referred to as scavangers.

• The level of HDL in serum is inversely related to the incidence of MI.
• HDL is cardioprotective and anti- atherogenic is referred to good cholesterol.
• HDL- Cholesterol appears to be the best independent predictor of coronary artery disease.
• HDL collects excess cholesterol iron tissues and transport it to liver and steroidogenic tissues. This
is called Reverse cholesterol transport.
117. HYPERLIPOPROTEINEMIA
• Fredrickson’s Classification of hyperlipoproteinemia are of 5 types

• Type I (familial lipoprotein lipase deficiency)- Deficiency of lipoprotein lipase or apo C-II.
• Elevated levels of chylomicrons
• Type IIa ( familial hypercholesterolemia)- Due to deficiency of functional LDL receptors.
• Four classes of mutation have been defined for LDL receptors- Class I (most common)- loss of
receptor synthesis
• Type IIb ( familial combined hyperlipedimia)- LDL and VLDL are increased
• Type III (familial dysbetalipoproteinemia)- Broad β- disease- Due to abnormalities in apo- E and
Chylomicron remnants and VLDL remnants(IDL) are increased.
• Type IV (familial hypertriglyceridemia)- Deficiency of apo-A- V.
118. Bile Acid Synthesis
• The primary bile acids are produced from cholesterol in liver.

• Primary bile acids are-
a. Cholic acid
b. Chenodexycholic acid
c. Glycocholic acid, glycochenodeoxycholic acid, taurocholic acid.
• Secondary bile acids produced from cholesterol in intestine.

• Secondary bile acids are-
a. Deoxycholic Acid
b. Lithocholic Acid
• Cholesterol converted to 7 Hydrocholesterol by 7 α- Hydroxylase.

• The first and rate limiting step by enzyme 7 α- Hydroxylase.
119. Lipoprotein Structure
• Free fatty acids (FAA) is metabolically most active of the plasma lipids.
• Non polar lipid contains cholesterol ester, cholesterol, phospholipid, triacylglycerol.
• Protein part of lipoprotein is apolipoprotein.
• Chylomicrons- These are principal form in which dietary lipids (exogenous lipids) are carried from
intestine to liver.
• Low density lipoproteins (LDL)- major source of cholesterol to peripheral tissues.
Electrophoresis-
• Chylomicrons have no mobility and remains at orginial position

• HDL has maximum mobility and move longest distance.
Ultracentrifugation-
• Chylomicrons are largest with maximum lipid contents.
120. Hypolipoproteinemia
• Abetalipoproteinemia-
• There is deficiency of apo-B containing lipoproteins i.e. chylomicrons, VLDL lDL, LDL.
• Low plasma levels of cholesterol and triacylglycerols occurs.
• HDL levels are normal.
• Deficient Vitamin E and fat soluble vitamins (vitamin A & K).
• Hypoalphalipoproteinemia (Tangier disease)
• Due to marked deficiency of major lipoprotein HDL (apo-A-I and apo-A-II)
• Enlarged tonsils
121. Regulation of Cholesterol Synthesis
• The rate limiting enzyme of cholesterol biosynthesis is HMG- CoA reductase.

• Cholesterol, mevalonate, bile salts or acids inhibits HMG CoA reductase.
• Insulin and thyroxine increase the activity of HMG CoA reductase
• Glucagon and Glucocorticoids decreases the activity of HMG CoA reductase.
• Hypolipidemic drugs (lovastatin, mevastatin) inhibits cholesterol synthesis by acting as competitive
inhibitors of HMG CoA reductase.
• Esterified form of cholesterol are-
1. Linoleic acid
2. Oleic acid
3. Palmitic acid
4. Arachidonic acid
• Esterification of cholesterol is catalyzed by two enzymes-

• In tissues- Increase in intracellular cholesterol activates Acyl cholesterol acyl transferase (ACAT)
• Cholesterol Excretion- Sterol (coprostenol)
122. VITAMIN A
• Vitamin A is a fat soluble vitamin.

• Retinoids- 3 biologically active vitamers (isomers of vitamin)
a. Retinol (alcohol)
b. Retinal (aldehyde)
c. Retinoic acid (acid)
• Lycopene- protect against prostate cancer.

• Retinal combines with light- sensitive protein opsin to form rhodopsin (in rods) and idopsin (in
cones).
• Retinol esters are transported to liver in the chylomicrons.
• Liver cells not only dispatch retinol with RBP but also store the surplus in the form of retinol esters.
• Sources of Vitamin A-
Fish liver oils (rich sources)
Halibut liver oil (richest sources)
Carrot (plant source)
123. Vitamin A Deficiency
• Clinical manifestations- Xerophthalmia (dry eye), Follicular hyperkeratosis

• Hypervitaminosis A can lead to rupture of lysosomal membrane.
• Acute toxicity- Pseudotumour cerebri
• Chronic toxicity- bone abnormalities and bony swelling.
• Single massive dose 100000 IU to children (6 month- 1 year) once in 6 months.
• Single massive dose 200000 IU to children (1_6 years) once in 6 months
• Required Daily Allowance of Vitamin A (μg of Retinol)
Children (1-6 yrs)- 400 pg/day

Men- 600 pg/day
Women- 600 pg/day
Pregnancy- 800 pg/day
Lactation- 950 pg/day
124. Vitamin D
• Vitamin D is a hormonal vitamin.

• It acts on intranuclear receptors.
• Vitamin D is also called as anti- rachitic factor.
• Vitamin D is synthesized in skin and metabolized to active metabolite calcitriol in liver and kidney.
a. Ergocalciferol (Vitamin D2)

b. Cholecalciferol (Vitamin D3)
• Vitamin D3 calcidiol (25 hydroxy cholecalciferol

• or 25-hydroxy vitamin D3) by 25 hydroxylase in the liver
• Calcidiol calcitriol by 1-α hydroxylation in kidney.
• The hydroxylation is the rate limiting step.
• Calcitriol (1, 25(OH)2 D3) is the biologically most active form of Vitamin D.
• When Ca+2 level is high, kidney produces the relatively inactive metabolite 24,25 Dihydroxy
Cholecalciferol (Calcitroic acid) excreted through urine.
125. Vitamin D- function, deficiency
1. Prevents infection by mycobacterium tuberculosis.

2. Only animal sources Liver, Egg yolk, butter and liver oils. Out of the food sources Fish liver oils are
the richest source
3. Sunlight
4. Vitamin D deficiency-
o Rickets in children
o Osteomalacia in adultsVitamin D Intoxication-
5. Vitamin D in excess is toxic (4000IU/day) .
Infants are sensitive to intakes of Vitamin D as low as 50 μg/day
126. Vitamin E & Deficiency

• Vitamin E is the stereoisomer of-
a. Tocopherols (most abundant)

b. Tocotrienols
• The most powerful naturally occurring antioxidant.

• Vitamin E is carried to liver in Chylomicrons.
1. Most important function in humans is to act as antioxidant.

2. Prevents oxidation of other antioxidant as carotenes, Vitamin A and Vitamin C.
3. Biologically most potent form is α- tocopherols.
4. Chain breaking antioxidants.
5. Free radical tapping antioxidant in cell membranes
6. Plasma lipoproteins by reacting with lipid peroxide radicals formed by peroxidation of
polyunsaturated fatty acids.
7. Prevents rancidity of fats due to its antioxidant action.
• Selenium decreases requirement of Vitamin E.

• Vitamin E Deficiency- Hemolytic anaemia, Dry skin
127. Vitamin K & Deficiency
• Vitamin K is the only fat soluble vitamin that acts as a coenzyme.

• Three forms of Vitamin K-
1. Vitamin K1- Phylloquinone (naturally occurring)

2. Vitamin K2- Menaquinone (naturally occurring)
3. Vitamin K3- Menadione
• Vitamin K2 is synthesized by intestinal bacteria.

• Vitamin K is as a cofactor for an enzyme carboxylase that catalyzes carboxylation of glutamic acid
residues on vitamin K-dependent proteins.
• Coagulation proteins- Prothombin fator (Factor II), Proconvertin (Factor VII), Christmas factor
(Factor IX), Stuart- Prower factor ( Factor X).
• Anticoagulation protein- Protein C.
• Matrix Gla protein via calcium ion.
Vitamin K deficiency-
• Elevated prothombin time, bleeding time.

• Newborn infants with their inadequate vitamin K stores may suffer from hemorrhagic disease of
newborn (HDN1).

HYPERVITAMINOSIS K- leads to Hemolysis
128. Vitamin B1 & Deficiency
• Thiamine is also called Aneurine.

• Thiamine has a role in metabolism of carbohydrates.
• Active form of thiamine is thiamine pyrophosphate (TTP) or Thiamine diphosphate.
• Thiamine is a coenzyme
• Thiamine Pyrophosphate is the coenzyme which functions for the decarboxylation reaction-
1. Pyruvate dehydrogenase- conversion of pyruvate to acetyl CoA

2. α-ketoglutarate dehydrogenase- conversion of α-ketoglutarate to succinyl CoA
3. Branched chain keto acid dehydrogenase- catalyses oxidative decarboxylation of Branched keto
Chain Amino acids.
4. Thiamine diphosphate is also the coenzyme for transketolase in pentose phosphate pathway.
Thiamine nutritional status is best assessed by erythrocyte or whole blood transketolase activity.
• Sources-
• Aleurone layer of cereals.
• Yeast is also good source of thiamine.
• Meat
VITAMIN B1 DEFICIENCY
• Deficiency of thiamine causes-
1. Beri Beri- 2 types
a)Wet Beri Beri
b) Dry Beri Beri- polyneuritis, muscle wasting
2. Wernicke’s encephalopathy with korsakoff psychosis
3. Lactic acidosis
• Recommended Daily Allowance of Vitamin B1- 1-1.5 mg/day

• Riboflavin is also called Warburg yellow enzyme of cellular respiration.
• Riboflavin is heat stable.
• Active forms of Riboflavin-
1. 1. FAD- flavin adenine dinucleotide

2. 2. FMN- flavin mononucleotide
• Flavin dependent (flavoprotein) enzymes are-
a) FMN dependent- L-amino acid oxidase, NADH dehydrogenase, monoamino oxidase.
Vitamin B2 Deficiency- clinical manifestations-
• Glossitis
• Angular stomatitis
• Seborrheic dermatitis
• Corneal vascularisation
130. Vitamin B3- metabolism
1. Vitamin B3 is also called as Nicotinic acid or nicotinamide.

2. Niacin can be synthesized tryptophan (1mg of the niacin formed from 60mg of tryptophan)
• Coenzymes involved in reactions-
1. Oxidoreduction reaction-
i) NAD+ linked dehydrogenases-
• Isocitrate dehydrogenase
• Malate dehydrogenase
• α-ketoglutarate dehydrogenase
• glutamate dehydrogenase
• glyceraldehydes-3- P dehydrogenase
• lactate dehydrogenase
• β-hydroxyl acyl CoA dehydrogenase
ii) NADP+ linked dehydrogenases-
• Glucose-6-P dehydrogenase in HMP shunt pathway

• Nicotinamide excreted in urine are N1 –methyl nicotinamide and N1 –methyl 2-pyridone 5-
carboxamide (2-pyridine).
• N-methyl nicotinamide metabolized to methylpyridone-2- and 4-carboxamide
• Nicotinic acid conjugated with glycine to form nicotinuric acid
• Nicotinic acid methylated to trignonelline.
• Daily recommended dose – 20mg/day
131. Vitamin B3 Deficiency
• Pellagra-
o Caused due to niacin deficiency
o Common in people consuming maize and sorghum (poor in niacin & tryptophan and rich in
leucine)
Clinical Manifestations-
• Characterized by 4Ds-
• Dermatitis, Diarrhea, Dementia and Death
• Casal’s necklace- rash form around neck
• Pyridine derivatives are-
a. Pyridoxine
b. Pyridoxial
c. Pyridoxamine
• Active form of pyridoxine is pyridoxial phosphate-PLP (for amino acid metabolism)

• Important PLP reactions-
1. Transamination
2. Decarboxylation
3. Non-oxidative deamination
4. Condensation
5. Transsulfuration
6. Tryptophan Metabolism
• Synthesis of niacin from tryptophan (can cause niacin deficiency)

• xanthurenic acid (xanthurenate) excretion in urine is increased in pyridoxine deficiency. Thus
pyridoxin may be used in xanturenic aciduria.
7. PLP is a cofactor for glycogen phosphorylase.

8. Pyridoxin can be used in oxaluria.
• Vitamin B6 Deficiency- Clinical Manifestations

• Neural dysfunction
• Anaemia
• Convulsion
• Pellagra
• Kidney stones
• Deterioration of parkinsonism
• PPL dependent conditions are- Homocystinuria, oxaluria, cystathioninuria and xanthurenic acid.
Biochemical Assay of Vitamin B6-
• Tryptophan load test

• Toxicity of Vitamin B6-
• High doses of pyridoxine can cause neurotoxicity.
• Also called as anti-egg white injury factor or Vitamin H.

• Synthesized by intestinal flora.
• Reactive form is CarboxyBiocytin.
• Biotin serves prosthetic group for carboxylation reaction.
• Biotin antagonist- Avidin(raw white egg), Streptavidin
• Biotin acts as a coenzyme
a) Acetyl CoA Carboxylase
b) Propionyl CoA carboxylase
c) Pyruvate carboxylase
Biotin Deficiency-
• Depression, Hallucination
• Anorexia
• Seborrheic and erythematous rash near nose, eyes, mouth.
• Alopecia

134. Vitamin B9 (Folic acid)
• Absorbed from upper part of jejunum.

• Active form of folic acid is Tetra Hydro Folic Acid (THFA)
• THF serves as a carrier of one-carbon (C1) unit during several biosynthetic reactions like nucleic acid
and amino acid metabolism.
• THF acts as a carrier of one carbon unit.
Sources of one carbon groups-
• The major point of entry of one carbon unit is Methylene THF.

• Serine is the most important source of one carbon units
• Serine Hydroxyl Methyl Transferase is the enzyme involved in pathway.
• Major circulating form of folic acid- methyl THF.
• As an acceptor of one carbon unit from various donors-
a. Serine to glycine conversion

b. Histidine breakdown
• As a donor of one carbon unit to various acceptors-
a. Conversion of glycine to serine
• 5-formyl –tetrahydrofolate is more stable and is used pharmaceutically.
Biochemical assessment of folate deficiency-
1. Blood level- normal level in serum is about 2-20 nanogram/ml

2. Histidine load test or FIGLU excretion test
3. AICAR excretion (amino imidazole carboxamide ribose 5 phosphate)
4. Peripheral blood picture
• Deficiency- megaloblastic ananemia
• It is also called as extrinsic factor of castle.

• It contains 4.35% cobalt by weight.
• Corrinoids are cobalt containing weight possessing corrin ring.
• Active form of cobalamin is methylcobalmine and deoxyadenosylcobalamine.
• Coenzyme role of Cobalamine-
a) Isomerisation of methylmalonyl CoA to succinyl CoA-

• methylmalonyl-CoA is accumulated and excreted in urine as methylmalonic acid (methylmalonate)
in vitamin B I2 deficieny i.e. methylmalonic aciduria.
b) Conversion of homocystein to methionine-
• Reaction catalyzed by cobalamin-dependent methionine synthase also called 5-

methyltetrahydrofolate- homocysteine methyltransferase.
Vitamin B12 Metabolism-
• It is absorbed in Ileum.
• The internal absorption of Vitamin B12 requires intrinsic factor (IF), secreted by parietal cells of
the stomach.
Transport of Cobalamin to the target tissues-
• Major Cobalamin transport protein in plasma is Transcobalamin II (TC II).
Sources of Vitamin B12-
• Animal origin only includes meat, eggs, milk and fish.

• Absent in plant foods.
• Synthesized in the intestine by the intestinal flora.
Vitamin B12 Deficiency-
• Vitamin B12 deficiency is caused due to-
1. Nutritional- strict vegetarians are at a risk.

2. Pernicious anaemia
3. Gastric- congenital absence of intrinsic factor or gastrectomy.
4. Intestinal- intestinal stagnant loop syndrome, Crohn’s disease.
5. Neuropathy- subacute combined degeneration(SCAD), demyelination
6. Fish tapeworm
• Deficiency of Vitamin B12 causes folate trap.
1. Megaloblastic anaemia
2. Homocysteinemia
3. Methyl Malonic Aciduria
4. Subacute Combined degeneration
5. Demyelination

136. Bile acid synthesis
• The primary bile acids are produced from cholesterol in liver.

• Primary bile acids are-
a. Cholic acid
b. Chenodexycholic acid
c. Glycocholic acid, glycochenodeoxycholic acid, taurocholic acid.
• Secondary bile acids produced from cholesterol in intestine.

• Secondary bile acids are-
a. Deoxycholic Acid
b. Lithocholic Acid
• Cholesterol converted to 7 Hydrocholesterol by 7 α- Hydroxylase.

• The first and rate limiting step by enzyme 7 α- Hydroxylase.
Type Found in Site of Synthesis Function

Apo A HDL, Chylomicrons Liver, intestine Major structural
Apo A- I protein of HDL, Major
activator of LCAT
Apo- II HDL, Chylomicrons Liver, intestine Inhibits lipoprotein
lipase
Apo B LDL, VLDL, IDL Liver Only apoprotein of LDL,
Apo B- 100 mediate uptake of LDL
by LDL receptors of
liver
Apo B-48 Chylomicrons, Intestine Structural protein of
chylomicrons remnants chylomicrons
Apo- C Chylomicrons, VLDL, Liver Inhibits CEPT, Activates
Apo C- I Liver HDL LCAT, LPL
Apo C- II Chylomicrons, LDL, HDL Liver Activates lipoprotein
lipase,
Apo C- III Chylomicrons, LDL, HDL Inhibits lipoprotein
Lipase
Apo- E (arginine rich) Chylomicrons, Liver Mediates uptake of
chylomicrons chylomicron remnants
remnants, VLDL, HDL and IDL by LDL
receptors in liver
• Most important apoprotein of HDL is Apo- I called alpha lipoprotein.

• Main apoprotein for LDL (beta lipoprotein) and VLDL is apo B- 100.
• Main apoprotein for chylomicrons is apo B-48.
138. Vitamin C- Scurvy
Vitamin C Deficiency-
1. Scurvy-
• Petechaie, ecchymosis, bleeding gums, joint effusion, fatigue.

• Perifollicular haemorrhages
• Hyperkeratotic papules
• Anemia
• Late stages characterized by edema, oliguria, neuropathy, death.
• Bowing of legs is seen in Scurvy.
• Radiological signs of scurvy are Winberger sign, Trimmerfeld zone, Frenkel's line , Pelican
spur, Bony thickening, Metaphyseal porosis, Metapyseal infarction, Metaphyseal calcification,
Epiphyseal separation, Cortical spur
2. Barlows Syndrome (Infantile Scurvy)- 6-12 months
139. Classification of Nutrients
MINERALS CLASSIFICATION
• Nutrients are classified into 2 major classes-
Macronutrients-
1. Proteins
2. Fats
3. Carbohydrates
Micronutrients-
i. Vitamins
ii. Microminerals (Trace elements)- less than 100mg/day
1. Copper
2. Iodine
3. Iron
4. Mangnese
5. Selenium
6. Zinc

iii) Macrominerals- more than 100mg/day
a) Sodium
b) Calcium
140. Hemochromatosis
• The iron storage pigment in tissues is called as hemosiderin (least in skin).

• Hemosiderosis is an acquired condition.
• Liver is the first organ to be affected & maximum deposition of iron by hemochromatosis.
• Conditions of Iron Overload States- classified as
I)Herediatry- hemochromatosis
• Iron loading-
i) Thalassemia major
ii) Sideroblastic anaemia
iii) Chronic haemolytic anaemia
• Antidotes for iron poisoning:Desferrioxamine is given parenterally (IM or IV), whereas deferiprone
and deferasirox are used orally.
141. Iron Deficiency
i)Iron deficiency anemia- microcytic hypochromic anemia
ii) Causes- Decreased iron absorption- diet, malabsorption of iron, surgery or gastrectomy.
iii) Lab diagnosis-
• Decreased serum ferritin

• Total iron binding capacity increased.
• Iron deficiency can be indicated by MCHC.

• Test to detect iron deficiency is serum ferritin.
• Mentzer index more than 13 suggests a diagnosis of iron deficiency anemia.
Treatment
• Red cell transfusion

• Oral iron therapy- 200mg per day (100- 150 mg per day)
• Parenteral iron therapy- iv iron,
• Total parenteral iron requirement can be calculated by : 4.3 x Body weight (kg) x Hb deficit (g/dl)
• Ferumoxytol delivers 510 mg of iron per injection, ferric gluconate 125 mg per injection, ferric
carboxymaltose 750 mg per injection, and iron sucrose 200 mg per injection.
• Iron dextran (highest risk of anaphylaxis).
142. STRUCTURE OF HEME
• Hemoproteins are haemoglobin, myoglobin, cytochromes (cytochrome C, cytochrome P450 ),

catalase.
• Haemoglobin is an allosteric protein.
• Each subunit of Hb is composed of protein part (globin) & non protein prosthetic group (Heme).
• Each Hb molecule is made up of-
Hb= 4 heme molecules + 4 polypeptide chains (2pairs of same polypeptide)
• The iron is held in the centre of porphyrin ring in ferrous form (Fe+2)
• 5th bond- between nitrogen atoms of histidine residue of globin chain called as proximal histidine.
• Distal histdine (His E7) reduces affinity of heme for carbon monoxide (CO).
• Each molecule of haemoglobin combine upto 4 molecules of oxygen.
143. Biosynthesis of Heme
• Heme is synthesized in all cells but mainly in bone marrow and liver.
• Organelle- cytoplasm and mitochondri
• Synthesis of ALA occurs in mitochondria (Rate limiting step)
• Synthesis of porphobilinogen, hydroxymethylbilane, uroporphyrinogen, coproporpyrinogen-
occurs in cytosol.
• Synthesis of protporphyrinogen occurs in mitochondria
• Formation of heme occurs in mitochondria.
144. Regulation & Factors of Heme Synthesis

• ALA synthase is the key regulatory enzyme in hepatic biosynthesis of Heme.
• ALA synthase occurs in hepatic and erythrocytes.
Factors That Heme Synthesis-
• Drugs- Barbiturates, Griseofulvin.

• Lead- inhibits catalyzed by ALA dehydratase and ferrochelatase.
• INH- decreases PLP.
• Intracellular buffer due to histidine residue.The NH2 group on intermediate histidine residues.
145. Metabolism of Bilirubin
EXAM POINTS-
• Metabolism of bilirubin occurs in liver.

• Metabolism process in three processes-
a) Uptake of bilirubin by liver cells
b) Conjugation of bilirubin with glucuronate in the endoplasmic reticulum.
c) Secretion of conjugated bilirubin in the bile.
146. Heme Catabolism
• Daily bilirubin formation in humans is approx 250-350mg.

• 1gm of haemoglobin yields 35mg of bilirubin.
• Site- reticuloendothelial cells of liver, spleen and bone marrow.
• Hemo oxygenase is green pigment, biliverdin is produced.
• Hemo oxygenase is the only source of endogenous CO in the body.
• Biliverdin Reductase (yellow) takes place in the cytosol.
• Bilirubin is transported to liver bound to serum albumin.
• Bilirubin is transferred to hepatocytes where it is bound to ligandin.
147. Structure of Hemoglobin
• A single heme consist of single iron in ferrous state (Fe+2).

Genetics of alpha and Beta chains-
• α-like globin genes on chromosome 16.

• β-like globin genes on chromosome 11.
Types of Hemoglobin-
• Embryonic haemoglobins
a) Hb Portland ?2γ2
b) Hb Gower I- ?2ε2
c) Hb Gower II- α2ε2
• Fetal Hemoglobins
a) Hb F- α2γ2
• Adult Hemoglobins
a) Hb A1 – α2β2
b) Hb A2 – α2δ2
Charateristics of Hemoglobin
• Slower electrophoretic mobility

• Increased resistance to Alkali Denaturation
• Decreased Interaction with 2, 3 BPG.
• Binding of 2, 3 BPG in the curve shifts ODC to right.
148. MYOGLOBIN
• Myoglobin is seen in muscle.

• It is rich in alpha helix.
• Myoglobin has similar structure like haemoglobin.
• It is a heme binding hydrophobic pocket.
• Myoglobin can bind only one molecule of oxygen.
• Myoglobin cannot show the phenomenon of cooperative binding.
• Oxygen- myoglobin dissociation curve is hyperbola.

149. Hyperbilirubenimia
• Sclera icterus in fetus bilirubin >15mg/dL
Congenital Hyperbilirubinemia
• Unconjugated hyperbilirubinemias
a) Glibert’s disease
b) Crigler- Najjar syndrome
• Physiological Jaundice
• Breast Milk Jaundice
• Lucey Driscoll Syndrome
Conjugated Hyperbilirubinemias
• Dubin Johnson’s syndrome- caused due to mutation of gene encoding MRP2.

• Rotor syndrome- defective bile excretion
• Benign recurrent intrahepatic cholestatsis
• Progressive Familial intrahepatic cholestatsis
150. Structure of Insulin
• Insulin is the first hormone to be extracted in pure form by Banting and Best.
• Sanger’s reagent was used for sequencing the protein.
Primary Structure of Insulin
• Primary structure consists of two polypeptide chains.

• Number of amino acids is 51 by disulfide bridges.
• Porcine and Human Insulin only in the terminal Amino acid of B chain.
• Stored in a complex Zn+2 ions.
151. DENATURATION OF PROTEIN
• Distruption of higher structures of protein (Primary, secondary and tertiary).

• During denaturation, peptide bond remains intact.
• Denaturation can completely disrupt secondary, tertiary and quaternary structures.
• Denatuartion is irreversible.
• Denaturation is randamization of conformation of polypeptide chain.
• Denaturation is always accompanied by loss of biological function.
• Dentatured proteins are less soluble and they precipitate.
• Denaturation agents are- 8M urea or 6 M guanidine chloride.
• Denaturation assume a random coil structure.
152. Separation Techniques of Protein
• Types of techniques are-
1. Salt fractionation
2. Ultracentrifugation
3. Electrophoresis
4. Chromatography
5. Ultra filtration
i) Salting In- 5% NaCl is used.
ii) Salting out- Excess Salt.
• Ammonium sulphate is most commonly used reagent for salting out in proteins.
• Chromatography- The most non-polar amino acids migrate the farthest, due to their greater
solubility in the organic solvent.
• Gel filtration chromatography or molecular sieving- Used for separation of molecules based on their
size are Hydrophilic cross linked gels like agrose (Sepharose), dextran ( Sephadex)
• Ion-exchange chromatography- Separation is made on the charge difference.
• The charged group commonly attached are
1. diethylaminoethyl (DEAE) group- the negatively charged proteins associate with positively charged
DEAE groups and replace chloride ions.
2. carboxylmethyl (CM) cellulase chromatography- negatively charged or neutral proteins have no
affinity for CM, move faster.
3. Affinity chromatography- based on the high affinity of specific proteins for specific chemical groups
called ligand. Specific protein molecules bind to specific ligand.
4. Hydrophobic interaction chromatography- hydrophobic ligand.
5. Electrophoresis- isoelectric net charge is zero and do not move.
• Electrophoresis is the most common method of protein separation in the clinical laboratory.
• Types of electrophoresis are-
1. Polyacrylamide gel electrophoresis (PAGE) - on charge and molecular weight.

2. Sodium dodecyl sulphate (SDS)—PAGE- based on molecular size, molecular weight.
3. Isoelectric focusing- on each protein has a different isoelectric point.
153. IMMUNOCHEMICAL METHODS IN PROTEIN
1. Double diffusion- concentration gradient is established for both antibody and antigen and the
technique is called ouchterlony technique. (widely used)
2. Crossed immunoelectrophoresis used in second dimension to drive antigen into gel containing
antibodies specific for the antigen interest
154. Diseases associated with Collagen
• Defect in Type I Collagen leads to osteogenesis imperfect, osteoporosis, Ehlers- Dahlos syndrome.
• Defect in Type II collagen leads to osteoarthritis.
• Defect in Type III collagen leads to Ehlers-Dahlos syndrome
• Defect in Type IV collagen leads to Alport Syndrome
• Defect in Lysyl hydroxylase leads to Ehlers- Dahlos Syndrome, Scurvy.
155. Ehler's- Danlos Syndrome
Classic EDS
• Type I EDS (Severe) and Type II EDS (Mild)
• Hyperelasticity of skin (Rubber Person Syndrome)

• Hypermobile joints
• Affect Type V Collagen and Type I Collagen.
Hypermobile EDS (Type III EDS)
• Joint hypermobility
Vascular EDS (Type IV EDS)- Most serious
• Type III collagen is affected
Type V EDS

• Inherited as an X-linked trait
EDS with Tenascin X defect seen in- Type III EDS
EDS due to enzyme defect-
• Arthrochalasic EDS (type VII EDS) or Dermatosparaxis

• Kyphoscoliotic
According to Villefranche Classification, EDS -
SUBTYPE DEFECT IN
Hypermobility Type III collagen, Tenascin X
Classic Type I and V collagen
Vascular Type III collagen
Kyphoscoliosis Lysylhydroxylase
Arthochalasis Type I collagen
Dematosparaxis ADAM metallopeptidase with thrombospondin
type I motif
156. Alport's syndrome
• X-linked disorder.
• Type IV collagen is affected.
CLINICAL FEATURES-
• Hematuria
• Sensorineural deafness
• Conical deformation of the anterior surface of the lens (lenticous).
• The pathognomonic feature of classic Alports syndrome lenticonus together with hematuria.
HISTOLOGICAL FEATURE-
• Abnormality in the structure of basement membrane and lamina densa.

• ACHONDROPLASIA- Most common cause of short limb dwarfism.

• STRICKLER SYNDROME- Characterized by degeneration of joint cartilage and vitreous body of eyes.
157. Protein Folding
• Auxillary Proteins assist protein folding is called Chaperones.

• Many Chaperones are also called as Heat Shock Proteins.
• They are induced by conditions that cause unfolding of newly synthesized proteins.
• Present in a wide range of species from bacteria to humans.
• Associated ATPase activity.
• Have a wide range of expressions
Molecular Chaperones are-
• HSP 70
• HSP 90
• HSP 40
Enzymes assist folding are-
• Protein Disulphide Isomerase

• Peptidyl Prolyl Isomerase
158. Ubiquitin
• Key molecule in protein degradation

• Attachment of Ubiquitin to Protein to be degraded is called Kiss of Death.
• Highly conserved protein
• Found in eukaryotic organisms
• Ubiquitin is a heat stable proteins
• Ubiquitin is found throughout the cell
• Ubiquitin conjugation is involved in DNA repair, embryogenesis, regulation of
transcription, apoptosis.
159. Prion Disease
PRION DISEASES (PROTEIN MISFOLDING DISORDER)
DISEASE HOST MECHANISM OF PATHOGENESIS

Kuru Fore people Infection through ritualistic
cannibalism
Creutzfeldt- Jakob disease (CJD) Humans
Sporadic CJD Humans
Gerstmann- Straussler- Humans Germ-line mutations in PrP gene

Scheineker (GSS) located in chromosome 20.
Fatal Familial Insomnia (FFI) Humans Germ-line mutation in PRNP
PRION RELATED PROTEIN DISEASE-
• Protein rich in α helix changes to protein rich in β sheet.

• Diseases like-
• Alzheimer’s disease
• Parkinson’s disease
• Huntington disease
• Fronto temporal dementia
• Amyloidosis
• Beta thalassemia
160. Plasma Cell Disorder
MULTIPLE MYELOMA
• M protein in serum or urine

• Bone marrow plasma cells
• Hypercalcemia
• Bone marrow plasma cells >30%
• Bence Jones protein is present
MONOCLONAL GAMMOPATHY OF UNDETERMINED SIGNIFICANCE
• Most common plasma cell disorder

• M protein in serum is
• Bone marrow clonal plasma cells <10%
SOLITARY PLASMACYTOMA OF BONE
• No M protein in serum and urine

• Single area of bone destruction

WALDEN STROMS MACROGLOBULINEMIA
• Malignancy of lymphoplasmacytoid cells that secreted IgM

• Hyperviscosity syndrome present
• Raynaud’s syndrome
• Comb’s test positive
POEMS SYNDROME
• Polyneuropathy
• Organomegaly
• Endocrinopathy
• Multiple myeloma
• Skin changes
HEAVY CHAIN DISEASES
• Gamma Heavy Chain Disease (Franklin’s Disease)
Lymphadenopathy in Waldeyer’s Ring
161. Glycoprotein
• Glycoprotein consists of protein to which short branched, oligosaccharides are covalently attached.
• Length of oligosaccharide chain is relatively short in glycoproteins.
• Carbohydrate chain is often branched in glycoproteins.
• Oligosaccharide chains of glycoproteins lack a serial repeating units.
• BIOLOGICALLY IMPORTANT GLYCOPROTEINS-
a) Hormones- TSH, LH, FSH
b) Enzyme- alkaline phsophatase
c) Structural protein- collagen
• MAJOR CLASSES OF GLYCOPROTEIN-
According to the glycosidic linkage between oligosaccharides and polypeptide-
a) O-linked glycosides
b) N-linked glycosides

c) GPI linked glycosides
• Glycopeptides bonds can be hydrolysed by glycosides
SYNTHESIS OF GLYCOPROTEINS
a)O-linked glycosides-
• Formation of O-glycosidic bond takes place in golgi apparatus.

• In O-linked glycolysation, oligosaccharide chain is added to hydroxyl chain of serine.
b) N-linked glycosides
• Oligosaccharide unit is synthesized in dolichol in the membrane of Endoplasmic reticulum.
c)]Glycosylphosphatidylinositol- anchored (GIP) glycoproteins- they are-
i) Acetylcholinestrase (red cell membrane)
ii) Alkaline phsophatase (intestinal, placental)
162. Dissaccharides
• Formula for diasaccharides is Cn (H2O) n-1

• Two monosaccharides units joined by glycosidic bond forms diasaccharides.
• [img id=7809]
• [img id=7810]
• Digestion of disaccharides occurs at small intestine
163. Polysaccharides
• Glycogen- Storage form of Glucose in animals, so called as animal starch.

• Glycogen present in muscle and liver.
• Homopolysaccharides- chitin, glycogen, starch, cellulose, iulin, dextran
• Dextran- used as a plasma volume expander. ( Eg. human albumin, dextran, hydroxyethyl starch
(hetastarch), degraded gelatin polymer.
• Dextrose a term often used in bed-side medicine, e.g. dextrose drip.
164. Mucopolysaccharides (Glycosaminoglycan)

• Glycosaminoglycans are unbranched heteropolysaccharides.
• Hyluronic acid (Hyluronan)- plays role in wound repair.

• Keratan sulphate- Glycoaminoglycan with no uronic acid.
• Heparin- Heparin is an anticoagulant
• Chondroitin Sulfate- Most abundant GAG
165. Mucopolysaccharidosis
MPS with no Mental Retardation
• Scheie Disease
• Morquio Disease [Keratan Sulphate and Chondroitin Sulphate]
• Maroteaux Lamy Disease
MPS with no corneal clouding
• Hunter's Disease
• Sanfilippo Disease
All MPS are Autosomal Recessive except Hunter Disease

Microbiology
1. Streptococcus
• Gram +ve cocci,arrangement in chains or pairs
Brown's classification:
1.α- hemolitic( green)
a. Streptococcus pneumoniae( optochin sensitive, bile soluble, capsule=>quellung+)

b. Streptococcus viridans(mutans,sanguis optochin resistant,no capsule, bile insoluble)
2.β- hemolitic(clear)
a. Streptococcus pyogens( group A, bacitracin sensitive)

b. Streptococcus agalactiae( group B, bacitracin resistant)
3. γ-hemolitic: Entrococcus
a. E. faecalis
b. E. faecium
Lancefield grouping
• Group A - S. pyogenes
• Group B - S. agalactiae
• Group C - S. equisimilis, S. equi, S. zooepidemicus, S. dysgalactiae
• Group D -E. faecalis, E. faecium, E. durans and S. bovis(most heat resistant > 60)
• Group E - Enterococci
• Group F, G & L - S. anginosus
• Group H - S. sanguis
• Group K - S. salivarius
• Group L - S. dysgalactiae
• Group M & O - S. mitior
• Group N - L. lactis
• Group R & S - S. suis
Other Streptococcus species are classified as 'non-Lancefield Streptococci'
CAPSULE
• Mucoid colonies are due to production of capsule of hyaluronic acid.
VIRULENCE FACTOR
M. protein
• Major virulence factor
Streptolysin O
1. Antigenic, causes hemolysis

2. Acitve in reduced form
Streptolysin S
1. Oxygen stable, soluble in serum
Pyrogenic exotoxin/Erythrogenic/Dick/Scarlational toxin - Superantigen
1. Associated with streptococcal toxic shock syndrome Et scarlet fever

2. Pyrogenic toxin A is plasmid mediated
3. Dick test - intradermal test to identify children susceptible to scarlet fever
4. Schultz-Charlton reaction - diagnostic test for scarlet fever
Streptokinase(Fibrinolysin)
1. Facilitates spread of infection

2. Streptokinase is produced from serotype A,C,K
DNAase or Streptodornase
• Liquefies thick pus

• responsible for thin serous character of streptococcal exudates

• Anti-DNAse,Streptodornase cleaves DNA
• Anti-hyaluronidase: retrospective diagnosis of pyoderma & glomerulonephritis
Hyaluranidase - Spreading factor
SPECIES OF STREPTOCOCCUS & ASSOCIATED DISEASE:
• Besides Str. pyogenes, streptococci belonging to group B, C, D, F, G and rarely H, K, 0 and R may
also cause human infections.
• Streptococcus causes destruction of skin grafts
Group B streptococci
• Str. agalactiae.
• Lives in female genital tract
• CAMP +ve
• It is the single most common cause of neonatal meningitis.
• Newborn infection acquired from mother's vagina during birth
DIFFERENTIAL DIAGNOSTIC TEST
• Catalase test is used to differentiate staphylococci from streptococci.

• Pneumococcus can be differentiated from streptococcus by Bile solubility test
2. Streptococcus Pneumonia
MORPHOLOGY:
• Lanceolate appearance
CULTURAL CHARACTERISTICS:
• Draughtsman or carom coin appearance

• Alpha-hemolytic colonies inhibited by optochin on blood agar and lysed by bile
Bile solubility test:
• Bile solubility is due to amidase
Optochin sensitivity:
• Disc impregnated with optochin

• Applied on a plate of blood agar inoculated with S.pneumonia

• Alpha-hemolytic colonies inihibited
• Wide zone of inhibition appears on incubation .
TOXINS AND VIRULENCE FACTORS:
The capsular polysaccharide
• Specific soluble substance

• Protect agianst Phagocytosis
• Antibody against it is IgG subclass 2
• Type 3 most virulent due abundant capsular material.
• Cell wall Substance:(C substance)
• Pneumolysin
• Autolysin
• IgA Protease
Quellung reaction:
• Used for rapid identification

• Pneumoocci mixed with specific/polyvalent antipolysaccharide serum
• Capsule becames swollen,sharply delineated and refractile
3. Streptococcus Pyogens: Morphology,Transmission, Antigenicity and Lysogeny
Biochemical reactions
• Senstivity to bacitracin(Maxted's observation).

• Catalase negative
• Not soluble in 10% bile.
• Hydrolyse PYR
• Ferment trehalose but not ribose.
Antigenic Structure
• Polysacchaide capsule:
• CellWall
• Hair-like pilli (fimbria): Important for attachment to epithelial cells.
LYSOGENY:
Toxins and Virulence Factors

Produce numerous exotoxins and exoenzymes
• Hemolysin
• Streptolysin
• Pyrogenic Exotoxin = Erythrogenic = Dick = Scadatinal Toxin
• Streptokinase (Fibrinolysin): Facilitates spread of infection.
• Spy Lep: A serine protease that cleaves and inactivate IL-8
• Deoxyribo nuclease (Streptodornase): Responsible for thin serous character of strep
• Exudates. Also called as DNAase.
• Nicotinamide Adenine Dinucleotidase (NAD-ase).
• Hyaluronidase: Favor spread of infection.
• Serum opacity factor: Lipoproteinase.
• Anti Streptolysin O titre used in retrospective diagnosis; > 200 units is significant.
4. Streptococcus Viridans
• Harm people with compromised immune systems.

• Infective endocarditis after tooth extraction is probably due to Streptococcus viridans
• Cause transient bacteremia following tooth extraction or other dental procedures
• Community acquired native valve endocarditis (Staphylococcus aureus ,most common and other
includes Str viridans, Str bovis, other non group A Streptococci)
• Viridans streptococci part of a mixed flora,from sites of sinusitis, brain abscess and liver abscess.
• Bacteremia occurs frequently in neutropenic patients, after bone marrow transplantation or high
dose chemotherapy for cancer.
5. Human Immunodeficiency Virus (HIV)
• Family retrovirdae; subfamily lentivirdae

• HIV prevalence can be assessed by Sentinel surveillance
• Oncogenic reterovirus
• Contain RNA genome and RNA-directed DNA polymerase (reverse transcriptase)
• Genome is diploid
• HIV contains Integrase , RNA directed DNA polymerase ,Ribonuclease
• Boiling, Ethanol, Cidex can destroy HIV in vitro
Group Specific Antigen (Gag)
• Codes for core and shell of HIV
Envelope (Env) gene

• gp120 and gp41 involved with fusion and attachment of HIV to CD4 antigen on host cells.
6. Replication & Transmission Of HIV
Primary HIV infection and Initial Viremia:
• During the asymptomatic latent phase of AIDS, the virus is actively proliferating
• Can be found in association with Follicular dendritic cells in lymph nodes
• Serve to trap HIV virions coated with anti-HIV antibodies.
• Sero conversion take place in 3-4 weeks
METHOD OF TRANSMISSION:
1. Sexual transmission
• Heterosexual transmission most common mode of transmission

• Risk of transmission from man to woman(most common50-70%)
2. Exposure to infected blood or blood products.
• Risk of HIV transmission is not seen with Plasma derived hepatitis B vaccine, Cryoprecipitate)(least
common> 1%)
• Use of contaminated clotting factors by hemophiliacs0.5%.
• Sharing contaminated needles (IV drug users> 25%).
• Health worker gets HIV from an accidental needle prick in1% cases
• Risk of getting HIV infection from transfusion of a unit of infected blood is > 95o/o.
3.Transplantation of infected tissues or organs.(But not with Skin scraping)
4.Mother to fetus
• Breast milk & perinatal transmission (30-40 %)

• Dependent on viral load and mother’s CD 4 count.
• HIV infection in child of a HIV +ve mother is 20-30%
• Possibility of vertical transfer of HIV infection if prophylaxis is given is 1% and if not the 25%
• Vitamin A deficiency increase risk of transmission
7. Diagnostic Techniques In HIV
DIAGNOSIS

• ELISA is the best screening test (Sensitivity > 99.9%)
• Western blot +ELISA=confirmatory test ( 99.9%)
Antigen detection p24
• p24 is the earliest viral marker

• p24 antigen capture assay (ELISA) is best for screening
• p24 antigen disappears from the blood after 6-8 weeks in HIV
Virus isolation
• Cultivation of patient CD4 + (Helper) T Lymphocyte with uninfected lymphocyte in presence of lL-2
T cell anergy
• Abnormal response of T cells to mitogens is a test used in HIV

• HIV causes immune suppression, it causes hypergammaglobulinemia
HISTOPATHOLOGY OF HIV:
• Disruption of centers ('moth-eaten appearance')

• Distinctive clustering of large follicular center cells
• Explosive follicular hyperplasia
WINDOW PERIOD
• The time period between primary infection and antibody detection is called window period
• Window period in HIV infection is 4-8 weeks
• During the Window period ELISA & western blot both are negative
• Associated with increased p24 antibody: basis for detection in window period.
• For p24 detection(antigen) - 16 days
• RNA PCR - 12 days
• Average incubation period of AIDS is 10 years
DISEASE MONITORING
• CD4+ cell counts

• HIV RNA - viral load
• Beta-2-microglobulin and Neopterin(concentration increase with advancing disease)
• Any HIV-infected individual with a CD4 + T Cell count of <200/microL has AIDS by defination,
regardless of the presence of symptoms or opportunistic disease
DIAGNOSIS OF HIV IN INFANTS:
• According to CDC recommendations, HIV screening of pregnant women is Opt out testing
• The infants continue to test positive for IgG antibodies for upto 18 months.
• Uptil 18 month of age this method of diagnosis cannot be used.
• Direct viral detection assays:
1. Detection of HIV DNA or RNA by PCR.

2. HIV p24 antigen
3. HIV culture
4. Immune complex dissociated p24 antigen.
Viral DNA by PCR is the preferred method in developed countries.
DIAGNOSIS OF AIDS ASSOCIATED DISEASES:

Pneumonia in AIDS:
• The cysts stained with methenamine silver
Penicillium marneffi:
• It forms yeast like cells that are often intracellular resembling histoplasmosis.
Candida tropicalis:
• Microscopy reveals capsulated yeasts
Tuberculosis:
• In tuberculosis in an AIDS patient the chest X-ray looks like Miliary shadow
8. AIDS Control Programmes
WHO case definition for AIDS:
• In an adult or adolescent (>12 years)
Major Signs:
• Prolonged fever more than 1 month

• Chronic diarrhoea > 1 month
• Weight loss > 10% of body weight
1097
• National helpline for HIV/AIDS

National Health Policy of India-2002
• Achieve zero level transmission of HIV/AIDS by 2010
National AIDS control Programme
• Providing 3 million people treatment by end of 2005 was "3 by 5" initiative.
• February 12, 2014 launched NACP VI, under the banner of NACO.
Highlights of NACP IV:
• Reversal of AIDS epidemic

• Targeting High Risk Groups (HRG) – truckers, migrants, pregnant women, etc
• Promotion of condoms (free distribution) in particular female condoms .
• Social protection.
STD control programme
• Diagnosis and treatment of STD one of the major strategies to control spread of HIV infection.
• For treatment of STDs, blue colored pack is used for treatment of Genital ulcer
HIV surveillance -
• HIV sentinel surveillance
School AIDS educational programme
• Training module called Learning for life prepared to bring an uniformity in approach
Anti-retroviral treatment (ART)
• 91 ART centres
• Combination of three potent drugs, given to the persons with advanced stage of AIDS.
• "Suraksha clinic" .
MILLENNIUM DEVELOPMENTAL GOAL:
• Goal 6: Combat HIV/AIDS, malaria and other diseases:
The Red Ribbon Express
• Seeks to spread awareness about HIV/AIDS

• Promote safe sex
• Reduce discrimination against AIDS victims in India, especially those in rural regions.
• NACO launched the Red Ribbon Express to commemorate World AIDS Day(dec 1).

Integrated counselling and Testing centres (ICICs)
• Established at :
i) Medical colleges iii) Sub-district level hospitals
ii) District hospitals iv) Community health centres.
o It is proposed to exend services to 24 hours PHCs.
9. WHO clinical staging of HIV/AIDS for children with confirmed HIV infection
WHO clinical staging of HIV/AIDS for children with confirmed HIV infection
Clinical stage 1
• Asymptomatic
• Lymphadenopathy
Clinical stage 2
• Unexplained persistent hepatosplenomegaty
• Papular pruritic eruptions
• otitis media, oton'hoea, sinusitis or tonsillitis
Clinical stage 3
• Persistent oral candidiasis (after first 6-8 weeks of life)
• Severe recurrent bacterial pneumonia
• Unexplained anaemia (9 per litre) and or chronic thrombocytopaenia (9per litre)
Clinical stage 4
• Pneumocystis pneumonia
• Recurrent severe bacterial chest infections (such as empyema, pyomyosrtts, bone or joint
infection or meningitis but excluding pneumonia)
• Oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs) Extrapulmonary
tuberculosisKaposi sarcoma (in adult)
• Progressive multifocal leukoencephalopathy
• Depression is most common psychological feature
Necrotizing Granuloma
• Numerous acid-fast bacilli are demonstrated by Ziehl-Neelsen staining within the cytoplasm of
epithelioid cells.
Progressive Multifocal Leukoencephalopathy
• Shows hemiparesis, ataxia, homonymous hemianopia, and cognitive deterioration.

• MRI of the brain demonstrates widespread areas of abnormal T2 signal in the white matter.
• An electroencephalogram is remarkable for diffuse slowing over both cerebral hemispheres.
• Brain biopsy reveals demyelination with abnormal giant oligodendrocytes, some of which contain
eosinophilic inclusions.
Misc
• HIV in children, characteristic finding is Recurrent chest infection

• Feature of HIV infection in childhood Failure to thrive is universal, Lymphadenopathy, P. Carinii
pneumonia, M.C. AIDS defining illness in children,
• Depression is the most common psychological features of AIDS
• Teratogenic effects are rare with HIV infections
10. Prevention Methods In HIV
• For contaminated medical instruments 2 % solution of glutaraldehyde is used.

• Strategies effective in preventing mother to child transmission of HIV are Antiretroviral
prophylaxis,Caesaren delivery & avoiding Breast feeding
• Put the blood contaminated dressing material directly in an appropriate bag and send for
incineration
• Target strategies in preventing the HIV transmission include Education, Treatment of STD & use
of Condoms
• Targeted intervention for HIV is done for Sex workers , Migrant laborers ,Homosexual
men, Truckers , IV drug users , Street children
• Community education behavioral change is aimed at AIDS control in India
• Universal (standard) precautions to be observed by surgeons for the prevention of hospital acquire
HIV infection include Wearing gloves and other barrier precaution,Washing hands on
contamination & Handling sharp instruments with care
• If a patient of Hemophilia to be taken for dental extraction patients should be screened for HIV
11. Treatment Modalities In HIV/AIDS Patients
• Octreotide is the drug of choice for diarrhea in AIDS

• Interferon is a Glycoprotein, produced by many mammalian cells, and used in the treatment of hepatitis,
papillomaviruses, hairy-cell leukemia and AIDS-related Kaposi's sarcoma

• Raltegravir is an integrase inhibitor which is used in combination with other antiretroviral agents in
treatment of patients with ongoing HIV-1 replicaiton.
• The drug efavirenz inhibits HIV 1 reverse transcriptase
• Ritonavir, Didanosine, Zidovudine comes under anti-HIV agents
• Rifampicin is contraindicated in AIDS as it induces metabolism of ritonavir, indinavir and saquinavir
• Protease inhibitor in HIV is Potent inhibitors of CYP3A4
• Saquinavir is a weak inhibitor of CYP3A4
• All protease inhibitors are substrates for P glycoprotein coded by MDR gene.a
• Zidovudine given for HIV in preganancy because Decreases the risk of vertical transmission
• For the prevention of parent to child transmission of HIV, the NACO's recommendation is to
give Niverapine 200 mg in active about to mother and syrup niverapine 2 mg/kg body weight to
newborn with 72 hours of delivery
• Ribavarin is the drug of choice for bronchitis with HIV
• AIDS patient presents with fistula - in- ano can be treated with seton
• The drug of choice for cytomegalovirus retinitis in HIV patients are ganciclovir or foscarnet
• Post exposure prophylaxis [PEP] for HIV should be given for a minimum period of 4 weeks
• Nevirapine drug is given as a single dose to prevent mother to child HIV transmissiona
12. HIV Involving Nervous System
• Progressive multifocal leukoencephalopathy is the least common cause of seizures in AIDS

• Pathologic features of brain in AIDS includes microglial nodule, Pericapillary aggregates of
multinucleated giant cells having generous or scanty neoplasm , Perivascular lymphocytic cuffing,
demyelination and infiltration of macrophages and multinucleated giant cells.
• Cryptococcus neoformans is the most common cause of acute meningitis in an AIDS patient
• Primary CNS lymphoma shows multicentric mass lesions in the brain and meninges derived from B-
lymphocytes
• Diffuse white matter pallor, Perivascular infiltrates of lymphocytes and macrophages, Foci of
necrosis, gliosis and / or demyelination, Microglial nodules, macrophages and multinucleated cells e
the Histopathological features of HIV encephalitis
• Perivascular lymphocytes & microglial nodules are seen in HIV encephalitis
• Primary CNS lymphoma is the Most common CNS neoplasm in HIV patient
• HIV associated neuronal loss occurs particularly in Hippocampus, Basal ganglia, Caudate nucleus.
13. Toxoplasma gondii: Toxoplasmosis
Clinical manifestation of toxoplasmosis
1.Adults
a) lmmunocompetant host

• M.C. clinical feature is cervical lymphadenopathy.
• Other less common manifestations are pneumonia, myocarditis
• Encephalitis- rare
2. Children
a) Congenital
• May present with hydrocephalus, microcephaly mental retardation, deafness, blindness, epilepsy.
• Chorioretinitis
• Intracerebral calcification may occur
• NOT infective in 3" trimester in pregnancy
b) Acquired
• C/Fs are
o Macular scarring
o Retinochoroiditis(Most common)
o Vitritis
Diagnosis of Toxoplasmosis
Serology
• Acute infection detected by presence of IgG by:

o Sabin Feldman dye test(gold standard)
o Avidity test-measure the strength of antigen-antibody reaction for IgG antibody
• IgA ELISA is more sensitive than IgM ELISA for detecting congenital infection.
Congenital infection
• Detection of IgM specific antibody in fetus

o Helpful in diagnosing congenital toxoplasmosis since it does not cross placenta.
Treatment of Toxoplasmosis
• Congenital infection
o Pyrimethamine and sulfadiazine
• Infection in pregnancy: Spiramycin (rovamycine) is DOC.
. LUNGS IN HIV
• AIDS patient most common mico-organism responsible for pneumonia is Pneumocystis carinii

• Mycobacterium tuberculosis is the Most common agent causing tuberculosis in AIDS patient in
tropical countries
• Mycobacterium tuberculosis can cause disease in HIV+ve patient with a CD4 count of 600/ cu.mm
• The most characteristic histopathological feature of pneumocystis carinii pneumonia in adults is
predominantly alveolar, foamy vacuolated, eosinophilic exudates.
• Respiratory system infections in HIV is seen with Streptococcus, H.influenzae, Pneumocystis carinii
• Chest X-ray findings in tuberculosis associated with HIV are Disseminated tuberculosis, Pleural
effusion, Hilar lymphadenopathy
15. AIDS defining Opportunistic infections and Neoplasms
Opportunistic Infections In AIDS:
Parasitic
• Cryptosporidiosis (most common in India)or Isosporidiosis (enteritis)

• Strongyloides stercoralis(common)
Fungal
• Candidiasis (esophageal, tracheal, or pulmonary)

• Cryptococcosis (CNS infection)
• Coccidioidomycosis (disseminated)
• Histoplasmosis (disseminated)
• Pneumocystis carinii
• Penicillium marneffei
• Aspergillosis (rare)
Neoplasm
• Kaposi sarcoma(Multifocal tumor of vascular origin)( HHV - 8 )

• Non Hodgkin lymphoma
• Primary lymphoma of brain
• Invasive cancer of uterine cervix
• Immunoblastic lymphoma (most common lymphoma)
• Primary Effusion Lymphoma (PEL)
• Plasmacytic lymphoma of the oral cavity
• Burkitt's lymphoma(EB virus)
Helminthic
• Strongyloides stercoralis

Other Opportunistic Infection In AIDS
• In AIDS, lymphadenopathy is most often due to Non specific enlargement of lymph node
Kaposi Sarcoma
• There are four types of Kaposi sarcoma:
1. The classic type/chronic KS/ European KS

2. HIV-associated/epidemic Kaposi sarcoma
3. Endemic/ African/ Lymphadenopathic Kaposi sarcoma
o Skin lesion are sparse.
4. Iatrogenic/transplant associated Kaposi sarcoma
o due to drug treatment causing immune suppression .
16. Kidney In HIV
• Focal segmental GN variant of Glomerulonephritis is associated with AIDS

• HIV associated nephropathy is a type of Collapsing glomerulopathy
• HIV infection is associated with focal segmental glomerulosclerosis, acute diffuse proliferative
glomerulonephritis, and mesangioproliferative glomerulonephritis, including IgA nephropathy,
MPGN, and membranous glomerulopathy.
• HIV infection, Hodgkins disease, and other Lymphoproliferative malignancies, Drug induced
Interstitial Nephritis( NSAIDS ,Rifampicin, Interferon) are the conditions associated with minimal
change disease
• HIV renal specific nephropathy is Focal Segmental Glomerulosclerosis
17. Eye, Endocrine system, Hematopoietic system, CVS and Dermatological system In HIV
• CMV retinitis is the most frequent and serious ocular opportunistic infection and is the leading
cause of blindness in AIDS patients.
• Viral, bacterial & fungal infection, Kaposi sarcoma, CMV retinitis, lymphoma are the Ocular
manifestation of HIV
• Commonest opportunistic organism to cause ocular inflammation in AIDS is Cytomegalovirus
• Central toxoplasma chorioretinitis , CMV retinitis, Candida endophthalmitis are the ocular lesions
may occur in patients suffering from AIDS
• Vision loss in HIV is commonly due to infection with Cytomegalovirus
18. Oral and GIT Manifestations Of HIV

CANDIDIASIS:
• White plaque-like material commonly involving tongue and buccal mucosa

• Dysphagia
o Indicates that the candidiasis involves the oropharynx
o or the esophagus
o as well as the mouth.
• Laboratory findings show :
o growth in cornmeal agar at 20 degree celcius,
o microscopy showing hyphae
o growth in human serum at 37 degree celcius show budding yeasts.
ORAL HAIRY LEUKOPLAKIA:
• White patch on the side of the tongue with a corrugated or hairy appearance.
• Virtually pathognomic of HIV disease in the context of HIV risk factors.
• It is caused by Epstein-Barr virus (EBV) .
Esophagitis
Intestinal Infection
Diahrrea in AIDS patient can be caused by:
Bacterial Salmonella, Shigella, Campylobacter jejuni
Fungal Histoplasmosis, Coccidiodomycosis Pencillosis
Protozoa Cryptospoidia(second most common), Microsporidia, Isospora

belli(most common)
Viral CMV,HIV,Enteropathy
• Agents transmitted venereally per rectum

o e.g., Neisseria gonorrhoeae, Treponema pallidum, Chlamydia
o may contribute to proctocolitis.
19. Chlamydia
INTRODUCTION:
• Obligate gram -ve intracellular bacterial parasite unable to grow in cell free media (against Koch's
postulates)
• They do not have peptidoglycan and N-acetylmuramic acid in cell wall.
• Most common organism associated with reactive arthritis is Chlamydia
• Elementary bodies are infectious
• Forms chlamydial microcolony called Inclusion body.
.Classification
• Classified into 4 classes
1. C. trachomatis
2. C.pneumoniae
3. C.psittaci
4. C.pecourum
Antigen
• Heat stable LPS(Lipopolysaccharide)

• Maior outer membrane protein/MOMP
RESISTANCE:
Molecular mimicry:Chlamydia induced INF-y inhibits INF-y dependent expression of MHC class-II proteins.
20. Diagnosis & treatment Of Chlamydia Infection
• Yolk sac inoculation is used for diagnosing chlamydia from tissue specimen.
NAATs:
• NAATs amplify and detect organism-specific genomic or plasmid DNA or rRNA

• FDA cleared for urethral swabs from men/women, cervical swabs from women, and urine from
both
• PCR and LCR: sensitive and specific methods for detecting cervical Chlamydia trachomatis infection
in women.
• Significantly more sensitive than other tests
Non-NAATs:
• Direct fluorescent antibody (DFA)

• Enzyme immunoassay (EIA)
• Detects bacterial antigens with an enzyme-labeled antibody
• Nucleic acid hybridization (NA probe)
• Detects specific DNA or RNA sequences of C. trachomatis and N. gonorrhoeae
• Gram staining:
• Presence of pus cells with absence of any microorganisms on gram stain
• Fries test (skin hypersensitivity test) was used for LGV (caused by chlamydia trachomatis).But it is
not used now because of high false positive results.
TREATMENT:
Treatment of Uncomplicated Genital Chlamydial Infections
CDC-recommended regimens
• Azithromycin 1 g orally in a single dose, OR

• Doxycycline 100 mg orally twice daily for 7 days
Treatment of chlamydial Cervicits:
• tetracycline
Treatment of Chlamydial Infection in Pregnant Women
CDC-recommended regimens
• Azithromycin 1gm as a single dose(latest )

• Erythromycin base 500 mg orally 4 times a day for 7 days, OR
• Amoxicillin 500 mg orally 3 times a day for 7 days
Treatment of Neonatal Conjunctivitis and/or Pneumonia
CDC-recommended regimen
• Erythromycin base or ethylsuccinate 50 mg/kg/day orally divided into 4 doses daily for 14 days
21. Vibrio cholerae
INTRODUCTION:
• John Snow (1813-1858) found the link between cholera and contaminated drinking water in 1854,
using spot map.
• Robert Koch Isolated V.cholrae in 1883
• Cholera is caused by Vibriocholera .01 and 0139
• Cholera belongs to category-B of bioterrorism
• Cholera is WHO notifiable disease
• Father of public health is Dr. John Snow
VIBRIO'S IN NATURE

• It is transported in Alkaline pH
• Man is the only natural
• Blood group O+ve are more susceptible
MORPHOLOGY & IDENTIFICATION:
• They appear curved gram negative aerobic rods and are motile
• Possesing a polar flagellum that shows Darting motility (shooting star)
• V. cholera is able to stay in GIT because of motility
• It is non halophilic
ANTIGENIC STRUCTURE & BIOLOGICAL CLASSIFICATION:
• V.cholrae has O lipopolysaccharide that confer serologic specificity

• Produces indole and reduces nitrates
V.cholrae - typing
• V.cholrae .01 has determinants that make possible futher typing
Vibrio cholerae .O1:
• Infectious dose: 106 – 108

• Incubation period 1-3 days (½-5 days
Epidemic V.cholerae is biotyped into
1. Classic
2. El Tor
El Tor Vibrio's:
• The El Tor biotype of vibrio cholerae was first isolated in Egypt

• 7th Pandemic of cholera was caused by El Tor
• El Tor vibrios has three serotypes- Ogawa(found in India), Inaba, Hikojima
• It is much harder than classical vibrios, capable of surviving in the environment much longer.
• The severity of illness is much less, with a large proportion of mild and asymptomatic infections.
Classical cholera vibria:
• Most severe diarrhea.

• The mortality rate of cholera, without treatment is between 25-50%.
• The incidence of mild and asymptomatic infections is more with El Tor vibrios than with classical
cholera vibrios.

V.cholrae- 0-139(Bengal V. cholera:
• V.cholrae 0139 is very similar to epidimologically & clinically V.cholrae .01 El Tor biotype
• V.cholrae 0139 Epidemic: The epidemic of cholera caused by V cholerae 0139 was discovered in
chennai
22. Vibrio cholerae Culture & Diagnosis
Holding and transport Media:
1. VR medium(Venkataraman Ramakrishan Medum)

2. Carry-Blair medium
3. Autoclaved sea water
• Transported in alkaline peptone water medium
Plating media
1. TCBS
• V.cholrae grows well on Thiosulphate citrate bile sucrose (TCBS ) agar
Growth Characteristics
• Vibrio's grow at a very high pH ( 8-5 – 9-5 ) and are rapidly killed by acid
• Quarantine period of cholera 5 days
DIAGNOSIS
Stool Examination
Specimen Collections
• Stool specimens are collected in acute stage of the disease. before the antibiotics are administered.
Transport:
• Stool culture:
• Use Cary Blair Transport media if available for transport.
• Use TCBS media for culture
Characteristics

• Mucus flecks from stool are cultured.
• Smears are not useful for diagnosis.
• Dark field microscopy shows rapidly motile vibrio's.
• Motility is inhibited by antiserum.
Serological Examination
• Confirmatory Tests for V.cholrae:

o V.cholrae organisms are further identified by slide agglutination tests using anti -0 group 1
or group 139 Antisera and by Biochemical reactions
Bio Chemical Reactions:
1. Catalase +ve
2. Oxidase +ve
3. Indole +ve
4. Nitrates reduced to Nitrites
5. Surcose fermenter
Characterstic V.cholrae( Classical ) V.cholrae (El Tor)
Hemolysis -ve +ve
Voges -proskauer test -ve +ve
Polymyxin sensitivity +ve -ve
Group IV phage Susceptibility +ve -ve
Chick erythrocyte Agglutination -ve +ve
23. Vibrio Cholera & It's Clinical Features
Manifestations
• Sudden onset of painless rice water diarrhea

• Electrolyte imbalance
• Shock.
Other Important pionts
• Acidosis
• Arsenic poisoning
o Can be detected from hair & nails long after death
o Confused with cholera
o Clinically present with rain drop pigmentation & mees line
PANCREATIC CHOLERA:
• It is a Pancreatic endocrine tumor,

• Commonly of the Delta cells
• Characterized by net secretion of salt and water by gut.
• Features of Pancreatic cholera :
o Severe watery diarrhea / flushing / weight loss
o Hypokalemia
o Hypochlorhydria
o Hypercalcemia
o Hyperglycemia
o Inordinate fecal water and electrolyte loss
o Achlorhydria
• Pancreatic cholera is synonymous with 'Verner Morrison Syndrome' or `WDHA Syndrome'
On laboratory evaluation there will be :
• Mild neutrophilic leukocytosis (neutrophilia)
24. Vibrio Cholerae Virulency
PATHOLOGY:
• Pathogencity of 0-139 vibrio is due to 0 antigen
TOXINS OF VIBRIO CHOLERA:
ENTEROTOXIN(CTX/CT/Choleragen/Permeability factor)
• Toxin production is determined by a filamentous phage integrated with bacterial chromosome.

• It is antigenically related to heat labile toxin of Escherichia
MECHANISM OF ACTION:
• Cholera toxin consists of 2 subunits

• Monomeric enzymatic moiety (A subunit):Further divided A1 and A2
• Pentameric binding moiety (B subunit)
• Ganglioside GM1 serves as a mucosal receptor for subunit B
• It promotes entry of subunit A into the cell

• Activation of subunit A1 which interacts with cytosolic proteins called ADP-ribosylation factors (ARF)
• ARF-A1 complexes catalyze ADP-ribosylation of a G-protein called GSa.
• ADP-ribosylated Gsa in turn binds to and stimulates adenylate cyclase
• This causes increased levels of intracellular cAMP
• cAMP inhibits the absorptive sodium transport system
• Activates the secretory chloride transport system
• Results in prolonged hyper secretion of water and electrolytes
25. Vibrio Cholera Transmission & Cholera Control
TRANSMISSION:
• Contaminated water (infectious dose = 109)

• Contaminated food(infectious dose = 103)
• Raw or undercooked seafood
• Rice, cereals, gruels left at ambient temperature
• Person to person transmission( not common)
• Human can be a healthy carrier with subclinical features
• The mechanisms by which cholera might be maintained during the intervals between peak cholera
seasons is Continuous transmission in man
• Fecal-oral transmission is possible
EPIDEMIOLOGY:
• Epidemiology of cholera in England was classified by John Snow

• Six Pandemics of Cholera occurred between 1817 – 1923.
• Most likely V.cholrae 01 of Classical type contributed to pandemics.
• Phage typing is useful as an epidemiological tool in cholera
• Epidemic in cholera is self limiting with abrupt onset
Cholera Control
• Patients isolated .
• Wells needs to be disinfected every Day
• Excreta disinfected
• The most effective disinfectant for general use is a coal-tar disinfectant with a Rideal-Walker (RW)
coefficient of 10 or more such as cresol.
• Notification
• Cholera is notifiable disease locally, nationally and internationally
• Notifiable to WHO within 24 hours of its occurrence by national government.
• Water control Boiling or chlorination(emergency sanitary).
26. Vibrio Cholerae Management

CHEMOPROPHYLAXIS:
• Treatment of Choice:Rehydration therapyDOC :single dose of doxycycline/tetracycline

• Mild to moderate rehydration:ORS
• For severe: IV fluid.Ringer lactate is best
• Oral Tetracycline tends to reduce stool output in cholera and shortens the period of excretion
of vibrio's
• TMP-SMX – antibiotic of choice for children.
• Furazolidone – antibiotic of choice for pregnant women.
VACCINES:
Killed vaccine
• Cholera vaccine effectiveness is 85% for 6 months which declines to 50% for 12 months
• Oral cholera vaccine is effective for 3 years
Two types of oral cholera vaccines are available:
• Dukoral (WC-rBS)
• Dukoral is a monovalent vaccine based on formation and heat-killed whole cells (WC) of V. cholerae
01 (classical and El Tor, Inaba and Ogawa) plus recombinant cholera toxin B Subunit.
• Shanchol and mORCVAX.
• NEWER VACCINES:Cholera vaccine is no longer required, nor recommended for the vast majority of
travellers by the Centres for Disease Control and Prevention (CDC).
o CDC – On Vaccination for Cholerae
27. Structure Of Immunoglobulin
STRUCTURE OF ANTIBODIES:
Immunoglobulin molecule:
• Represents hetero-tetrameric quarternary structure between 4 polypeptide (2 heavy + 2 light)

chains
CONSTANT REGION/CARBOXY TERMINUS
• Fc fragment of Ig
• Determines the biological properties of Ig
o Complement fixation
o Placental transfer
o Skin fixation
o Catabolic rate
Amino terminus/Variable unit/FAB/ANTIGEN BINDING SITE
• Antigen binding site
Heavy chain
• have high molecular weight i.e 50,000-77,000d

• Composed of 450 amino acid.
• Class specific antigenic determinants of an immunoglobulin is associated with H-chain

• H chain consist of 1 variable (VH) and three domains in constant region (CH1, CH2,
• CH3
• Highly variable zones
• 3 in L and 4 in H chain
• Involved in the formation of antigen-binding sites.
• Sites on the hypervariable regions which make actual contact with the epitope
• Are called complementarity determining regions or CDR's
• CH2 region in IgG & IgM binds C1q in the classical complement sequence
28. Immunoglobulin A
STRUCTURE:
• Secretory IgA (SIgA) is dimeric formed by two monomers joined by J chain

• Synthesized by plasma cells.
PROPERTIES:
• It is 2nd highest serum Ig

• Major secretory Ig (Mucosal or Local Immunity)
• SIgA plays an important role in local immunity against respiratory and intestinal pathogens
• IgA does not fix complement but activates alternative complement pathway
• Predominant type of immunoglobulin in human milk
LOCATION:
• IgA is found in peyer's patch

• IgA is the main immunoglobulin in secretions such as
o milk
o saliva
o tears
o secretions of the respiratory, intestinal, and genital tracts.

Clinical Conditions Associated:
• IgA nephropathy may occur following an episode of mucus membrane infection of the respiratory
or gastrointestinal tract.
• Henoch-Schonlein purpura is characterized by the deposition of IgA around the vessels
IgA DEFICIENCY:
• In Protein Energy Malnutrition IgA is reduced the most

• In malnourished subjects(e.g.kwashiorkar), secretory IgA is generally reduced.
• Therefore infections tend to be severe and recovery delayed
• It may be acquired by :
o Congenital infections such as toxoplasmosis, rubella, CMV
o Treatment with phenytoin
29. Immunoglobulin M
PROPERTIES:
• Earliest Ig synthesized by fetus
STRUCTURE:
• IgM molecules are polymers of five four-peptide subunits

• Pentamer
• Contain J chain which forms disulfide bond with hinge region
Functions
• Fc piece of IgM Fixes complement

• IgM is responsible for opsonisation
Clinical Importance:
• First to appear following infection and disappear early

• Hence their demonstration in serum indicates recent infection - primary immune response
• Does not cross placenta and hence its detection is useful in IU and congenital infections
30. Immunoglobulin E
Properties

• Only heat labile Ig (inactivated at 560C in 1 hour)
• Antibody with least serum concentration IgE(0.0004)
• Binds to basophils and mast cells (Does not require Ag binding)
Functions
• Responsible for anaphylactic type of hypersensitivity
Elevated IgE levels
• Seen in type I allergic conditions (asthma, hay fever, eczema, children living in unsanitary conditions
with high load of intestinal parasites
• Main defence against helminthic infestations
31. Immunoglobulin G
INTRODUCTION:
• Capacity, of producing IgG starts at 6month age

• Major serum Ig (80%)
• Persists for many years after exposure
• Half-life: 23 days
• Small intestine (Most probably) Most abundant immunoglobin in blood
• IgG1 - maximum serum concentration
STRUCTURE:
• IgG molecules contain

• Two gamma heavy chains of a given subtype
• Two light chains (either kappa or lambda).
• The 2 in IgG2 indicates the subclass to which the molecule belongs.
• IgG2 contains two gamma2 chains (since a given B cell can only form one type of heavy chain).
PROPERTIES:
• Major serum Ig about 85% of imunoglobulin

• Can cross placenta as have receptor on placenta
• The Fc piece of IgM & IgG fixes C1
• Can Fixes & can activate complement (± IgG4)
• Serum IgG4 is elevated at least twofold higher than 135 mg/dL in those with autoimmune
pancreatitis.

32. E.coli:Structure and Virulency
PHYSIOLOGY & STRUCTURE:
• Gram-negative, facultative anaerobic rods, Peritrichous flagella

• Fermenter; oxidase negative
• Non-pathogenic amoebae
• Preferred bacteriological indicator of faecal contamination of water
• E.coli gets attached to a surface with the help of lectin( P blood group antigen binding Microbial
adhesion proteins)
Antigenic Structure
Somatic antigen O 1. Lipopolysaccharide in nature

2. Heat stable
3. Antibodies to O-antigen
4. are predominantly lgM
Capsular antigen K 1. Heat labile

2. Responsible for attachments of bacteria to epithelial cells.
Flagellar antigen 1. Associated with virulence
• Serotyping based on these three antigens is:

• Early 'O' group (1, 2,3,4, etc):
• Later'O'group (25,55,85 etc): Enteropathogenic strains
• O157:H7 (common)is negative (clear colonies) on sorbitol MacConkey agar & MUG tests
• non-O157 serotypes may be sorbitol positive
Toxin
• Hemolysins .
• Enterotoxins: Important in pathogenesis of diarrhea
• Heat-stabile :Activates cGMP
• Heat-labile enterotoxins
• Shiga toxins STEC /Verocytotoxin
33. STAPHYLOCOCCI
INTRODUCTION:

• Gram positive cocci
• Ogston discovered Staphylococcus in 1881
CLASSIFICATION:
• Based on pathogenecity:
• Pathogenic:- includes only one i.e., S.aureus
• Non-pathogenic:- includes S.epidermidis, S.saprophyticus, S.albus, S. citrus, S.hominis,etc.
• Based on coagulase production:
• Coagulase positive: S. aureus
• Coagulase negative: S. epidermidis, S. saprophyticus
• Based on Novobiocin susceptibility(for cogulase -ve group)
+ve -ve
S. epidermidis S. saprophyticus
S. hemolyticus S. saprophyticus
S.hominis
S. logdunesis
S. schleiferi
• Infection by coagulase negative Staphylococci are due to Staphylococcus epidermidis
34. Staphylococcus aureus: Pathogenesis, Clinical Syndromes
CLINICAL SYNDROMES:
• Conjuctivitis
CUTANEOUS INFECTIONS:
• Bullous Impetigo:
• It is characterized by watery bristles, which become pustules and then honey coloured crust
• Botryomycosis
DEEP INFECTIONS:
• Osteomyelitis
• Both acute & chronic osteomyelitis is caused by S.aureus
• Periostitis

• Endocarditis:
• It is an inflammation of the inner layer of the heart, the endocardium
• Prosthtetic valve, tooth extraction may be the aggrevating factor in Infective endocarditis by s.
aureus
• Endocarditis occurs when bacteria enter bloodstream, travel to heart, and lodge on abnormal heart
valves(Prosthetic valve endocarditis ) or damaged heart tissue.
• Myocardial abscess is most common in acute endocarditis caused by Staphylococcus aureus
• Septic arthritis( in children)
• Pneumonia( In patient with bronchiectasis)
Staphylococcal pneumonia
• URTI , pyoderma or other associated purluent disease

• Most common pathogen causing, pulmonary infection in cystic fibrosis in infants & young children
is Staphylococcus aureus
• Sore throat
• Pneumatocoele
• Chest radiograph shows patchy areas of consolidation and multiple bilateral thin walled air
containing cysts
Exfoliative diseases:
• ‘Staphylococcal skin scalded syndrome’previously called dermatitis exfoliativa pemphigus

neonatorum
• Lyell’s disease
• Ritter’s disease
TOXIC SHOCK SYNDROME:
• Caused when Toxin shock syndrome toxin (TSST) liberated by S.aureus enters bloodstream
• It is a multisystem illness, that occurs due to superantigen
STAPHYLOCOCCUS FOOD POISIONIG:
• Caused when consuming food in which S.aureus has multiplied and pre-formed endotoxin
• Intradietic toxin is responsible for intestinal symptoms.
• Commonly occurs with dairy products
• Optimum temperature for toxin production is 37°C
• Incubation period is 1-6 hours
• Gastroenteritis within 4-6 hrs of consumption of cooked food indicates the cook to be in the carrier
state of staphylococcus
• Staphylococcus appear in stool

35. Staphylococcus aureus: Diagnosis, Prevention and Treatment
Bacteriological Investigation:
• Sputum: to diagnose lower respiratory tract infection
MRSA:
• Most strains of S.aureus, even those acquired in community, are penicillin resistant
• Resistance is attributable to beta-lactamase production due to genes located on extrachromosomal
plasmids.
• Some are resistant to the newer beta-lactamase resistant semisynthetic penicillins,
o methicillin
o oxacillin
o nafcillin
TREATMENT:s
• Oxacillin is the drug of choice for penicillinase resistant staphylococcus

• Transfer of drug resistance in staphylococcus is by Transduction & Conjugation
• MRSA are susceptible to Vancomycin, Teicoplanin and Linezolid
• Drug of choice for Methicillin resistant staphylococcus aureus is (MRSA) is vancomycin
(glycopeptide)
36. Corynebacterium Diphtheria
INTRODUCTION:
• Gram-positive
MORPHOLOGY:
• Appear in short chains (“V” or “Y” configurations) or in clumps resembling “Chinese letters”.
• Metachromatic granules
o Give Club shape
o Present of at one or both ends
o Also called volutin or babes-Ernst granules.
o Special stains like albert [ malachite green & toludine blue], neisser or polychrome
methylene blue are used for staining.
CULTURAL CHARACTERISTICS:
• Tellurite blood agar:

o Black colonies due to reduction of tellurite to tellurium.
o Colonies appears after 48 hrs.
• Tinsdale agar
o Brown halo surrounding the colony is differentiating feature.
Diphtheria Toxin
• Heat Labile Polypeptide exotoxin

• Production iron concentration dependent.
• Toxin is phage mediated
• Have both local and systemic effect.
37. Mycobacterium Tuberculosis
• M.tuberculosis, M.bovis, M. bovis bacille Calmette-Guerin (BCG), M.africanum, M.microti, and

M.canettii forms mycobacterium tuberculosis complex
• Type IV hypersensitivity to Mycobacterium tuberculosis antigen may manifest as Phlyctenular
keratoconjunctivitis
• Cell wall of M.tuberculosis has high lipid content
• Mycolic acids and LAM in M.tuberculosis form waxy coat(this LAM is also used for diagnosis
of M.tuberculosis.)
• M.tuberculosis Lacks exotoxins or endotoxin
• M.tuberculosis is a non- sporing, aerobic, gram negative bacteria that measures 0.5-3 micon m
• The normal time required to culture mycobacterium TB is 4-8 weeks
• Mycobacterium tuberculosis was discoverd by Robert koch
• The medium used for Mycobacterium tuberculosis is Lowenstein jensen medium
• Mycobacterium tuberculosis is niacin positive
• The single most common cause of pyrexia of unknown origin is Mycobacterium tuberculosis
• Mycobacterium tuberculosis infection in humans is most commonly because of inhalation
• Live TB bacilli culture is by MGI
38. Salmonella Typhi
• An increased frequency of infections due to salmonella has been reported among patients with
achlorhydria
• The infectious dose of Salmonella typhi causing typhoid fever is 103 - 106 colony forming units.
• Selenite F broth is an enrichment media for Salmonella & shigella
• S.typhi do not produce gas
• Incubation period of salmonella typhi is 3-21 days
• Blood culture in S.typhi is + ve in 3-7 days
• Vi antigen found in Salmonella Typhi & paratyphi
• Salmonella can enter through the shell if eggs are left on contaminated chicken feed or feces and
grow inside.
• S.typhi need tryptophan as a growth factor
• Salmonella infection is most commonly caused by contaminated water, milk and/or food
• Deoxycholate citrate agar (DCA) medium is used in differentiation of Salmonella from lactose
fermenter
• Salmonella is non-lactose fermenting bacteria
• Salmonella have human reservoir
39. Clostridium Perfringens
• The spores are usually wider than the rods

• Spores located terminally or sub terminally.
• Cl. perfringens is considered as an ideal bacteriological indicator as acceptability aspect of water
• Spores are rarely seen in culture media or material from pathogenic lesions, a characteristic
morphologic feature
TOXINS:
12 distinct types of Preformed enterotoxins elaborated:
• α toxin-
o lethal,dermonecrotic & hemolytic( principle toxin)
ENZYMES
• Hemolysin
o shows double zone of hemolysis
• Lecithinase
o produce opacity around colonies
o by spliting lecithin into phosphorylcholine and diacylglycerol
o appear opalescence in serum or egg yolk media.
40. Clostridium Tetani
• The main reservoir of cl. tetani:soil and intestine of animals and humans
• The main mode of transmission: trauma and contaminated wound
MORPHOLOGY :
• Gram positive Bacillus

• Non capsulated
• Sporing
• Obligatory anaerobe
• Drum stick appearance
• Spherical & terminal spores
• Motile by peritrichate flagella except type IV which is non motile.
• Tetanus spores are highly resistant to:
o boiling and autoclaving for 15 minutes at 120 ( Heat)
CULTURAL CHARACTERSTICS:
• Incubation period of clostridium tetani:

o 6-10 days
• Robertson's cooked meat broth.
o Grows well
o Shows Swarming growth.
• Produces 2 toxins -
o tetanolysin (hemolysin)
o tetanospasmin(neurotoxin)
• Tetanotysin (hemolysin)
• Tetanospasmin:
o block release of inhibitory neurotransmitters glycine and GABA of spinal cord
o Acting pre-synaptically → aboliƟon of spinal inhibiƟon → spread of uncontrolled impulses
initiated elsewhere in the CNS
41. Clostridium Botulinum
INTRODUCTION:
• Category A Bioterrorism's agent

• Causes a disease of Neuromuscular transmission called botulism
TOXINS:
• Gene for botulinum toxin is encoded by a bacteriophage

• All varieties neuotoxic except C2 cytotoxic.
• Site of action:
o Peripheral cholinergic nerve endings.
o Blocks release of Acetylcholine.
• Principal causes of human illness.

o A, B, and E

o Rarely F
• Type C(non-neurotoxin) produces limberneck in birds.
CLINICAL FINDINGS:
Food borne botulism
• Source
o Preformed toxin is important in food poisoning.
o Canned food eaten without cooking.
• Symptoms
o Begin 18–24 hours after ingestion of the toxic food
o Cranial Nerve involvement
o Dysphagia, diplopia, dysarthria are seen
o Signs of paralysis are progressive
o Death occurs from respiratory paralysis or cardiac arrest.
Infant botulism
• Due to ingestion of subterminal spores

• Sudden infant death syndrome (SIDS) following administration of honey is due to Clostridium
botulinum
• Floppy infant syndrome is seen commonly due to infection with Clostridium botulism
o poor feeding
o weakness
o signs of paralysis ("floppy baby").
Wound botulism
• Toxin is produced in wound.
42. Clostridium difficile
MORPHOLOGY:
• Gram-positive, rod-shaped, spore-forming bacteria.

• Anaerobic
• Inhabits the microflora of intestines of humans
• Spores are subterminal
RISK FACTORS:
• Prolong antibiotic therapy

• Pantoprazole increases the risk
• Associated with use of rectal thermometer
VIRULENCE :
• Two major toxins -toxins A and B

• Fiud is leaked leading to whitish yellow plaque formation over, colon known as Pseudomembranous
colitis.
SIGNS & SYMPTOMS:
• Watery diarrhea (at least three bowel movements per day for two or more days)
• fever, loss of appetite, nausea, abdominal pain/tenderness .
• May cause crohn's disease
DIAGNOSIS:
• 3 unformed stools per 24h for 2days

• Toxin A or B detected in the stool
• Pseudo membranes seen in colonoscopy
• There is also a disctinct odor when the feces contains Clostridium difficile.
CONTROL & TREATMENT:
• In mild cases of Clostridium difficile infection, Metronidazole is administered.

• In severe cases, treatment can begin with the administration of Vancomycin but can also require
surgical intervention.
43. Herpes Simplex Virus
MORPHOLOGY:
• Core containing large double-stranded DNA genome
PATHOGENESIS
• The initial infection

o inapparent
o occurs through a break in the skin or mucous membranes, such as in the eye, throat, or
genitals.
HSV includes

• HSV-1
• HSV-2
• HSV 1 and 2 have only about 50 percent genomic homology.
• However, they share most other characteristics.
• HSV 1 On chick embryo CAM,form smaller pock
• HSV 2 Form larger pock
CLINICAL MANIFESTATION:
• Mucocutaneous manifestations
• Face most common site
o gingivostomatitis
o herpes genitalis
o herpetic keratitis
o dermal whitlows.
o Herpes Gladiatorum
• Encephalitis
o Herpes Simplex Virus is the commonest cause of sporadic encephalitis
• Neonatal herpes simplex virus infection and herpes simplex virus encephalitis shows:
o fever
o followed by headache
o confusion
o focal seizures
o Alterations in behaviour
o Olfactory hallucinationand right hemiparesis.
o Mollaret meningitis is also caused by herpes simplex-2
• Meningitis
o Mollaret's Meningitis
• Eye Infection
o Type 1 herpes simplex virus is usually
o Follicular conjunctivitis
o Decreased corneal sensations
o dendritic and geographical ulcer
o Accompanied by stromal keratitis in more severe infection.
• Genital lesions
o Type 2
o Bilateral lesion
o women: Cervix and Urethre
o Males: Penis
• Latent infection often persists at the initial site despite high antibody titers.
• Recurrent disease triggered by
o temperature change
o emotional distress
o hormonal factors.

DIAGNOSIS:
• MRI
o shows bilateral frontotemporal hyperintense lesion in herpes encephalitist
• EEGmembrane.
o Periodic temporal lobe spikes on a background of slow or low amplitude activity on EEG
• Herpes simplex virus produces small white shiny non-necrotic pocks on chick embryo
chorioallontoic
TREATMENT:
• Acyclovir is effective for Herpes simplex (thymidine kinase enzyme)

• Valaciclovir and famciclovir are all licensed therapeutics.
• Acyclovir treats herpes simplex encephalitis
44. Prion
INTRODUCTION:
• Prions are most resistant organisms to antiseptics & sterilization.

• Prions are best killed by Sodium hydroxide
• Prions are Encoded by viral genome
• Prion protein diseases is Commonly manifested as dementia
• Prion diseases/transmissible spongiform encephaloathies (TSEs)
• Family of rare progressive neurodegenerative disorders
• Affect both humans and animals,known as "mad cow disease" in cattle
• “Creutzfeldt -Jakob disease” (CJD) in humans.
Classification
Group A
• Infection of sheep caused by lentiviruses e.g. visna maedi
Group B = Subacute Spongioform viral encephalopathies/Prion
• Comprise prion (infectious protein) diseases of the CNS
1. Scrapie
2. latrogenic Creutzfeldt -Jakob disease ;
Infection from prion contaminated human growth hormone, duramater graft, corneal transplant

3. Kuru (human):Infection through ritualistic cannibalism
4. Variant (CJD):Infection from bovine prion (Eating BSE infected beef)
5. Familial CJD:Germline mutation in PRNP
6. Sporadic CJD:Somatic mutation or spontaneous convention of PRPc into PRPsc
7. Fatal familial insomnia:Germline mutation in PRNP
8. Gestmann Strausster Scheinker:Germline mutation in PRNP
9. Bovine spongiform encephalopathy
10. Transmissible mink encephalopathy
Mechanism
Patient with prion disease

PRPsc protein(Primary structure same as PRP)
More B sheets, little alpha helix
Resistance to protease
Accumulation
• Prions propagate by transmitting a misfolded protein state

• Alteration in the conformation of the protein
• Normal α-helix structure is converted to β-sheet structure.
• Acts as a template to guide the misfolding of more protein into prion form.
Group C
Subacute sclerosingpanencephalitis (SSPE)
• Delayed sequel to infection with defective measles virus
• SSPE also seen in RubeIIa infection
Progressive multifocal leukoencephalopathy (pML)
• Caused by JC virus(papovavirus)
• Affect elderly persons whose immune process is impaired .
CLINICAL FEATURES:
• Prion protein diseases is Commonly manifested as dementia
45. Polymerised Chain Reaction

INTRODUCTION
• PCR is a method of enzymatic amplification of a target sequence of DNA.

• It is sensitive, selective (specific)
• Extremely rapid means of amplifying any desired sequence of double stranded DNA,
o Can be as short as 50-100 base pairs (bp)
o As long as 10 kbp.
• DNA to be amplified is replicated by DNA polymerase of Thermus aquaticus (Taq).
• Taq polymerase is used because
o it is thermostable
o not denatured at a temperature upto 95°C
o (in PCR DNA is to be heated to 94°-95° C for separation of strands).
Materials required:
• Two primers:
• each about 20-35 bases long
• With sequence complementary to the sequence immediately adjacent to the DNA segment of
interest ( flanking sequence) .
• Divalent cations, magnesium or manganese ions; generally Mg2+ is used,
• DNA polymerase (e.g., Taq polymerase) which can sustain high temperature
• A large number of free deoxynucleotides (dNTPs)
• The target DNA fragment.
METHOD:
• SYBR Green Dye is used monitor PCR reactions

• PCR occurs in following steps -
1. Isolation of target DNA sequence.

2. Primers construction.
3. Denaturation of DNA.
4. Annealing of primers to single stranded DNA .
5. Chain extension by DNA polymerase and deoxyribonucleotides (dNTP)
USES:
• The most sensitive method for detecting cervical chlamydia trachomatis infection
• Prenatal diagnosis of Hemophilia
• HIV can be detected and confirmed
46. Epstein Barr Virus

Introduction
• Oncogenic
• The DNA is surrounded by a protein nucleocapsid.
DISEASE ASSOCIATION:
• Infectious Mononucleosis
• Lymphoproliferative disease and CNS lymphoma in the immunosuppressed.
• X-linked lymphoproliferative syndrome
• Malignancies caused by EBV includes
o Burkitt’s lymphoma
o Hodgkins disease
o Post transplant lymphoma
o Tcell lymphoma
o Nasopharyngeal carcinoma
o Gastric carcinoma
o Leiomyosarcoma
• Oral leukoplakia in AIDS patients
• G.B syndrome
• Transverse myelitis
• Glandular fever
• Chronic interstitial pneumonitis with pleural effusion in AIDS patients.
Hematologic complications
• hemolytic anemia
• thrombocytopenia
• neutropenia
Neurologic involvement:
• aseptic meningitis
• lymphocytosi
• encephalitis
• isolated neuropathy such as Bell palsy
• Guillain-Barré syndrome.
PATHOGENESIS:
To infect cells, EBV uses a cell surface receptor (CR2,CD21) found primarily on
• B lymphocytes
• Nasopharyngeal epithelial cells.

Primary reservoir of EBV in the body
• Latently infected B cells
Epstein Barr virus causes autoimmunity by Polyclonal B cell Activation
DIAGNOSIS:
• Leucopenia
• Raise in TLC
• Lymphocytosis
• more than > 70 % atypical lymphocytes(CD8 + cells)
• Thrombocytopenia
Serological testing:
• Paul Bunnel test

• EBV specific antibody test
• Nucleic acid hybridization
47. Hepatitis B Virus
• Serological marker present during window period in hepatitis B infection is Anti HBc
• Anti HBs is the protective antibody present after recovery from hepatitis B or immunization.
• First antibody to appear in plasma/blood in acute hepatitis B is Ig M Anti HBc
• Recumbent stage of Hepatitis B is characterized by Anti HBc
• The presence of hepatitis B surface antigen means actively replicating virus, and in the context of
the history of recent needle-stick injury, this likely represents a hepatitis B infection.
• Hepatitis B virus is least likely to cross placenta
• Highest transmission of hepatitis B from mother to fetus occurs if the mother is infected during IIIrd
trimester
• 10-15% of anti-HBe- positive mothers transmit HBV infection to their offspring
• HBsAg + HBeAg suggest highly infective stage
• Incubation period of HBV is 45 to 180 days
• HBV present in India is Ayw, Adr
• Reverse transcriptase of HBV is coded on p gene
• P gene is the longest DNA of hepatitis B virus
• HBcAg is found within the nuclei of infected hepatocytes and not usually in the peripheral
circulation in Hepatitis B' infection
• The serological marker of acute Hepatitis B infection is HBsAg+Core antibody
• Acute Hepatitis B can be earliest diagnosed by IgM anti HBc ab
• Epidemiologic study of Hepatitis B is by Anti HBc
• Active replication in Hepatitis B infection is indicated by HBeAg
• Hbs Ag a component of HBV causes glomerulonephritis
• Early diagnosis of active hepatitis B infection is done by IgM HBcAg antibody
• Serological markers for active viral replication include HBe Ag, presence of DNA polymerase and
circulating HBV DNA.
• HBsAg is also known as australian antigen
• E antigen (HBeAg) of hepatitis B virus is a product of C gene
• DNA polymerase of HBV is encoded by P gene
• Super carrier of HBV shows HbsAg + HBeAg + HBV DNA
48. Shigella
• People with blood group O has increased susceptibility to shigella
CULTURAL CHARACTERISTIC:
Culture media:
• High selective
• Deoxycholate citrate agar
• Hektoen agar/SS agar
• Mannitol ferment
• Subgroup D: S. sonnei: only one serotypes(lactose non-fermeter)
• Shigella dysenteriae: most serious form of bacillary dysentery (Shiga toxin)
49. Mycobacterium leprae
MYCOBACTERIUM LEPRAE
• Mycobacterium leprae, also known as Hansen's bacillus spirally.

• Bacterium causes leprosy (Hansen's disease).
MORPHOLOGY
• Less acidic 5 % sulphuric acid used for decoulration.

• Globi appear in Virchow’s Lepra cells or foamy cell(undifferentiated histocytes)
CULTIVATION
• Not possible
• Can be propagated in foot pad of mice
• Granulomas appear at site of inoculation

• For experimental work, Lepra bacilli are best cultured in Armadillos
• Generation time/Doubling Time 12-14 days
• Average may be 8-14
50. Leprosy- Epidemolgy,Vaccination,NTLEP
LEPROSY
• Chronic granulomatous disease.
Epidemiological determinants of leprosy
Agent:
• M. leprae
Source of infection:
• Multibacillary cases (most important), subclinical infections.

• The current view is all patients with active leprosy considered infectious.
Transmission
• Long contact with leprosy patient can transmit the disease.

• Insect can transmit the disease.
• Transplacental spread not seen
Primarily affect
• Skin
• Peripheral nerves
• Nasal mucosa
Not affect
• Female genital tract
Cell mediated immunity
• Deficient
Prevalence

• Decreasing in past decade .
Incidence
• Between 10-20 years.

• Most sensitive index of transmission in leprosy is incidence
Infectivity
• Highly infectious (communicable) disease

• An infectious patient can be rendered non-infectious by treatment with dapsone for about 90 days
• Or with rifampicin for 3 weeks.
• Local application of rifampicin (drop or spray) might destroy all the bacilli within 8 days.
Country Commonest leprosy
India, Africa TT(polar tuberculiod)
Southeast Asia BT
Mexico Lepromatous(LL>BL)
LEPROSY VACCINE
• Protective effect of BCG vaccine against leprosy and ICRC bacillius
National Leprosy Eradication Programme (NTLEP)
• Launched in 1983
AIM
• Achieve control of leprosy

• Eradicating the disease by the turn of the century.
• The aim was to reduce case load to I or less than 1 per 10000 population.
HOW
• Through early detection of cases

• Dapsone monotherapy on an ambulatory basis.
SET centres
• Established if prevalence leprosy Is 1-5

Revised strategy (NLEP) was based on
• Early detection of case

• Short term multi-drug therapy
• Health education
• Ulcer and deformity care
• Rehabilitation activiti
• NLEP provided :
a .Domiciliary treatment in endemic districts through specially trained staff
b.In moderate to low endemic districts, services through mobile leprosy treatment units and primary
health care persons.
51. Rabies Virus
RABIES VIRUS
• Produce infection that is almost fatal to humans.

• Neurotrophic virus
• There are two types of strains(antigenically similar)
1. Street virus
2. Fixed virus
STUCTURE
• Negative polarity(RNA), non-segmented

• Linear single stranded
• Enveloped RNA virus and is bullet-shaped..
MODE OF TRANSMISSION
• Bite of rabid dogs or other animals (Most common)

• Non bite exposure
1. Licks or aerosols
2. Transplantation of cornea.
INCUBATION PERIOD
• The incubation period is exceptionally variable.

• Ranging from fewer than 10 days to longer than 2 years.

• Usually 1–3 months.
CLINICAL MANIFESTATIONS
• Replicates initially in muscle.

• Then enters peripheral nervous system.
• It spreads to CNS gray matter.
• Negri bodies are found in neurons.
• Pathognomonic lesion is the Negri body, an eosinophilic cytoplasmic inclusion in brain.
• Particularly in the hippocampus, cerebral cortex, cerebellum, and dorsal spinal ganglia.
Five general stages are recognized in humans
• Incubation
• prodrome,
• acute neurologic period
• coma
• Death
Speed of rabies virus axon is 3 mm per hour
SENSETIVE TO
• Ethanol
• Soap
• Iodine Preparations
• Detergents
• Quaternary ammonium Compound
• Lipid Solvents such as ether, chloroform and acetone
INACTIVATED BY
• Phenol
• UV irradiation
• Formalin
• Sun Light
• Beta propiolactone (BPL)
• Thermal inactivation (one hour at 500 C and 5 min at 60°C)
DIAGNOSIS
• Rabies is diagnosed by detection of rabies virus antigens by immunofluorescence.

52. Rabies :Transmission and Clinical features
RABIES
• It is the communicable disease which is always fatal.(100% morality)

• Rabies is an enzootic and epizootic disease of world-wide importance.
• Diseases under international surveillance (WHO)
DISTRIBUTION
• Water appears to be the most effective natural barriers to rabies.

• In India, Lakshadweep and Andman & Nicobar islands are free of the disease.
• A Rabies free area has been defined as one in which no case of indigenously acquired rabies has
occurred in man or any animal species for 2 years.
• Countries where rabies is not found
1. Australia
2. china (Taiwan)
3. Cyprus
4. Iceland
5. Ireland
6. Malta
7. Japan
8. Newzealand
9. Britain
MODE OF TRANSMISSION
• Bite of rabid dogs or other animals (Most common)

• Non bite exposure
1. Licks or aerosols
2. Transplantation of cornea.
PATHOGENESIS
• Enters the peripheral nervous system (PNS) directly

• Migrates to the brain.
• It replicates within muscle tissue, where it is safe from the host's immune system
• Enters the nervous system through the neuromuscular junctions.
• Produces acute inflammation of the brain.
• Rabies prominantly infect neurons
• Brain stem encephalitis
• Centrifugal spread to other tissues including
• salivary gland
• heart
• adrenal gland
• skin
• Coma and death soon follow.
TYPES
Furious, or encephalitic rabies
• This occurs in 80 percent of human cases.

• The person experience hyperactivity
• headache, fever, irritability, restlessness and anxiety.
• Dilated pupils
• Muscle pain
• Vomiting
• Salivation
• Hydrophobia
• Phase coninue
• Coma
• Death
Paralytic or "dumb" rabies
• Patient experiences depression

• Paralysis followed by a coma.
• Death eventually results from respiratory arrest.
SYMPTOMS
Five stages
• incubation
• prodrome
• acute neurologic period
• coma
• death
Why does rabies cause a fear of water?
• Intense spasms in the throat are triggered when trying to swallow.

• Even the thought of swallowing water can cause spasms.
53. Rabies :Diagnosis and Negri bodies

DIAGNOSIS OF RABIES
• Detection of antigens by immunofluorescence.

• The specimens collected are :
1. Antemortem
2. Corneal smear
3. Skin biopsy from neck or saliva
4. Postmortem
5. Brain biopsy
• A definitive diagnosis Negri bodies in the brain or spinal cord.

• Rabies virus specific antibodies detection in serum and CSF.(devlop late)
• Indirect fluorescent antibody test
• Rapid fluorescent focus inhibition (RFFIT)
• Reverse-transcription polymerase chain detection of rabies virus nucleic acid in the saliva.
• It is done during early CNS infection.
NEGRI BODIES
• Negri bodies are practically pathognomic for rabies

• Composed of fibrillar matrix and virus particles
STRUCTRE
• Deeply eosinophilic inclusions

• Seen in hematoxylin and eosin stained sections.
• Consists of a mass of nucleocapsids
• Intracytoplasmic membranes.
SITE OF OCCURENCE
• Ammon's horn of neurons of the brain stem(Hippocampus)

• Purkinje cells of the cerebellum
• Can be seen in axons(infection spread from here)
• Found away from the inflammatory, nonspecific lesions
DETECTION
• Immunofluorescence of biopsy sample
54. Rabies: Pre-exposure and Post-Exposre Prophylaxis

INTRODUCTION
• Devloped by Louis Pasteur

• Rabies vaccine is prepared from fixed strain of virus.
TYPE OF RABIES VACCINE
• Devloped by Louis Pasteur

• Semple Vaccine grown in neural tissue of embryonated Hen's egg .
• Duck embryo Vaccine
• killed sheep vaccine
• HDCV vaccine (safest)
1. Chick embryo fibroblast

2. Vero continous cell line
3. Human dipliod cell vaccine
PRE-EXPOSURE VACCINATION
GIVEN TO
• People at high risk of exposure to rabies

• Laboratory staff working with rabies virus
• Veterinarians, animal handlers and wildlife officers
SCHEDULE
• Given on days 0, 7 and 21 or 28

• 1 or 0.5 ml/dose depending on the vaccineor i.d. (0.1 ml/inoculation site)
REGION OF ADMINISTRATION
• Deltoid area of the arm(adult)

• Anterolateral area of the thigh (children).
• Never administered in the gluteal area( in lower neutralizing antibody titres)
ADVERSE REACTION
• Well tolerated
• Minor Adverse reactions
• local pain
• erythema
• swelling
• Puritis
• Neurological comlication with semple vaccine.

• Duck embryo Vaccine allergies
POST-EXPOSURE PROPHYLAXIS
CATEGORY(as per WHO) FEATURES TREATMENT
I • Touching/feeding suspect • None

animals
• skin is intact
II • minor scratches without • Immediate vaccination

bleeding from contact • Local treatment of
• broken skin wound
III • More bites, scratches, licks • Immediate vaccination

on broken skin • Adminstration of rabies
• Contact that breaks the skin immunoglobin
• Exposure to bats • Wound treatment
• Thorough washing of the wound with soap/detergent and water

• Application of ethanol or an aqueous solution of iodine or povidone.
• Standard WHO Intramuscular regimen- 0, 3, 7, 14, 28 (one dose each at day 0, 3, 7, 14, 28)
• Reduced Multisite Intramuscular regimen — 2-1-1 (two dose on each arm on day 0, one dose each
at day 7 & 21)
• Intradermal schedules : 2 site = 2 2 2 0 1 1 (At 2 sites on day 0, 3, 7 and single site on day 28, 90)
• Intradermal schedules: 8 site = 8-0-4-0-1-1 (on 8 sites at day 0, on 4 sites at day 7, on one site at day
28 & 90)
VACCINATED PREVIOUSLY
• 3 doses of IM HDC vaccine on day 0, 3, 7 are recommended if :
1. The patient's antibody titre is not known.

2. The antibody titre < 0.5 IU/ml.
3. The bite is severe.
• Only 2 doses are recommended if

o Antibody titre is more than 0.5 IU/ml.
o The bite is not so severe
Dosage HRIG
• The dose for HRIG is 20 IU/kg body weight
• For ERIG and F(ab’)2 products 40 IU/kg body weight.
• Administered into and around the wound site.
• Standard WHO Intramuscular regimen- 0,3,7,14,28 (one dose each at day 0,3,7,14,28)
• Reduced Multisite Intramuscular regimen — 2-1-1 (two dose on each arm on day 0, one dose each
at day 7 & 21)
• Intradermal schedules : 2 site= 2 2 2 0 1 1 (At 2 sites on day 0,3,7 and single site on day 28, 90)
• Intradermal schedules: 8 site= 8 0 4 0 1 1 (on 8 sites at day 0, on 4 sites at day 7, on one site at day
28 & 90)
• Pre exposure prophylaxis — 0,7,28
• Post exposure prophylaxis for those already immunized- 0,3,7
55. Lepra Reaction And Erythma Nodosum Leprosum
Type I Reversal reaction/lepra reaction /Jopling Type I
Type lV delayed hypersensitivity.
• Common in patients between the two poles of the leprosy spectrum with immunologically
unstable borderline forms
• Higher incidence in BB and BL patients as compared with BT patients.
Manifestations
• Inflammation within previously involved macules,papules and plaques

• Skin lesions suddenly becomes reddish, swollen, warm, painful and tender
• The rest of skin is normal
• MC nerve trunk involved - Ulnar at elbow
• Most characteristic microscopic feature of type I reaction is Edema.
Cytokines involved
• Increased activity of T helper (Th)-1 lymphocytes expressing IL-2 and IFN-γ
Treatment:
Treatment of lepra reactions Type 1 Type 2

according to severity
Mild NSAIDS NSAIDS
Moderate Nsaids , Corticosteroids NSAIDS , Clofazimine, Thalidomide,
Chloroquine

Severe NSAIDS . Thalidomide , Corticosteroids ,
Corticosteroids Parenteral antimony
• DOC glucocorticoids
• Clofazimine also given
• Thalidomide - ineffective.
• Irreversible nerve damage can set in less than 24 hours
• So treat promptly with steroids
• Foot drop d/t involvement of common peroneal nerve
Type II lepra reaction - Erythema Nodosum Leproticum/Jopling Type II:
• Type III hypersensitivity reaction occurs exclusively in BL, LL .

• Usually follows therapy (sulfone syndrome) but may precede therapy.
Manifestations
• Red, painful, tender, cutaneous nodules (deep) appear that are not associated with leprosy
patches.
• ENL may appear commonly on face, arms, legs.
Central role in pathobiology:
• TNF
• Tumor necrosis factor-alpha play a central role in the pathobiology of type II lepra reaction/ ENL.
Treatment
• Mild - antipyretics alone

• Moderate to severe - Ist drug to be used glucocorticoids
• DOC: thalidomide
• Clofazimine - More active than in Type I.
56. Leprosy- Diagnosis
Lepromin test
• Not diagnose leprosy nor inditicate prior contact.
SMEAR SAMPLE
• A minimum of seven sites should be examined

1. Smears from 4 skin lesion
2. Smears from both ear lobes
3. One nasal swab
• ample from the skin should be obtained from the edges of the lesion rather than from the centre.
Uses
• To classify the lesion
Tuberculiod Positive
Lepromatous Negative
Borderline Variable
• To assess the prognosis
1. Positive is Good prognosis

2. Negative is Bad prognosis
3. Conversion to lepromin positive during treatment is evidence of improvement.
• To assess the resistance of individuals to leprosy.

• BCG vaccination can convert lepra reaction from negative to positive
SLIT SMEAR
Leprosy type Slit Smear Infectivity

Tuberculoid AFB may be found from margin -ve
Boderline AFM found infective

Lepromatous Teeming with AFB infective
57. Leprosy:WHO Classification ,WHO Disability grading
WHO Clasiification
• Paucibacillary(tuberculiod)
• Multibacillary(lepromatous)
Paucibacillary (PB) Multibacillary (MB)

Tuberculoid Leprosy Lepromatous Leprosy

Severity • Can be extreme
• Without treatment, the patient will die
Mild
Unique Signs and Symptoms • Many erythematous macules,papules
or nodule
• Few erythematous or • extensive tissue destruction(e.g:nasal
hypopigmented plaques cartilage,bones,ears)
• flat centres and raised,demarcated • diffuse nerve involvement with patchy
borders sensory loss
• peripheral nerve damage with • lack of nerve enlargement.
complete sensory loss
• visible enlargement of nerves.
Distribution of lesions • Symmetrical
• Asymmetrical
Occurs When • Infected person unable to mount a
cell-mediated immune response to the
• Infected person able to mount a bacterium
robust, cell-mediated immune
response to the bacterium
Defined by WHO as • >5 patches associated with leprosy.
•1-5 patches associated with

leprosy
Person Infectious? Possibly
No
PROGNOSIS Cure from disease possible, however, underlying
disease complications (such as limb damage due
Good to infection) may not be reversible or require
reconstructive surgery
Lepromin test
Positive Negative
Erythema Nodosum Leprosum
Absent Usually present
Treatment
• Paucibacillary leprosy
• should be treated for 6 months with dapsone 100 mg/day unsupervised plus rifampin 600 mg/
month supervised.
• Multibacillary leprosy
• hould be treated for 12 months with dapsone 100 mg/day unsupervised, clofazimine 50 mg/day
unsupervised, and rifampin 600 mg plus clofazimine 300 mg/month supervised.
• Follow-up in paucibacillary leprosy 2 years
• Follow-up in multibacillary leprosy 5 years
• In paucibacillary leprosy, the multidrug therapy is stopped after 6 months of treatment regardless
of the presence of clinically active disease".
WHO DISABILITY GRADING FOR LEPROSY

Hand and Feet
• Grade0:no anaesthesia,no visibledeformityordamage.

• Grade1:anaesthesia present,but novisibledeformity ordamage.
• Grade2:visible deformityor damagepresent.
Eyes
• Grade0:no eyeproblem dueto leprosy;no evidenceof visualloss.

• Grade 1:eye problems dueto leprosy present,but visionnotseverely affected asa result
ofthese(vision: 6/60 or better)
• Grade2:severevisualimpairment(vision:worset THAN 6/60.Lagopathalmos, iridocyclitis and
coroneal opacities
58. Leprosy Classification-Madrid and Ridley and Jopling Classification
Ridley and Jopling Classification(Clinical, bacteriological, immunological, histological classification
SYMPTOMS HISTOLOGICAL FEATURES

• Epithelioid cells
TUBERCULIOD • lymphocytes
• giant cells form noncaseating
• Can be either one large red patch with well- granulomas.
defined raised borders or a large • Dermal nerves are destroyed.
hypopigmented asymmetrical spot Normal skin organs (e.g., sweat
• Non caseating granuloma in nerve glands, hair follicles) are lost.
• Lesions become dry and hairless • ENL reaction seen
• Loss of sensation may occur at site of some • Bacilli are frequently absent
lesions • Max. no. of CD4 - T cells (TH -1)
• Tender, thickened nerves with subsequent
loss of function are common
• Spontaneous resolution may occur in a few
years or it may progress to borderline or rarely

• neural involvement occurs early
• BT leprosy, granulomas are

Boderline Tuberculiod epithelioid, with a preponderance
of lymphocytes. Dermal nerves are
• Similar to tuberculoid type except that lesions mostly destroyed. Bacilli may be
are smaller and more numerous scanty or absent.
• -Normoesthetic and symmetrical lesions
• -Disease may stay in this stage or convert back
to tuberculoid form, or progress
• granulomas are epithelioid

Boderline Boderline • dermal nerves may be visible
• bacilli are seen more often than in
• Numerous, red, irregularly shaped plaques BT leprosy
• Sensory loss is moderate
• Disease may stay in this stage, improve or
worsen
• Asymmetrical thickening of
• several nerves.
• Several hypoesthetic macules on skin
• Lesions looking like inverted saucers are
common
• histiocytes form granulomas

Boderline Lepromatous • dermal nerves are visible,
• bacilli are seen in greater number.
• Numerous lesions of all
kinds, plaques, macules, papules and nodules.
• Hypoesthetic
• Symmetrical nerve thickening; glove and
stocking anesthesia
• epidermis is normal
Lepromatous • rete flattened.
• clear space separates the
• Early nerve involvement may go unnoticed epidermis from diffuse
• Normoesthetic, small, symmetrical and granulomatous reaction

numerous lesions of all kinds, plaques, with macrophage
macules, papules and nodules • large, foamy histiocytes (Virchow
• Early symptoms include nasal stuffiness, or lepra cells); and many
discharge and bleeding, and swelling of the intracellular AFB, which are
legs and ankles frequently found in globi
• Epithelioid cells and giant cells are
not found.
• Granulomas are most numerous
around blood vessels, nerves, and
skin appendages.
• Plasma cells are found
• Dermal nerves are easily visible.
• Max. no. of CD8 - T cells
If LL Left untreated, the following problems may occur:
• Leonine facies, Saddle nose

• Ear lobes thicken, upper incisor teeth fall out
• Photophobia (light sensitivity), glaucoma and blindness
• Testicles shrivel causing sterility and enlarged breasts (males)
• Internal organ infection causing enlarged liver and lymph nodes
• Renal lesion occurs,membranous glomerlonephritis .
• Voice becomes hoarse
• Slow scarring of peripheral nerves resulting in nerve thickening and sensory loss.
• Fingers and toes become deformed due to painless repeated trauma.
NERVES INVOLVED
• Propioception is carried by Goll & Burdech tract (posterior column)

• Which is not involved in leprosy
• Temperature & pain lost earlier than touch & pressure.
• Commanly involved nerves are:
1. Posterior tibial (most common)

2. Ulnar (2" most common, most commonly Vt abscess)
59. Streptococcus Pyogens: Clinical manifestation, Diagnosis and Treatment
DISEASES:

• Infections typically begin in the throat or skin. The most striking sign is a strawberry-like rash
1. Pharyngitis (strep throat)

2. Localized skin infection (impetigo)
3. Erysipelas and cellulitis
4. Necrotizing fasciitis
5. Scarlet fever
6. Streptococcal toxic shock syndrome
7. Autoimmune-mediated complications( rheumatic fever and acute
postinfectious glomerulonephritis).
60. Streptococcus Pneumonia :Clinical Manifestations , Diagnosis and treatment
DISEASES:
NON-INVASIVE DISEASES:
• SINUSITIS(MC)
• OTITIS MEDIA (middle ear)(MC)
• PNEUMONIA (lungs)(lobar & community acquired commonly)
1. Complication :Empyema
INVASIVE DISEASES( bacteremia)
• MENINGITIS (CNS)
• ENDOCARDITIS (CVS)
• PERITONITIS (body cavity)
• SEPTIC ARTHRITIS
• UVEITIS
• SUBDURAL EMPYEMA
• OTHERS (appendicitis, salpingitis, soft tissue infections)
Produce milk borne diseases
Commonest Post splenectomy infection
Australian syndrome
Concurrence of pneumococcal pneumonia,endocarditis and meningitis.
Diagnosis:
• Gold standard diagnosis:pathological examination of lung tissue.

• Gram staining and culture of CSF or sputum.
• Biomarkers:Prolactin levels increase and Passive agglutination testing(CRP)
Treatment
Amoxicillin for otitis media/sinusitis/pneumonia
Ceftriaxone +vancomycin for meningitis
Ceftriaxone/cefotaxime +vancomycin for endocarditis
Pencillin resestance due to alteration in pencillin binding protien.
61. Chlamydia trachomatis
Introduction
• MC cause of
1. STD worldwide
2. Opthalmia neonatorum
3. Epididymitis
4. Post-gonococcal urethritis
5. Inclusion conjunctivitis of neonate
6. Adult form is called as "swimming pool disease
LIFE CYCLE
• Chlamydia trachomatis occurs in two forms during its life cycle(biphasic)
Elementary body.
• Extracellular
• Infectous
• Inactive
Reticulate body (RB).
• Active replicative form.

• Inhibit lysosomal fusion.
• C trachomatis also inhibits apoptosis of epithelial cells
• Thus enabling completion of its replicative cycle.
• Reticulate body divides by binary fission
• Chlamydial microcolony formed know as inclusion body
SEROTYPES

15 serotypes are known:
D to K-Inclusion Conjuctivitis
Clinical manifestations
Trachoma
Stages
• Trachoma dubium
• Protrrachoma
• Established trachoma(stages I to IV)
Details
• In established trachoma,
o superior epithelial keratitis
o sub epithelial keratitis
o pannus, or superior limbal follicles
o Ultimately the pathognomonic cicatricial remains of these follicles, known as Herbert's
pits—small depressions covered by epithelium at the limbo corneal junction.
• With disease progression, there is:
o tissue necrosis
o granulation tissue deposition
o scar formation leading to blindness
o Lacrimal duct obstruction and distortion of the eyelids.
o Loss of an adequate tear system
o Cornea becomes vulnerable to dehydration and opacification.
GENITAL INFECTIONS
Genital chlamydiasis
• Mostly asymptomatic
• MC of nongonococcal and postgonococcal urethritis
• Men:
• urethritis (non-gonococcal)
• epididymitis
• proctitis
• conjunctivitis
• Reiter's syndrome
• Women: Salphingitis due to chlamydia and gonnorrea are common causes of tubal block resulting
in infertility
• acute urethral syndrome
• bartholinitis
• mucopurulent cervicitis
• endometritis
• salphingitis(infertility)
• pelvic inflammatory disease
• conjunctivitis
• perihepatitis (Fitz-Hugh-Curtis syndrome)
• Reiter's syndrome
• Gram stained smears of urogenital exudates show significant number of neutrophils
Lymphogranuloma venereum (LGV)
• Primary lesion: small painless papulovesicular lesion on external genitalia

• Secondary stage: lymphadenopathy
• in males inguinal nodes are most commonly involved
• in females intrapelvic and pararectal nodes
• Frei's test: intradermal test for LGV
Reiter’s Syndrome
• triad of recurrent conjunctivitis, polyarthritis and urethritis in men or cervicitis in women

• Associated with HLA B 27
Treatment
STD: Azithromycin DOC
Trachoma
• Tetracycline
• Erythromycin
• Rifampicin
62. Chlamydia pneumoniae and Chlamydia psittaca
CHLAMYDIA PSITTACOSIS
• Human infection is acquired from inhalation of aerosols liberated from birds (parrots) dropping and
nasal discharge.
• IP : 7-14 days
• Usual presentation is pneumonia
• Others: Meningoencephalitis, Arthritis , Splenomegaly ,Thrombophlebitis, Pericarditis, Typhoid like
syndrome, Hepatomegaly, Pulmonary infarction, Endocarditis, Horder's spot, GI symptoms
Treatment
• Tetracycline(DOC) or Erythromycin
CHLAMYDIA PNEUMONIAE
• TWAR strain (Taiwan Acute Respiratory)

• Risk of atherosclerosis, asthma, sarcoidosis.
• The group specific antigen is responsible for the production of complement fixing antibodies
in Chlamydia pneumonia
63. SYNTHESIS OF IMMUNOGLOBULINS
SYNTHESIS OF IMMUNOGLOBULINS:
• After antigenic stimulation, B-cells form plasma cells

• Which secrete immunoglobulin
• The secretory component of immunoglobulin molecule is formed by epithelial cells of lining mucosa
• All immature B cells carry Ig M immunoglobulins on their surface and most also carry Ig D
• Genes for various chains
C gene for the gamma heavy chain on chromosome 14
C gene for the kappa light chain on chromosome 2
C (constant) regions of the heavy chains gene One chromosome
V gene for the kappa light chain on chromosome 2
C gene for the epsilon heavy chain on chromosome 14
V gene for the lambda light chain. chromosome 22
The C gene for the kappa light chain. on chromosome 2
• Differential RNA processing decides whether an immunoglobulin will remain membrane bound or
secreted.
64. HUMAN IMMUNOGLOBULINS CLASSES

HUMAN IMMUNOGLOBULINS CLASSES:
Isotype:
• Immunoglobulin isotype class switching is determined by Constant region of heavy chain
Idiotypes
• Found in the hypervariable region of the Fab portion
65. E. coli: Clinical manifestations
DISEASES:
Bacteremia
• UTI is MC source of. E.coli bacteremia leading to septic shock (within 2month)
• Ascending cholangitis
Pnenumonia
• No. 2 MC cause of nosocomial pnenumonia
Urinary tract infection
• Most common cause of bacterial UTIs

• Catheter induced UTI
• Emphysematous pyelonephritis
• Malakoplakia often associated with urinary tract infection by E.coli(shows characteristic polygonal
granular cells ,Michaelis gutmann bodies, leukocytes and few RBCs )
Neonatal meningitis
• Usually with strains carrying the K1 capsular antigen

• Intraabdominal infections (associated with intestinal perforation)
Organism Disease Pathogenesis

Enteropathogenic E. • Site of action • Plasmid-mediated
coli (EPEC) • Small intestine • adheres to the mucosa of
• Infant diarrhea in upper small intestine
underdevelopedcountries • Causes disruption of the
• watery diarrhea brush border microvilli (
• vomiting adhesion to HEP-2 cells)
• nonbloody stools • Histopathology with
disruption of normal
microvillus structure
• Malabsorption and diarrhea
Enterotoxigenic E. • Site of actionTraveler's diarrhea • Plasmid-mediated

coli (ETEC) • Small intestine • heat-stable
• Transmitted by feco-oral route • heat-labile enterotoxins
• Infant diarrhea • Stimulate hypersecretion
• Developing countries of fluids and electrolytes
• waterydiarrhea
• vomiting
• cramps
• nausea
• low-grade fever
Enterohemorrhagic E. • Site of actionInitial watery • Mediated by cytotoxic

coli (EHEC) diarrhea Shiga toxins (Stx-1, Stx-2),
• Large intestine which
• Later grossly bloody diarrhea • Disrupt protein synthesis
• Hemorrhagic colitis(O157:H7 is • A/E lesions
the serotype) • Destruction of intestinal
• Abdominal cramps microvillus
• Progress to hemolytic uremic • Resulting in decreased
syndrome (HUS) absorption
• Also produces
Verocytotoxin
Enteroinvasive E. coli • Site of actionDisease in • Plasmid-mediated invasion

(EIEC) underdevelopedcountries • Destruction of epithelial cells
• Large intestine lining colon
• fever • Shows Sereny test is positive
• cramping
• watery diarrhea
• May progress to dysentery with
scant, bloody
• Stools
Enteroaggregative E. • Site of actionInfant diarrhea in • Plasmid-mediated

coli (EAEC) underdeveloped countries • Aggregative adherence of
• Small intestine rods ("stackedbricks")
• Traveler's diarrhea • shortening of microvilli
• Persistent watery diarrhea • Mononuclear infiltration
• vomiting • Hemorrhage
• Dehydration • Decreased fluid absorption

• Low grade fever
66. E. coli Diagnosis and Treatment
DIAGNOSIS:
• EMB agar—Selective and Differential

o E. coli forms blue-black colonies with a green metalic sheen. (due to lactose fermentation)
Methods for detection of ETEC enterotoxins
Assay LT ST
In vivo tests ± +
Ligated rabbit deal loop
+ ?
Read at 6 hours
Read at 18 hours
Infant rabbit bowel + +

Infant mouse intragastric (4 hours) - +
Adult rabbit skin (vascular permeability) + ?
In vitro tests
Tissue culture tests

Rounding of Y1 mouse adrenal cells - -
Elongation of chinese hamster ovary (CHO) + ?
cells
Serological tests
ELISA + (ST-ELISA with monocolonial antibody)
Passive agglutination tests, passive + -

immune hemolysis, precipitin (Eiken's) test
Genetic tests

DNA probes + +
Lactoferrin
• Binds to iron and makes it unavailable for E.coli

• Acts a defence mechanism against infections
67. Staphylococcus aureus: Morphology,Culture and Biochemical reaction
STAPHYLOCOCCUS AUREUS:
• Natural habitat:-Nostril (30%)and skin
Morphology:
• Shows Transient colonization

• For phage typing23 phages of staphylococcus aureus are used
• Catalase positive, beta-hemolytic staphylococcus
BIOCHEMICAL REACTION:
• Catalase positive; oxidase negative

• 3-lactamase production in Staphylococci is under plasmid control
68. Staphylococcus aureus: Virulence and Toxin
• About 30% of general population are healthy nasal carriers

• Epidermolysis and TSS toxin are superantigens
• Toxic shock syndrome is Staphylococcus infection is due to superantigen, Leucocidin and Hemolysin
• Staphylokinase enzyme produced by Staphylococcus aureus that dissolves fibrin clots
• Toxins of Staphylococcus are Enterotoxin
• Staphylococcus aureus remains in the skin for longer period because of Hyaluronidase
• Methicillin resistance is chromosome mediated
69. COAGULASE - ve STAPHYLOCOCCI
Staph epidermidis / albus
• Predilection for growth on implanted foreign bodies

• Common source of stich abscess.
STAPHYLOCOCCUS SAPROPHYTICUS :
• Causes 0%-20% of acute urinary tract infections in young, sexually active females & acute cystitis
S.lugdunensis and S. schleiferi
• Produces serious infections than do other CoNS.

• native valve endocarditis and osteomyelitis
70. Corynebacterium Diphtheria: Clinical manifestation, Complications, Diagnosis and Treatment
Introduction
• Most common in children of 2-5 years.
Incubation period
• 2-5days
Mode of transmission
• Droplet spread
Types
1. Faucial(commonest )
2. Laryngeal
3. Nasal
4. Conjunctival
5. Otitic
6. Vulvovaginal
7. Cutaneous mainly around mouth and nose
Respiratory Diphtheria
• MC type Tonsillopharyngeal (Faucial)

• Complications
• Mechanical complication
• Pseudomembrane may extend to the larynx
• Lead to laryngeal obstruction, asphyxia and death.
• Systemic effects

• Myocarditis
• Peripheral polyneuropathy of descending type.
• First muscle involve in paralysis - palatopharynges.
• Ciliary paralysis occur but not pupillary paralysis
• Most common ophthalmic effect of diphtheria is Isolated ocular palsies
Cutaneous Diphtheria
• Punched out ulcers

• Caused by non-toxigenic strains.
Invasive infection
• Rare
DIAGNOSIS:
Culture:
• Respiratory diphtheria diagnosis clinical

• Cutaneous diphtheria requires lab confirmation.
• The throat swabs are inoculated.
Virulence tests:
• Virulence testing may be done by:

o In vivo: Guinea pigs and rabbits- by subcutaneous or intracutaneous.
o In vitro: Eleks gel precipitation test ( test for toxigenicity)and tissue culture tests
• Schick test:
o Done to demonstrate circulating diptheria antitoxin.
o Skin test based on neutralization reaction
CONTROL ARM TEST ARM INFERENCE

No Reaction No Reaction Immune

No Reaction Positive
Red flush of 1-5 cms diameter, Susceptible to
generally appears within 24-36 hr infection
reaching its maximum develop-
ment by 4-7 day.
This fadesslowly
Red flush but less circumscribed Pseudo positive Allergic type
than positive fades by 4th day Red flush equally in both arms interpreted as
less circumscribed Schick type
Pseudo positive reaction Show positive reaction Susceptible
Combined reaction
TREATMENT:
• Erythromycin DOC
• Procaine penicillin G .
• Patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.
• Diphtheria antitoxin is given intradermal
• Post exposure prophylaxis in health care professionals is not indicated in infections with diphtheria
71. Shigella : Clinical Findings, Pathogenesis, Lab Diagnosis and Treatment
Introduction:
• PERSON TO PERSON TRANSMISSION

• Gut pathology is due to toxin
INFECTIVE DOSE:
• 10-100 VIABLE BACILLI
Toxins:
• Endotoxin
• LPS
• Cause irritation of bowel.
• Shigella Dysenteriae-
• Produces heat labile exotoxin (Shiga bacillus exotoxin)
• Affect gut and CNS:
• Show neurotoxicity on blood vessel of CNS
• Cytotoxicity = Verotoxin I or Shiga like toxin
• Toxins produce early, non bloody voluminous diarrhea.
CLINICAL SYMPTOMS:
• Shigella Associated with hemolytic uremic Syndrome

• Ranges from asymptomatic infection to severe bacillary dysentery
• Two-stage disease: watery diarrhea changing to dysentery with frequent small stools with blood
and mucus, tenesmus, cramps, fever
• Early stage:
• Watery diarrhoea attributed to the enterotoxic activity of Shiga toxin
• Fever attributed to neurotoxic activity of toxin
• Majority of lesion are in distal colon.
COMPLICATIONS
• HUS
o Schistocytes are suggestive of hemolytic-uremic syndrome (HUS)
DIAGNOSIS
• Sampling: fresh stool, mucus flakes and rectal swabs

• Selenite F broth(0.4%) is used as enrichment and transport media (for 9-12hours)
• Total blood count reveals anemia and thrombocytopenia, and schistocytes
• Increase blood urea nitrogen(BUN)
• Invasive test for shigella is Rabbit ileal loop
TREATMENT:
• Oral rehydration therapy (No antibiotics) for mild to moderate dehydration.

• Ciprofloxacin, Fluoroquinol, Azithromycin, Pivmecillinam, Ceftriaxone
• DOC for multiresistant Nalidixic acid.
72. Clostridium Perfringens: Clinical manifestation, Diagnosis and Treatment

Anaerobic myositis or myonecrosis or gas gangrene
• Several species found in association:

o Anaerobic streptococci & facultative anaerobes (E.coli,Stap,Proteus)
o Cl.perfringens is most frequently encountered(60%)
Non-traumatic gas gangrene
• Hematogenous seeding of normal muscle with histotoxic Clostridia principally

• Most serious complication of clostridial invasion of healthy muscle tissue (rhabdomyolysis)
Food poisoning:
• Usually caused by Type A strains(produces heat resistance spores)

• Cytotoxin mediated
Gangrenous appendicitis
Necrotizing enteritis
Biliary tract infection:
Gasterointestinal enteritis necroticans
• Associated with C.perfringens type A
Emphysematous cholecystitis
Urogenital infections(myoglbinuria)
LABORATORY DIAGNOSIS:
• Specimen:
o Wound swabs
o human faeces
o necrosed tissue
o muscle fragments,
o exudates from active parts etc.
• Microscopy:
o Gram +ve, non-motile, capsulated bacilli.
o Spores are rarely observed in Cl.perfringens
• Culture:
o On RCM→ meat turned pink but not digested
o On blood agar → target hemolysis
• Nagler’s Reaction
o Rapid detection of Cl.perfringens from clinical sample
• Reverse CAMP Test:
o CAMP +ve Group B Streptococcus is streaked in SBA & Cl.perfringens is streaked
perpendicular to it “arrowhead”(enhanced) hemolysis is seen between growth of
Cl.perfringens & Group B streptococcus
73. ANTIGEN ANTIBODY REACTION AND PRECIPITATION REACTION
Antigen antibody reaction
1. Primary Stage
o Formation of Ag-Ab complex
o Ag-Ab combined by weaker intermolecular forces
o van der Waals,
o ionic bond
o H2 binding
2. Secondary stage
o agglutination
3. Tertiary stage (reaction):
o Leads to tissue damage
Precipitation reaction
Mechanism of precipitation.
• Marrack (1934) proposed the lattice hypothesis

• When antigen and antibody exist in optimal proportions formation of lattices (cross-links).
Method
• Soluble antigen combines with its antibody in the presence of electrolytes (NaCI)
• At a suitable temperature and pH
• Antigen antibody complex forms an isoluble precipitate.
Plot in a curve
• Three zones are detected ,If

o Varying amounts of Ag are mixed and incubated with Constant volume of antisera
1. Zone of Ag excess :
o insufficient Ab
o Too small complexes to precipitate
2. Equivalence zone :
o Large lattice is formed
o Visible precipitates
3. Zone of Ab excess :
o not enough Ag
o Too small complexes to precipitate.
Types
1. Ring test
o e.g. Ascoli's thermoprecipitin test and streptococcal lancefield grouping.
2. Slide flocculation test
o VDRL test of syphilis
o Antigen and antibody complex are suspended..
o The flocculation can be observed by using microscope
3. Tube test
o Kahn test of syphilis
4. Immunodiffusion/Counter Current immunoelectrophoresis
o e.g. Elek test for toxigenicity in diphtheria (double diffusion).
5. Electroimmunodiffusion
o e.g. rocket electrophoresis for quantitative estimation of antigen.
74. AGGLUTINATION
Agglutination
• Sensitive than precipitation reaction for detecting antibodies.
Agglutination is of following types:
1. Slide agglutination
o used for blood grouping and cross matching.
2. Tube agglutination
o Widal test Brucellosis
o Weil-Felix reaction
o Paul Bunnel test
o cold agglutination
o Streptococczs MG test.
3. Antiglobulin
o Coombs test
o used for detecting incomplete Ab of brucellosis
o anti- Rh Ab.
4. Passive agglutination test
o used to detect Ab
o by adsorbing soluble Ag on carrier particles so precipitation reaction converts into
agglutination test
o more convenient and more sensitive.
o e.g. Rose waller test, test detecting RA factor by using amboceptor.
5. Latex agglutination test
o latexfixation test
o for detection of ASO, CRP, RA factor
o HCG; Streptozyme test.
o Rapid test for acute Pyogenic meningitis
6. Reversed passive agglutination
o Estimation of antigen by adsorbing antibody to carrier particles.
Heterophilic agglutination reaction
• Some organisms of different class or species share closely related antigens.

• When serum containing agglutinin (antibody) of one organism gives agglutination reaction with
antigen of other organism.
• Examples are
o Streptococcus M.G. agglutination test for primary atypical pneumonia.
o Weil - Felix reaction for typhus fever
o Paul Bunnell test fin- IMN.
75. TYPE I HYPERSENSITIVITY
Introduction
• Rapidly developing immunological reaction

• Occur within minutes
• Wheal & flare reaction
• Combination of an antigen with antibody bound to mast cells in individuals previously sensitized to
the antigen.
• Mast cells are the most important cells.
• Eosinophils are the most important cells in the late phase reaction .
• Histamine is the most important mediator.
• IL-4 is essential for turning on IgE secreting B cells.
• PAF is the most important cytokine in the initiation of late phase reaction.
• Most potent eosinophilic activating cytokine is IL-5.
Examples
• Urticaria
• angioedem
• hay fever
• some forms of asthma
• eczema
• Anaphylactic shock
• Casoni's test
• Theobald Smith phenomenon
• Schultz Dale phenomenon
• Prausnitz Kustner (PK) reaction
Type I hypersensitivity test
• Injection is given subcutaneously or intradermally (usually in the forearm).

• The site is examined after 20 minutes.
• Examples Casoni's test, sensitivity testing of drug.
76. TYPE II HYPERSENSITIVITY
Introduction
• Antibody mediated/Cytotoxic Hypersensitivity

• Depends on the abnormal production of IgG or IgM directed against tissue antigens
Three different antibody-dependent mechanisms :
Opsonization and complement and Fc receptor-mediated phagocytosis
• Most common
• Example —*Transfusion reactions, Erythroblastosis fetalis
Complement and Fc receptor mediated inflammation
• Examples Glomerulonephritis, vascular rejection in organ grafts.
Antibody mediated cellular dysfunction
• Antibodies directed against cell surface receptors .

• Examples: Graves disease and Myasthenia gravis
The type V reactions
• By antibody dependent cellular cytotoxicity (ADCC).

• The type V reactions are sometimes considered as a subtype of the type II hypersensitivity.
• Example: membranous glomerulonephritis seen in SLE

Examples
• Transfusion reactions
• Erythoblastosis fetalis (Hemolytic disease of neontates)
• All hemolytic anemia or agraulocytosis or thrombocytopenia
• Pemphigus syndrome
• Bullous pemphigoid
• Pernicious anemia
• Thrombotic phenomenon
• Acute rheumatic fever
• Some forms of vasculitides and certain drug reactions.
• Phagocytosis of tumor cells or parasite .
• Some role in graft rejection
• Thyrotoxicosis / Grave's disesas
• Myasthenia gravis
77. TYPE III HYPERSENSITIVITY
Introduction
• Immune complex diseases

• Usually involve IgA antibodies.
• Large amounts of circulating antigen can form immune complexes:
o which are not easily cleared by phagocytic cells
o Deposited in organs
o Activate complement
o Cause inflammatory damage.
Glomerulonephritis
Insect bites
Arthus reaction:
• Deposits of immune complexes
Hyperacute graft rejection
• Pre-existing antibody against donor graft antigens can cause

• This form of rejection occurs within minutes or hours after transplantation
Serum sickness

• following the injection of an anti-toxin
SLE
• Antinuclear antibody specific for SLE is Anti ds DNA
Hypersensitivity pneumonitis
• Immunologically mediated response to an extrinsic antigen

• involves
o immune complex (Type III)
o cell mediated (Type IV) hypersensitivity reactions.
Other Examples
• Rheumatoid arthritis
• lnfective endocarditis
• PAN
• Henoch-Schonlein purpura
Type III hypersensitivity Test
• Toxin is given intradermally and this toxin reacts with circulating antitoxin
• Produce local type of type III hypersensitivity, i.e. Arthus reaction.
• Example Schick test.
78. TYPE IV HYPERSENSITIVITY
Introduction
• Cell-Mediated) Reactions/Delayed-type hypersensitivity/antibody-independent

• Involve reactions by memory cells.
• Reactions are delayed by one or more days (delayed type hypersensitivity).
• Delay is due to migration of macrophages and T cells to site of foreign antigens.
• Reactions are frequently displayed on the skin: itching, redness, swelling, pain.
Peak action time
• after 24 hours
Initiated by
• activated T-lymphocytes.
Includes
1. Delayed type hypersensitivity - mediated by CD-4 T cells.

2. T-cell mediated cytotoxicity - mediated by CD8- T cells.
Examples
• Tuberculin test
• Lepromin test
• Fairleys (Schistosomiasis) test
• Frie's (LGV) test
• Granulomatousinflammation
• Contact dermatitis
• Defence against intracellular pathogen
• Type I lepra reaction
• Graft rejection
• Resistance to virus infection
• Reaction against tumour cells
Type IV hypersensitivity Test
• Injection is given intradermally on the flexor aspect of the forearm.

• The site is examined after 48-72 hours.
• Induration of greater than 10 mm is considered as positive.
• Examples Tuberculin test, Lepromin test
79. INTERLEUKINS
Interleukins
• T helper —1 (TH1) secretes IL-2 and interferon

• T helper — 2 (TH2) secretes IL-4, IL-5, IL-6, IL-13
Interleukin-1
• IL1 antagonist is Anakinra

• Principally secreted by :
o macrophages
o monocytes
o epithelial cells.
• Other sources are:
o B lymphocytes
o fibroblasts

o endothelial cells.
• Immunological effects-
o Activation of T cells for the production of IL - 2.
o B cell proliferation and antibody synthesis
o Neutrophil chemotaxis and increased PMN release from bone marrow.
o Increases body temperature (important endogenous pyrogen).
Interleukin-2
• Induces the proliferation of responsive T-cells.

• Plays important part in :
• activation of naïve CD 4+ T cells
• initiation of cell mediated immune response
• Produced by T helper cells 1.
Interleukin-3
• Secreted by T helper 2 cells

• Regulates blood-cell production .
Interleukin-5/Eosinophil differentiation factor (EDF)
• It regulates eosinophil growth and activation
lnterleukin-7 (IL-7)
• Produced by spleen and bone marrow stromal cells.

• It acts as B and T cell growth factor.
IL28B
• harboring genetic variation in IL28B

• patients with hepatitis C may not respond well to treatment with interferon
80. Neisseria gonorrhoeae :Basics
• Neisseria gonorrhoeae is an exclusive human pathogen

• Some strains of Neisseria gonorrhoeae may cause disseminated disease
• Acute urethritis is the most common manifestation in males in Neisseria gonorrhoeae
• Gonococcus can be identified by being fermentation of glucose
• The electron transport system of Neisseria is located on Cytoplasmic membrane
• Differentiating feature of Neisseria gonococcus from Neisseria meningitides is Maltose
fermentation
• The virulence factor of Nisseria gonorrhoeae includes M proteins
• Nisseria gonorrhoeae Cause stricture of urethra
• Nisseria gonorrhoeae Involves seminal vesicles and spreads to epididymis
• Drug of choice for Nisseria gonorrhoeae is ceftriaxone
• Selective media for N. gonorrhoeae is Thayer martin media
• Genus neisseria is Gram negative diplococci
81. Neisseria gonorrhoeae : Clinical manifestations
• Exclusive human pathogen

• Some strains may cause disseminated disease
• Acute urethritis is the most common manifestation in males
• N. gonorrhea causes Salpingitis and Cervicitis
• Asymptomatic carriage of gonococcal infection in female is commonly seen endocervix
• Gonococcal vaginitis occurs in in children
• Most patients present with symptoms of dysuria in gonococcal urethritis
• Gonococcal infection spreads by ascending route and Involvement of adjacent structures
• Vagina is not affected by gonococcal infections
• Chlamydia trachomatis can be isolated in up to 50% of women with gonorrhoea and because
women treated for gonorrhoea only may soon go on to develop Chlamydia or pelvic inflammatory
disease (PID), any woman receiving treatment for gonorrhoea should also be treated for Chlamydia
• Recurrent Neisseria infections are predisposed by late complement component deficiency
• Complement necessary for neisseria infection are C5, C6 and C7 gonococcal urethritis
82. Neisseria gonorrhoeae :Diagnosis and Treatment
• Best site to obtain a swab in asymptomatic gonorrhea should be endocervix.

• Gonococci produces beta lactamase, rendering penicillin treatment ineffective.
• For uncomplicated gonococcal infection ceftriaxone is DOC (along with azithromycin or doxycyclin
to cover chlamydial infection)
83. Clostridium tetani: Clinical manifestations
Infection is acquired by
• Not transmitted from person to person , i.e. herd immunity is not protective
• Minimum lethal human dose of exotoxin is 2.5 ng/kg.
• Seen more often in the summer season and in hot, damp climates with soil rich in organic matter.
• Wounds contaminated with fecal matter and soil are most prone
Symptoms
• Symptoms are due to the effect of toxin.

• Tetanospasmin (neurotoxin) is responsible for tetanus.
• Median time of onset after injury is 7 days.
• Period of onset in tetanus refers to the time between first symptom to spasm
• Sinus sardonius:
o Spasms of facial and buccal muscles.
84. Clostridium tetani : Diagnosis, treatment and Prevention
Diagnosis of tetanus
1. Muscle enzyme levels may be raised
Treatment of tetanus
1. Antimicrobial therapy
2. Antitoxin :-
o Human tetanus immune globuline (TIG) is the preparation of choice.
o Administered within time it neutralizes tetanus toxin and significantly lowers the mortality
o Serious wound + uncertain about immunization should receive both
1. Tetanus toxoid (active immunity)
2. Tetanus immune globulin (Passive immunity)
Prevention
Active immunization
• Protective level of antitoxin > 0.01 IU/ml serum

• Active immunity offered by tetanus toxoid is effective in 100% of the patients
• Adsorbed toxoid are more beneficial
• Should never freeze
• Monovalent Vaccine:
o 2 dose of purified tetanus toxoid (IT) should be given at interval of 1-2 month
o Ist booster after 1 year of 2nd dose.
o 2nd booster after 5 years of 3rd dose.
Combined Vaccine :
• DPT .
Passive immunization :

• Human tetanus hyperimmunoglobulin (TIG) is best prophylactic to use.
• Toxin already bound to neural tissue is not affected.
Combined active and passive immunization:
• Patient is given TIG in one arm

• TT in other arm
• Followed by another dose of TT 6 weeks later and third dose 1 year later.
• TIG contraindicated during pregnancy.
• The purpose of antitoxin is for immediate temporary protection
• The purpose of tetanus toxoid is for long lasting protection
• TT is useful even after 12 hours have elapsed following injury.
Pregnancy
Primigravida
• Tetanus toxoids appear safe during pregnancy

• 0.5 ml tetanus toxoid is given at 6 weeks interval for 2 times
• The first one to be given between 16-24 weeks.
Multigravida (completely immunized in last 5 years):
• 1 booster dose is sufficient
Multigravida (partially immunized in previous pregnancy in last 5 years):
• 2 doses, 1 month apart, after I trimester.
Multigravida (unimmunized in previous pregnancy in last 5 years):
• 2 doses, I month apart, after I trimester
Multigravida (completely immunized in previous pregnancy earlier than 5 years):
• 2 doses, I month apart, after I trimester.
85. Bacillus Anthrax
Morphology
• Bacilli arranged in Bamboo stick/box car like appearance.

• On staining with polychrome methylene blue, it shows M'Fadyeans reaction; which represents
capsular material.
• Spores -
o Used in biological warfare or bioterorism.
o Formed in culture or soil but never in animal body.
o Not cause bulging of vegetative cells (in comparison of clostridia spores).
Culture
• Selective medium:
o PLET medium.
• OnAgar plates -
o frosted glass appearance seen.
o On microscopy it has Medusa head appearance.
• On Gelatin stab -
o characteristic Inverted Fir tree appearance.
VIRULENCE FACTORS :
1) Capsular polypeptide -
• Basis of live attenuated anthrax spore vaccine.
2) Anthrax toxin
Complex of three fractions :
a) The edema factor (EF or factor I)
b) The protective antigen factor (PA or factor II)
c) The lethal factor (LF or factor III)
86. Bacillus Anthrax:Clinical manifestation, Diagnosis and treatment
Introduction:
• Anthrax is a zoonoses
• "Man is relatively resistant to infection with B. anthracis"
• Few as one to three spores may be adequate to cause disease in some setting
• According to The Workmen's Compensation Act, 1923, Antrax is considered an occupational disease
Forms
1. Cutaneous anthrax
• Cutaneous anthrax is most common.
• The whole area is congested and edematous
• The lesion starts as macule
• Progress through papular and vesicular or pustular stages
• Formation of an ulcer with a blackened necrotic eschar.
• The lesion is painless.
• Its called malignant pustule.
• Hide porter's disease.
• Cutaneous anthrax generally resolves spontaneously
• But 10-20% of untreated patients may develop septicemia.
2. Pulmonary anthrax
• Woolsorters' disease
• Occupational hazard for people who sorted wool
• Most dangerous form of inhalational anthrax
• It causes hemorrhagic pneumonia.
3. Intestinal anthrax(rare)
• Laboratory Diagnosis
• Mc-Fadyean's Reaction
• Blood films containing anthrax bacilli are stained with polychrome methylene blue stain for few
seconds
• Examined under microscope
• Amorphous purplish material is noticed around bacilli.
• This represents the capsular material and is characteristic of anthrax bacilli.
• Culture Characteristics of Bacillus anthracis
• On agar plate: Frosted glass appearance
• On gelatin stab culture: Inverted fir tree appearance
• Ascoli's thermoprecipitin /Elek's gel precipitation test
• Penicillin G is the DOC
87. Bacteriophage
Introduction
• Viruses that infect bacteria.
Types of phages
• Lytic or virulent phages

• Temperate or prophages
• Temperate phages, on the other hand, can penetrate the bacterium and enter a dormant state
called “lysogeny’ in which most viral genes are repressed.
Example
• Lysogenic conversion in corynebacterium diptheria converts it into pathogenic bacteria.

• After lysogenic conversion, C. diphtheria acquires the ability to produce toxin.
• Lysogenic conversion is also seen in salmonella typhi and clostridium botulinum.
• Exogenous genetic material can be introduced into the bacterial cell by three methods:
Transformation
Conjugation
Transduction
• Occurs when bacteriophage carries a piece of bacterial DNA from one bacterium to another.
• Confined to transfer of chromosomal DNA, episomes and plasmid may also be transduced.
• Plasmid is a DNA molecule that is separate from and can replicate independently of chromosomal.
Just as there are two types of phages, there are two types of transduction.
• Lytic phages cause generalized transduction.

• Temperate phages cause specialized transduction.
Transmit of extrachromosomal genes
• Bacteriophages can also transmit extrachromosomal genes (plasmids)

• Penicillinase resistance in staphylococcus is a classical example of plasmid mediated drug resistane
transmitted by transduction or bacteriophages.
• Lysis of bacteria occurs due to replication of bacteriophage in the bacteria, in lytic cycle.
Phage Assay
• Used for titrating number of viable bacteriophage and for purification of phages.
88. Proteus bacilli
Proteus differs from other enterobacteria:
• by presece of enzyme phenylalanine deaminase
Features

• Peritrichous flagellae
• Show Pleomorphism
• gram negative
Culture
• Swarming growth on solid media

• Swarming growth is due to motility of bacteria.
• P. mirablis and P. vulgaris
• Dienes phenomenon is used to detect swarming of proteus.
Infections
• UTI (20-30% of complicated UTI)

• Pneumonia (primarily in hospitalized patient)
• Intraabdominal infections
• Soft tissue abscess
• Xanthogranulomatous pyelonephritis
Renal Stones
• Magnesium-ammonium-phosphate stones
• Secondary to urinary tract infection
Diagnosis
Urease test
• Distinguish Proteus organisms, which produce urea, from other enteric bacteria.
Urine
• Alkaline urine
• Cloudy with plenty of pus cells
Weil felix reaction
• The basis of the test is the sharing of an alkali - stable carbohydrate antigen by some rickettsiae and
by certain strains of proteus
• P. vulgaris OX - 19 and OX - 2 and P. mirabilis OX - K.
Treatment

• Proteus mirabilis is often inhibited by penicillins
89. Bordetella pertussis
Morphology
• Capsulated
• It is a strict human pathogen
Culture
• Bordet-Gengou glycerine potato-blood agar medium is commonly used.

• Contains a high percentage of blood (20%–30%) to inactivate inhibitors in the agar.
• Mischulow's charcoal agar
• Produces bisected pearls or mercury drops colonies.
• Confluent growth present and "aluminium paint" appearance.
• Culture films have Thumbprint appearance
Virulent Factors
1. Pertussis toxin
2. Filamentous hemagglutinin (FHA) secreted protein:
• Piracy of Adhesins
3.Tracheal cytotoxin
90. Bordetella pertussis: Clinical manifestations and diagnosis
Introduction
• Whooping cough is caused by B. pertussis.

• < 5% cases it is caused by B. parapertussis.
Source of infection:
• Case of pertussis (not carrier).
Secondary attack rate :
• High, i.e. 90%.
Age group:

• Disease of infants and young children (< 5 years of age).
• Infants are susceptible to infection from birth because maternal antibody does not give them
protection.
Mode of transmission:
• By droplet infection and direct contact.

• The role of fomites in the spread of infection appears to be very small, unless they are freshly
contaminated.
lncubation period:
7 - 14 days.
Clinical features
• Catarrhal stage:
• Infectivity is maximum .
• Paroxysmal stage: -
• Post-tussive vomiting
• Mucus Plug.
• Vomiting with cough.
• Episodes are often worsen at night and interfere with sleep.
• Most complication occur during paroxymal stage.
• Paroxysm is precipitated by noise, eating and physical contact
• Leukocytosis due to absolute lymphocytosis is characteristic in late catarrhal or paraoxysmal stage
• Convalescent stage
Complications of Pertussis
• Respiratory -
• Patchy Atelectasis
• Subcutaneous emphysema
• Neurological-
• Persistent seizures
• Paraplegia
• Ataxia: Not of cerebellar origin. There is no involvement of the cerebellum in Pertusis
Diagnosis:
• Presence of recurrent bouts of severe cough followed by an audible whoop suggests a diagnosis of
pertusis.
• Culture of nasopharyngeal secretions remains the gold standard of diagnosis.
• Best specimen is collected by nasopharyngeal aspiration.
• DNA detection by polymerase chain reaction (PCR) increased sensitivity and quicker results.

Lymphocytosis
• Lymphocytes often have a weird “clefted” appearance"
91. Bordetella pertussis: Control of whooping cough
1. Management of cases and contacts
Cases:
• Erythromycin is the DOC.
2. Prevention by active immunization
• There are two vaccines:
1. Whole cell vaccine
• The adverse effect with pertussis (used in DPT)

• Local pain, swelling, redness
• Fever
• Convulsion
• Anaphylaxis
• Hypotensive, hyporesponsive episode
• infant death syndrome, and autism.
• Pertussis vaccination can complicate the already apparent abnormalities and their management.
Contraindication
• Progressive neurological disease (Relative)

• Immediate anaphylaxis
• Encephalopathy
• Contraindicated in individual > 7 year age.
Acellular vaccine
• Five antigens purified from the organism:

• Chemically or genetically detoxified pertussis toxin (PT toxoid).
• Filamentous hemagglutinin
• 69k Da outer membrane protein ( also known as pertactin)
• Fimbrial-2antigen
• Fimbrial-3 antigens.
• May provide protection against disease but not prevention against infection.
• It can create career form in adults which can affect the infants.
Immunization:
• The pertussis component in DPT vaccine is not recommended after the age of 6 years.
Threshold level of herd immunity:
• 92-94%
Secondary attack rate of pertussis :
• SAR in unimmunization household contacts of pertussis 90 %
92. Brucella
Introduction
• Brucella is agent of biological warfare.

• Bruce identified the causative agent of Malta fever in 1887.
Morphology
• noncapsulated
Sensitive to
• sunlight
• Heat
• Pasteurization destroys brucella
• Transmitted by unpasteurized milk
Culture
• B. Abortus require 10% CO2for growth(capnophilic)

• Other three species can grow in air.
• Erythritol has a specially stimulating effect
• The biphasic culture medium used for Brucella culture is Castaneda medium.
Classification
• Brucella abortus (cattle)

• B suis(hogs)

• Br Cants (dogs)
• B melitensis (Sheep, goat and camel )
93. Brucellosis
Cause:
• Brucella
• Most virulent cause of brucellosis: B. melitensis .
• mediterranean fever/Malta/undulant fever.
Source:
• Sheep, goats,camels.
Route of transmission:
• Occupational exposure
• Infected meat (slaughterhouse workers)
• placentae of infected animals (farmers, veterinarians)
• Ingestion of untreated milk or milk
• products, raw meat (blood)
• inhalation
• transplacental
• during breasffeeding
• during sexual activity.
Symptoms
• fever, chills, diaphoresis, headaches.

• Pancarditis
• lymphadenopathy
• Hepatosplenomegaly
• GBS syndrome
• Abortion or IUD
• Death is usually a consequence of cardiac involvement.
Diagnosis
Laboratory diagnosis of Brucellosis
Culture

• Blood culture is the most definitive method for the diagnosis of Brucellosis.
• Castaneda method of blood culture recommended.
Serological tests
MercaptoEthanol (2-ME) agglutination test
• Differentiate active from inactive Brucellosis.

• Determining the adequacy of antibiotic therapy
• Adequate therapy reduces the IgG antibody level but not the IgM antibody level.
Polmerase chain reaction (PCR)
For diagnosing animal infection -
• Rapid plate agglutination

• Rose Bengal card
• milk ring test
Treatment
• Adults: Streptomycin + doxycycline.
94. Rickettsiae
Morphology
• Gram negative
• Pleomorphic coccobacilli
• Obligate intracellular organisms
Culture
• Rickettsiae are unable to grow in cell free media.

• Exception to this rule, R. Quintana
• Can be cultivated in Mouse fibroblast
Rickettsial Diseases
• Rickettsia tsutsugamushi is a small gram-negative, obligate intracellular organism causing scrub

typhus
• Rickettsial pox is caused by Rickettsia akari
• 'Louse' is the insect vector for Rickettsia prowazekii.
• Rickettsial pox, caused by Rickettsia akari, is transmitted to humans by the house mouse mite
Liponyssoides sanguineus.
Important Points:
• Most severe
• Rocky mountain spotted fever
• Most mild
• Rickettsia pox
• Symptoms
• fever
• headache
• malaise
• Prostration
• hepatosplenogy
Rash is seen in
1) Epidemic typhus
2) Endemic typhus
3) Scrub typhus
4) Rocky Mountain spotted fever
5) Indian tick typhus
Lymphadenopathy is seen in
1) Scrub typhus
2) Rickettsial pox
Eschar is seen in
1) Scrub typhus
2) Rickettsialpox
3) Indian tick typhus
Mortality
• 20% of Rocky Mountain Spotted fever

• 30% for epidemic typhus.
• Become localized chiefly in vascular endothelial cells
• The overall pathological features of the rickettsial diseases are due to the damage of vascular
endothelium.
Weil felix reaction

• This reaction is an agglutination test in which sera are tested for agglutinins to 0 antigens of certain
nonmotile proteus strains OX -19, OX - 2 and OX - K.
OX 19 ln epidemic and endemic typhus
OX-2 In rocky mountain spotted fever

OKX In scrub typhus
No value Q fever, Trench fever, Rickettsial pox

False positive Typhoid, liver diseases, Proteus infection Pseudomonas,Borelia,S. typhi
• Treatment
• Tetracyclines (e.g., doxycycline are DOCs)
95. Treponema Pallidum
Morphology
• Motile by endoflagella, which are polar flagella.

• Discovered by Schaudinn and Hoffman
• The causative agent of syphilis
• Does not fulfil Koch's postulate.
Staining
• Fontana's method is useful for staining films.
Cultivation
• Do not grow in artificial culture media.

• Obligate intracellular organism.
• Reiter strain (T phagedenis) -
• Non-pathogenic treponeme, can grow in artificial culture.
Susceptibility
• It is killed in 1-3 days at 0-4°C

• Transfusion syphilis can be prevented by storing blood for at least four days in the refrigerator
before transfusion.
Antibodies:

• Reagin antibody:
• Responsible for Wasermann reaction, Kahn test, and VDRL.
• Antibody to group antigen
• Antibody to species-specific antigen
• T pallidum has hyaluronidase:
• Enhances, invasiveness of the organism.
96. Treponema Pallidum :Syphilis
Introduction
• Most common STD in India is

• herpes genitalis (20%)
• followed by chancroid (11%),
• viral warts/HPV (11%)
• syphilis (11%)
• gonorrhea (9%)
Incubation period:
9-90 days(primary syphilis)
1.Venereal Syphilis
(a) Primary syphilis
• Primary chancre is well defined punched out ulcer with following characteristics:
• Single lesion
• Painless
• Avascular (non-bleeding)
• Firm inducation
• Usually superficial (but may be deep)
• Well circumscribed with elevated round or oval edges
• Cartilagenous consistency
• Lymphadenopathy:
• painless
• firm
• nonsuppurative.
• Sites of involvement are :
• penis in heterosexual males
• rectum, anal canal
• mouth in homosexual males
• cervix and labia in females.
(b) Secondary Syphilis:
• Bilateral symmetrical asymptomatic localized or diffuse mucocutaneous lesion

• macule, papule, papulosquamous and rarely pustule
• Non-tender generalized lymphadenopathy
• Highly infectious condylomata late, in warm moist intertriginous areas
• Moth-eaten alopecia, arthritis, proteinuria
(c)Tertiary Syphilis:
• Gumma, neurosyphilis/tabes dorsalis

• Ostitis, periostitis
• Aortitis, aortic insufficiency, coronary stenosis and nocturnal angina
2. Congenital Syphilis
(a) Early Congenital Syphilis:
• Snuffles (rhinitis)is the earliest feature.

• Lesions are vesiculobullous and snail track ulcers on the mucosa
(b) Late Congenital Syphilis:
• Characterized by Hutchinson's triad

• interstitial keratitis
• 8th nerve deafness
• Hutchinson's teeth i.e. pegged central upper incisors
• Saddle nose, sabre tibia, mulberry molars
• Bull dog's jaw (protrusion of jaw)
• Rhagades (linear fissure at mouth, nares)
• Frontal bossing, hot cross bun deformity of skull
• Clutton's joint(painless swelling of joints, most commonly both knee)
• Palatal perforation
• Higaumenakis sign (periostitis leads to unilateral enlargement of sterna end of clavicle)
General paresis of insane
• Is a form of neurosyphilis, peaks in incidence 10 to 20 years after untreated Treponema pallidum

infection

97. Treponema Pallidum: Diagnosis and Treatment
• Treponema pallidum isolation from CSF is maximum in the secondary stage of syphilis.
• Infection leads to lifelong immunity.
• Penicillin is the only recommended agent for treatment of syphilis in pregnancy.
• If the patient has a documented penicillin allergy, desensitization and penicillin therapy should be
given.
• Seropositive infant not treated at birth if mother received penicillin in 3rd trimester
• Biological False positive/ BFP serological test for syphilis may be encountered in:
• Viral Hepatitis, SLE, and Leprosy.
• Primary or secondary syphilis - Benzathine penicillin G 2.4 million units intramuscularly (IM) in a
single dose
• Congenital syphilis can be best diagnosed by IgM FTA- ABS
• Most sensitive diagnosis during secondary stage of syphilis is VDRL.
• Treponemal Test
• Fluorescent treponemal antibody-absorption (FTA-ABS)
• Microhemagglutination assay T pallidum (MHA-TP)
• T pallidum hemagglutination (TPHA)
• FTA-ABS-Confirmatory test
• TPI (Treponemal pallidum immobilization) test(most specific)
• Non-treponemal tests
• RPR (Rapid plasma reagin)
• VDRL
98. Parvovirus
Parvovirus
• Smallest virus.
• Not a cultivable virus
Pathogenesis of parvovirus
• Affects erythroid progenitors.
Transmission
• Vertical (transplacental) transmission rates are estimated to be :

• 30% or higher.
• Transmission is primarily by :
• respiratory route
• Also through blood.
Clinical manifestations:
Erythema infectiosum (fifth disease)
• Fifth of the Childhood Viral Rash

• The main symptomatic manifestation
• Erythema infectiosum also known as fifth disease or slapped check disease.
• Child present with facial rash (slapped cheek appearance)
• Preceded by lowgrade fever.
Polyarthropathy syndrome
• Uncommon among children but occurs in 50% of adults.
Aplastic crisis
• Asymptomatic Transient reticulocytopenia precipitated in certain cases of Ch Hemolytic Anemia

• Ex – Sickle Cell Anemia , Hereditary Spherocytosis
Pure red cell aplasia/chronic anemia
• chronic anemia with reticulocytopenia
Hydrops fetalis
• Cause nonimmunohydrops fetalis if infection occur in first 20 weeks of pregnancy
Maternal infection can result in:
• Hydrops fetalis
• Fetal death due to severe anemia.
Diagnosis
• Done by the detection of B19 IgM and IgG antibodies.

• IgM is detected at the time of rash in erythema infectiosum
• IgG is detected on the 7th day.
Treatment
• No antiviral is effective against parvovirus.

99. Pox Virus
• Class:
• Orthopoxvirus
Variola
• Enveloped ds DNA virus

• Elementary bodies :
• Paschen bodies
Vaccinia
• Employed as a vector for the development of recombinant vaccine

• Vaccine vectors(are used experimentally )
• Recombinant poxviruses
• Influenza virus
• Adenoviruses
• Eosinophillic inclusion bodies:
• Guamieri bodies
• Demonstrated in stained preparation.
Cultivation of Poxvirus
• Both Variola and Vaccinia grow on CAM producing pocks.
Antigenic cross-reactivity
• All pox virus share a common antigen nucleoprotein (NP)

• This antigen is used to prepare vaccines which can be used both in smallpox and cowpox.
Small pox eradication:
• Smallpox was declared eradicated on 8th May 1980.

• Edward Jenner introduced vaccination for smallpox with live cowpox virus in 1798.
• The epidemiological factors which led to smallpox eradication are as follows:
• Highly effective, heat stable and easily administrable vaccine that confers long-term protection.
• Lifelong immunity after recovery from the disease.
• Persons with sub-clinical infection did not transmit the disease.
• No known animal reservoir
• No long term carrier of the virus.
• Easily detectable clinical cases
• International cooperation
Molluscum contagiosum (MC)

• Caused by :
• molluscum contagiosum virus (MCV).
• MCV has no nonhuman-animal reservoir (infecting only humans).
• Types
• There are four types of MCV, MCV-1 to -4
• MCV-1 is the most prevalent
• MCV-2 is seen usually in adults
• Transmission:
• Direct skin or mucous membrane contact (eg. touching & sexual contact)
• via fomites.
• Characteristic lesion:
• Umbilicated papule containing a grayish central plug (pore)
• On face & genitals in children
• Treatment :
• Watchful waiting, curettage, and cryotherapy
• The virus cannot be grown in eggs, tissues culture or animals.
100. Influenza virus
Morphology
• Belong to orthomyxoviridae → Envelope, RNA virus

• Contain single-stranded RNA which is segmented → 8 pieces
Types
• There are three viral subtypes

• based on RNP and M protein antigens
• Type A → Causes all pandemics and most of the epidemics
• Type B → Sporadic and epidemics
• Type C → Causes endemic infection
• Types of influenza viruses are circulating in the world -
• A (H1N 1)-causes swine flu
• A (H3 N2)
• B
• H7 N9 of type A (caused an epidemic of avian influenza in China in 2013)
• A(H5 N 1)-
• causes bird flu or avian influenza
• 1997 bird flu pandemic
Culture
• In embryonated egg cultivation for influenza virus site of inoculation are:-

• Allontoic cavity or amniotic cavity
Antigenic structure
a.Internal Antigen:
b.Surface Viral or V antigen:
• Antigenic variation is highest in type A, less in type B and not seen in type C
• Two types:
Antigenic drift Antigenic shift
Gradual and sequential change in genome Abrupt, drastic and discontinuous variation
occurring at regularly at frequent intervals resulting in a novel virus
New antigen related to previous antigen New surface antigen not related to previous
Inaccurate viral RNA polymerase frequently Due to genetic reassortment between 2 strains,
produces point mutations in certain error-prone presumably during coinfection of a single host.
regions in the genes.
Cause periodic epidemics Causes major epidemics and pandemic
• V antigen composed of at least 2 virus-coded protein:
Hemagglutinin:
• Cause hemagglutination.
• 16 subtypes
Neuraminidase
• Receptor destroying enzyme (RDE)

• Cause elution.
• 9 subtypes
• Source of infection:
• Case or subclinical case
Mode of transmission:
• Droplet infection by respiratory route

• Influenza affects all ages and both sexes.

Incubation period:
• 18-72 hour
Prevalence:
• Data regarding the prevalence of influenza is not adequate
Cyclic trend:
• Influenza shows cyclic trend :

• With epidemic occurring every 2-3 years in case of influenza - A
• Every 4-7 years in case of influenza-B.
• Pandemics are caused by only influenza - A every 10-15 years.
101. Influenza virus: Clinical manifestations, Complications, Diagnosis, Treatment and Prevention
• H1N1
• causes swine flu is also known as swine influenza, hog flu, and pig flu.
• Swine Flu pandemic in 2009
• causes serious systemic manifestations
• Most infections are subclinical
• Fever, cough, rhinorrhea, fatigue, and headache.
• Vomiting in type B seen.
• There is no viremia
• A pandemic of H1N1 is suspected when :
• Cases are spread over 5 or more cities
Complications
• Pneumonia:
• M.C. by str. pneumoniae
• Occurs most frequently in high-risk individuals with chronic pulmonary and cardiac disease and in
elderly individuals
• Worsening of COPD
• Encephalitis
• Reye's Syndrome:
• with type B virus
• GB. Syndrome
• G I Symptoms (gastric flu):
• With type B virus

In India, facilities for isolation of influenza virus are available at the following institutes:
• Govt. of India, Influenza Centre, Pasture Institute, Coonor, South India

• Haffkine Institute, Mumbai
• School of Tropical Medicine, Kolkata
• All India Institute of Medical Sciences, New Delhi
• Vallabhai Patel Chest Institute, Delhi
• Armed Forces Medical College, Poona
H1NI influenza pandemic phases:
• Six phases
• H1NI influenza pandemic is in phase 6
Prevention
a. Killed vaccine:
• Contains H, N antigens
• Guillain-Barre syndrome (ascending paralysis) rarely seen.
b. Live attenuated vaccines:
• Administered as nose drops so induce both local and systemic immunity
c. New Vaccines
• Split virus vaccine (subvirion vaccine)

• Neuraminidase specific vaccine (sub-unit vaccine contains only N-antigen)
Mild problems following inactivated flu vaccine:
• Soreness, redness, or swelling where the shot was given

• Hoarseness
• Sore, red or itchy eyes
• Cough
• Fever
• Aches
• Headache
• Itching
• Fatigue
School Closure:

• School holidays reduced the reproduction number of Influenza H1N1 by 14-27% in different regions
of India
• Significant impact of school holidays on spread of pandemic influenza virus
Treatment
Type A & B
• Specific antiviral Neuraminadase inhibitor oseltamivir and zanamivir

• The dosage of Oseltamivir for children
0 – 1 month of age 2 mg/kg BID x 5 days
>1 month – 3 months 2.5 mg/kg BID x 5 days
> 3 month – 1 year 3 mg/kg BID x 5 days
• Zanamivir is indicated in individuals > 5 year of age only
Type A
• Admantone agent amantadine and rimantidine .
102. Avian Influenza
Introduction:
• Has not become an epidemic till now.

• Human to human transmission is rare; this is the most important reason.
Avian Influenza
• Primarily infect birds

• Also known as 'Bird flu' or 'Highly pathogenic avian influenza'
• Causative agent:
• H5N1 (Type A Influenza virus)
• Avian Influenza is a Pandemic:
• Origin from Hong Kong (1997)
• Aquired by close contact with domestic birds
• Cause widespread infection in the human body instead of infection being limited to the lung.
• Fortunately, the transmission of the current H5N1 virus is inefficient
Treatment:
• Drug of choice:
• Oseltamivir (Tamiflu) 75 mg BD x 5 days
• contraindicated in infants
Vaccine Avian Influenza:
• This inactivated influenza virus vaccine

• Two-dose regimen.
• One 90 microgram dose is given intramuscularly, in the upper arm
• Second 90 microgram dose is given in the same manner, 28 days later.
103. Respiratory Syncytial Virus (RSV)
Morphology
• SS negative-sense RNA virus

• The viral envelope has two glycoproteins :
• G protein:
• By which virus attaches to cell surface
• F- protein ( Fusion protein:
• which bring about the fusion between viral and host cell membranes.
Types
• RSV can be subtyped into:

• Type A
• Type B
Clinical Manifestations:
• RSV infection leads to a wide spectrum of respiratory illnesses.

1. In infant cause:
• pneumonia
• bronchiolitis
• tracheobronchitis.
• In this age group, illness begins most frequently with rhinorrhea, low-grade fever, often
accompanied by a cough and wheezing.
2. In adults, the most common symptoms are:
• a common cold, with rhinorrhea
• sore throat
• cough.
• It causes severe pneumonia in elderly.

3. Sinusitis, otitis media, and worsening of chronic obstructive and reactive airway disease are also
associated with RSV infection.Diagnosis
For Bronchiolitis:
Chest X-ray shows:
• Hyperinflation
• Multiple areas of interstitial infiltration
Bud tree Appearance:
• MC cause of tree in bud (bronchiectasis) appearance is Mycobacterium tuberculosis

(endobronchial).
• Most common specific cause of tree in bud appearance in HSL (bone marrow) transplant patients is:
• CMV (30-70%) > RSV (18%) > M. tuberculosis (5-6%) > Pneumocystis > Invasive aspergillosis.
Treatment
• Oxygen: Mainstay of therapy.

• Aerosolized ribavirin is used in the treatment of bronchiolitis with RSv
Prevention
• Palivizumab:
• Humanized monoclonal antibody
• Directed against an epitope in the A antigen site on the F surface protein of RSV.
• Licensed for the prevention of RSV infection in high-risk infants and children.
• Once-monthly intramuscular injections (15 mg/kg) for 5 months beginning at the start of the RSV
season
104. Rotavirus: Classification, Structure, composition and properties
• Rotavirus is a double-stranded RNA virus belonging to the family Reoviridae.

• Under electron microscope, Rotavirus looks like a wheel.
• The RNA is enclosed in a triple layered, non enveloped icosahedral capsid.
• It is one of the commonest cause of watery diarrhoea in children.
• Oral rehydration therapy is the most appropriate treatment of choice.
• Segmented genome is found in Rotavirus
• One unique feature of rotaviruses is the ease with which the 11 RNA segments can undergo
reassortment.

105. Rotavirus: Pathogenesis, Clinical symptoms, laboratory diagnosis, and Treatment
• Rotavirus is the major cause of diarrhea in infants and children under the age of 2
• Rotavirus, a double-stranded RNA virus, infects only the mature villous cells in the duodenum.
• Rota B cannot be grown in cell culture
• Viral enterotoxin is detected as a possible of mechanism pathogenesis in Rotavirus.
• Rotavirus can be diagnosed by immunofluorescence antigen in a stool ,antigen in stool by ELISA.
• Electron microscopy is helpful in diagnosis of Rotavirus.
• Best vaccine for rotavirus infection is Genetic reassortment
• Roatvirus vaccination causes intussusception .
• Viral enterotoxin is detected as a possible of mechanism pathogenesis in
106. Hepatitis A Virus
• Hepatitis A spreads by feco-oral route.

• Incubation Period:
• 2-4 weeks with a mode of ~1 month from exposure to symptoms regardless of the route of
infection
• Best test to diagnose prodrome of Hepatitis A is IgM anti-HAV.
• Vaccination
• Minimum age: 12 months
• Killed HepA vaccine(available in India): Start the 2-dose HepA vaccine series for children aged 12
through 23 months; separate the 2 doses by 6 months.
• Live attenuated H2-strain Hepatitis A vaccine: Single dose starting at 12 months and through 23
months of age
• For Travellers: Normal human immunoglobulin in a dose of 0.02-0.05 mg/kg of body weight.
107. Hepatitis C Virus
• HCV spread by blood

• HCV is flavivirus.
• Progression to chronicity is seen with hepatitis B and Hepatitis C
• Type I MPGN is commonly associated with persistent hepatitis C infection
• Extrahepatic Manifestations of Hepatitis C include lichen planus, glomerulonephritis, and
cryoglobulinemia
• A course of Interferon plus Ribavarin is the recommended treatment of choice for Relapsers after a
previous course of standard monotherapy with interferon or combination
interferon/ribavarintherapy

108. Hepatitis E and Hepatitis D
Hepatitis E (HEV)
• HEV is non-enveloped, positive-sense, single stranded RNA genomic ,HAV like virus
• Most common cause of sporadic Hepatitis amongst adults in India
• Most common cause of epidemic Hepatitis amongst adults in India
• Most common cause of Fulminant Hepatitis amongst pregnant women
• Worst prognosis in pregnancy
• Most common route of transmission is, fecoral route
• Hepatitis B, C and D are essentially spread by parenteral routes.
• Hepatitis A & E are non parenteral hepatitis.
• HDV superinfection of a person with chronic Hepatitis B (HBV) has the worst prognosis with a high
likelihood of fulminant hepatitis and death.
• HEV most common type of hepatitis responsible for epidemics in India.
• Hepatitis E usually affects adults.
Hepatitis D (HDV) or Delta virus
• It is defective RNA virus dependent on the helper function of HBV for its replication and expression.
109. Dengue Fever
Dengue Fever
Caused by :
• Four serologically related virus termed dengue 1, 2,3 4.

• Type II is most virulent
Morphology:
• Group B (flaviviruses) Arboviruses

• All are enveloped SS RNA virus belongs to flavivirus family
Diseases transmitted by:
• Ae. aegypti mosquito is vector.

• Bite chiefly during the day.
• Aedes prefer an artificial collection of water (stagnant water)
Manifestations of Dengue infection

A) Undifferentiated fever
B) Classical dengue fever
• Break bone fever

• Saddleback fever
• Fever Returns to normal after 5-6 days
• Or subside on about the 3rd day
• Rise again after 5-8 days after onset
• Rashes
C) Dengue Hemorrhagic fever -
• Caused by infection with more than one dengue virus.
Criteria for clinical diagnosis of DHF
• Clinical diagnosis
Fever Acute onset, high continuous lasting 2-7 days.
Hemorrhagic manifestations Petechiae, purpura, ecchymosis
Epistaxis, gum bleeding
Hematemesis and/or melaena
Tourniquet test is used in diagnosis of

dengue haemorrhagic syndrome (DHS).
Liver Enlargement of liver
• Laboratory diagnosis
• Diagnosis of Dengue fever can be made earliest by:
• NS-1 antigen detection
• X-ray of the chest (may demonstrate pleural effusion).
Polymerase chain reaction Early symptomatic phase
Hemagglutination - inhibition (HI) Sensitive but not specific.
Neutralization test (NT) Most sensitive and specific

Complement fixation test (CFT) Can be used for patients with current infection Limited
value
IgM - ELISA IgM antibodies are indicative of recent infection.
• Treatment
• Blanket/ mass treatment
• Immediate treatment of choice for severe hypotension in Dengue shock syndrome
• plasma volume replacement is most urgent, IV crystalloids are used for that purpose.
110. Chikungunya
• Chikungunya is emerging infection in India .

• Belongs to
• Family: Togaviridae
• The main virus reservoirs are monkeys, but other species can also be affected, including humans.
• Transmitted to humans by virus-carrying Aedes mosquitoes (generally Aedes aegypti mosquitoes).
• Chikungunya is an Abroviral infection.
111. Candida
Candida
• Yeasts like fungus

• Most common cause of fungal infections worldwide.
• Inhabiting 80% of everyone's intestinal tract, colon, and mouth with no problems.
Morphology:
• It is dimorphic.
• In Gram-stained smears, Candida appears as gram positive budding yeast cells (blastoconidia)
• Pseudohyphae showing regular points of constriction.
• Spores form on the pseudohyphae called chlamydospores
• C. albicans can take on either a unicellular (yeast) or multicellular (hyphae, pseudohyphae) form.
Culture:
• Germ tube positive:

• Form germ tubes within two hours when incubated in human serum at 37°C
• Reynolds - Braude phenomenon /Germ tube test
• They grow rapidly on simple media as oval budding cells at 25° to 37°C
• Candida shows mycelia and chlamydospores on corn meal agar
• Growth is inhibited by Griseofulvin
Host predisposing factors:
• Long-term antibiotic therapy eradicating resident bacterial flora

• Age:
• Infants
• Elderly are more susceptible
• Disorders Which may predispose to mucocutaneous infections:
• Diabetes mellitus: Most common risk factor.
• Cushing's syndrome
• Addison's disease
• Hypothyroidism
• Immunodeficient conditions, inborn or acquired predispose to systemic infections
• Women on contraceptives (oral or IUCD), pregnancy, menopause are more at risk of vaginitis
• Neutropenia is the most prominent risk factors for invasive candidiasis
112. Candida: Clinical Manifestations
A. Mucocutaneous candidiasis
• Most common organism causing fungal infection of oral cavity

• Oral thrush/Pseudomembranous candidiasis.
• The patch of creamy white pseudomembrane on the buccal epithelium, gums or the palate.
• Erythematous candidiasis
• Stomatitis
• Hyperplastic oral candidiasis:
• White plaques in mouth especially on cheeks and tongue.
• Cannot be easily removed.
• Median rhomboid glossitis
• Cheilitis
• Oesophagitis:
• Extension of oral candidiasis (thrush) into the oesophagus.
• Lesion are in distal 3rd of esophagus. Diagnosed by biopsy
• Pruritis ani, occur as result from long-term antibiotic therapy or extension of intestinal candidiasis.
• Vaginitis
• Balanitis
B. Cutaneous candidiasis
• Candida paronychia:
• Common in patients whose hands are frequently immersed in water.
• The nail fold becomes red and swollen and there is loss of cuticle with detachment of nail fold from
nail plate.
• Candida onychomycosis:
• Chronic paronychia leads to onychomycosis.
• The commonest type of candida onychomycosis is distal and lateral subungual onychomycosis
(DLSO).
• Intertriginous candidiasis
• Chronic mucocuatenous candidiasis
• Diaper rash.
• The commonest fungal lesion of the eyelid
• Candidial granuloma:
C. Systemic candidiasis
• Bronchial and pulmonary candidiasis

• Meningitis: Most patients have underlying conditions such as IV catheter, antibiotic or cytotoxic
therapy.
• Endocarditis: Previously damaged or prosthetic valve
• Urinary tract infections:
• This can occur in disseminated candidiasis, diabetes, pregnancy or catheterization.
• It is more common in females.
• Hepatosplenic candidiasis/Chronic disseminated candidiasis
• Mostly occur in the neutropenic patient.
• Septicemia
• Arthritis
113. Candida: Diagnosis and Treatment
• Pseudohyphae of candida with budding yeasts are present on this potassium hydroxide preparation
• Ketoconazole would treat both dermatophysis and candidal infection
• Drug of choice in systemic candidiasis is Amphotericin
• Drugs used for candidiasis include Fluconazole, Nystatin, Clotrimazole, Itraconazole
• Different species of Candida can be identified by following tests:
• Chlamydospore formation on Cornmeal Agar (Dalmau plate)
• Germ tube test (Reynaud Braude)
114. Pneumocystis jiroveci Pneumonia
Introduction
• Opportunistic fungi.
• Cannot be cultured
Taxonomic classification of Pneumocystis as a fungus is based on factors:
• Analysis of gene sequence for ribosomal RNA, mitochondria, proteins and major enzymes
• Presence of b-1, 3 glucan in the cell wall
• The efficacy of antifungal drugs that inhibit b-glucan synthesis.
Two distinct forms:(seen in tissue)
• Thin walled trophozoites.

• Thick walled spherical or elliptical cysts
• Contain four to eight nuclei.
• Cyst can be stained with silver stain. toulidine blue, calcoflour white.
Persons at risk for Pneumocystic disease (Pneumocystosis)
• AIDS
• Patients receiving Immunosuppressive therapy (especially Glucocorticoids) for cancer, organ
transplantation etc.
• Children with primary immunodeficiency diseases
• Premature malnourished infants (immunodeficient)
Clinical Manifestations
• diffuse interstitial pneumonia

• fever
• non-productive cough
• dyspnea on exertion
• tachypnea
• Profound weight loss
• fatigue
• impaired oxygenation
Lab Diagnosis
• Pneumocystis infection is usually diagnosed by sputum examination

• Histopathological Findings:
• Methenamine silver, toludine blue stain cell wall
• Wright-Gietnsa stain the nuclei.
• Immunofluorescence with monoclonal antibodies; more sensitive
• The most characteristic is predominantly alveolar, foamy vacuolated, eosinophilic exudates.
• Fiberoptic bronchoscopy with BAL:
• forms the mainstay of diagnosis for Pneumocystic Pneumonia
• demonstrates small, "hat- shaped" structures in alveoli /Cup shaped cyst
• Transbronchial biopsy and open lung biopsy
• Chest X-Ray
• B/L diffuse infiltrate in perihilar region.
Treatment
• DOC cotrimoxazole
Prophylaxis is indicated for
• Patients with CD4- cell counts of< 200

• History of oropharyngeal candidiasis
Secondary prophylaxis is indicated for
• Both HIV infected and non HIV infected patients.

• Who have recovered from pneumocystosis.
• Primary and secondary prophylaxis may be discontinued in HIV infected persons once.
• CD4+ counts have risen to > 200 and remained at that level for 3 months.
First choice agent for the prophylaxis
• Trimethoprim, sulphamethoxazole.
Other agents used in prophylaxis.
• Dapsone, pentamidine.
115. Histoplasma capsulatum
Histoplasma capsulatum
• A dimorphic fungus
• Non encapsulated
Source of Infection:
• Infection is acquired by inhalation of microconidia (small spores) in dust contaminated with bird or
bat dropping
Culture:
• On Sabourauds agar,

• White cottony mycelia growth appears, with large (8-20 micrometer) thick walled, spherical spores
with tubercles or finger-like projections.
Pathology:
• fungi inhaled in spore form

• lungs are locally infected
• Microconidia reach the alveoli and initiate a granulomatous reaction.
• infection disseminates hematogenously
• Histoplasmosis/Darling's disease/ Cave's disease /Caver's disease.

• Endemic fungal infection
Symptoms
• Asymptomatic
• Mild (acute primary pulmonary histoplasmosis).
• fever
• cough
• chest X-ray finding of hilar adenopathy due to caseation necrosis or calcification
• which mimics TB
• with or without 1 or more areas of pneumonitis are typical features.
• Chronic pulmonary histoplasmosis or chronic fibrocavitary pneumonia
• Related to mediastinal fibrosis
• Disseminated disease
• fever and malaise
• seen in immunocompromised
• Mimic disseminated TB
• Adrenal glands are the most commonly involved organs
• adrenal glands are usually symmetrically enlarged
Diagnosis
• Culture:
• Tuberculate spore is diagnostic
• Millary mottling on X-ray chest
116. Entamoeba histolytica
• N-acetylglucosamine is the host receptor for Entamoeba histolytica

• Entamoeba histolytica belongs to supergroup Amoebozoa
• Mature cyst of Entamoeba histolytica has 4 vesicular nuclei.
• Nuclear structure retains characteristics of trophozoite in mature cyst
• Trophozoites
• Colonise in the colon
• The presence of red blood cells in the cytoplasm (erythrophagocytosis) is diagnostic of E. histolytical
as it is the only intestinal amoeba to exhibit this characteristic.
• The nuclear membrane is lined with a single layer of uniformly distributed fine chromatin granules.
• Karyosome is central in position (not eccentric).
• The pathogenicity of Entamoeba histolytica is indicated by isoenzymes pattern
• Cultures media used for cultivation of E.histolytica are: -
• Boeck and Drbohlav's medium
• Jones medium
• Philip's medium
• Balamuth's medium
• Shaffer and Frye's medium
• Diamond's medium
117. Entamoeba Histolytica: Clinical Manifestations
• The main reservoir for entamoeba histolytica is man
Mode of Transmission:
1. Faecal-oral route
2. Oral-rectal contact
3. Transmission through vectors ( flies, cockroaches and rodents)
• Amebiasis most frequently involves the cecum and ascending colon, followed in order by the
sigmoid, rectum, and appendix.
• Cutaneous amoebiasis
• Direct infection from liver
• Granulomatous ulceration and granulomatous mass may occur in the peri-anal region.
• Characteristic feature of amoebic ulcer
• Flask shaped
• Undermined edge
• Amoebic liver abscess :
• In the tropics 2-10% of the individuals infected with E. histolytica suffer from hepatic complications
• Liver abscess is the most common extra-intestinal manifestation of amoebiasis.
• Common in :
Most common in right lobe liver/right posterior-superior region
Portal vein is in direct continuation with the right tributary.
• Pus in amoebic liver abscess is not due to suppuration, but is a mixture of sloughed liver tissue and
blood
• Pus is chocolate coloured, classically called anchovy-sauce
• Abscess wall good for culture
• Pleuropulmonary infection is the most common complication.
• Most common cause of amoebic lung abscess is direct spread from liver
• Amoebic liver abscess ruptures most commonly into pleural cavity
118. Entamoeba Histolytica: Diagnosis and Treatment
• Amoebic liver abscess can be diagnosed by demonstrating trophozoites in the pus.

• Ultrasonography is the preferable initial diagnostic test for liver abscess
• Invasive amoebiasis can be best diagnosed by ELISA
• The presence of red blood cells in the cytoplasm (erythrophagocytosis) is diagnostic of E. histolytica
as it is the only intestinal amoeba to exhibit this characteristic.
• cysts are resistant to readily attainable levels of chlorine, disinfection by iodination (Tetraglycine
hyperiodide) is recommended.
Drug therapy for Amoebiasis
1. Asymptomatic carrier (asymptomatic cyst passers)
• Diloxamide furoate is the DOC.
2. Luminal amoebicides:
• Diloxamide furoate, iodoquinol, paromomycin.

• Effective in amoebic colitis.
3. Tissue Amoebicides:
• Emetine, chloroquine, effective in extraintestinal amoebiasis

• Metronidazole is effective in both conditions
119. Leishmania
Epidemiology
• Location
• tropical and subtropical countries
• mostly a disease of the developing world
• Reservoir of Leishmaniasis in India in acute visceral leishmaniasis

Forms
Amastigote forms
• Seen in human infections

• Leishman-Donovan bodies:
• Intracellular Amastigotes microscopically seen.
• Wthin blood and spleen monocytes
• Less commonly, in circulating neutrophils and in aspirated tissue macrophages
Promastigote forms
• Seen in the gut of sand fly Phlebotomus argentipes.

• It is also seen when grown in laboratory on artificial culture media.
• It is a spindle shaped structure measuring 15-20 um by 1-2 um.
• It has a flagellum arising from the axoneme and coming out of the anterior end.
• Blepheroplast and a vacuole in the anterior end
• Nucleus is round to oval and central in location.
• The nucleus is red and the kinetoplast is bright red on Leishman stain
Culture
• L. donovani can be cultured in N.N.N. (Novy, Macneal and Nicolle) medium.

• In N.N.N. medium amastigote form changes into promastigote form.
Transmission
• phlebotomine sand flies
• Leishmania donovani
• Causes a visceral disease called Kala azar.
• Immune-complex-mediated mesangio-proliferative glomerulonephritis seen
• Leishmania tropica:
• Causes Oriental sore (cutaneous leishmaniasis) On the skin
• Post kala azar dermal leishmaniasis:
• Leishmania brazilensis
• Espundia
• muco cutaneous leishmaniasis/nasopharyngeal leishmaniasis
Diagnosis
• Blood smear
• stained with Giemsa or Leishman's stains
• Direct visualization of the amastigotes
• In aspirates of bone marrow, spleen, liver or lymph nodes, makes the diagnosis
• Aldehyde test
• Supportive hematological tests.
Treatment
Pharmacologic
• Drug used for Leishmaniasis (Kala azar) -

• Sodium stibogluconate (DOC)
• Pentamidine
• Amphotericin B
• Ketoconazole
• Miltefosine
• Paromomycin
• Allopurinol.
• miltefosine
• for visceral and cutaneous
• fluconazole
• effective in treating cutaneous leishmaniasis
120. Dry Heat Sterilization
Burning or incineration
• For contaminated cloth

• Hospital dressing is best disposed by incineration
• animal carcasses
• pathological materials
• Human anatomical waste
• Cytotoxic drug
• incineration and disposed of by secured landfills.
• Double-chamber pyrolytic incinerators :designed to burn infectious health care waste.
Hot air oven:
• The holding period of 160oC for one hour is used to sterlize

• glassware,
• scalpels
• all glass syringes
• swabs
• liquid paraffins
• dusting powder
• fats
• grease
• For cutting instrument
• Temperature of 150oC for 2 hours is required
• 170oC for holding period of 20 minutes.
121. Moist Heat Sterilization
Temperature below 100oC:
• For pasteurization of milk

• Holder method
• 65oC for 30 min
• Flash Process
• 72oC for 15 sec
• Pasteurization kills nearly 90% of the bacteria in milk
• Including the more heat resistant - Tubercle bacilli
• It does not kill bacterial spores.
• It does not kill the thermoduric bacteria.
• Pasteurization of milk is determined by:
1. Phosphatase test
• Alkaline Phosphatase (ALP) is an enzyme naturally present in all raw milk
• Used as an indicator of proper milk pasteurization.
• Complete pasteurization will inactivate the enzyme .
2. Coliform count
3. Standard plate count
Steam under pressure /Autoclave/steam sterilizer (>100oC)
• Most effective sterilizing agent for

• dressing
• instruments
• laboratory wares
• media and pharmaceutical products
• aqueous solutions.
• Not for sharp instruments
• Done at:
• Temperature of 121oC
• keeping chamber pressure of 15lb per square inch
• For 15 min.
• 126oC
• 20lbs psi
• for 10 min
• on 133oC
• 30 lbs psi
• for 3 min.
• Biological indicators
• Sporesof Bacillus stereothermophilus (Geobacillus stearothermophilus) are used.
• Spores of Bacillus subtilis and Bacillus pumilis are also used.
122. Mucormycosis
Introduction:
• Opportunistic mycosis caused by fungi of class zygomycetes.

• Mucor and rhizopus species are the most common
Epidemiology
Risk factors
• acidosis
• diabetic ketoacidosis
• leukemia
• AIDS
• DM
• lymphomas
• Long-term desferroxamine therapy
• Immunosuppression due to steroids or cytoxic drugs
Associated conditions
• Central artery occlusion (Orbital mucormycosis)
Symptoms
• Intitially, the disease runs a subtle course with only fever and rhinorrhea.
• Later on, it invades the orbit and intracranial cavity:
• It has marked predilection for vascular invasion:
• leading to widespread thrombosis, tissue necrosis, and gangrene.
• Characteristic nasal finding:
• Dark necrotic turbinate
• Surrounded by pale mucosa blackish discharge and crusts.
• M/C site is middle turbinate followed by middle meatus and septum.
Laboratory
• irregular, non-septate hyphae branching at wide angles

• filamentous
Pharmacologic
• amphotericin B (must act quickly)
123. Adenovirus
Classification
• Group: Group I(ds DNA)

• Family:Adenoviridae
Morphology
• DNA virus
• double-stranded and linear
• non-enveloped
• Space vehicle (hexagonal shape) shaped
Disease conditions
respiratory disease in children :
• Serotype- 1,2,5,6
• MC in children with rhinitis
• ARD in military recruits
• serotypes 4,7,21
• Common cold/coryza:
• MC cause
• acute respiratory disease:
• Serotype 4,7
• in adult MC
• Follicular (swimming pool)conjunctivitis
• Serotypes- 3,7
• Epidemic keratoconjunctivitis(shipyard eye)
• Serotypes- 8,19,37
• gastroenteritis
• Serotypes- 40,41
• Hemorrhagic cystitis
• Serotypes-11,21
• Pharyngoconjunctival fever
• Serotypes-3,7
Oncogenic virus:
• Type 12 and 15 produces sarcoma

• When inoculated into baby hamster
• However there is no evidence relating to natural malignancy in human.
124. Aspergillosis
Introduction
• Aspergillus fumigatus is the most common cause of aspergillosis.

• Aspergillus is a mould with septate
• Dichotomous branching hyphae.
• Ability of A. fumigatus to grow at 45oC helps to distinguish it from other species.
• Not a contagious disease
Clinical manifestations of aspergillosis
1. Allergic bronchopulmonary aspergillosis:
• occurs in patients with preexisting asthma or cystic fibrosis.
2. Endobronchial saprophytic pulmonary aspergillosis (Aspergilloma):
3. Invasive Aspergillosis
4. Allergic sinusitis
• Most common cause of fungal sinusiti
5. Aspergillosis in AIDS
6. Extrapulmonary
• Otomycosis
• Aspergillus Niger 90% cases
• Endophthalmitis
• Satellite lesions in eye
Hypersensitivity Reaction to Aspergillus
• Bronchial Asthma, ABPA and Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis)
In Atopic Individual
• Allergic Bronchial Asthma and ABPA

• The immune response is IgE mediated
In Non atopic Individuals
• Extrinsic Allergic Alveolitis (Hypersensitivity penumonitis)

• Not IgE mediated.
• May be mediated(type IV) or immune complex (Type III) reactions.
Diagnostic features of allergic bronchopulmonary aspergillosis (ABPA)
• Main diagnostic criteria

• Clinical history of Asthma
• Pulmonary infiltrates (transient /fleeting or fixed)
• Peripheral eosinophilia (> 1000 /,uL)
• Immediate skin reactivity to Aspergillus antigen (wheal and flare response)
• Serum precipitins to A. fumigatus
• Elevated serum IgE levels(>100Ong/ml)
• Central /proximal bronchiectasis
• Secondary diagnostic criteria
• History of brownish plugs in sputum
• Identification/culture of A., fumigatus from sputum
• Late skin reactivity to aspergillus antigen - CMDT
• Elevated IgE (and IgG) class antibodies specific for A. fumigatus
Histopathology
• Microscopically, the fungus may appear as a tangled mass within the cavity.
• The organisms are identified by their characteristic morphology—
• Thin septate hyphae with dichotomous branching at acute angles
• Stain positive for fungal stains such as PAS and silver impregnation technique.
• The wall of the cavity shows chronic inflammatory cells.
Treatment
• First choice drug for aspergillosis :

• Voriconazole/Amphotericin B
• Second choice drug for aspergillosis
• ltraconazol
125. Nocardia
Morphology
• Gram positive
• Show true branching both in culture and in stains from clinical lesions.
• Aerobic
Staining
• Nocardia is an acid fast organism

• Acid fast stains commonly used for staining of Nocardia are:
• Ziehl - Neelson stain
• Differentiated from Actinomyces by Ziehl Neelsen (Z.N.) stain
• Kinyon acid fast stain
• Fite faraco stain
• Mucin stains can also stain Nocardia.
• Examples of mucin stain are ?
1. Mucicarmine stain
2. Alcian blue stain
Culture
• Use paraffin as carbon source so paraffin baiting is used for isolation.
• MC species associated with invasive disease N. asteroids

• Manifestation divided into:
• Respiratory tract disease
• MC is pneumonia.
• Extrapulmonary dissemination
• MC site brain
• Usually supratentorial
• Subacute abscess
• Typical manifestation is subacute abscess usually supratentorial.
• Actinomycetoma
• Disease begins as a papule or a nodule
• Slowly progress into multiple abcesses and sinus tracts ramifying deep into the tissue
• X-ray of the foot shows destructive changes in the underlying bone
Treatment
• Trimethoprim-Sulfamethoxazole-
• DOC
126. DERMATOPHYTES
Introduction
• Infect only superficial keratinized tissue

• Skin(stratum corneum), hair and nails.
• Cause a variety of clinical conditions, collectively known as dermatophytoses, tinea or ring worm.
Classification:
• Three genera:
• Trichophyton
• Causes black dot ring worm
• Microsporum
• Epidermophyton
Distribution:
• M. distortum
• Australia, USA
• Not in India
Morphology
• In lesions appear as :
• Hyphae
• Arthrospores
• On sabouraud's agar form :
• Septate hyphae
• Asexual spores (micro and macroconidia)
• Differentiation is based mainly on macroconidia.
Trichophyton Microsporum Epidermophyton

Site Hair, Hair Skin
Skin Skin Nail
Nail
Microconidia Abundant Single Absent
(multicellular)
Arranged in clusters along
hyphae
Macroconidia Relatively scanty Single Groups of 2 or 3
Elongate Multicellular Club shape/pear

shaped
Blunt ends Spindle shaped
Pencil/Cylindrical shaped
• Clinical Manifestation
Dermatophytoses Causative agent

Tinea capitis Microsporum, Trichophyton most species
Favus T. schoenleinii T. violaceum, M. gypseum
Tinea barbae T. rubrum, T. mentagrophytes, T. verrucosum
Tinea imbricata T. concentricum

Tinea corporis T. rubrum and any other dermatophyte
T. cruris (Tock itch) E. floccosum, T.rubrum

T pedis (Athlete's foot) E. floccosum, T rubrum
Ectothrix hair infection Microsporum species, T. rubrum
Endothrix hair infection T. schoenleinii, T. tonsurans, T. violaceum(INDIA)
• Treatment
• Topical antifungal agents
• Oral griseofulvin is DOC.
• 3 months duration for fingure nail dermatophytosis.
127. Blastomycosis

• Blastomycosis is a chronic infection caused by Blastomyces dermatitidis.
• B. dermatitidisis dimorphic fungi
• B. dermatitidis yeast like
• Infection is largely confined to the North American continent
• "North American blastomycosis".
• Clinical manifestations:
• Self limited pneumonia
• Skin lesions
128. Mumps Virus
Mump Virus
• Paramyxovirus.
Source of infection
• Clinical and subclinical cases

• Incubatory carrier seen
• Man is the only natural host
Incubation period
• 14-18 days
Clinical manifestation
Parotitis
• Most common manifestation of mumps (in all age groups)

• 30-40% of infections are sub-clinical
• Characteristic presentation is pain and swelling in either one or both parotid glands.
Orchitis
• 2nd most common manifestation of mumps

• Seen in postpubertal males.
• Half of these infections result in testicular atrophy, and in rare cases sterility can follow
Aseptic meningitis
• Common manifestation of mumps more common in children .

Dacryoadenitis
• Most common ocular manifestation of mumps.
Complications of mumps
• Sterlity
• Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.
• Mild forms of meningitis.
• Oophoritis (inflammation of ovaries).
• Pancreatitis , manifesting as abdominal pain and vomiting
• Encephalitis, very rare
• Profound (91 dB or more) but rare sensorineural hearing loss, uni- or bilateral.
• Acute unilateral deafness occurs in about 0.005% of cases
• Thyroiditis, neuritis, hepatitis, myocarditis etc.
Mumps vaccine
• 95 % effective live attenuated vaccine.

• Widely-used live attenuated mumps vaccine strains include :
• The Jeryl-Lynn
• Contraindicated in pregnancy
• Routine immunization:
• For children over 1 year of age
• Either alone or in combination with other virus vaccines
• A second dose is recommended for children at 4-6 years of age i.e., before starting the school
129. Measles
Introduction
• Maximum incidence in 6m-3 year age group
Virus
• A paramyxovirus
• Only one strain causes infection
• Nucleocapsid proteins
• Protect the genome RNA from nuclease digestion
• Recognize the location in the cell membrane for budding
Transmission

• Spread through respiration
• Contact with fluids from an infected person's nose and mouth
• Either directly or through aerosol transmission
• Highly contagious
SAR
• Approximately 80%.
• Formula to Calculate SAR
• No. of exposed persons developing the disease within the range of incubation period/Total number
of exposed”susceptible” contacts*100
Incubation period
• An asymptomatic incubation period occurs nine to fourteen days from initial exposure
Infectivity
• Infectivity lasts from two to four days prior

• Until two to five days following the onset of the rash (i.e. four to nine days infectivity in total).
Isolation
• After the appearance of rash, prophylactic isolation of measles case is necessary for a minimum of 5
days
Prodromal/Pre-eruptive stage
• Koplik's spot
• A day or two before the appearance of rash
• Appear on the buccal mucosa opposite the first and second upper molars.
• Pathognomonic enanthem of measles.
Eruptive Stage
• Rash appears on the 4th day from fever.

• It begins at hairline and behind the ear,and spreads downward rapidly.
• Fever usually resolves by 4th day after the onset
Post measles stage
Complications

• Pneumonia is the most common life-threatening complication
• Mortality in developing countries may be as high as 10 to 15%
• Otitis media
• Most common complication
• Acute encephalitis (and rarely subacute sclerosing panencephalitis)
• The mortality rate in encephalitis associated with measles is about 10-20 %
• Rarest complication
Warthin–Finkeldey cell :
• Giant multinucleate cell found in hyperplastic lymph nodes

• Seen early in the course of measels
• Under the light microscope, these cells consist of a large, grape-like cluster of nuclei
130. Measles- Vaccination and WHO's measles elimination strategy
Measles vaccine :
• Type:
• Live attenuated, lyophilized (Freeze dried) vaccine
• Route:
• Subcutaneous
• Age of administration in National Immunisation schedule (India):
• India started 2-dose vaccination strategy for measles
• 9 months (can be lowered to 6-9 months in epidemics & malnutrition)
• Second dose of measles is also given at 16-24 months.
• Diluent for Reconstitution:
• Distilled Water or sterile water
• Use within 1hr after reconstitution with diluent
• Side effect
• Measles (& MMR) vaccine can lead to Toxic Shock Syndrome
• Measles vaccine is contraindicated in pregnancy
• Measles vaccine also contains:
• Sorbitol and hydrolyzed gelatin as stabilizers
• Small amount of neomycin as preservative
• People with a history of an anaphylactic reaction to neomycin, gelatin or other components of the
vaccine should not be vaccinated
• In epidemics measles:
• Vaccine is to be given within 3 days of exposure
• Duration of Protection: Lifelong
• IP of vaccine-induced measles: 7 days
Immunoglobulin
• Measles immunoglobulin is also available for post exposure prophylaxis.
• Non immunized pregnant women coming in contact with measles may be protected by:
• Intramuscular injection of 5ml of immune serum globulin within 3 days of exposure.
Elimination
• WHO defines elimination of measles as the absence of endemic measles for a period of 12 months
in the presence of adequate surveillance.
• One indicator of measles elimination is a sustained measles incidence < 1/100, 000 population.
• In 2005, the World Health Assembly set a goal:
• Achieving a 90% reduction in global measles mortality by 2010 as compared with level in 2000.
• WHO's measles elimination strategy comprises a three part vaccination strategy, i.e. :-
i) Catch-up
• One-time, nationwide vaccination campaign targeting usually all children aged 9 months to
• 14 years regardless of history of measles disease or vaccination status.
ii) Keep-up
• Routine services aimed at vaccinating more than 95% of each successive birth cohort.
iii) Follow-up
• Nationwide vaccination every 2-4 years
Epidemic of measles :
• Occur if proportion of susceptible children is > 40%

• Measles is introduced in a virgin community, it infects > 90% of children
• Vaccination age can be lowered to 6 months in epidemics.
• Measles shows a cyclic trend with epidemic every 2-3 years.
• Eradication of measles requires vaccine coverage >95%
131. Giardia lamblia
Giardia intestinalis/ Giardia lamblia
• Inhabit duodenum, jejunum & upper ileum

• Infection is common in:
• Selective IgA deficiency
• G. intestinalis exists in 2 stages – trophozoite & cyst

Morphology of Giardia lamblia trophozoite
• Pear shaped, rounded anterior end, posterior end pointed (looks like monkey face)
• Bilaterally symmetrical:
• 2 nuclei, 2 axostyles, 4 pairs of flagella (2 anterior, 2 posterior, 2 ventral, and 2 caudal)
Morphology of Giardia lamblia cysts
• 4 nuclei present, either clustered at on end or present in pairs at opposite ends
Infective form
• Mature cyst passed in feces of man
Routes of transmission
• Feco-oral
• Ingestion of contaminated water – most important
• Ingestion of contaminated food
• Person to person – day care, nursing homes, mental asylums (poor hygiene)
• Sexual – sexually active homosexual males
Pathology
• Do not invade tissues

• Feed on mucous secretions
• May localise in biliary tract to avoid the acidity of duodenum
• Cause inflammation of duodenum & jejunum
• Cause malabsorption as the parasite coats the mucosa & damage epithelial brush border
• Stool contains large amounts of mucous & fat but no blood
132. Giardiasis
Giardiasis
• Acute:
• Self-limiting infection
• Acute watery diarrhea
• Abdominal cramps
• Bloating
• Flatulence
• Stool is profuse & watery in earlier disease
• Frothy
• Voluminous, foul-smelling & greasy(steatorrhoea) later
• Chronic
• Chronic diarrhea with malabsorption syndrome
• Steatorrhoea
• Chronic Recurrent intestinal giardiasis/Intractable diarrhea
• Common variable deficiency is associated with it.
• Hypogammaglobulinemia
• Reduction in all classes of immunoglobulins
• But sometimes only IgG is reduced.
• Traveller's diarrhea
Laboratory Diagnosis
Microscopy
• The gold - standard for diagnosis of giardiasis is:

• Microscopic demonstration of the trophozoite, cyst or both in faeces.
• Direct Wet Mount
• Trophozoite with falling leaf motility in saline mount
Sting Test
Treatment
• Nitroimidazole derivatives –
• Metronidazole
• Tinidazole drugs of choice
Milk
• Human milk is protective against Giardiasis

• Bile salt stimulated lipases kill amoeba and Giardia.
133. Cryptococcus neoformans
Cryptococcus neoformans
• Most common cause of fungal meningitis:

• In immuno-compromised patients (such as people with AIDS).
Morphology
• Yeast with prominent polysaccharide capsule.

• Unicellular
• Possess urease.
• It reproduces by budding
• It does not produce pseudohyphae
Serotypes
• Four capsular serotypes - A, B, C and D

• Abundant in pigeon droppings :
• Contain serotype A and D.
• Eucalyptus tree contains serotype B.
Culture:
• Sabouraud’s dextrose agar

• Temp:
• Room temperature or 37 °C.
Pathogenesis
• Cryptococcus has predilection for lung and meningis.
Virulence Factors of Cryptococcus neformans
• Capsule:
• Anti-phagocytic
• Phenoloxidase:
134. Cryptococcosis
Risk Factors
• Cryptococcosis is most often seen in immune-compromised patients with impaired T cell immunity
• AIDS
• Solid organ transplantation (Renal transplant)
Cryptococcal meningitis:
• Hematogenous spread results in subacute or chronic meningitis or meningoencephalitis

• Lung infections:
• Primarily cause lung infection
• Reactivation of old healed lesion may occur.
• Cryptococcal lung lesions do not calcify.
• Skin and other infections:
• Sometimes skin, lymph nodes, bones are involved.
• Superficial skin lesion.
Laboratory diagnosis
• Maltese cross pattern under polarised light is seen
India ink preparation
• Differentiates cryptococcus from other fungus.

• Demonstration of heavily capsulated yeast cells in CSF, exudates and urine establishes the
diagnosis.
Identification:
• Identified by urease production and carbohydrate assimilation test
Detection of Antigen:
• Latex agglutination test is most useful in detection of cryptococcal polysaccharide antigen.
Treatment
• Cryptococcal meningitis :
• Treated for two weeks with intravenous Amphotericin B
135. Poliomyelitis
Clinical manifestation:
• Few suffer from minor illness, very few suffer from meningitis and less than 1% suffer from
major paralytic disease
1. Asymptomatic illness:
• In most of the infection is asymptomatic and self-limiting

• 99% cases
2. Abortive poliomyelitis:

3. Non paralytic poliomyelitis
4. Paralytic Poliomyelitis:
• Less than 1% patients suffer from major paralytic poliomyelitis

• Paralysis in polio is asymmetric, descending, non-progressive and LMN type.
• Flaccid paralysis: motor neuron damage
• Lower motor neuron lesion of the anterior horn cells of the spinal cord and affects the muscles of
the legs, arms and/ or trunk
• Bulbar paralysis: respiratory paralysis
5. Post-poliomyelitis muscle atrophy
6. Death is rare. And if occur it is due to respiratory paralysis
• Lab diagnosis:
• Specimen: nasal secretion, faecal samples, throat swab, CSF
• Electron Microscopy: virus detection
• Virus isolation from stool
• Prevention and control:
1. Vaccination
i. Inactivated Polio Vaccine (Salk type – killed):
• Effective against all serotype of poliovirus

• Produces circulatory antibody
• Does NOT require stringent refrigeration
• NOT effective in an epidemic
ii. Oral Polio Vaccine (Sabin type – live):
• Developed by Albert Sabin in 1962

• The vaccine contains :-
1. Over 300,000 TCID 50 of type 1 poliovirus
• Dose 2 drop (0.1 ml)
• Schedule in National Immunization Programme of India.( 5 doses)
Dose Age
1. OPV-0 (Zero dose)- At birth

2. OPV-1 -6 weeks
3. OPV-2 -10 weeks
4. OPV-3 - 14 weeks
5. OPV-B (Booster dose) - 16-24 months
• On administration, the virus multiplies in the intestine
• Induces intestinal and systemic immunity
• Intestinal immunity prevents infection of intestine by Poliovirus
• Vaccine virus is excreted in the feces and can infect the unimmunized and induce immunity
• Thus widespread herd immunity results, even if only approximately 66% of the community is
immunized (100% coverage is not required).
• In endemic countries monovalent oral poliovirus type I vaccine (MOPvI) is introduced to eliminate
the last reservoir of poliovirus
• Nevertheless, several studies show that among breastfed infants who are fed OPV in the first three
days of life, 20-40 percent develop serum antibodies and 30-60 percent excrete vaccine virus.
• Molar concentration of certain salts MgC12, Na2So4 protect polio virus from heat inactivation
• As it prevents heat inactivation mgCl2 can be added to polio vaccine so that it can be stored at a
higher temperature.
Complications of OPV
• In the course of their multiplication in vaccinated children, and rare cases of vaccine associated
paralytic polio have occurred in -
• Recipients of the vaccine
• Thier contacts
Vaccine derived polio virus (VDPV)
Types of VDPV:
• c-VDPV: Person-to-person transmission in community

• i-VDPV: Isolates from immunodeficient persons
• a-VDPV: Ambiguous from health person or sewage isolates
IM injections and increased muscular activity lead to increased paralysis
136. Polio Virus
• Poliovirus 1:
• Most common and virulent type.
• Frequently isolated from patients with poliomyelitis and causes epidemics
Mode of transmission
• Human are the only natural host for Poliovirus

• primarily by: Faeco-oral route by Ingestion of virus contaminated food and water
• In the faces, the virus is excreted commonly for 2 to 3 weeks, sometimes as long as 3 to 4 months
• Droplet infection, inhalation
Reservoir of infection
• Man is the only reservoir. Most infections are subclinical and play a dominant role in spread of
infection.
• It is estimated that for every clinical case, there may be 1000 subclinical cases in children and 75 in
adults.
Period of communicability
• 7 to 10 days before and after onset of symptoms.
137. Haemophilus influenzae
Habitat
• Mucous membrane of the upper respiratory tract of humans.
Morphology
• Slender, short, gram-negative rods or coccobacillus

• Capsules are present and important in pathogenicity.
Cultural characteristics
• Requires 2 accessory growth factors:

• A head stable growth promoting substances present in Red Blood Cells (X-Factor)
• A heat labile vitamin like substances (V-Factor).
Antigenic Properties
• Major surface antigen

• Capsular polysaccharideOuter membrane protein (OMP)
• Major antigenic determinant
• Based on which, it is typed into six capsular types a to f
• While noncapsulated strains are nontypable
• Isolates from acute invasive infections belong to 'b" mainly.
• Lipo-oligosaccharide
• Serotyping of H. influenzae ie done by agglutination or quelling reaction
Pathogenicity
Haemophilus influenza b (Hib)
• Major cause of childhood infectious disease.

• Meningitis: Primary bacteremia
• M.C invasive disease of H influenza
• children age 5 months to 5 years.
• MC Complication of its meningitis - Subdural effusion
• Post-splenectomy infection(rare)
• Pneumonia
• Acute epiglottitis
• Arthritis.
• Acute bacterial rhinitis:
• MC cause of bacterial rhinitis
Non-Capsulated influenzae (Nc-hi)
• Causes otitis media, conjunctivitis and sinusitis

• Causes chronic bronchitis in adults
Treatment
• DOC for H. influenzae meningitis Cs Third generation cephalosporin.

• Ceftriaxone or cefotaxime
138. Pulse Polio and Polio eradication
Polio Epidemic
• An epidemic of polio is defined as 2 or more local cases caused by same virus type in any 4 week
period.
• So, it has following features -
i) 2 or more cases of polio
ii) Caused by same virus type
iii) Within 4 week period

Pulse polio immunization (PPI)
First Round of PPI
• On 9th Dec 1995 and 20th Jan 1996.
Polio Free
• As of 25th Feb 2012 India was removed from the list of polio endemic countries by the WHO
• On 27th March 2014, the Regional Certification Commission of WHO certified South-East Asia
Region of WHO, which includes India, as polio free.
• Each region can consider certification only when all countries in the area demonstrate the absence
of wild poliovirus transmission for at least three consecutive years.
AFP Surveillance
• Cases of AFP are classified as Polio if :

• Wild polio virus is isolated from any stool specimen.
• Cases of AFP without isolation of wild polio virus may be classified as 'polio compatible' if :
• Stool specimens were inadequate and
• Residual weakness was present 60 days after onset of paralysis or 60-day follow-up was not done
(due to death or absence)
• WHO recommends the immediate reporting and investigation of every case of AFP in children aged
less than 15 years, and collection of 2 stool samples (not 3 samples) for analysis
• In India, even a single case is treated as an outbreak and preventive measures are initiated, usually
within 48 hours of notification of the case.
• Throat swab (pharyngeal swab) and stools are the samples from which poliovirus can be isolated
for diagnosis.
Total probability of full or partial recovery following polio :
• P (full or partial recovery)= P(full recovery)+ P(partial recovery)
139. Neisseria Meningitidis
• Ferments glucose and maltose with acid production is the differentiating feature of Neisseria
gonococcus from Neisseria meningitides
• Neisseria meningitides can penetrate normal cornea
• It is most common organism which can contaminates crowded army camps
• Lipopolysaccharide is responsible for the production of overwhelming septicemic shock
complicating bacteremia
• Most common cause of meningitis in children
• Meningitis with rash is seen.
• Fulminant meningococcemia (purpura fulminans or Waterhouse - Friderichsen syndrome caused by
N meningitides
• A quadrivalent vaccine constituted by polysaccharides of serotypes A,C,Y and W-135 : for children
and adults
• Penicillin DOC for meningococcal infections
140. Campylobacter jejuni
Morphology
• Gram negative
• Comma shaped
• Motile with a single polar flagellum → DarƟng or tumbling moƟlity
Biochemical reactions
• Catalase and oxidase positive
Source:
• Cattle, Chicken, Dogs etc
Campylobacteriosis
• Symptoms (within 2-5 days of exposure):

• Watery foul smelling diarrhea (may be bloody)
• Nausea and vomiting (may seen)
• Cramping
• Severe abdominal pain
• Fever
Campylobacter infections are also associated with some autoimmune diseases:
1. Guillain-Barré Syndrome
2. Reactive arthritis
3. Reiter’s syndrome
Laboratory diagnosis:
Specimen:
• Diarrhoeal or dysenteric specimen containing blood, pus and mucus.

Culture
• Compylobacter jejuni is thermophilic, growing well at 42°C.

• Inoculated plates are incubated under
• Microaerophilic conditions
• With an atmosphere of 5% 02, 10% CO2 and 85% N2 at 42°C.
• . Plating media commonly used are
• Skirrow's medium
• Butzler's medium
• Campy BAP medium
• Stool examination shows coma shaped organism with RBC and WBC
141. Plasmodium
• Infective form Sporozoites

• Mode of transmission The mosquito ingests gametocytes in its blood meal.
• Bite of an infected mosquito, Anopheles stephensi and Anopheles culicifacies
• Anopheles stephensi is the major malaria vector in India
Phases of Development in Man
Inside the liver (tissue phase)
• Pre-erythrocytic schizogony
• Exo- erythrocytic schizogony
• Cause of relapse.
• This Phase is absent in P falciparum.
Inside the RBCs (erythrocytic phase)
• Erythrocytic schizogony
• Gametogony
Morphological forms seen in Humans
In RBCs :
• Trophozoites – ring form/Band forms
Incubation period
• P. vivax, P. ovale,P. falciparum:10 to 14 days)

• P. malariae:18 days to 6weeks
• Fever is the hallmark symptom of malaria and is induced when the erythrocytes rupture and
merozoites are released.
• Plasmodium falciparum It infects RBCs of all ages
• P vivax and ovale – young
• P malariae –old
• Causes rosetting, sequestration
142. Bacillus cereus
Diarrheal Syndrome
• Associated with proteinaceous foods, vegetables, sauces and puddings

• Incubation period: 8 - 24 h (average of 10 -12 h)
• Profuse watery diarrhea, abdominal pain and occasional nausea
• Clinical illness very similar to C. perfringens food poisoning
Emetic Syndrome
• Associated with rice (particularly fried rice)

• Incubation period: 0.5 - 5 h
• Nausea, vomiting and occasional diarrhea
• Clinical illness very similar to S. aureus food poisoning
143. Plasmodium: Clinical Features (Malaria)
Genetic factors protecting against Malaria
• Sickle cell anaemia –

• Sickle-celled RBCs are removed by the spleen before the development of schizonts
• Duffy blood group negative individuals –
• Duffy blood group Ag is the receptor for the attachment of merozoites of P.vivax
• Newborn infants –
• Natural protection for 1st few months of life due to high conc. of HbF in their RBCs.
• Para amino benzoic acid of breast milk prevent the infection
Clinical features
• P. falciparum:
• Malignant tertian = Pernicious malaria
• The most virulent plasmodium species.

Symptoms
• Quartan malaria – every 72 hrs

• Tertian malaria - every 48 hrs
• The major organs that are directly involved due to parasitic infestations are
• Spleen, Liver, Brain.
• The organs which are involved secondarily
• Heart (Hypoxic lesions)
• Lung (Pulmonary edema)
Falciparum Malaria
• Multiple infections of the red blood cell

• More than one parasite (from 2 to 6) invading a single red blood cell is very common with P
falciparum.
• Most pathogenic of human malaria species
• Does not affect heart or lungs.
• Severe falciparum malaria is associated with
1. Pernicious malaria /cerebral malaria
2. Blackwater fever
3. Anaemia
4. Hypoglycaemia
5. Hypotension
6. Complications in pregnancy
Black waters Fever
• Sometimes seen in falciparum malaria
Recurrences in Malaria
1. Recrudescence –
• Seen in P. falciparum & P.malariae

• Recurrence of sexual parasitemia after completion of treatment
2. Relapse
• Occurs due to a special form of parasites – hypnozoites.

• Hypnozoites are the sporozoites that remain dormant after infecting liver
• Seen in P. vivax

144. Toxoplasma gondii
• The parasites reproduce in the cat's small intestine and form oocysts, which are thick-walled cysts
containing zygotes.
• Human, sheep, pig etc intermediate host.
Transmission
• The freshly passed oocyst is not infectious.

• It becomes infectious only after development in soil or water for few days-
• Infective forms
1. Sporulated oocyst from contaminated soil with cat faeces.
2. Tissue cyst containing bradyzoites in undercooked pork, beef or meat.
• Transmission Routes
1. Ingestion of sporulated oocyst (Sporocyst) or tissue cyst containing bradyzoites (most common)
oral route.
2. Blood transfusion.
3. Kidney or heart transplant.
4. Transplacental transmission.
• First trimester-
• The incidence of transplacental infection is lowest (15%
• But the disease in the neonate is most severe.
• Third trimester,
• Incidence of transplacental infection is greatest (65%)
• But the infant is usually asymptomatic at birth.
145. Plasmodium: Diagnosis
• Microscopy – detecting & identifying malarial parasites in peripheral blood films.

• Concentrating parasites in venous blood by centrifugation when they cannot be found in blood
films
• Using a rapid malaria Ag or enzyme detection test
• Other tests – Hb, PCV, Blood glucose, total WBC & platelet count.
Thin films :
• To confirm the Plasmodium species
Identifying Blood Film
• Look for the different morphological forms of parasite in blood smear:

1.Trophozoites / ring forms
2.Schizont(Not seen in Plasmodium falciparum)
3.Gametocytes
Schüffner's dots
• Exclusively found in Plasmodium ovale and Plasmodium vivax

• Morphologic alterations in infected host erythrocytes that are visible as multiple brick-red dots
Maurer's dot:
• Fine granular precipitates or irregular cytoplasmic particles present in red blood cells infected with
the trophozoites of Plasmodium falciparum
Immunochromatographic test
• Three tests are available commercially

• Detects HRP2 Ag (Histidine-rich protein) or specific pLDH (parasite lactate dehydrogenase) or Pan
malarial plasmodium aldolase
• Both HRP2 & pLDH are produced by the parasites during their growth & differentiation in RBCs.
146. Malaria: Treatment
Stage specificity of antimalarial drugs
1. Pre-erythrocytic schizogony
• Drugs acting on this stage will prevent infection of RBC and clinical attack of malaria causal
prophylaxis.
• Drug are
• Proguanil & Tetracycline → for falciparum.
2. Primaquine for all species
• Slow acting are →

• Pyrimethamine, proguanil, sulfonamides, tetracyclines.
3. Gametogony
• Primaquine & artemisinins → for all species

• Chloroquine & quinine → for P.vivax
4. Exoerythrocytic schizogony
• Primaquine is the only drug which acts on exoerythrocytic schizogony.
Treatment of falciparum malaria
• Artemisinin derivatives are the drug of choice for any type of falciparum malaria
i)Uncomplicated
ii)Complicated/severe/cerebral
• Amongst artemisinin derivatives, artesunate is the DOC.

• Other drugs used for severe/complicated/cerebral falciparum malaria: Artemether , Quinine ,
Quinidine.
Chemoprophylaxis of malaria
• Chloroquine
• DOC for chemoprophylaxis in chloroquine sensitive P. falciparum areas.
• Chloroquine 300 to 310 mg once weekly, and Proguanil 200 mg once daily
• Atovaquone/Proguanil
• Used in areas with chloroquine or mefloquine-resistant P. falciparum.
• Doxycycline
• Used in areas with chloroquine or mefloquine-resistant P. falciparum.
• Mefloquine
• Used in areas with chloroquine-resistant P. falciparum
• Hydroxychloroquine
• Alternative to chloroquine in areas with chloroquine-sensitive P. falciparum
Drugs for chloroquine resistant malaria
• Sulfadoxine +Pyrimethamine + Artesunate(DOC)

• Artemether + Lumefantrine
• Quinine + Tetracycline or doxycycline +Primaquine
• Halofantrine
• Mefloquine + Artesunate
Treatment of resistant falciparum malaria in children
i) Child < 8 years of age
• Quinine + Clindamycin
• Or Atovaquone + Proguanil
Treatment in pregnant women

• If plasmodium is sensitive to chloroquine chloroquine is the DOC.
• For chloroquine resistant strains Quinine
147. Nipah Virus
• Nipah virus (NiV) infection is a newly emerging zoonosis that causes severe disease in both animals
and humans.
• Family: Paramyxoviridae
• Seen in India, outbreak 2001 West Bengal.
• Nipah virus is associated with epidemics of Encephalitis
148. Toxoplasma gondi - Structure, Life Cycle and Transmission
Toxoplasma Gondi
• Obligate Intracellular Parasite Protozoan

• Three Forms
• Trophozoites
• Tissue Cysts
• Oocytes
Trophozoites- Toxoplasma gondi
• Non Infectious seen during Acute Stage

• Stained by GIEMSA STAIN
• Can Invade all nucleated cells and form rapidly multiplying tachyzoites
• Crescentic parasites distend the cells which are called psuedocyst or pseudo colony
Tissue Cyst- Toxoplasma gondi
• Formed during Chronic Phase in various organ ( CNS & Muscles)

• Contains slowly multiplying rounded parasite called Bradyzoites
• Stained by SILVER STAIN
Oocyte-- Toxoplasma gondi
• Develops in intestine of DEFINITIVE HOST (Cat)

• Contains two sporocysts with sporozoites inside

LIFECYCLE- Toxoplasma gondi– Important Points
• Most Cats Shed Oocytes in Feces only once in a lifetime for 1-2 weeks
• Oocytes Becomes infective only after 5 days (After Sporulation)
Transmission in Humans- Toxoplasma gondi
• Human, sheep , pig (etc) are intermediate host

• Ingestion of sporulated oocytes or tissue cysts containg bradyzoites is Most Common Route
• Blood Transfusion / Renal / Heart Transplant
• Transplacental Transmission
• Incidence of Transplacental Transmission in 1st Trimester is 15% but Leads to severe disease
• Incidence of transpalcental transmission in 3rd Trimester is 65% but mostly asymptomatic
149. Sterilization Methods( Radiation,Chemical Agents and Sporicidal Agents)
Important Definitions
• Sterilization: the process by which an article, surface or medium is freed of all living microorganisms
(vegetative or spore state)
• Antisepsis: prevention of infection, by inhibiting the growth of bacteria in wounds or tissues
Vapour phase disinfectants
1. Ethylene oxide.
• It is used to sterilize heat labile articles such as bedding, textiles, rubber, plastics, syringes,
disposable petri dishes, complex apparatus like heart-lung machine, respiratory and dental
equipments.
• Efficiency testing is done using Bacillus subtilis var niger.
2. Formaldehyde gas
• For fumigation of operation theaters and other rooms
3. Beta-propiolactone
Formaldehyde
• Active against the amino group of protein molecule

• Bactericidal, sporicidal and virucidal
• 2 % solution ,Cidex is used for sterilization of fiberoptic scopes (cystoscope,bronchoscope)

Gluteraldehyde
• It is a high-level disinfectant
• Disinfectant for heat-sensitive equipment such as dialysis instruments, surgical instruments, suction
bottles, bronchoscopes, endoscopes, ear, nose, and throat instruments,spirometry tubing,
transducers, anesthesia and respiratory therapy equipment and reuse of laparoscopic disposable
plastic trocars .
• Concentrations -Solutions range in concentration from 2.4 – 3.4%.
Radiation
• Non ionizing - UV rays and IR rays

• Ionizing (Cold sterilization) - X-rays, gamma rays(most common), Cosmic rays
• Materials which are destroyed by heat such as rubber or plastic disposable goods, disposable
syringes, surgical catgut, bone and tissue grafts, adhesive dressings are sterilised by ionising
radiations
Dyes
• Acridine and aniline dyes
Halogens
• Chlorine is used commonly as hypochlorites

• Sterilization & disinfection of blood spills is done by Sodium hypochlorite.
Complete sterlizing agent (with sporicidal activity) : -
• Ethylene oxide
• Prophylene oxide
• Ozone
• Glutareldehyde
• Formaldehyde
• Halogen (sodium hypochlorite, Iodine,Hydrogen peroxide,phenol and cresol, Iodophore, chlorine)
• Peracetic acid
• P-propionolactone
• Chlorhexiding
150. Disinfectant
Disinfectants
• Destroy some, but not necessarily all organisms.

• The category is further divided into subcategories:-
i) High level disinfectants
• Examples are :-2% gluteraldehyde, 8% formaldehyde, 6-10% hydrogen peroxide and ethylene oxide
gas.
ii) Intermediate level disinfectants
• Examples are :-0.5% iodine, 70-90% ethanol and isopropanol, chlorine compounds (hypochlorite),
some phenolic compounds and iodophor based disinfectants.
iii) Low level disinfectants
• Examples are :- quarterly ammonium compounds, mercurials,some phenolic compounds and

iodophores.
• Quaternary ammonium compounds are cationic detergents.
Determination the efficacy of a disinfectant
There is no reliable test available to determine the efficacy of a disinfectant.
• This is due to the number of parameters which influence disinfectant activity.

• Traditionally in such tests phenol is taken as the standard.
• Phenol coefficient:It is a measure of the bactericidal activity of a chemical compound in relation to
phenol.
Two important tests are :-
i) Rideal-Walker test
ii) Chick-Martin test
• In this, the disinfectant acts in the presence of organic matter (dried yeast or feces).
• Phenol is taken as standard
151. Hemolytic Streptococci- Group A, B, C, D and F
Group B Streptococci/Baby strep
• Streptococcus agalactiae colonizes in the genital tract of some women

• It produces two types of infection in the new born :
1. Early onset (within a week of birth) Infection is acquired from the maternal vagina

2. Late onset (2nd to 12th weeks) Infection is obtained from the environment
• Can cause neonatal meningitis and sepsis( MC cause)
• Biochemical test: S. agalactiae gives CAMP test positive, resistance to bacitracin and can hydrolyze
the hippurate.
• Diagnosis: is made by isolation and identification of organism from sterile site.
• The demonstration of gram positive organism in pairs or chain in buffy coat or other sterile fluid
indicates infection.
Group C Streptococci
• Group C beta hemolytic streptococci currently include S. dysgalactiae subsp. equisimilis and other
related strains
Group D Streptocci
• Include enterococci (e.g., Enterococcus faecalis and Enterococcus faecium) and nonenterococci (S.
bovis).
• Enterococci are members of normal flora of the colon.
• A beta hemolytic bacteria
• Resistant to vancomycin shows growth in 6.5% NaCI
• Non bile sensitive
• They can cause urinary, biliary and cardiovascular infections.
• There is a significant association between S. bovis bacteremia and endocarditis with carcinoma of
the colon and other colonic diseases.
152. Actinomyces and Actinomycosis
Actinomyces
Characterized by
• Contiguous spread,
• Suppurative and granulomatous inflammation, and
• formation of multiple abscesses and
• sinus tracts that may discharge sulfur granules
Morphology
• Anaerobic
• Thin, branching (filamentous)
• Gram positive bacillus.
• Morphologically Actinomyces colonies form fungus-like branched networks of hyphae
• Microaerophilic, grow best anaerobically. VERY fastidious.
Clinical manifestations:
Actinomycosis
• A disease characterized by the formation of abscesses in the mouth,lungs, or the gastrointestinal

tract
• Characterized by multiple abscesses and interconnecting sinus tracts that contain granules
of microcolonies imbedded in tissue elements
Cervicofacial
• Most common form of actinomycosis.

• The infection generally evolves as a chronic or subacute painless or painful soft-tissue swelling or
mass involving the submandibular or paramandibular region.
Thoracic
• This is an indolent, slow process involving the pulmomonary parenchyma and pleural space.
Abdominal
• The inflammatory process is a chronic, localized, and is preceded by the breaking of the integrity of
the gastrointestinal mucosa by intestinal perforated
• The ileocecal region is involved most frequently
Pelvic
• This is observed in women who had prolonged use of IUD, and may also occur from extension of
intestinal infect
Central nervous system (CNS)
• Rare
Treatment
• 1st choice-Penicillin or amoxicillin for six to twelve months
153. K. pneumoniae, K. ozaenae and K.rhinoscleromatis
K. pneumoniae
Morphology

• Gram negative
• Short, plumb , rod shaped
• Encapsulated
• Friedlander's bacillus
Predisposing Factors
• Chronic alcoholics
• Diabetics
• Chronic lung disease
Klebsiella Pneumonia
• Klebsiella pneumoniae is a well-recognized cause of community-acquired lobar pneumonia

associated with cavitation
• It is found typically in alcoholic males over 40 years of age with underlying diabetes or obstructive
lung disease.
• Consolidation Pattern-Lobar Consolidation
• Positive air bronchogram sign
• Lobe predilection-Commonly involves posterior segment of the rightupper lobe (Bulging fissure
sign)
• Abscess formation rare but more common than streph
• Pleural effusion common (empyema)
• Cavitation is common
• Pneumatoceles may be seen (These are multiple thin walled air containing cysts.)
• Bulging fissures in lungs is seen
Diagnosis
Voges–Proskauer or VP is a test
• Most commonly seen in cases of Klebsiella Pneumoniae.
Treatment
• ESBL +ve Klebsiella pneumoniae is resistant to cephalosporins, aminoglycosides, tetracyclines, and

TMP-SMX.
• It is sensitive to amikacin or carbapenems.
K. ozaenae
• Causes atrophic rhinitis (Ozaena)

• Associated with laryngitis sicca/Laryngitis atrophica which is common in females
K. rhinoscleromatis
• Causes rhinoscleroma
154. H. aegyptius and H. ducreyi
H. ducreyi
Morphology
• Saftey pin appreance
Chancroid
• Causes ulcus molle (soft chancre) a tropical venereal disease .

• Painful, soft ulcers with ragged undermined margins develop 1–2 weeks after inoculation (usually
seen in prepuce and frenulum in men and vulva, cervix, and perianal area in women)
• The infection locus presents as a painful, readily bleeding ulcer occurring mainly in the genital area.
• Regional lymph nodes are quite swollen.
• Suppurating buboes seen
Diagnosis
• Identification of the pathogen by means of microscopy and culturing are needed to confirm the
diagnosis.
• School of fish appearance or rail road track appearance
H. aegyptius (possibly identical with biovar III of Haemophilus influenzae)
• Causes a purulent conjunctivitis occurring mainly in northern Africa, in particular Egypt.
155. Helicobacter pylori
Morphology
• Spiral-shaped
• Gram-negative
• Motile bacterium with lopotrichous flagella, 5-6 flagella
• Microaerophilic.
Epidemology

• All children in developing counteries have immunity by five years of age
• "Today, helicobacters colonise the stomach of half the human population of the world".
• Developed countries -30%
• Developing countries > 80%
• H. pylori is usually acquired in childhood but immunity does not develop.
• Low socioeconomic status is a risk factor for H. pylori positivity.
Biochemical test
• Oxidase, Urease and catalase-positive
Culture
• Incubated at 37oC in microaerophilic condition.

• Media -Skirrow's medium, chocolate medium
Diseases
• Duodenal Ulcer(commonest cause)

• Gastric (Stomach) Ulcer
• Non-Ulcer dyspepsia Weird Syndromes (associated with acne rosacea, gulf veterans syndrome,
chronic fatigue syndrome and chronic halitosis)
• Stomach Cancer
• MALT Lymphoma
Laboratory diagnosis
Noninvasive tests
1.Serology
• Detect an immune response by examining a blood sample for antibodies to the organism (ELISA).
2.Urea breath test
• A urea solution labelled with C14 isotope is given to pt.

• The C02 subsequently exhaled by the pt contains the C14 isotope and this is measured.
• A high reading indicates presence of H. pylori.
3. Faecal antigen test.
4.Polymerase chain reaction (PCR)
5. Urease Test

• Urease activity in the stomach qualitatively detects active infection with a sensitivity and specificity
of more than 90 percent.
Invasive testing
Treatment
• No treatmnet for asymptomatic
1st line:Regimen 1
• 14 days
• PPI(proton pump inhibitors) BD
• Clarithromycin 500 mg BD
• Amoxicillin 19 BD (or Metronidazole 500 mg BD in penicillin allergic)
1st line: Regimen 2- 10 days
• PPI BD
• Amoxicillin 1g BD (days 1-5)
• Days 6-10 Clarithromycin 500 mg + Metronidazole 500 mg both BD
2nd line
• Omeprazole, Bismuth, Tetracycline, iletronidazole (OBTM)
Treatment assessment test-
Stool antigent test, Urea test, biopsy based test.
156. Non-Venereal Treponematosis- Bejel, Yaws and Pinta
Endemic syphilis: (Bejel)
Caused By
• Treponema pallidum endemicum
Yaws( Frambesia, plan, parangi, bubas)
Introduction
• Caused by T. palliilun subspecies T. pertenue

• Yaw is a chronic contaginous non- veneral disease .
• "As in syphilis, secondary and tertiary manifestations follow in yaws, but cardiovascular and
neurological involvement is rare."
• Modes of transmission
i) Direct contact ( most common)
• Transmitted by direct contact with infectious lesions often during play or group sleeping.
• This is enhanced by disruption of skin.
ii) Indirect contact ( uncommon route) :
• Clinical manifestations
• Incubation period of yaws is 3-5 weeks.
A) Early yaws :-
• Primary lesion or mother yaw is extragenital lesion
B) Late yaws ( secondary yaws) :- Manifestations of late yaws are:-
i) Extensive destructive lesions of skin and bone.
ii) Hyperkeratosis of palms and soles.
iii) Osteits and periostitis.
iv) Hydroarthosis.
Treatment
• Penicillin
Pinta
• Causesd by-T.carateum (Learn Cap).
Diagnosis
• Yaws & Pinta cannot be differentiated serologically.
157. Transfer of genetic information

Gene transfer
• Gene transfer refers to the process of genetic material (e.g. DNA) being sent and received among
two organisms-* Donor sends and recipient receives the genetic material.
1. Horizontal gene transfer (HGT) or lateral gene transfer
• Conjugation
• Transduction
• Transformation.
a. Conjugation
• Mating of two bacterial cells, during which DNA is transferred from the donor to the recipient cell
• The mating process is controlled by anF (fertility) plasmid (F factor), which carries the genes for the
proteins required for conjugation.
• The role of plasmids in conjugation was first described by Lederberg and Tatum in E coli
• Plasmid may be R factor, which codes for transferrable multiple drug resistance.
b. Transduction
• Transfer of cell DNA by means of a bacterial virus (bacteriophage, phage).
c. Transformation
• Transfer of DNA itself from one cell to another
2. Vertical gene transfer
• This process is not important in bacteria.
158. Acanthamoeba
Acanthamoeba
• Free living amoeba

• Neuropathogenic amoeba
• Acanthamoeba does NOT depend upon a human host for the completion of its life-cycle
Modes of transmission

• Through contamination of traumatized skin or eye
C/Fs
a) Granulomatous amoebic encephalitis (GAE)
• Meningitis caused by acanthamoeba species is chronic in nature
b) Keratitis/Chronic amoebic keratitis
• In contact lens users commonest cause of keratitis

• Patients presents with severe eye pain, photophobia, tearing, and blurred vision.
• The characteristic clinical signs are indolent corneal ulceration, a stromal ring, and perineural
infiltrates.
• Radial keratoneuritis
Diagnosis:
• KOH mount is useful for recognition of acanthamoeba cysts.

• Calcofluor white stain: stains cysts of acanthamoeba bright apple green under fluorescence
microscope.
• Lactophenol cotton blue stain can demonstrate acanthamoeba cysts.
• Culturing on non-nutrient agar with an overlay of E scherichia coli. may show trophozoites within
48 hours.
Treatment
• For keratitis Polyhexamethylene biguanide PHMB (Drug of choice)
159. Naegleria fowleri
Naegleria fowleri
• Free living amoeba

• Neuroparasite
Clinical features
Primary amoebic meningoencephilitis
• Common in young adults and children.

• Incubation period 2 - 15 days (5 days)
• Headache, high fever, nausea, vomiting, meningismus.
• Cranial nerve palasies 3rd, 4th and 6th
• Most patients die within a week (95%).
Diagnosis
• Detection of motile amoeboid trophozoites in wet mounts of C.S.F.
160. Trypanosoma cruzi and Trypanosoma brucei
Trypanosoma brucei
• Causative organism of sleeping sickness.
Host
• Definitive host - Man

• Intermediate host-Tsetse fly
Infective form
• To men-Metacyclic form (metacyclic trypomastigote)
C/Fs
• Sleeping sickness
• Lymphadenopathy, particularly of the posterior triangle of the neck- Winter bottom sign
Trypanosoma cruzi
• T. cruzi causes American trypanosomiasis or Chaga's disease
Transmission
• Transmitted to humans and other mammals by an insect vector, the blood-sucking insects of the
subfamily Triatominae (family Reduviidae) most commonly species belonging to the Triatoma,
Rhodnius, and Panstrongylus genera.

161. Leptospira
Host
• Zoonoses
• Leptospira affects wild and domestic animals worldwide.
• Man is an accidental host.
• Rats and small rodents are the main reservoirs of Leptospira.
Media used for isolation
• Korthof medium
Modes of transmission
1. Direct contact
• Transmission of leptospires may follow direct contact with urine, blood or tissue from an infected
animal.
2.Indirect contact
3. Droplet infection
• Through inhalation by breathing air polluted with droplets of infected urine.

• Direct man to man infection is rare.
Clinical features
• Incubation period of Leptospirosis is 1-2 weeks.

• Vasculitis is responsible for the most important manifestations of the disease, mainly affect the
kidney and liver.
Leptospirosis may present as one of the two clinical types:
(1) Anicteric form
• It is mild form and accounts for 90% of cases of leptospirosis.

• It presents as acute influenza like illness, with fever, chills, headache, myalgia, vomiting, sore
throat and pulmonary involvement like cough, hemoptysis and chest pain.
(2) Icteric form
• It is severe form and accounts for 5-10% of cases of leptospirosis.

• It is also called icterohemorrhagic fever or hepto-renal syndrome/Weils' disease

Diagnosis of leptospirosis
1. Microscopic Demonstration
• Dark-field microscopy or by immunofluorescence or light microscopy after appropriate staining

used
2.Isolation of leptospires (Culture)
3. Serology
• Microscoplc agglutination test [MAT](Gold Standard)

• Macroscoplc agglutlnation test
4.Complement fixation (CF)
5.Slide agglutination assays
6.Molecular diagnosis-PCR
7. Molecular typing
Treatment of leptospirosis
• Mild cases Doxycycline or amplicillin or amoxicillin

• Moderate or severe Penicillin G or ampicillin or amoxicillin or erythromycin
162. Mycoplasma
Mycoplasma: habitat, morphology, culture and biochemical characteristics
• Mycoplasma are pleuromorphic smallest living organism, also known as Pleuropneumonia like
organism (PPLO).
• Medically important species are: Mycoplasma pneumoniae, M. hominis, M. genitalium
Morphology:
• Smallest pleuromorphic bacteria

• They lack cell wall so they are pleuromorphic and do not stain with conventional bacteriological
stains.
• Cholesterol containing cell membrane

Mycoplasma pneumoniae (Eaton agent)-Mycoplasmal pneumonia
• Also called Primary Atypical Pneumonia/ Walking pneumonia
Diagnosis
• Specimens – throat swabs, respiratory secretions and sputum.
Microscopy
• Stained with Giemsa.
Isolation of Mycoplasma (Culture) –
• Need cholesterol for growth

• Typical “fried egg” appearance of colonies .
• Colonies best seen with a hand lens after staining with Diene’s method.
• Serum cold antibody
Serological diagnosis
• PCR
Other test
• Raised ESR
Ureaplasma urealyticum
• Hydrolyzes urea
Genital infection
• Caused by M. hominis & U. urealyticum

• Transmitted by sexual contact
• Cause of nongonococcal urethritis (NGU)
• Men - Nonspecific urethritis, proctitis, balanoposthitis & Reiter’s syndrome
• Women –PID, cervicitis, vaginitis
• Also associated with infertility, abortion, postpartum fever, chorioamnionitis & low birth weight
infants
Treatment
• Tetracycline, Erythromycin & Clarithromycin – drug of choice

• Resistant to antibiotics which interfere with bacterial cell wall synthesis.
163. Mycobacteria other than Tuberculosis-MOTTS/Atypical mycobacteria
Runyon Classification of Mycobacteria:
TB complex
• M tuberculosis
• M africanum
• M bovis
Photochromogens
• M asiaticum
• M kansasii
• M marinum
• M simiae
Scotochromogens
• M flavescens
• M gordonae
• M scrofulaceum
• M szulgai
Nonchromogens
• M avium complex
• M celatum
• M haemophilum
• M gastri
• M genavense
• M malmoense
• M nonchromogenicum
• M shimoidei
• M terrae
• M trivale
• M ulcerans
• M xenopi
Rapid growers
• M abscessus
• M fortuitum group
• M chelonae group
• M phlei
• M smegmatis
• M vaccae
Diseases
Mycobacterium marinum/M.balanei
• Aquarium granuloma/ Fishtank granuloma/swimming pool granuloma
M. chelonae, M.fortuitum M.abscessus
• Rapidly growing atypical mycobacteria causing lung infections
Saprophytic mycobacteria not associated with human illness.
• M. phlei
• M. smegmatis
• M. gordona
• M. paratuberculosis
M. Kansasii
• Produce pulmonary and systemic disease indistinguishable from tuberculosis
Mycobacterium bovis
• Equally pathogenic to M tuberculosis for humans.
Mycobacterium ulcerans
• Causative organism for Buruli ulcer disease.
164. Legionella
LEGIONELLA
Morphology
• Gram negative
Culture

• Has fastidious requirements and grow on complex media such as buffered charcol, yeast extract
(BCYE) agar.
Mode of transmissions :
1) Aerosolization
• Inhalation of aerosols produced by cooling towers, air conditioners and shower heads which act as
disseminators.
2) Aspiration
• Predominant mode of transmission
3) Direct instillation in to the lung
Source
• Water
Serotypes
• L. pneumophila serogroup 1 (SG 1) accounts nearly all severe infections.
Predisposing factors
• Depressed cell-mediated immunity
Pathogenesis of legionella infection
• Cell-mediated immunity is the primary mechanism of host defense against Legionella

• Alveolar macrophages readily phagocytose Legionella.
• The attachment of the bacteria to phagocytes is mediated via Fc receptors and complement
receptors, which attach to the bacterial major outer-membrane protein.
• Binding to these receptors promotes phagocytosis but fails to trigger an oxidative burst.
C/F s
• Legionnaire disease
• Pontiac fever
Diagnosis
• Legionella is grown on complex media such as Buffered Charcoal Yeast Extract agar (BCYE) with
alpha ketoglutarate at pH 6.9, temp 35°C and 90% humidity..

Treatment
Legionnaire's disease
• Azithromycin are DOCs
Prevention
• Some outbreaks have been aborted by hyperchlorination, by correcting malfunctions in water

systems, or by temporarily elevating the system temperature above 70°C.
• The installation of silver and copper ionization systems similar to those used in large swimming
pools has been effective as a last resort in hospitals plagued with recurrent nosocomial
legionellosis.
165. Genetic Mechanism of Drug Resistance
• The most common mechanism of resistance is production of neutralizing enzymes by bacteria

• Penicillinase production is transmitted by transduction is plasmid mediated
• Methicillin resistance is due to change in PBP.
• Complete elimination of target is the mechanism by which enterococci develop resistance to
vancomycin
• Alteration of target lesions leads to development of resistance to antibiotics in Streptococcus
pneumoniae
• Drug resistance in Tuberculosis is due to mutation and Rpo B Gene responsible for resistance to
rifampicin
• Mechanism of resistance to erythromycin
1. Alteration in ribosomal binding site
2. Plasmid mediated
3. Efflux proteins
166. Pseudomonas aeruginosa
Morphology
• Motile by polar flagellum

• Non capsulated but many strains have mucoid slim layer especially the organisms which are
isolated from cystic fibrosis patient.
Culture
• Obligate aerobe
• Optimum temperature for growth is 37 degree and is able to grow at temperature as high as 42° C
• Colonies emit a distinctive, musty, mawkish, earthy or sweet grape-like odour or corn tocolike
odour.
• Cetrimide agar is a selective media.
Biochemical Reactions
• Oxidase test positive

• Glucose is utilized oxidatively ⇒ Oxidative reaction in of media
Diseases
Respiratory infections
• Pneumonia in neutropenic cancer patients undergoing chemotherapy; diffuse broncho pneumonia,

infection in cystic fibrosis patients
• Green-tinged sputum seen (due to the formation of blue and green pigments by P. aeruginosa)
Bacteremia and septicemia
• Causes hospital acquired Gram negative bacteremias in immunocompromised patient and in severe
burns.
• Accounts for 25% of hospital acquired BSI caused by Gram negative bacilli.
Ear infections
• Causes otitis externa and”swimmer’s ear”
Central nervous system infections
• Meningitis
Urinary tract infection
• Causes hospital-acquired UTI related to urinary tract catheterization, instrumentation or surgery.

• Pseudomonas aeruginosa is the third leading cause(12%) of all hospital-acquired UTIs.
Endocarditis
Bone and joint infections
Gastrointestinal infections
• In immunocompromised host.
Skin and soft tissue infections

• Ecthyma gangrenosum
• It is often seen in immunocompromised patients such as those with neutropenia
• Ecthyma gangrenosum presents as a round or oval lesion, 1.0 to 15 cm in diameter, with a halo of
erythema
Diagnosis
• Specimen can be pus, urine, blood, CSF, tissue, etc

• Gram staining- Gram negative bacilli and pus cells will be seen
• Culture the specimen on Blood agar and MacConkey agar plates. Incubate overnight at 37° C
• MacConkey agar. Pale colonies on MaConkeyAgar, fruity odour, pigment (greenish, brownish)
• Oxidase positive test
• Confirm by OF test and Arginine dihydrolase test
• Antibiotic susceptibility testing by Kirby Bauer disc diffusion method
Drugs acting against Pseudomonas.
• Penicillins - Piperacillin, Carbenicillin, Ticarcillin, Mezlocillin.

• Cephalosporins - Ceftazidime, Cefoperazone, Cefepime.
• Carbapenems - lmipenem, meropenem
• Monobactams - Aztreonam.
• Aminoglycosides - Tobramycin, Gentamycin, Amikacin.
• Fluroquinolones - Ciprofloxacin, Levofloxacin, Norfloxacin.
• Other - Polymixin B, Colistin.
NOTE:
• For most of the infection of pseudomonas, treatment of choice is the combination of an

antipseudomonal plactam and an aminoglycoside.
• Antibiotic resistance to Pseudomonas Aeroginosa strains from contact lens wearer largely results
from the ability of these strains to form 'slime enclosed microcolonies' or biofilms.
• Biofilm grown cells show increased resistance to biocides and antibiotics through multiple
resistance mechanism.
167. Yersinia pestis
Morphology
• Gram-negative
• Saftey pin appreance
• Pleomorphic
• Most are motile under 30 degrees C. and non-motile at 37 degrees C
MACROSCOPIC APPEARANCE
• Stalactite growth in ghee broth
Transmission
• Wild rat main reservoir

• The primary carriers of the pathogen are the Oriental rat flea, Xenopsylla cheopis, and infected
rodents.
Disease
Three forms of the plague
Bubonic plague
• Most common
• Human acts as dead end host
• Easily diagnosed by the presence of extremely swollen and tender lymph glands called “buboes”
that can grow to the size of an egg, and typically arise in the groin, neck and armpits.
• Absence of visible cellulitis
• Disease becomes evident 2-6 days after infection
• High fevers, chills, headache, and extreme exhaustion.
• Development of gangrene in the extremities, lending it the name “Black Death”.
Septicemic plague
• Necrosis
• Develops secondarily to bubonic plague, and is a result of direct invasion of the bloodstream
without involvement of the lymph nodes.
• Due to the lack of buboes, symptoms generally resemble the flu and make diagnosis difficult.
• In severe cases, seizure and shock can take place.
• Death rates for this form are 40% for treated cases and 100% for untreated cases.
Pneumonic plague
• The most serious form of infection is the which is 100% lethal if not treated within the first 24
hours.
• Man to man transmission.
Treatment
• Yersinia pestis is very susceptible to streptomycin and chloramphenicol

• DOC chemoprophylaxis-Tetracycline
Misc.
• Bioterrorism Agent Category A agent

• Notifiable diseases
• Survival in cold environment also favours Yersinia pestis.
168. Vibrio - V. parahaemolyticus, V. alginolyticus, Vibrio Vulnificus, Vibrio Mimicus
Halophilic vibrios
• Require higher concentration of sodium chloride.

• They are natural inhabitants of seawater and marine life.
• Major halophilic vibrios that are known to cause infections in humans are Vibrio parahemolyticus,
Vibrio alginolyticus and Vibrio vulnificus
• Most halophilic-Vibrio alginolyticus
V. parahaemolyticus
• Display a safety pin appearance due to the accumulation of dye at the poles of the cells
• It is the causative agent of food poisoning due to sea fish.
• Usual signs are abdominal pain, diarrhea, vomiting and fever.
V vulnificus
• Vechile- Shellyfish
• Acute gastroenteritis
• People may develop a blistering dermatitis sometimes mistaken for pemphigus or pemphigoid.
169. Pasteurella multocida
Pasteurella multocida (Pasteurella septica)
Morphology
• Gram-negative, nonmotile.
Epidemiology and pathogenesis
• Cat and dog bites frequently become infected

• P. multocida is the most commonly cultured bacterium from infected bite wounds.
• Apart from bites, scratches and licks, close contact has also been sufficient for infection.
Disease in humans
• Infection typically produces cellulitis and/or abscesses at the site of the bite or scratch
• Usually 3 to 6 hours after inoculation
• Occasionally, the local infection can progress to necrotising fascitis, septic arthritis and
osteomyelitis.
Diagnosis
• Diagnosis is made on the basis of bacterial culture from infected tissues or secretions.
• Pasteurella grows readily on chocolate and sheep-blood agar media, but fails to grow on
MacConkey agar, the usual medium for Gram-negative bacteria.
170. Borrelia burgdorferi and Lyme disease
Transmission and Life cycle
• Transmitted to humans by Ixodes ticks.

• These small, dark-colored ticks have a 2-year life cycle made up of four developmental stages: egg,
larva, nymph, and adult.
• The natural reservoir hosts are rodents, deer and other mammals.
• Adult and nymph stages can infect humans.
• Ticks feed on mice and then deer.
• No deer, no disease.
Lyme disease
Stage 1
• Begins with the characteristic skin lesion, erythema migrans, at the site of the tick bite (~80-90% of
patients).
• Erythema migrans starts as a red papule at the site of the bite, which gradually expands to a round
lesion with red borders and partial central clearing.
Diagnosis
Serologic laboratory testing
• ELISA or immunofluorescence assay as a screening test

• Followed by a Western blot for confirmation(If ELISA +ve)
171. Borrelia and Relapsing Fever
Introduction
• Relapsing fever is caused by spiral-shaped bacteria of the genus Borrelia and sub-species Relapsing
Fever Borrelia (RFB).
• Borrelia readily undergoes antigenic variations in vivo and this is believed to be the reason for the
occurrence of relapses in the disease
Relapsing Fever can be divided into
Louse-borne relapsing fever
• Caused by a single Borrelia pathogen, B. recurrentis.

• Transmitted by louse
• No other known animal reservoir of B. recurrentis exists
Soft tick-borne relapsing fever
• The disease is caused by B. crocidurae, B. duttoni, B. persica, B. latyshervi, and B. hisponica, B.

venezuelensis, B. mazotti, B. hermsii, B. turicatae, and B. parkeri.
Hard-tick relapsing fever
• Infections are currently known to be caused by B. miyamotoi.
• Severe for most tick-borne relapsing fever; headache, neck stiffness, arthralgia, myalgia,
ecchymosis, epistaxis, and petechiae.
• Complications include ARDS, decreased sensorium, myocarditis, hepatitis, abortion or stillborn and
death.
Serologic laboratory testing
• ELISA or immunofluorescence assay as a screening test

• Followed by a Western blot for confirmation
• PCR
Treatment
• For decades, penicillins and tetracyclines have been the treatment of choice in relapsing fever.

172. Sporothrix schenckii
Sporothrix schenckii
• Thermally dimorphic fungus

• Lives on vegetation.
• Some times 'asteroid bodies' are seen in the lesion of sporotrichosis, composed of a central fungus
cell with eosinophilic material radiating from it.
• Commonly seen in sub himalyan regions and farmers
Traumatic implantation
• The conidia or hyphal fragments of S schenckii are introduced into the skin by trauma(rose or pulm
thorns/phagnum moss)
• Patients frequently recall a history of trauma associated with outdoor activities and plants.
C/Fs
Sporotrichosis
I) Cutaneous (skin) sporotrichosis
• Most common form of this disease.

• About 75% of cases are lymphocutaneous; ie, the initial lesion develops as a granulomatous nodule
that may progress to form a necrotic or ulcerative lesion.
• Meanwhile, the draining lymphatics become thickened and cord-like.
• Multiple subcutaneous nodules and abscesses occur along the lymphatics.
• Usually cutaneous sporotrichosis lesions occur in the finger, hand and arm.
2) Pulmonary sporotrichosis
3) Disseminated sporotrichosis
Diagnosis
• In the clinical laboratory, round or cigar-shaped budding yeasts are seen in tissue specimens. In
culture at room temperature, hyphae occur bearing oval conidia in clusters at the tip of slender
conidiophores (resembling a daisy).
173. Coccidioides immitis
Coccidioides immitis

• It is a dimorphic fungus with septate hyphae.
• Fungus causing endemic mycosis -Coccidioidomycosis
Has two forms.
• White fluffy mould on most culture media(Sabouraund's agar)

• Nonbudding spherical form-a spherule, in host tissue.
• C. immitis reproduces in host tissue by forming small endospores within mature spherules.
• Fungus is identified by its appearance by the formation of thick-walled barrel shaped spores,
called arthrospores.
• Most of the infections are asymptomatic Asymptomatic pulmonary nodule.

• Many persons develop a self limited influenza like fever Valley fever or desert rheumatism. -
Acute pneumonia
174. Cytomegalovirus (CMV)
Classification
• Enveloped
• Linear, double-stranded DNA virus
Transmission and Diseases associated
Transmission Patient Disease

In utero- Fetus Infected with no defect
Most commonly infects in last Severe cytomegalic inclusion

trimester diseases:
Most common cause of congenital Jaundice

viral infection
Hepatosplenomegaly(Most
coomon)
Thrombocytic purpura
Pneumonitis
CNS damage

Death
Birth process Babies Hetrophile negative

mononucleosis
Milk
Reactivation in transplanted organ Transplant patient Interstitial Pneumonitis
Reactivation or new infection AIDS patient CMV retinitis
Diagnosis
1. Physical exam-Fever, cervical lymphadenopathy, hepatosplenomegaly and maculopapular rash
2.Labs
• Lymphocytosis with atypical lymphocytes

• Thrombocytopenia
• Transaminitis
• Negative heterophile antibody
• CMV-specific immunoglobulin M (persists for 4-6 months)
• CMV-specific immunoglobulin G (2-3 weeks)
• Ig G antibody test is of little diagnostic value as positive results also reflects maternal antibodies.
• CMV viral DNA in blood by polymerase chain reaction in neonate
• Nucleic acid detection from the intraocular fluid in CMV retinitis
3. Histology
• A large cell containing a large basophilic intranuclear "owl's eye" and intracytoplasmic inclusion
bodies.
Drugs
• Gancyclovir
• Gancyclovir used intravitreally for retinitis
• Valganciclovir

175. Varicella Zoster
Characteristics
• DNA
• double-stranded
• linear
• enveloped
Transmission
• Respiratory secretions
Pathogenesis
• Molecular biology remains latent in trigeminal and dorsal root ganglia reactivation due to
immunocompromised state or stress
Presentation
Chickenpox
Infectious period
• 2 days before and 5 days after the onset of rash.

• Risk of neonatal chicken pox is maximum if maternal infection occurs near delivery ( 5 days before
delivery or 48 hours after) and it is very severe.
Secondary attack rate is high
• 70-90 %
• C/Fs - has two stages
1. Pre-eruptive stage
2. Eruptive stage
• Rash is symmetrical
Centripetal in distribution
• Rash is plemorphic, that is, all stages of rash (Papule, vesicle and crusts) may be seen
simultaneously.

Scab does not contain virus.
Predisposing factors for reactivation of VZV : -
• Old age
• Lymphoreticular malignancy. e.g., Hodgkin's disease
• HIV infection
Shingles (varicella-zoster/Herpes zoster)
• Reactivation of latent infection

• Latent infection in trigeminal ganglion
• Occurs in old age 60 years or above
• Ramsay Hunt Syndrome - due to reactivation in geniculate ganglion of facial nerve
• Facial nerve involvement is least
Complications
• Meningeal irritation
• Pnemonia in adults
• Transverse myelitis
• Cutaneous dissemination
• Patient's with hodgkin's disease and non hodgkin's lymphoma are at greatest risk for progressive
hespes zoster.
• Bacterial superinfection(Most Common i children)
• Pneumonia
• Meningitis (rare complication)
• Encephalitis may be seen in children and immunosuppresion
• Reye syndrome
• Intrauterine complications in the fetus
• Blindness
• Cutaneous scarring in a dermatomal distribution
• Limb hypoplasia
A) Microscopy
• Tzank smear - multinucleated giant cells

• Cowdry type A intranuclear inclusion bodies
B) Virus Isolation
C) Serology

• Tests are :
• Fluorescent antibody to membrane antigen (FAMA)
• Enzyme-linked immunosorbent assay (ELISA)most sensitive
• Immunofluorscent test.
• Immune adherence hemagglutination
D) PCR for detection of VZV DNA
Treatment
• Acyclovir
Vaccination
• Live attenuated vaccine
176. Coxsackievirus
Morphology
• Genus Enterovirus
Types
• The coxsackieviruses were subdivided into groups A and B based on their pathology in newborn
mice.
Both strains cause
• Asymptomatic
• Mild fever
• Common cold
• Rashes
• Aseptic meningitis
Coxsackie A
• Herpangina
• Fever
• Sore throat
• Small vesicles on the back of the throat
• Hand, foot, and mouth syndrome
1. Fever
2. Oral vesicles
3. Lesions on hands, feet, buttocks
4. Caused by coxsackie A16, A5, A10
Coxsackie B
• Myocarditis and pericarditis in infants(MC cause)

• Associated with 50% of myocarditis cases
• Biopsy of myocardium shows lymphocytes
• Most common cause of pericarditis
• Pleurodynia
• Pleuritic pain
• Fever and headache
• Bornholm disease
Isolation
• It is necessary to employ suckling mice for the isolation of coxsackie viruses.

• Inoculation is usually made by intracerebral, subcutaneous and intraperitoneal route.
177. Ebola Virus
Classification
• Filovirus
Characteristics
• "filo"-viridae
• Category A bioterrorism agent
Incubation period
• 2-21 days.
• It kills up to 90% of people who are infected.
Diseases
• Hemorrhagic fever

178. Differences between Exotoxins and Endotoxins
• Exotoxins can be toxoided.

• Exotoxins are protein in nature, heat labile and has antigenic property.
• Exotoxin has mostly enzymatic activity
• Endotoxin is lipopolysaccharide complex.
• Endotoxin has no enzymatic activity
179. Human PapillomaVirus (HPV)
Classification
• Virus
• DNA
• Non-enveloped
• Papovaviridae family.
• Human papillomavirus
Risk Factor
• Most important risk factor is multiple sexual partners.
Presentation
Cutaneous warts
• Serotypes 1, 2, and 4
• Hands, fingers, and soles of feet
• Multiple papillomatosis most common manifestation in childrens.
Anogenital warts (condylomata acuminata)
• Serotypes 6 and 11
• Low risk HPV
Cervical intraepithelial neoplasia
• Serotypes 16, 18, 31, and 33 are preneoplastic

• High risk HPV
• Can progress to squamous cell carcinoma or spontaneously resolve
Diagnosis
• Koilocytic cells seen on biopsy or Pap smear

• Characteristic nuclear alterations and perinuclear halo seen with HPV infection in the cervical
squamous epithelial cells.
Vaccine
Two types
1. Quadrivalent :- containing HPV types 6,11,16,18

2. Bivalent :- containing HPV types 16,18
Efficacy
• Most of the time, rates of vaccine efficacy exceed 90%.
Recommended for
• Girls and young women 9-26 years of age.
Administration
• The quadrivalent vaccine is administered intramuscularly as three separate doses, with second dose
given at 2months after the first dose and the third dose 6 months after the first dose.
180. Culture medium
• Nutrient broth is basal medium

• Alkaline peptone water for cholera
• M tuberculosis - LJ medium
• Pseudomonas's selective media is Cetrimide agar
• Enriched media are blood agar, Chocolate agar, Monsour's taurocholate , Tetrathionate broth and
Lowenstein-Jensen media.
• Selenite F broth is an enrichment media for Salmonella and Shigella.
• TCBS Agar is highly selective for the isolation of V. cholerae and V. parahaemolyticus as well as
other vibrios
• Thayer - martin medium for selective medium for meningococcal infection and N. gonorrhoeae.
• Selective medium for Naegleria fowleri is nutrient agar rich with E coli
• Selective medium for shigella hektoen agar
• Loffler's medium os enriched media
• Mac Conkey's Agar is differential medium
• Transport medium are used for stool specimen :- Cary Blair medium, buffered glycerol saline or
Stuart medium.

181. Innate Immunity
Important components of the innate Immune system.
• Cells Macrophages, Dendritic cells, NK cells, NK-T cells, Neutrophils, Eosinophils, mast cells,
basophils, epithelial cells.
• Complement components → Classical and alternaƟve pathway.
• Antimicrobial peptides Defensins, Cathelin, probiotics.
• Pattern recognition receptors.
• Cytokines.
• Natural killer cells/NK cells are a type of cytotoxic lymphocyte that constitutes a major component
of the innate immune system. they play a major role in the rejection of tumors and cells infected by
viruses. They kill cells by releasing small cytoplasmic granules of proteins called perforin and
granzyme that cause the target cell to die by apoptosis.
• Neutrophils and monocytes (the precursors of tissue macrophages) migrate from the blood into
inflammatory sites during innate immune responses. Macrophages and neutrophils are phagocytic
cells that engulf a microbial pathogen after it has been identified by the innate immune system.
• Conserved antigenic patterns in bacteria such as unmethylated CpG DNA, flagellin, lipid and
carbohydrate structures in the bacterial cell wall serve as danger signals to activate innate
immunity, resulting in local inflammation and the influx of the macrophages, neutrophils, and
dendritic cells.
182. Adaptive/Acquired immunity
Functions of AI include:
• Recognition of "non-self" antigens in the presence of "self".

• Generation of responses that are tailored to maximally eliminate pathogen-infected cells.
• Development of immunological memory, in which pathogens are "remembered" through memory
B cells and memory T cells.
Immunological memory/Immunity is of two types:
• Active memory
• Passive memory
Active immunity has immunological memory. Passive-active immunity is useful for the exposure of
Rabies, Hepatitis B, Varicella-zoster.
In some diseases passive immunization is often undertaken in conjunction with inactivated vaccine
products, to provide both:
• Immediate (but temporary) passive immunity.

• Slowly developing long-lasting active immunity.
The disease in which simultaneous active and passive immunization is used: Tetanus Diphtheria Rabies
Hepatitis B
In measles also, both active and passive immunization is used, but not simultaneously. Because the antibody
response to live attenuated measles vaccine is diminished in persons who receive immunoglobulin can currently.
So, the person passively immunized should be given a live measles vaccine 8-12 weeks later.
Both active and passive immunity is used:
Simultaneously Tetanus, rabies, Diphtheria, Hepatitis B.

At the different time Measles.
The duration of passive immunity is approximately equal to the half-life of the immunoglobulin
injected, which varies from disease to disease,
Example:7 days in case of anti-tetanus serum.
183. Lymphoreticular system
Cells of a Lymphoreticular system (four types)
• Lymphocyte- T- lymphocyte and B-lymphocyte.

• Null cell/ LGL
• Phagocytic cells Macrophages
• Dendritic cells.
The main functions of the lymphoreticular system are the removal of senescent cells and production of immune
cells. The human body contains 1012 lymphocyte out of which 109 are renewed daily. Mature B and T cells before
they encounter antigen are called Naive cells.
1) T-lymphocytes
• Found in the parcortical area of lymph nodes and periarteriolar sheaths of the spleen.
• Antigen binds to the TCR [T cell receptor] which is responsible for signal 1.
• All lymphocyte contain CD-3 molecule which are involved in transduction of signal 1.
• Other surface molecules or co-receptors include CD 2, CD 4 or CD 8, CD 11a, CD 28. Antigen interaction
with T lymphocytes precipitates the release of lymphokines, substances that modulate other aspects of the
immune response., CD 40.
• CD 4 is expressed on 50% of T cells which help to produce immunoglobulins, while 30% expressed CD 8,
they are strict aginst virus infected cells
• All T cells express T cell receptors, and either CD4 o CD8.NOT BOTH.
• Antigen interaction with T lymphocytes precipitates the release of lymphokines, substances that modulate
other aspects of the immune response.

Mature T cells should recognize only foreign antigens combined with self-MHC molecules in order to mount an
appropriate immune response.
2) B-Lymphocytes
• 10-20% of peripheral lymphocytes

• responsible for humoral immunity
• present in bone marrow, peripheral lymphoid tissue, e.g. lymph node (superficial cortex), spleen(white
pulp), tonsils and extra lymphatic organs e.g- GIT.
• In spleen and Lymph node it forms lymphoid follicles, Unlike T cell, it responds to free Antigen.
• B cell act as Antigen presenting cells.
• other molecules are complement receptor, Fc receptors, CD 21 (receptor of EBV),
• CD 40 (essential for interaction of T and B cell which cause B cell maturation so a mutation in CD 40 ligand
cause immunodeficiency called X-linked hyper-IgM syndrome).
• first Ig class to appear on the B cell surfaces is IgM.
3) Null cell/Large Granular Lymphocyte (LGL)
They are classified as:
• ADCC lymphocyte
• NK cell- two types 1) LAK- lymphokine-activated killer cell 2) NK/T cells-
• Antibodies do not induce proliferation of NK cells. NK cells express CD3, CDI6 & CD56 and also but less
commonly CD2 & CD8.
4) phagocytic cells
• it is of two types
1) mononuclear macrophages of blood and tissue
2) Microphages
These are polymorphonuclear leucocytes of blood-neutrophil, eosinophils and basophil, they do not have any role in
specific immune processes.
Dendritic cells
• These are antigen-presenting cells to T cell during a primary immune response.

• Bone marrow-derived cells of the lineage
• They have little or no phagocytic activity.
these are of three types.
• Interdigitating dendritic
• Langerhans cells.
• Follicular dendritic cells.

Pharmacology
1. MEFLOQUINE
• Effective with a single dose.

• Mefloquine is contraindicated with Halofantrine/Quinine.
• Causes QT-lengthening.
• Drug for prophylaxis of malaria in chloroquine-resistant P.falciparum is Mefloquine.
• Mefloquine can be safely administered in a baby with glucose-6-phosphate dehydrogenase
deficiency.
• Mefloquine is generally considered safe for young children and pregnant women.
• Mefloquine causes neruopsychiatric reactions & convulsions.
• Hence, not prescribed as prophylaxis for patients with major psychiatric disorders.
• Prophylaxis of malaria:
• Among travellers to areas with multidrug resistance:
• 5 mg/kg (adults 250 mg) per week is started 1–2 weeks before travel till 4 weeks after return
from endemic area.
• Chemoprophylaxis in an Englishman visiting chloroquine and mefloquine-resistant malaria region is
done with Doxycycline.
2. ISONIAZID (INH)
• Isoniazid inhibits phenytoin metabolism & can precipitate its toxicity.

• Cross-resistance of Isoniazid is seen with Ethionamide.
• Side -effects of Isoniazid are Peripheral Neuropathy, Hepatitis, Optic Neuritis.
• Peripheral neuropathy during use of Isoniazid might be prevented by using Pyridoxine.
• Multidrug resistance (MDR) TB is defined as resistance to Rifampicin and isoniazid.
• XDR(Extensively Drug-Resistant TB) is defined as resistance to INH and rifampicin as well as to all
fluoroquinolones and one of the injectable drugs (capreomycin, kanamycin, amikacin).
• For diagnosis of MDR TB, currently, drug sensitivity testing is done for Rifampicin, Isoniazid,
Streptomycin, and Ethambutol.
• Dose of Isoniazid in children is 10-20mg/kg when given daily.
• Is mainly Bactericidal Drug.
• Isoniazid & rifampicin reach into caseous material fo necrotic wound.
• Most effective drug against extracellular Mycobacteria.
• Peripheral neuritis due to isoniazid is due to the formation of Hydrazone complex.
• Drug of choice for TB prophylaxis.
• Metabolized by Acetylation.
• In a patient with suspected tubercular anterior uveitis, diagnosis is confirmed by a positive
response to isoniazid test.
• Lupus-like picture can be caused by Isoniazid, Hydralazine & Procainamide.
• A poverty-stricken mother suffering from active tuberculosis delivers a baby.
• Breastfeeding + INH + BCG vaccination would be most appropriate.
3. HALOPERIDOL
• Involuntary movements of this hands, feet, lips, and tongue will increase initially as the
medication is decreased
• Haloperidol toxicity can cause Akathisia
• Long QT is seen as effect of overdosing of haloperidol.
• The most common side effect reported with treatment with haloperidol is Akathisia
• Depot preparations are available for Haloperidol.
• A week after the initiation of Haloperidol the patient shows be restlessness, fidgety, irritability and
cannot sit still at one place can be treated with beta-blockers.
• Acute drug dystonia shows abnormal movements like induced persistent deviation of neck on one
side is seen with haloperidol.
• Tongue protrusion, oculogyric crisis, stiffness and abnormal posture of limbs and trunk without loss
of consciousness for last 20 minutes after administration of haloperidol suggest acute dystonia.
• Hyperpyrexia, muscle rigidity, akinesia, mutism, sweating, tachycardia, high BP after administration
of haloperidol suggest Neuroleptic malignant syndrome.
• Drug treatment of schizophrenic is haloperidol.
• Treatment of morbid grief showing Preoccupation with the memory of deceased is Haloperidol.
• Effect of dopamine on kidney is blocked by Haloperidol.
• Extrapyramidal syndrome like side effects are seen in haloperidol.
4. DAPAGLIFLOZIN
DAPAGLIFLOZIN
• Dapagliflozin acts by inhibiting SGLT-2 transporter.

• Dapagliflozin is an SGLT-2 inhibitor drug.
• A single daily dose of dapagliflozin produces continuous glucosuria lowering blood glucose
levels, thus results in rapid weight loss, tiredness & increased incidence of urinary tract
infections & genital infections

5. INFLIXIMAB
• Infliximab is a TNFα inhibitor drug.

• Infliximab is mainly indicated in severe active fistulating type of Crohn's Disease (CrD) & in severe
Ulcerative Colitis (UC).
• Infliximab is chimeral monoclonal antibody against TNFα, which binds & inactivates TNFα.
6. TICLOPIDINE
• Ticlopidine acts by altering surface receptors on platelets (mainly P2 Y12).

• Mainly inhibits ADP irreversibly & fibrinogen-induced platelet aggregation.
• Active metabolite of ticlopidine blocks ADP irreversibly & interferes with platelet activation.
• Ticlopidine decreases ADP mediated cAMP activation.
• Ticlopidine is a prodrug converted to an active metabolite by CYP2 C19 in liver.
• The most common adverse effect with ticlopidine is bleeding, neutropenia & thrombocytopenia.
7. GLYCERYL TRINITRATE
• CCF, oesophageal spasm & cyanide poisoning can be treated by Nitrates

• Nitroglycerine causes methemoglobinemia, vasodilatation, hypotension & tachycardia.
• Nitrates act in CCF by decreasing preload.
• Nitrates decrease myocardial oxygen consumption by direct reduction of myocardial oxygen
consumption, dilation of capacitance vessels & decreasing heart size.
• Long-term nitrate usage decreases its own effect due to SH group in enzyme.
• NTG is given by sublingual route because of hepatic first-pass metabolism.
• Treatment of stable angina include nitrates & CCBs.
• DOC in an acute attack of Prinzmetal's angina is Nitrates.
• Aggravation of angina symptoms is seen in Idiopathic hypertrophic subaortic stenosis
on administering nitrates.
• Best time to administer long-term nitrates for nocturnal angina is evening.
• GTN can be used as "Transdermal patch".
• Tachycardia due to nitrates with angina pectoris is blocked by Beta-blocker.
8. DIGOXIN
• Digoxin toxicity may result from the concurrent administration of digoxin with Amiodarone,
quinidine, verapamil, spironolactone, Furosemide, Hydrochlorothiazide.
• Digoxin toxicity is increased by Renal impairment, Hypercalcemia hypokalemia & Hypomagnesemia

• Digoxin induced arrhythmia shows Paroxysmal Atrial Tachycardia with variable AV
block, Ventricular Bigeminy & May be used to treat Atrial Fibrillation
• Most effective method of treatment of Digitalis toxicity is Digoxin Antibody - Digibind.
• Dose of digoxin is altered in Old age,Renal disease & Hypercalcemia
• Therapeutic plasma level of digoxin is 0.5-1.5 ng/ml
• Half-Life of Digoxin is 40 hrs(26-45hrs)
• Diuretics, amphotericin
B, corticosteroids, Quinidine, Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaol
in-pectin are the drugs showing interaction with digoxin.
• Interaction occurring when quinidine and digoxin are given together - Quinidine decreases
excretion of digoxin
• Interaction occurring when quinidine and digoxin are given together - Quinidine displaces digoxin
from protein binding sites & decreases excretion
• Digoxin is contraindicated in Hypertrophic obstructive cardiomyopathy.
• Digoxin is useful in Complete heart-block with CHF.
• Digoxin induced arrhythmia can be treated with Lignocaine
• Dose of digoxin in child 0.04-0.06 mg/kg
• Atrial Fibrillation is treated by digoxin
• Digoxin is distributed in heart, kidney & skeletal muscles.
• On changing maintenance dose of digoxin the new steady state plasma digoxin concentration
would be achieved in approximately 1 week.
9. ATROPINE
• Atropine is used as Mydriatic, Cyclopegic & Preanaesthetic medication

• An antidote for Mushroom poisoning, Organophosphates poisoning & Carbamates poisoning.
• Percentage of atropine in "Atropine eye drops" as cycloplegic is 1%
• Atropine is most sensitive to mucous & pharyngeal secretions.
• Atropine is derived from Atropa belladonna.
• Atropine cause relaxation of lower oesphageal sphincter.
• Atropine in anterior uveitis causes rest to ciliary muscle, increases antibody supply & prevents
posterior synechia formation.
• Atropine therapy in elderly may be hazardous because risk of elevating intraocular pressure in
patients with glaucoma
• Atropine should never be started when patient is cyanosed due to danger of respiratory arrest.
• Atropine is useful in organophosphate poisoning because is a competitive antagonist of
acetylcholine
• Rise of body temperature, Decrease bowel sound,Decreased salivary secretion & Increased A-V
conduction are the effects of atropine
• Atropine when used as a pre-medication causes Skin flush,Prevents bradycardia & Dryness of
mouth
• Atropine-mechanism of action in organophosphate poisoning is that it Acts on central and
peripheral cholinergic receptors
• Treatment of atropine toxicity Physostigmine
• Agent used for dilatation of pupil in children is atropine
• Mydriatic used in 3 years old child for refraction is 1 % Atropine ointment
• Drug of choice for increased IOT in acute anterior uveitis is atropine
• Atropine is drug of choice in Iridocyclitis.
• Features of atropine poisoning are Mydriasis, Confusion & Hallucinations.
• Atropine is contraindicated in glaucoma
• A farmer visiting an orchard gets unconscious, excessive salivation, constricted pupils and
fasciculation of muscles. Treatment is started with: Atropine
• Atropine and acetylcholine show Competitive antagonism
10. OCTREOTIDE
• Drug of choice for diarrhea in AIDS is Octreotide

• Octreotide is used in Insulinoma, Glucagonoma & Carcinoids
• Octreotide is useful for Acromegaly, variceal bleeding,secretory diarrhea & Suppresses growth
Hormone secretion.
• Octreotide can be used in the management of acute pancreatitis
11. BROMOCRIPTINE
• Bromocriptine is indicated in Prolactin-secreting adenomas, Amenorrhea, Galactorrhea

& Acromegaly.
• Bromocriptine is used in Type II DM, Hepatic Coma & Cyclical mastalgia.
• Prolactinoma is treated with Alpha-Bromocriptine.
• Bromocriptine is dopaminergic agonists used for parkinsonism which has the potential to cause
retroperitoneal fibrosis.
• Bromocriptine is contraindicated during breast milk feeding.
• Bromocriptine is dopamine agonist that decreases prolactin release.
• To suppress lactation in mother with rheumatic fever, Rx of choice is Bromocriptine.
12. HALOTHANE
• Halothane has least analgesic effect.

• Sensitizes myocardium to catecholamines.
• Pleasant smelling gas causing postoperative hepatitis.
• Portal flow is maximally reduced.
• Halothane can cause malignant hyperthermia.

• Methoxyflurane should NOT be used in a patient with previous history of halothane induces
hepatitis.
• Halothane causes centrilobular necrosis in liver.
• Best uterine relaxation is seen with Halothane.
• Halothane potentiates competitive neuromuscular blockers.
• Halothane is contraindicated in patients with Cardiac arrhythmia.
• Presence of trifluoroacetic acid (TFA) in urine indicates that volatile anaesthetic agent used
was Halothane
• In 2 months, old infant undergoing surgery for biliary atresia halothane should be avoided.
• Halothane corrodes metal in vaporizers and breathing systems.
• Postoperative jaundice is because of use of Halothane.
13. THIOPENTONE
• Fall in intracranial tension, decreases oxygen consumption of brain & decreases metabolic rate of
the brain are seen as an effect of thiopentone
• Dose of thiopentone is 2.5%
• Sodium carbonate is added to improve solubility of thiopentone.
• Thiopentone is Cerebro protective
• Thiopentone is contraindicated in porphyria
• Thiopentone on extravasation or intraarterial injection cause intense pain and even necrosis.
• Thiopentone is indicated in case of head injury.
• Thiopentone is indicated in increased intracranial tension.
• Thiopentone does not trigger malignant hyperthermia.
• Sodium Thiopentone is ultra short-acting due to rapid redistribution.
• Thiopentone is commonly used in narcoanalysis.
• Intravenous thiopentone produces rash, pain, spasm
• Intraarterial injection of thiopentone causes vasodilation, necrosis of vessel wall, hypotension
• Anaesthesia used in Duchenne muscular dystrophy for tendon lengthening procedure is induction
with intravenous thiopentone and N20; and halothane for maintenance.
• Thiopentone is highly distributed to body fat that is an anaesthetic agent lacking analgesic effect.
• Action of i. v. thiopentone is terminated by redistribution.
14. PROPOFOL
• Propofol intravenous induction agent is most suitable for day care surgery.
• Safe inducing agent in malignant hyperpyrexia is Propofol
• Propofol is associated with less residual impairment and low incidence of postoperative nausea
and vomiting.
• Propofol intravenous anaesthetic agent is highly protein bound & lipid soluble.
• Propofol is painful on injecting intravenously, because of oil preparations.
• Propofol has no muscle relaxant property.
• Propofol undergoes hepatic metabolism.
• Propofol is safe in porphyria, anti-emetic effect, pleasant sedation & recovery.
• Propofol, Fentanyl, Isoflurane are most preferred for short daycare surgeries.
15. ISOFLURANE
• Isoflurane is the anaesthetic agent of choice in renal failure.

• Isoflurane as an inhalational agent is used in patients with raised intracranial tension.
• Isoflurane is a pungent volatile anaesthetic agent.
• Fluoride content is least in Isoflurane
• Isoflurane has the least effect on myocardial contractility & is least cardiotoxic.
• Desflurane is a structural analogue of isoflurane
• In Coronary artery bypass grafting (CABG) surgery maintenance of anaesthesia is achieved
by Isoflurane
• Alcoholic liver failure requires general anaesthesia AOC isoflurane.
16. SEVOFLURANE
• Sevoflurane is anaesthesia of choice for anaesthetic induction in children.

• Is fastest acting inhalational agent
• Sevoflurane isanaesthetic without epileptogenic potential.
• Sevoflurane rises intracranial pressure.
• Sevoflurane is indicated in elective urology surgery in pediatric patient.
• Sevoflurane MAC is higher than isoflurane & Potency more than cardio depressant than isoflurane.
• MAC is 2%
• Blood gas coefficient of Sevoflurane is higher than desflurane
• In a child with intestinal obstruction with deranged liver function test, the anaesthetic of choice
is Sevoflurane.
17. FLUOXETINE
• Drug of choice for OCD is Fluoxetine

• Fluoxetine is a potent reuptake blocker of Serotonin
• In a patient with palpitations, breathlessness, sweating and a fear of impending death. Has one
episode of such attacks every week. There are no identifiable triggers for the episodes. Fluoxetine is
the Drug of choice.
• Loose stools - Common side effect of Fluoxetine therapy
• Non-sedating antidepressant is Fluoxetine
• Mode of action of fluoxetine Inhibition of axonal uptake of 5HT.
• Side effect of Fluoxetine is Weight gain, Anxiety, Sweating & Diarrhoea
• Drug of choice in depression in old person is Fluoxetine.
18. CLOZAPINE
• Clozapine is the drug of choice for the schizophrenic patient with poor oral absorption.
• Clozapine is indicated in a patient with schizophrenia & tardive dyskinesia.
• Least extrapyramidal side effects are seen in Clozapine.
• Clozapine may precipitate seizure & agranulocytosis.
• Clozapine should be discontinued if WBC (leukocyte) count <3000/mm3.
• Clozapine should not be used along with carbamazepine.
• Clozapine's action is more on D1 receptors than D2 receptors.
• Patient of schizophrenia on CPZ (chlorpromazine) develops auditory hallucination should be treated
with Clozapine.
• Clozapine is an antipsychotic drug with least extrapyramidal effects.
• Clozapine shows highest potential to cause metabolic syndrome.
19. LITHIUM
• Amiloride is the drug of choice in lithium-induced polyuria

• Abnormality to check if lithium is given to a pregnant female cardiac anomaly.
• Drug of choice in Bipolar MDP is lithium.
• Treatment of choice in acute Bipolar disorder - Lithium.
• Lithium is drug of choice in a Vascular headache, Neutropenia & Major depression.
• Lithium may produce Hypothyroidism.
• 0.8 – 1.2 meq/l is the therapeutic level of Lithium in serum.
• An appropriate pre-Lithium work-up includes Serum creatinine, Thyroid-stimulating hormone (TSH),
Serum electrolytes.
• The current agent of choice for treatment of bipolar affective (manic-depressive) disorder is Lithium
carbonate
• The commonest side effect of lithium is a tremor.
• Congenital Anomaly produced by lithium therapy is Heart Block.
• Ebstein's anomaly is caused by lithium toxicity.
• Most common cardiac adverse effect of lithium is Arrhythmia.
• Lithium directly affects sodium.
• Psoriasis is exacerbated by lithium.
• Lithium toxicity is treated by increased hydration, sodium bicarbonate & Hemodialysis.
• The absolute contraindication to lithium is the Renal failure.
• Most common renal sequel of lithium toxicity is Nephrogenic DM.

• Lithium potentiates the action of nondepolarizing muscle relaxants so 2 days before administration
of the muscle relaxant should lithium be stopped.
20. HEPARIN
• Protamine is chemical for heparin antagonism.

• Pregnant patient with prosthetic valve should be switched to heparin in 36 weeks.
• Drug used in heparin overdose is Protamine sulphate.
• Lepirudin is recommended for the treatment of Heparin-Induced Thrombocytopenia.
• Haemorrhage secondary to heparin administration can be corrected by the administration
of Protamine sulfate
• NSAIDs have increased effect when given with heparin.
• Heparin causes reversible alopecia.
• Heparin releases Lipoprotein Lipase & Non Teratogenic.
• LMWH shouldn't be used for treatment of Heparin Induced Thrombocytopenia (HIT) syndrome.
• Heparin Induced Thrombocytopenia (HIT) syndrome causes both arterial and venous thrombosis.
• Heparin Induced Thrombocytopenia (HIT) syndrome occurs commonly in about a week of heparin
therapy
• Calcium is recomended as dietary supplements is recommended for a pregnant lady on Heparin.
• In Heparin induced thrombocytopenia (HIT) Thrombocytopenia is not severe usually & will not lead
to bleeding. Marked thrombocytopenia < 20,000 is rare.
• The antibody responsible for heparin induced thrombocytopenia is Antiheparin / PF4 antibody
• The best suited anticogulant for osmotic fragility test is heparin
• Heparin is a mucopolysacchride
• Heparin Acts by activating anti-thrombin III
• Heparin Requires aPTT monitoring in patient
• Most commercial preparations of heparin now utilize pig intestinal slimes
• For treatment of Deep vein thrombosis with heparin activated partial thromboplastin time is
monitored to adjust dosage
• Low molecular weight heparin inhibits Factor Xa
• Low molecular weight heparin therapy is associated with Less chances of bleeding & given as single
dose per day
• Low molecular weight heparin has Easy filterability by glomerular capillaries
• As compared to unfractionated heparin, low molecular weight heparin Are absorbed more
uniformly when given subcutaneously
• LMWH (Low Molecular Weight Heparin) has higher and predictable bioavailability.
• PT; aPTT monitoring is not required in LMWH
• LMWH (Low Molecular Weight Heparin) has more favorable pharmacokinetic.
• Heparin interferes with pH of ABG
• Heparin is given in mesenteric vein thrombosis
• For prophylaxis of deep vein thrombosis used is Heparin.
• Heparin inhibits active form of factor X, XI, XII.

• Laboratory monitoring of Anti-factor Xa activity is desirable with low molecular weight heparin
therapy.
• Parameter which should be tested before starting heparin therapy is Activated partial
thromboplastin time.
21. PILOCARPINE
• Acquired nasolacrimal duct obstruction is caused by Pilocarpine

• Pilocarpine is used to treat glaucoma by improving drainage of aqueous humor.
• Punctate stenosis, Follicular conjunctivitis & Posterior synechia are the Side effects of Pilocarpine
• Drug of choice for acute congestive glaucoma is 1-2% pilocarpine
• Cause of anisocoria may be due to Pharmacological blockage
• In primary open-angle glaucoma pilocarpine, eye drop lower the intraocular pressure by its direct
action on the Longitudinal fibres of the ciliary muscle/Sphincter pupillae muscle
• Pilocarpine is not used in young adults as it causes Myopia
• Combination of pilocarpine and epinephrine use in glaucoma treatment may inhibit Pigmented
pupillary cyst
• Drug contraindicated in iridocyclitis is pilocarpine
• Pilocarpine is used in Primary, Open Angle Glaucoma, Acute Angle Closure Glaucoma & Chronic
Synechial Angle Closure Glaucoma
• Pilocarpine acts on trabecular meshwork and affects the aqueous outflow
• Accommodation spasm, Blurred vision, Miosis are side effects of topical pilocarpine solution
• Alcohol, salicylates and pilocarpine can be used as Diaphoretics
22. SODIUM CROMOGLYCATE
• Sodium cromoglycate is a form of therapy in spring catarrh

• Topical sodium cromoglycate is useful in the treatment of Vernal keratoconjunctivitis
• Inhaled sodium cromoglycate is of benefit in preventing exercise-induced bronchial spasm
• Sodium cromoglycate Inhibits degranulation of mast cells
• Sodium cromoglycate is not a bronchodilator
• Sodium cromoglycate acts as mast cell stabilizer.
23. LEUKOTRIENE ANTAGONIST
• Montelukast mechanism of action is Competitive inhibition of leukotriene synthesis

• Montelukast is leukotriene antagonist
• The leukotriene receptor antagonist used in bronchial asthma is Zafirlukast
• Leukotrienes antagonists are effective in aspirin-induced asthma.
24. ACYCLOVIR
• Acyclovir inhibits viral polymerase activity to inhibit herpes virus replication

• Bell's palsy patient comes on day 3 can be treated with Oral steroids + Acyclovir
• Drugs of choice for corneal herpes is Acyclovir
• Ideal time for starting post-exposure prophylaxis with acyclovir in a person exposed to varicella is 7-
9 th day
• Indication of Acyclovir in pregnancy is in Disseminated herpes, Chicken-pox in first trimester &
Prophylaxis in recurrent herpes
• HSV encephalopathy is treated with acyclovir
• Acyclovir inhibits DNA synthesis and viral replication
• Oliguria causing drug is Acyclovir
• Acyclovir is nephrotoxic
• Systemic acyclovir in herpes zoster is useful When started immediately after the onset of rash
• Mechanism of Acyclovir resistance Thymidine kinase.
• Herpes resistant to acyclovir is treated by Foscarnet.
25. NITRIC OXIDE
• Nitric oxide is produced from endothelium.

• Nitric oxide helps to regulate vascular tone & shows important role in penile erection.
• Present in low concentration in cigarette smokers.
• Nitric Oxide (NO) is a novel neurotransmitter which is considered to have an effect in the
pathophysiology of Mood Disorders.
• Nitric oxide is synthesised from arginine.
• Nitric oxide is an important mediator of vasodilation.
• The primary action of the neurotransmitter Nitric oxide (NO) in the gastrointestinal tract is
gastrointestinal smooth muscle relaxation.
• Vasoactive intestinal polypeptide and nitric oxide inhibit the lower oesophagal sphincter.
• Mechanism of action of Nitric oxide is through cGMP.
• Drugs which increases nitric oxide are Glycerine trinitrate, Hydralazine, Sodium nitroprusside.
• Inhaled nitric oxide is used for reducing pulmonary hypertension.
• Platelet adhesion is inhibited by Nitric oxide.
• Inhaled nitric oxide is used to decrease pulmonary artery pressure in adults and infants.
26. LINEZOLID
• Platelet count should be monitored in patient receiving linezolid therapy.

• Optic neuropathy, Pancytopenia & Lactic acidosis are side effects of Linezolid.
• In Methicillin-resistant Staphylococcus - aureus (MRSA) linezolid can be given.
27. ZIDOVUDINE
• Zidovudine for mother (36 weeks) and child (6 weeks) therapy can be offered to reduce the chance
of transmission of HIV to the newborn.
• Zidovudine causes myopathy as a side effect.
• Severe hepatotoxicity associated with steatohepatitis, most likely a result of mitochondrial toxicity,
is being recognized with zidovudine.
• Zidovudine + Lamivudine + Indinavir for 4 weeks is the recommended regimen for post-exposure
prophylaxis of HIV Infection.
• Resistance to zidovudine develops due to mutations in reverse transcriptase.
• Zidovudine + Lamivudine + Nevirapine drugs are supplied free of cost to the government Hospital
by NACO.
• Co-administration of Indomethacin, Aspirin & Trimethoprim are not preferred with zidovudine.
28. CISPLATIN
• Chemotherapy for dysgerminoma is Cisplatin, etoposide, bleomycin.

• Cisplatin is used in treatment of ovarian carcinoma.
• Cisplatin is one of the most emetogenic chemotherapy agents.
• Treatment of squamous cell carcinoma of anal canal is Cisplatin-based chemotherapy followed by
radical radiotherapy.
• Cisplatin is used in lung cancer is also used in ovarian carcinoma.
• Important chemotherapy agent used for the thymoma treatment is Cisplatin.
• Anticancer drug causing nephrotoxicity is cisplatin.
• Cisplatin is associated with secondary leukaemia.
• Cisplatin causes tacrolimus toxicity.
• In oesophageal ca, Cisplatin is used as a Neoadjuvant chemotherapy agent.
• Cisplatin is used in metastatic testicular carcinoma.
• In carcinoma cheek, Cisplatin is the best drug for single drug chemotherapy.
• Predominantly sensory neuropathy is caused by Cisplatin.
29. DRUGS CAUSING GYNAECOMASTIA
• Biclutamide causes gynaecomastia.

• Digitalis, Cimetidine & INH causes gynaecomastia.
• Impotence, Galactorrhea & Gynaecomastia are the side effects of cimetidine.
• Metaclopramide long term use can cause parkinsonism, galactorrhoea and gynaecomastia.
• Spironolactone causes hirsuitism and gynaecomastia
• Testosterone, Estradiol, Lutenizing hormone are useful while investigating a case of gynaecomastia.
• Ketoconazole & Digoxin causes gynaecomastia
30. TRASTUZUMAB
• Trastuzumab has a specific activity in a subset of female breast cancers.

• Trastuzumab shows a better response in combination with paclitaxel.
• Trastuzumab is used in metastatic breast cancer.
• Trastuzumab is a monoclonal antibody produced by injecting HER-2 antigen.
• Trastuzumab causes dilated cardiomyopathy.
31. PYRAZINAMIDE
• Pyrazinamide is a bactericidal drug.

• Hyperuricemia is a recognized side effect of pyrazinamide.
• Pyrazinamide precipitates gout.
• Pyrazinamide is anti-tubercular drug not given in liver disease.
• First line ATT in children - Streptomycin & Pyrazinamide.
• Maximum liver toxicity is seen with Pyrazinamide anti -TB drug.
32. Clozapine
• Clozapine is the Drug of choice for schizophrenic patient with poor oral absorption.
• Resistant schizophrenia is indication for use of clozapine
• Agranulocytosis, seizure are common side effects of clozapine
• Drug of choice for the treatment of negative symptoms of schizophrenia is clozapine
• Clozapine has highest potential to cause metabolic syndrome
• Extrapyramidal side-effect least seen with Clozapine
33. RIFAMPICIN
• Treatment of choice for HIV and TB:

• Rifampicin + Ritonavir.
• Rifampicin acts by DNA dependent RNA polymerase.
• Rifampicin is microsomal enzyme inducer.
• Rifampicin may cause OCP failure.
• Rifampicin is bactericidal in nature.
• Rifampicin enhances warfarin metabolism.
• A tuberculosis patient with only rifampicin resistance will be treated under Cat IV.
• During rifampicin treatment, some patients will have mild elevation in the bilirubin with normal
transaminases due to hepatic adaptation.
• Rifampicin does not require dose reduction in patient with renal failure.
• Rifampicin reaches inside of caseous material.
• Rifampicin is most active against both dormant & non-dormant bacilli.
• Rifampicin is most effective antitubercular drug against slow multiplying intracellular mycobacteria.
• Rifampicin shows harmless orange colour to urine, sweat, tears, contact lenses.
• Contact lens staining occurs in rifampicin.
• Hepatotoxicity is the major side effect of rifampicin.
• MDR tuberculosis is defined by resistance to isoniazid and rifampicin.
• Rifampicin is not used with ritonavir, indinavir and saquinavir.
• The treatment of contacts of meningococcal meningitis is by rifampicin.
• Dose of rifampicin in RNTCP is 450mg given three times in a week.
• First line anti-tubercular drugs are same in children and adults INH, rifampicin, ethambutol,
pyrazinamide, and streptomycin.
• For treatment of paucibacillary leprosy drugs used are rifampicin & dapsone.
• Toxic amblyopia is produced by rifampicin.
• Rifampicin is associated with side effects as respiratory syndrome, cutaneous syndrome, Flu
syndrome and abdominal syndrome.
• Maximum sterilising action is shown by rifampicin.
• Rifampicin is obtained from Bacteria Streptomyces mediterranei.
• Gene responsible for resistance to rifampicin - Rpo B gene.
34. ETHAMBUTOL
• Ethambutol is not a hepatotoxic antitubercular drug.

• Ethambutol is bacteriostatic.
• Under the RNTCP, for diagnosis of MDR TB, currently, drug sensitivity testing is done for Rifampicin,
Isoniazid and Ethambutol.
• In ethambutol toxicity, there will be loss of ability to see green colour.
• Retrobulbar neuritis is seen with ethambutol.
• Hyperuricemia is seen with ethambutol.
• Ethambutol is avoided in children as it causes visual disturbance
• Antitubercular drug causing gout is ethambutol.
35. AMINOGLYCOSIDE
• Aminoglycosides cause non-oliguric renal failure.

• Deafness might be seen in TB patient, who has regularly been injecting intramuscular injection of
streptomycin.
• In treatment of Pseudomonas infections, carbenicillin is frequently combined with Gentamycin.
• Streptomycin should not be used with d-tubocurarine.
• Old age, Hypokalemia, Aminoglycoside administration in recent past increase the risk of
aminoglycoside renal toxicity.
• Enterococcus faecalis when isolated in the blood, requires the synergistic activity of
penicillin with aminoglycoside for appropriate therapy.
• Streptomycin used in treatment of plague, brucellosis
• Streptomycin is protein synthesis inhibitor & are nonplant toxin.
• Streptomycin single dose is more effective than multiple small doses because of its concentration-
dependent lytic effect.
• Streptomycin is useful in treatment of Granuloma venerum.
• Streptomycin require dose adjustment in renal failure
• Streptomycin is a glycoside.
• Mechanism of action of streptomycin is inhibition of translation.
• Framycetin is not available for parenteral use.
• An aminoglycoside with an outstanding feature of being little or not affected by majority of
inactivating enzymes is Amikacin
• Widest spectrum aminoglycoside is Amikacin
• Aminoglycoside class of drugs causes hearing loss by damaging Outer hair cells of basal turn.
36. ANTI-TUBERCULAR TREATMENT REGIME
• Dots Plus regime consist of 6Km Ofx Eto Cs ZE + 18 Ofx Eto CsE
• To be termed as cured a patient who was initially smeared positive and completed treatment
should have a negative smear result on at least 2 occasions of which one should be at treatment
completion.
• ND2 regime – For sputum -ve pulmonary not seriously ill patients and extrapulmonary not seriously
ill patients – 12(HE)
• In DOTS continuation phase drugs are given in a multi-blister combi-pack.
• DOTS medication is to be taken in presence of a health worker
• Alternate day treatment is recommended in DOTS.
37. METRONIDAZOLE
• Drug of choice in bacterial vaginosis is Metronidazole.

• Treatment for Trichomonas vaginalis is Metronidazole.
• Treatment of choice in Gardenella vaginitis in pregnancy Metronidazole.
• A lady presented with a creamy white vaginal discharge having fishy odour,
• The clinical scenario is of bacterial vaginosis that can be treated with Metronidazole.
• Patient presenting with abdominal pain, diarrhea taking clindamycin for 5 days.
• Treated with metronidazole symptoms subsided.
• Causative micro-organism will be Clostridium difficile.
• A patient presents with lower gastrointestinal bleed.
• Sigmoidoscopy shows ulcer in the sigmoid. Biopsy from this area shows flask-shaped ulcers.
• Treatment will be Metronidazole
• Metronidazole causes flushing, vomiting, dizziness and rashes after taking alcohol.
• Best drug for anaerobic infections is Metronidazole.
• Metronidazole used in the treatment of Clostridium difficile associated diarrhoea.
• IV Metronidazole is used in the treatment of Pseudomembranous enterocolitis, Anaerobic bacterial
infection & Amoebiasis.
• Metronidazole is a Radiosensitising substance.
• An elderly male presented with a headache, fever and hemiparesis of right side.
• On further examination and investigation a diagnosis of brain abscess was made.
• Treatment of choice is combination of cephalosporin and metronidazole.
38. KETOCONAZOLE
• Anti-histamines associated with an increased risk of cardiac arrhythmias in patients receiving

erythromycin or ketoconazole & Terfenadine.
• Ketoconazole would treat both dermatophytosis & candidal infection.
• Ketoconazole is Cyt. p450 inhibitor.
• Ketoconazole is effective in the treatment of pityriasis Versicolor.
• Ketoconazole is used for medical adrenalectomy.
• Ketoconazole decreases the efficacy of testosterone.
39. CHLORAMPHENICOL
• A young male presents with meningococcal meningitis and allergy to penicillin can be treated with
chloramphenicol.
• Chloramphenicol resistance in Pseudomonas aeruginosa is due to active efflux pumping out of drug.
• Gray baby syndrome is caused by Chloramphenicol.
40. AZITHROMYCIN
• A patient with discharge per vagina was evaluated and on endocervical biopsy, chlamydia was
found. Treatment to be given in this case is Azithromycin and contact tracing.
• A young boy presented with high fever shows clinical features suggestive of Legionnaires'
Disease. Treatment of choice is Azithromycin.
• The drug of choice to treat Chlamydia infection in pregnancy is Azithromycin.
• Mass treatment with azithromycin is indicated if the prevalence of trachoma follicles (TE) in 1-9
years population is more than 10%.
• A 30-year-old male presents with pneumonia and diarrhoea five days after discharge from hospital.
The drug of choice for treating him is Azithromycin.
• 24 years old male complains of mild urethral mucoid discharge after sexual contact with a sex-
worker. Examination is normal. Drug used to treat such a patient is Azithromycin.
• Treatment of granuloma inguinale is Azithromycin.
41. SULPHONAMIDE
• Brinzolamide is contraindicated in patients with allergy to sulphonamides

• Sulphonamides precipitate attacks of acute intermittent porphyria
• Sulfadiazine is a sulfonamide which can be used orally, as it is rapidly absorbed & rapidly excreted.
• Sulphonamides can precipitate kernicterus in the newborn
• Longest acting sulphonamide is Sulphadoxine
• Sulphonamide injection causes decrease in folic acid by Competitive inhibition
• Topical Sulfonamides - Sulfacetamide sodium, Mafenide, silver sulfadiazine.
• Due to sulphonamide erythema, multiformis may occur
• Salazopyrin is used for the treatment of ulcerative colitis
42. COTRIMOXAZOLE
• Cotrimoxazole is effective against P carinii

• T/t of choice for grade IV vesicoureteric reflux with recurrent UTI Cotrimoxazole
• In cotrimoxazole, sulphamethoxazole and trimethoprim are in the ratio of-5: 1
• The drug with a definite risk of hemolysis in patients with G6PD deficiency is Cotrimoxazole
• Cotrimoxazole therapy is to be given in HIV infected patients irrespective of the presence of
symptoms if the CD4 count is less than 200.
43. DOXYCYCLINE
• Doxycycline can be used in renal failure without dose adjustment.

• Doxycycline is least Nephrotoxic.
• Antibiotic treatment of choice for treating cholera in an adult is a single dose of Doxycycline.
• Doxycycline drug of choice for Non-Gonococcal Urethritis.
• Doxycycline is the drug of choice in Mycoplasma infection.
• Doxycycline is the drug of choice in typhus fever.
• Drug of choice for scrub typhus - Doxycycline (100 mg bd orally for 7-15 days)
• Doxycycline is the drug of choice in Brucellosis.
• Doxycycline acts by inhibiting protein synthesis.
• Doxycycline has the maximum propensity for photodermatitis.
• Chemoprophylaxis in an Englishman visiting chloroquine and mefloquine-resistant malaria region is
done with Doxycycline.
• A 19-year old male presents with several comedones, papules and pustules on face and trunk.
• The drug of choice for the patient would be Topical retinoic acid + Oral doxycycline.
44. TETRACYCLINE
• Tetracyclines are known to have teratogenic effects.

• Tetracyclines inhibits protein synthesis by binding to 30S ribosomal subunit, and prevents the
attachment of aminoacyl tRNA to the mRNA – ribosome complex.
• Tetracycline is the drug of choice for chemoprophylaxis of cholera.
• Drug of choice in rhinoscleromatosis is Tetracycline
• Fatty change in liver is seen with use of Tetracycline
• Rate of newly synthesized osteoid mineralization can be best estimated by Tetracycline
• Tetracycline injection causes palsy of radial nerve
• Tetracycline causes Pseudotumour cerebri
• Treatment of granuloma inguinale is Tetracycline
• The drug of choice for chemoprophylaxis in contacts of a patient of penumonic plague is
Tetracycline
• Drug of choice of trachoma is Tetracycline
• Tetracycline ointment for mass prophylaxis 0.1%
• Drug of choice for lymphogranuloma venerum is Tetracycline
45. DAPSONE
• Dapsone is used in treatment & therapeutic diagnosis of dermatitis herpetiformis.

• Both Dapsone & Systemic steroids drugs are used in generalised lichen planus.
• Rifampicin, dapsone and clofazimine are used if HIV infected patient develops multibacillary
leprosy.
• Hemolytic anaemia is the commonest side effect of Dapsone.
• Dose of Dapsone is 1-2 mg/kg.
• WHO regime for paucibacillary leprosy is 100 mg Dapsone daily + Rifampicin monthly (600 mg).
• Fixed drug eruption (FDE) is an adverse cutaneous reaction to an ingested dapsone.
46. PENICILLIN

• Treatment of S. aureus infection with penicillin is often complicated by the production of
penicillinase by S. aureus
• Carbenicillin is NON- RESISTANCE TO β-LACTAMASE
• Syphilis, Anthrax and Bacterial meningitis are therapeutic uses of penicillin G
• Antipseudomonal penicillins include the carboxypenicillin and the ureidopenicillins.
• Penicillin Binding Proteins (PBPs) are essential for cell wall synthesis
• Penicillin Binding Proteins (PBPs) act as carboxypeptidases and transpeptidases
• Alteration in PBP's is the primary bases of resistance in MRSA
• β- Lactamase production is the most common mechanism of resistance to Penicillin
• Alteration in permeability/penetration of antibiotic causes resistance only in Gram-negative
bacteria
• β-Lactamase production causes resistance in both Gram-positive and Gram-negative bacteria
• Penicillin would be LEAST effective in treating Mycoplasma pneumonia
• Enterococcus faecalis when isolated in the blood, requires the synergistic activity of penicillin plus
an aminoglycoside for appropriate therapy
• Plant penicillin is Endrin
• Penicillins inhibits cell wall synthesis
• Methicillin is Acid Labile penicillin
• Penicillinase-resistant penicillin Methicillin
• The dosage of benzylpenicillin in the treatment of primary syphilis is 2.4 MU single i.m.
• Treatment for clostridial myonecrosis is Penicillins
• Penicillin is Drug of choice for Treponema Pallidum
• Penicillin is Drug of choice for thoracic actinomycosis
• Penicillin in high doses can cause convulsions
• The clinical presentation of fever, altered sensorium and purpuric rashes, is highly suggestive of
meningococcal meningitis is treated with Penicillin
• TOC for penicillin-resistant gonorrhoea Ceftriaxone
• Presence of fever, jaundice and renal failure in a sewage worker (contact with rat urine) suggests a
diagnosis of Wen syndrome or Icterohemorrhageic fever caused by leptospirae. Penicillin G
(intravenously) is the recommended agent.
• Treatment of spreading streptococcal cellulitis is Penicillin
• Treatment of contaminated wound in Gas Gangrene is Penicillin
• Rapidly spreading infection of the external auditory canal with the involvement of the bone and
presence of granulation tissue point towards malignant otitis externa treated with Penicillin
• Penicillin is used in the treatment of quinsy
• Piperacillin is an anti-pseudomonal drug of penicillin-class
• Dose and duration of benzathine penicillin for prophylaxis of rheumatic fever is 1.2 MU every 4
weeks
47. CLASSIFICATION OF ANTI-MICROBIALS
• Vancomycin, Aztreonam & Cephalexin inhibit bacterial cell wall synthesis

• Bacteriocidal agents include cephalosporin
• Anti-pseudomonal action is a characteristic of Cefoperazone
• Tacrolimus (Fk-506) is macrolide antibiotic
• Tetracycline, Chloramphenicol, Erythromycin inhibit protein synthesis
• Bacteriostatic anti TB drug Ethambutol
48. AMOXICILLIN
• Amoxicillin is used in H. pylori.

• The MOST frequently implicated antibiotic among the causes of DILI is Amoxicillin -clavulanic acid.
• The most frequently implicated antibiotic among the causes of drug-induced liver injury
is Amoxicillin-clavulanic acid.
• Drug of choice for prevention of infection by animal bite Amoxicillin/clavulanate.
• Moraxella catarrhalis is resistant to Amoxicillin.
• Advantages of amoxicillin over ampicillin are better bioavailability & faster action.
• The incidence of diarrhoea is lower.
• Food does not interfere with its absorption.
49. CEPHALOSPORIN
• Strain i.e beta-lactamase producing and resistant to chloramphenicol, of H. influenzae isolated

from CSF in a known case of meningitis, can be treated with Third-generation cephalosporin.
• Ceftazidime, Cefodizime & Cefoperazone belongs to third generation Cephalosporin
• Cefoperazone has got antipseudomonal effect
• Cephalosporin act by inhibiting cell wall
• Cefepime, Cefpirome belongs to fourth generation Cephalosporin
• Cephalosporin that does not require dose reduction in the patient with any degree of renal
impairment is Cefoperazone
• Cephalosporin is Bacteriocidal agents
• A third-generation cephalosporin, such as ceftriaxone or ceftazidime is DOC for the treatment of
meningococcal infections.
• Ureaplasma is naturally resistant to cephalosporin
• When allergic to penicillin Cephalosporins is contraindicated
• ESBL are lactamases that mediate resistance (by hydrolyzing) to extended spectrum (third
generation) cephalosporins, penicillins and monobactams (e.g. aztreonam).
• IIIrd generation is resistant to beta-lactamases from gram-negative bacteria
• Ceftriaxone is administered parenterally
• Cefamandole can cause Disulfiram-like reaction
• Cephalosporins with antipseudomonal activity:- Ceftazidime, Cefoperazone, Cefepime
• Cephalosporin causing thrombocytopenia is Ceftazidime
• Ceftobiprole has activity against MRSA (Methicillin Resistant Staphylococcus Aureus)
• First generation cephalosporins are active against Gram-positive bacteria
50. ACETYLCHOLINESTERASE (AchE) INHIBITORS
• Positive edrophonium test is most sensitive test for diagnosis of myasthenia gravis.
• Neostigmine is a quaternary ammonium compound.
• Neostigmine antagonizes nondepolarizing blockade by decreasing acetylcholine breakdown at
motor end plate, preventing K+ efflux from cell & depolarization of motor end plate.
• Neostigmine helps in urinary retention.
• Neostigmine is given to reduce post operative paralytic ileus.
• Neostigmine is given to reduce effect of depolarising muscle relaxation.
• Donepezil is used in treatment of alzheimer dementia.
• Rivastigmine (cholinesterase inhibitor) should not be used with drugs that have cholinergic
antagonistic activity like tricyclic antidepressants (TCA) as combination is counterproductive.
• Neostigmine is used for reversing adverse effect of DTC + pancuronium.
• Shortest acting anticholinesterase is Edrophonium.
• Rivastigmine & Donepezil are drugs used predominantly in management of dementia.
51. ORGANOPHOSPHATES POISONING (OPP)
• Muscarinic signs of OPC poisoning can be remembered as SLUDGE- BBB: Salivation, Lacrimation,
Urination, Defecation, Gastric upset, Emesis, Bronchospasm, Blurred vision (Miosis), Bradycardia.
• Delayed onset polyneuropathy after organophosphorous poisoning is seen after 2-4 weeks.
• Fatality rate of organophosphorous poisoning in India is 15-30%.
• In organophosphorous compound poisoning, organophosphorous compound is a
Phosphorylated enzyme irreversibly inhibit cholinesterase.
• Most specific test for organophosphorous poisoning is Plasma cholinestrase level.
• Organophosphate inhibits Esteratic site of AchEs.
• Antidote for organophosphorous poisoning is Atropine.
52. SYMPATHETIC RECEPTORS
• Adreneric β receptors having lipolysis property in fat cells is Beta -3.

• Alpha 2 agonist cause analgesia & not hyperalgesia.
• Salmeterol is long acting beta-2-agonist.
• Beta-2-agonist causes a brief spell of hyperkalemia followed by hypokalemia.
• Beta-2-agonist doesn't cause hypoglycemia.
• Alpha-2-agonist causes Sedation, Glaucoma & Hypertension.
• Beta-1 receptors in heart stimulates its contractions.
• Beta-2 receptors are present in smooth muscles.
• Beta-1 receptors stimulation releases renin.
• Beta blockers are used to treat hyperthyroidism (Not hypothyroidism).
53. GLAUCOMA PHARMACOLOGICAL MANAGEMENT
• Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment
of glaucoma because it Produces no miosis
• Drug of choice for open angle glaucoma Timolol
• Acetazolamide s contraindicated in sulfonamide hypersensitivity
• Brimonidine can cause drowsiness
• A patient with glaucoma is being treated with systemic beta blocker should not be
given Levobunolol
• Acute angle closure glaucoma first line treatment Iv mannitol
• Drug used in refractory glaucoma Alpha agonist
• Latanoprost used topically in glaucoma primarily acts by Increasing uveoscleral outflow
• Main MOA brimonidine in glaucoma Decreased aqueous secretion
• Drug kept as a last resort in the management of primary open angle glaucoma is Oral acetazolamide
• Selective alpha 2 agoinst used in glaucoma is Brimonidine
• Atropine should be avoided in angle closure glaucoma
• Pain in absolute glaucoma is best relieved by Retrobulbar injection of steroid
• Drug CONTRAINDICATED in glaucoma patients suffering from bronchial asthma is Timolol
• Combination of pilocarpine and epinephrine use in glaucoma treatment may inhibit Pigmented
pupillary cyst
• In primary angle-closure glaucoma pilocarpine lowers the intraocular pressure by its direct action
on the Sphincter pupillae muscle
• In primary open-angle glaucoma pilocarpine eye drops lowers the intraocular pressure by its direct
action on the Longitudinal fibres of the ciliary muscle
• In a hypertensive patient with glaucoma Dipivefrine is contraindicated
• Treatment of malignant glaucoma includes Topical atropine, IV mannitol & Vitreous aspiration
54. EPINEPHRINE
• In the beginning of resuscitation efforts, 0.5 mg of epinephrine is

administered subcutaneously Alpha-1 receptors in vascular smooth muscle, beta-1 receptors in the
heart, and beta-2 receptors in bronchial smooth muscle are responsible for the beneficial effect of
epinephrine in this patient.
• Epinephrine secreted by Pheochromocytoma to cause its clinical manifestations.
• Epinephrine is formed from Tyrosine.
• Epinephrine stimulates gluconeogenesis.
• Actively bleeding peptic ulcer can be managed endoscopically by injection therapy
using epinephrine with concentration 1 in 10,000.
• Insulin secretion is inhibited by Epinephrine.
• In surgical stress Epinephrine is increased.
• Stress-induced hyperglycemia is due to Epinephrine.
• Epinephrine action in liver is Glycogenoloysis.
• Epinephrine causes hyperglycemia by increased glucagon & Decreased insulin secretion.
• Mechanism of action of epinephrine in cardiopulmonary resuscitation is Increase SA node activity.
• Drug of choice for anaphylactic shock is Adrenaline.
• In Anaphylactic shock epinephrine given by Intravenous route.
• A child presents with hepatomegaly and hypoglycemia. There is no improvement in blood sugar
even after administration of epinephrine in Von girke's disease..
• Bupivacaine toxicity treated with Epinephrine.
• Epinephrine treats Uveitis glaucoma,Open angle glaucoma & Neovascular glaucoma.
• Epinephrine reduces aqueous production and increases outflow facility.
• Sympathomimietic causing increase in mean blood pressure, heart rate and cardiac output on
intravenous infusion is Adrenaline
• IV dose of 1:10000 concentration of epinephrine in pre term baby is 0.2 ml
• Adrenaline is secreted by Adrenal medulla.
• Metyrosine inhibits the rate limiting step in synthesis of epinephrine.
55. BETA ADRENERGIC RECEPTOR ANTAGONIST / BETA-BLOCKERS
• Beta blockers are contraindicated in Decompensated CCF, Asthma , Atherosclerosis

• Beta blockers are antiarrhythmic agents TYPE II
• Acebutol, Atenolol & Metoprolol are cardioselective beta blocker
• Beta blockers are contraindicated in Asthma
• Atenolol is longer acting than metoprolol
• Labetalol has both alpha and & beta blocking action
• Nadolol has longest half life
• Sotalol is contraindicated in renal failure
• Beta blocker without local anaesthetic effect is Atenolol
• Beta blockers are contraindicated in Sick sinus syndrome
• Combination use of beta blockers and calcium channel blockers cause Heart block
• Contraindication of topical beta blockers asthma
• First line drug choice for management of hypertension in patients with angina Beta Blockers
• Effect of beta blocker's on heart are Decrease in heart rate, Decreases cardiac output
& Precipitates heart failure
• First line drug for primary open angle glaucoma is Beta blockers
• Shorest acting beta blocker Esmolol
• Mechanism of action of timolol is Nonselective beta blocker
• Beta blockers mask all effects of hypoglycemia Sweating, Palpitations, Dizziness
• Lipid insoluble beta blockers Are long acting
• Lipid insoluble beta blockers are Incompletely absorbed orally
• Lipid insoluble beta blockers Do not cross blood brain barrier

56. INSULIN
• Insulin performs glycogen synthesis, glycolysis & lipogenesis.

• Insulin clearance closely resembles G.F.R.
• Human insulin differs from beef insulin by 1 amino acid residue.
• Rapid infusion of insulin causes hypokalemia.
• Insulin is required for transport of glucose, amino acid, K+ & Na.
• In fetus, the insulin secretion begins by 3rd month.
• Increased ratio of insulin to glucagon causes decreased levels of cyclic AMP.
• Insulin promotes lipogenesis by decreasing intracellular cAMP, increasing the transport of glucose
into cell & increasing activity of acetyl-CoA carboxylase.
• Insulin secretion was seen in Glucose, Vagal stimulation & Acetylcholine.
• Insulin activate lipoprotein lipase to aid fat metabolism.
• Insulin facilitates glucose uptake in Liver, RBC & Kidney.
• Insulin acts on glucose metabolism by permeability across cell membrane against glucose gradient.
• Sulfonylurea is shifted to insulin in pregnant lady because Insulin does not cross placenta.
• Newer insulins are neutral.
• Regular insulin can be given through IV.
• Lispro, Aspart & Glulisine are short & rapid-acting insulin.
• Long-acting insulin is Insulin glargine.
• NPH insulin is an intermediate-acting insulin.
• Glargine is never mixed with other insulins.
• Oedema, Hypoglycemia & Lipodystrophy are side effects of insulin.
• Fetal growth is maximally affected by Insulin.
• Caudal regression in a newborn is specific for maternal insulin dependent diabetes mellitus.
• Percentage of the dose given as basal insulin in bolus basal regimen in children is 25-50%.
• Infusion of insulin + glucose fastest way to reduce the hyperkalemia.
• The drug of choice in a 50-year-old patient presenting with hyperglycemia and ketoacidosis
is Regular Insulin.
• Recombinant human insulin is made by cDNA of pancreatic cell.
• Chromium is required for proper effects of Insulin.
• Plasma half-life of insulin is 10 minutes.
• Glucose-6-phosphatase is increased in low insulin/glucagon level.
• Insulin secretion is normally stimulated by GLP-1.
• Insulin secretion is decreased by Somatostatin.
• Crystallization and storage of insulin requires Zn++.
57. DOPAMINE
• The strategy for therapy for dopamine deficiency in the substantia nigra of individuals with
Parkinson’s disease is indicated by provision of metabolites in the tyrosine pathway.
• Neurotransmitter related to schizophrenia pathology is dopamine.
• The efferent fiber bundle of the substantia nigra transmits dopamine to Corpus striatum.
• Dopamine is the major neurotransmitter in substantia nigra.
• Slow IPSP in autonomic is generated by dopamine.
• Adrenaline, noradrenaline and dopamine act through seven pass receptor.
• Dopamine shows positive ionotropic effect.
• Dopamine improves renal perfusion.
• Dopamine causes vasoconstriction.
• Effect of dopamine on kidney is blocked by Haloperidol.
• Dopamine is preferred in treatment of shock because of renal vasodilatory effect.
• Prolactin secretion will be inhibited by dopamine.
• Bromocriptine,Ropinerole & Pramipexole are dopaminergic agonists used for parkinsonism.
• Dopamine neurotransmitter is depleted in Parkinson's disease
• Drug most useful in cardiogenic shock is dopamine.
• Dopamine is preferred over dobutamne in treatment of renal shock because of renal vasodilatory
effect.
• Anti-psychotic drugs act through Dopamine D4 receptor blockade.
• Dopamine at 1-2 Microgram/ Kg/ min produces renal vasodilatation.
• Dopamine receptor with inhibitory action is D2.
58. ORDER OF KINETICS
• Zero order kinetics is independent of plasma concentration.

• Zero order kinetics is otherwise known as saturation kinetics.
• In zero order kinetics constant amount of drug eliminated per unit time.
• Zero order kinetics occur in Phenytoin,Tolbutamide, Propranolol and Ethanol at high dose.
• In first order kinetics a constant proportion of plasma concentration is eliminated.
• In first order kinetics rate of elimination is directly proportional to drug concentration.
• In first order kinetics clearance is constant.
• Elimination after 4 half lives in first order kinetics is 93%.
• Elimination after 3 half lives in first order kinetics is 87.5%.
• For drugs with first order kinetics the time required to achieve steady state levels can be predicted
from half life.
• First order kinetics is elimination of the drug is proportional to the serum concentration.
59. FIRST PASS METABOLISM
• A drug administered through oral route undergo high first pass metabolism.
• High first pass metabolism causes for less bioavailability.
• High first pass metabolism is seen in Lignocaine, Propranolol & Salbutamol.
• Isosorbide mononitrate bypasses first pass metabolism.
• Sublingual route escape first pass metabolism.
• Theophylline escape first pass metabolism.
60. CHOLINERGIC RECEPTORS
• Action potentials on the alpha motor neuron release acetylcholine (Ach) from the axon terminal
• Cholinergic receptors on the muscle endplate are cation channels
• Alpha motor neurons excite, and Renshaw cells inhibit, the muscle endplate
• In Myasthenia gravis, antibodies are present against Nicotinic Receptor
• Nicotine receptor sites include Adrenal medulla, Skeletal muscle & Sympathetic ganglia
• Carbachol has maximum nicotinic effect
• Muscarinic antogonists Decrease gastric secretions, Decrease respiratory secretions & Fascilitates
AV conduction
• Oxybutynin acts by Muscarinic receptor inhibition
• D-tubocurarine is a skeletal muscle relaxant that acts by competitive inhibition of NM receptors at
neuron-muscular junction.
• Dry mouth during antidepressant therapy is caused by blockade of Muscarinic acetylcholine
receptors
• Bupropion is Nicotinic receptor antagonist
• Drug used for muscarinic symptoms seen in cobra envenomation is Neostigmine
• Acetylcholine acting on nicotinic receptors produces Contraction of skeletal muscle
• Nicotinic cholinergic receptors are ionic channel
• Varenicline acts by Partial nicotine receptor agonist
• Muscarinic cholinergic receptors are seen at Stomach, CNS , Glands
61. ALPHA ADRENERGIC RECEPTORS
• Alpha 1a blocker used for BHP without any effect on blood pressure - Tamsulosin
• Dale's vasomotor reversal is due to Alpha blocker
• Prazosin, Indoramin & Idazoxan are alpha blocker
• Clonidine is Alpha 2 receptor agonist
• In a hypertensive patient with glaucoma, Alpha blocker is given
• Alpha-1 agonist used as Nasal decongestant
• Selective alpha 2 agonists used in glaucoma - Brimonidine.
62. ENZYME INHIBITION (COMPETITIVE, NON-COMPETITIVE AND UNCOMPETITIVE)
• The presence of a noncompetitive inhibitor can Lead to a decrease in the observed Vmax
• A competitive inhibitor of an enzyme will Bind to the same site as the substrate
• In competitive inhibition Vmax is unchanged but Km increased
• Disopropyl phosphorofluoridate (DFP) reacts with serine proteases irreversibly and therefore
is Non-competitive inhibitor
• In noncompetitive antagonism Km value decreased; V max decreased
• Atropine is useful in organophosphate poisoning because it is a competitive antagonist of
acetylcholine
• Non-competitive inhibitor of carbonic anhydrase is Acetazolamide
• Non-depolarizing muscle relaxants are Competitive inhibitor of acetylcholine
• Imatinib and suntinib are competitive inhibitors of tyrosine kinase
• If V max decrease to 80% due to an inhibitor and Km is same as before Non competitive type of
inhibition
• Cyanide affects respiratory chain by Non-competitive irreversible inhibition
• Substance which binds to substrate other than catalytic enzyme is Non-competitive inhibitor.
63. GLUCOCORTICOIDS
• Drug causing hyperglycemia is Glucocorticoid

• Glucocorticoids causes Muscle wasting, Diabetes mellitus, Osteoporosis,Peptic
ulceration, Cataracts
• Induction of thymic involution, Production of surfactant by type II alveolar cells & Functional
hypothalamopituitary axis depends on production of maternal or fetal glucocorticoid
• Glucocorticoids given to a case of Preterm Labour help in reducing Respiratory distress
syndrome, Intraventricular hemorrhage, Necrotising enterocolitis
• Stress-induced hyperglycemia is due to Glucocorticoids
• Oral candidiasis can occur as a side effect of inhaled glucocorticoids in bronchial asthma
• Glucocorticoids act in inflammation by ↑ LipocorƟn
• Cortisone has least glucocorticoid activity
• Compared to hydrocortisone, maximum glucocorticoid activity is seen in Hydrocortisone
• Short acting glucocorticoid is Hydrocortisone
• Longest acting glucocorticoids is Dexamethasone
• The primary goal of glucocorticoid treatment in rheumatoid arthritis is Suppression of inflammation
and improvement in functional capacity
• Glucocorticoids drug produce neutrophilia
• Betamethasone is the most potent glucocorticoid
• Glucocorticoids induces apoptosis in a cell
• Pregnenolone is Common precursor of mineralocorticoid, glucocorticoids and sex steroids
• Intracellular receptors are used by glucocorticoid
• Chemical process involved in conversion of progesterone to glucocorticoids is Hydroxylation
64. MINERALOCORTICOID

• Mineralocorticoid receptors are present in Hippocampus, Kidney, Colon
• Metabolic alkalosis is seen in Primary mineralocorticoid excess
• Mineralocorticoid deficiency causes metabolic acidosis
• Mechanism of hypokalemia in Gitelman syndrome is Mineralocorticoid Excess
• Apparent mineralocorticoid excess is due to 11-13 hydroxysteroid dehydrogenase
• Least mineralocorticoid activity is seen in Methylprednisolone, Dexamethasone, and Triamcinolone
• Spironolactone is a mineralocorticoid antagonist
• The diuretic group that does not require access to the tubular lumen to induce diuresis
is Mineralocorticoid antagonist
• Most potent mineralocorticoid is Aldosterone
• Mineralocorticoid with no glucocorticoid activity Desoxycorticosterone acetate (DOCA).
65. ASPIRIN
• At usual therapeutic doses (blood levels), expected effects of aspirin include efficacy greater than
acetaminophen as an anti-inflammatory agent.
• Aspirin is contraindicated in Warfarin.
• In low doses, aspirin inhibits cyclo-oxygenase.
• Important effects of aspirin include reduction of fever, prostaglandin synthesis in inflammed tissues
& Respiratory stimulation.
• Aspirin irreversibly inhibits platelets.
• Aspirin is useful in prevention of heart attack and stroke.
• Aspirin is contraindicated in Peptic ulcer.
• In aspirin poisoning most important step is Fluids.
• Aspirin and NSAIDS are most commonly involved in Anaphylactoid reaction.
• Aspirin hypersenstitivity is seen along with Nasal Polyposis.
• Mechanism of action of Aspirin in MI is Thromboxane A2 synthesis inhibition
• Low doses of aspirin used in myocardial infarction act by Inhibiting cyclooxygenase
• Antiplatelet action of aspirin is due to Decrease thromboxane A2 synthesis.
• Aspirin is associated with Reye's Syndrome.
• An elective surgery is to be done in a patient taking heavy doses of Aspirin. Management consists
of Stopping aspirin for 7 days and then do surgery
• A patient is on aspirin shows Prolonged BT
• Aspirin + Low molecular weight Heparin is recommended in a woman with Antiphospholipid
Antibodies and history of prior abortions / still birth.
• Low doses of aspirin therapy is essentially advised for IUGR, Post myocardinal infarction & Pre
ecclampsia.
• Aspirin reduces risk of TIA.
• Anti-inflammatory dose of aspirin is 3 - 6 g/d.
• Chemically aspirin is Acetyl salicylic acid.

66. K+ SPARING DIURETICS
• In patients with decompensated cirrhosis on diuretic therapy with tender gynaecomastia, the best
diuretic to substitute is Amiloride (10-40 mg/day) for spironolactone
• The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal
hypertension is Furosemide 160 mg and spironolactone 400 mg
• Antiandrogen is the MOST important adverse reaction of spironolactone therapy
• Spironolactone, Eplerenone & Triamterene drugs act as potassium-sparing diuretics
• Triamterene is only slightly soluble and may precipitate in the urine, causing kidney stones.
• Spironolactone should NOT be given with ACE inhibitors
• Spironolactone alters cardiac mortality
• The primary site of action of triamterene and spironolactone is the Distal tubule and collecting
duct.
• Eplerenone & Spironolactone are Aldosterone antagonist
• Spironolactone is the first drug to be given for Cirrhotic edema
• Mainstay of treatment of Nephrogenic Diabetes Insipidus is Thiazide / Amiloride diuretics and salt
restriction
• Spironolactone is least commonly used in Hypertension
67. LOOP DIURETICS
• Hyperglycemia, Hypomagnesemia, acidosis, Hypokalemia, Ototoxicity & Hyperuricemia are adverse

effects can be caused by Loop Diuretics
• The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal
hypertension is Furosemide 160 mg and spironolactone 400 mg
• Loop diuretic is the mechanism of action of bumetanide
• Loop diuretics are most likely to result in contraction alkalosis
• Loop diuretics act on Thick ascending limb
• Ethacrynic acid causes increased concentration of Na' & Cl- in urine with normal bicarbonate
• Furosemide is used in pulmonary edema
• Ethacrynic acid is not used due to Ototoxicity
• Loop diuretics interact with cefotaxime
• IV fluid with furosemide is given in Hypercalcemia
• Drug of choice for acute left ventricular failure is I/V Furosemide
• Furosemide is excreted unchanged in urine
• Diuretics of choice for acute pulmonary edema is Loop diuretics
• The site of action of the loop diuretic furosemide is Thick ascending limb of loop of Henle
68. PARACETAMOL
• Paracetamol poisoning produces Metabolic acidosis

• Vesiculobullous lesion healed with hyperpigmentation on the glans soon after taking tablet
paracetamol for fever suggest Fixed drug eruption
• In cases of moderate to severe poisoning of paracetamol, N-acetyl cysteine (mucomyst) should be
given orally within 24 hours of overdose to prevent hepatic damage.
• Paracetamol is one of the safest NSAIDs produces very little GI toxicity and can be administered in
patients intolerant to other NSAIDs.
• Kit B given at subcentre is Paracetamol
• Sterile pyuria may occur due to Paracetamol
• A patient presented with vomiting, pain in abdomen, jaundice and encephalopathy. There is a
history of attempt to commit suicide. Poisoning suspected is Paracetamol
69. PHENYTOIN
• Phenytoin follows zero order kinetics

• Phenytoin is a potent microsomal enzyme inducer
• Phenytoin is Highly protein bound
• Phenytoin with increasing dose, the T 1/2 increases
• Dilantin (Phenytoin) is known to cause folic acid deficiency
• FOS phenytoin is Used for generalized tonic-clonic seizures
• FOS phenytoin is a Prodrug
• FOS phenytoin is Highly protein bound
• Phenytoin acts on voltage-sensitive neuronal Na+ channels
• Phenytoin Used by slow IV injection in status epilepticus
• In Phenytoin Kinetics change from 1st order to 0 order over therapeutic range
• A lady having epileptic seizure with phenytoin therapy and become pregnant, Treatment
is Tapering to lowest level of phenytoin and continue pregnancy
• Adverse effect of phenytoin include gingival hyperplasia, Lymphadenopathy, Ataxia & Hirsutism
• Pseudolymphoma is a manifestation of Phenytoin
• Fetal hydantoin syndrome is caused by Phenytoin
• Phenytoin toxicity shows Gum hypertrophy
• Toxic epidermonercrolysis is caused by Phenytoin
• Fosphenytoin route of administration Intravenous
• Exanthema is caused by Phenytoin
70. BENZODIAZEPINE
• Diazepam poisoning is treated by Flumazenil

• Benzodiazepine antagonist Flumazenil
• Benzodiazepines of choice in elderly and those with liver disease Lorazepam, Orazepam
& Temazepam
• Shortest acting benzodiazepine is Triazolam
• Benzodiazepine without anticonvulsant property is Temazepam
• To avoid future recurrence of seizure attacks Oral Diazepam 6 hourly is given
• Alprazolam is an anxiolytic benzodiazepine with antidepressant action
• IV diazepam shows Coronary dilatation
• Inverse agonist of benzodiazepine receptor is Beta carboline
• Midazolam causes Anterograde amnesia, tachyphylaxis during high dose infusions & Decreased
cardiovascular effects as compared to propofol
71. Anti-Parkinsonism Drugs
• Carbidopa is used in the treatment of Parkinsonism because It decreases peripheral utilization of L-

dopa
• Contraindication to breast milk feeding is Bromocriptine therapy for mother
• Bromocriptine Inhibits prolactin release
• Bromocriptine, Ropinerole & Pramipexole are dopaminergic agonists used for parkinsonism
• Pyridoxine abolishes the therapeutic effect of levodopa by enhancing peripheral decarboxylation of
levodopa
• In Parkinsonism, phenothiazines reduce the efficacy of levodopa
• Levodopa is a prodrug
• Levodopa can cause On-off phenomenon
• Entacapone enhances the bioavailability of levodopa
• Rotigotine is intended to be delivered through transdermal patches, so as to ensure a slow and
constant dosage in a 24-hour period.
• Antiparkinson drug known to cause cardiac valvular fibrosis is Pergolide & cabergoline
• Drug of choice for drug-induced parkinsonism Anticholinergic
• Benzhexol is Drug of choice in drug-induced Parkinsonism
• Drug of choice for the initial treatment of parkinsonism is Ropinirole
• Central anticholinergics are used in treatment of Akathisia, Parkinsonism & Acute dystonia
• Bromocriptine is used in Type II DM, Parkinsonism, Hepatic Coma & Cyclical mastalgia
• Rotigotine is Dopamine agonist
• Patient on treatment on carbidopa + levodopa for 10 yrs now has weaned off effect should be
given Rasagiline
72. Histamine & Histaminic receptors
• Histamine causes Arteriolar dilatation, Increased permeability of venules & Constriction of large
arteries
• Histamine is found in Mast cells
• Histamine Increases gastric acid secretion
• The role of histamine in acute inflammation mediates increase in Related to arousal and blood
pressure,vascular permeability, chemotaxis, Release of pain causing substances
• HCL secretion is stimulated by Histamine
• Increased permeability in acute inflammation is due to Histamine
• Vasoactive amines, involved in inflammation are Histamine
• H1 blockers are useful as Anti-allergic
• Pulmonary vasodilatation is caused by Histamine
• Triple response is due to Histamine
73. MONOCLONAL ANTIBODY
• In monoclonal antibody production, monoclonal cells are differentiated from Myeloma cell lines
• Bevacizumab is Monoclonal antibody against VEGF
• Herceptin (trastuzumab) prescribed in breast cancer is a monoclonal antibody produced by
injecting her-2 antigen
• Monoclonal antibody against VEGF is Bevacizumab
• The monoclonal antibody useful in the treatment of PNH is Eculizumab
• Monoclonal antibody Produced by hybridoma technology
• Monoclonal antibody Used for blood grouping
• Monoclonal antibody Requires in small quantity
• Cetuximab and rituximab are Chimeric monoclonal antibodies
• Cardiomyopathy is caused by Trastuzumab
• DENOSUMAB a monoclonal antibody against RANKL receptor is used in the treatment
of Osteoporosis
• HER2/neu overexpression in Ca breast Responds well to monoclonal antibodies
• Rituximab is an anti-cancer drug comes under monoclonal antibodies
• Rituximab is a Chimeric monoclonal antibody against CD-20 B cell antigen
• Most common side effect of Rituximab is infusion reaction
• Rituximab is First FDA drug approved for resistant lymphomas
74. VALPROIC ACID (SODIUM VALPROATE)
VALPROIC ACID (SODIUM VALPROATE)
Augmented release of inhibitory neurotransmitter GABA,
• Increased GABA levels in blood.
Highly effective and DOC:
• Absence seizure
• Myoclonic and atonic seizures
Interactions:
Effects of concurrent usage:
• Mutual induction of metabolism - with Carbamazepine

• Administration with clonazepam contra-indicated
Adverse effects:
Hepatotoxicity (Fulminant hepatitis):
• Asymptomatic rise in serum transaminase.

• Metabolite "4-pentanoic acid" - causes hepatotoxicity
Treatment:
• Carnitine - ameliorate mitochondrial enzyme deficiency
Intake during pregnancy:
• Neural tube defects in offspring.
75. ANTI-THYROID DRUGS
ANTI-THYROID DRUGS:
• Inhibit thyroxine synthesis

• Drugs included: Propylthiouracil, Methimazole & Carbimazole.
• Blocks thyroxine synthesis by,
• Inhibits thyroid peroxidases.
• Inhibit iodination of tyrosine residues in thyroglobulin.
• Inhibit coupling iodotyrosine residues forming T3 & T4.
• Actions unaffected include, T3 & T4 action in peripheral tissues & pituitary.
• Transfer across placenta & milk (less with propylthiouracil).
• Adverse effects include congenital malformations (Specific to carbimazole) & Aplasia
cutis congenita.
Propylthiouracil:
• MOA: Peripheral conversion of T4 to T3 inhibited.

• Major advantage:
• Highly plasma protein bound.
• So less trans-placental & milk diffusion.
• No active metabolite.
• Hence, No congenital malformations associated.
Carbimazole:
• Antagonize propylthiouracil.
• Plasma t1/2 : 6-10 hrs.
• 3 times more potent.
• Duration of action: 12-24 hrs.
• Major disadvantage:
• Active metabolite - Methimazole.
• Increased trans-placental & milk diffusion.
Effects in Pregnancy:
Congenital malformation:
• Scalp or patchy hair defect (aplasia cutis congenita).

• Choanal atresia.
• Hypoplastic or absent phalanges (low set fifth finger).
• Minor facial anomaly (Flat face, low set ears & upper lip traction).
Indications:
• Thyroid Storm:
• Thyrotoxicosis in Grave's disease & Toxic Nodular Goitre in pregnancy
Contraindications:
• In pregnancy
• Carbimazole:
• Hyperthyroid pregnant women.
• Causes Aplasia Cutis Congenita.
Advantages of anti-thyroid drugs:
1. Hyperthyroidism in Pregnancy:
• DOC: Propylthiouracil (low doses).

• Less transfer across placenta & milk.
• High plasma protein binding ability.
• No risk of congenital malformations.

2. Preferences over surgery / I131
76. CYCLOSPORIN
CYCLOSPORIN
• Specific T-cell Inhibitor/ Calcineurin Inhibitor

• Inactivates calcineurin.
• Acts by selective inhibition
• Suppress responses of primed helper T-cells
• Hence, useful in auto-immune diseases
• Bile-independent.
• Prevents graft rejection, unaffecting host's immune system.
• No toxic effects on bone marrow & RE system.
Adverse effects:
• Nephrotoxicity
• Post-transplant hypertension
• Hyperuricemia, hyperkalemia & hypomagnesemia
• Hirsutism
• Gum hyperplasia
• Tremor
• Seizures
Indicated in:
• Prevention and treatment of graft rejection reaction.

• Routinely used in renal, hepatic, cardiac, bone marrow.
• Autoimmune diseases - Second line drug.
• Severe rheumatoid arthritis, uveitis, IBD, psoriasis.
• Aplastic anaemia.
Drug interactions:
• Enhanced toxicity when given along with Vancomycin, Amphotericin B, & NSAIDS.
77. DOSE RESPONSE CURVE
DOSE-RESPONSE CURVE

• Best mode to study response of wide number of drugs in population is DRC.
• ED50 refers to Effective Dose of a drug.
• ED 50 is a measure of Potency.
• Therapeutic index is a measure of the margin of safety of a drug.
• Therapeutic index = Median lethal dose/Median effective dose.
• LD 50/ ED 50
• The maximum effect of a drug is defined by Efficacy.
• Efficacy is more important for choice of a drug.
• In non-competitive inhibition, potency is reduced.
78. THERAPEUTIC DRUG MONITORING
THERAPEUTIC DRUG MONITORING
THERAPEUTIC WINDOW:
• Is the minimum dosage necessary for a patient to benefit from the main effects intended of a
specific drug.
TDM testing is performed for drugs with lower therapeutic index.
• Eg: Digitalis, aminoglycosides, Gentamycin, TCA's, theophylline, Lithium, anti-epileptics,

Immunomodulators & antiarrhythmics.
TDM testing is not performed for whose drugs whose effect are easily measured.
• Eg: Anti-hypertensives - Via BP monitoring.

• Anti-coagulants (Warfarin) - Bleeding time monitoring.
• Anti-Diabetics - Metformin.
79. ANTI-CHOLINERGIC DRUGS
ANTI-CHOLINERGIC DRUGS
ATROPINE:
• Atropine is derived from Atropa belladonna.

• Atropine is used as Mydriatic, Cycloplegic & Preanaesthetic medication
• An antidote for Mushroom poisoning, Organophosphates poisoning & Carbamates poisoning.
• Percentage of atropine in "Atropine eye drops" as cycloplegic is 1%
• Atropine is most sensitive to mucous & pharyngeal secretions.
• Atropine is useful in organophosphate poisoning because is a competitive antagonist of
acetylcholine
• Mydriatic used in 3 years old child for refraction is 1 % Atropine ointment
• Drug of choice for increased IOT in acute anterior uveitis is atropine
• Atropine is drug of choice in Iridocyclitis.
• Pirenzepine is an Antiulcer drug.
• Hyoscine is most effective agent to prevent motion sickness.
• Valethamate is an anticholinergic which is tertiary amine.
• Tropicamide - Short-acting mydriatic.
• Hyoscine - More potent mydriatic action.
• Oxybutynin - Maximum risk of dry mouth.
80. DRUG DISTRIBUTION
DRUG DISTRIBUTION
• Loading dose depends on volume of distribution.

• Apparent volume of distribution of a drug exceeds total body fluid volume if a drug is sequestrated
in body tissues.
• Dosage of drug is determined by volume of distribution, half-life & lipid solubility.
81. NEWER ANTI-DIABETIC DRUGS
NEWER ANTI-DIABETIC DRUGS
1. Incretins:
• Incretin - Acts on pancreatic β-cell Anticipatory insulin release.
Ex:
• glucagon-like peptide-1 (GLP1)

• glucose-dependent insulinotropic polypeptide (GIP)
• vasoactive intestinal peptide (VIP)
• pancreozymin-cholecystokinin.
MOA:
• Enhances insulin release by increasing cAMP formation in β cells.

• In DM type-2 - GLP-1 secretion is reduced.

Action of GLP-1 -
• Little stimulatory effect on insulin secretion (at normoglycemic concentration) - Hence, GLP-1 has
lower risk of causing hypoglycemia.
• Other actions:
Suppress glucagon secretion.
Preserves islet cell integrity & decreases its apoptosis.
Delays gastric emptying causing reduced appetite
Properties of GLP-1:
• Endogenous GLP-1 rapidly broken - By dipeptidyl peptidase-4 (DPP-4).

• pharmacologically, incretins can be employed -
• Via GLP-1 receptor agonists
• Via DPP-4 inhibition - Oral active inhibitors of DPP-4 enzyme - Indirectly acting insulin
secretagogues.
2. GLP-1 receptor agonists:
• Acts by mechanism similar to GLP-1.

• Administered subcutaneously.
• Ex:
• Exenatide & Liraglutide.
• Latest drugs - Albiglutide & Dulaglutide.
Advantages - Promote weight loss.
Adverse effect - Nausea (Common)
Contra-indication - Family history of medullary thyroid cancer or MEN-2.
Individual drugs –
Liraglutide -
• Longer acting (once daily)

• Does not require dose adjustment in renal failure
• Also used for obesity management.
Exenatide -
• Twice daily
• Dose adjustment needed (should be reduced).
3. DPP-4 Inhibitors:
MOA:
• Prolongs endogenous GLP-1 action, by inhibiting GLP-1 metabolism through DPP-4.

• Orally effective.
• Eg: Sitagliptin, vildagliptin, saxagliptin, alogliptin, empagliflozin & Linagliptin.
Advantages - Do not cause nausea or weight loss.
Disadvantages:
• Require dose adjustment in renal failure except linagliptin.

• Vildagliptin - Cause hepatitis.
4. Sodium-glucose co-transporter-2 inhibitors (SGLT-2 inhibitors):
MOA:
• SGLT-2 inhibitors act by inhibiting this transporter Causing glucosuria in diabetics causes
weight loss.
• Effective orally.
• Efficacy reduced in renal failure.
• Eg: Dapagliflozin & canagliflozin.
Adverse effect - Increased incidence of UTI & genital infections.
Dapagliflozin:
• Higher rates of breast & bladder cancers.

• After single daily dose Produce round-the-clock glucosuria & lowers blood glucose levels.
• Glycosuria predisposes to,
• Urinary & genital infections
• Electrolyte imbalance
• Increased urinary frequency.
5. Dopamine D2 agonist:
Bromocriptine mesylate:
• An adjunct to diet & exercise.

• Improves glycemic control in type -2 diabetes.
• MOA: Dopamine alters insulin resistance - By acting on hypothalamus.
• Bromocriptine targets D2 receptors.
6. Amylin analogs/ Amylin:

Drugs included - Pramlintide:
• Synthetic analog of islet amyloid polypeptide (IAPP).

• Administered by subcutaneous route.
• Approved for both type 2 & type 1 DM treatment.
MOA:
• Decreases glucagon secretion

• Delays gastric emptying
• Decreases appetite
• Can cause hypoglycemia & weight loss.
82. ORAL HYPOGLYCEMIC DRUGS
ORAL HYPOGLYCEMIC DRUGS
• Insulin secretagogues - Drugs include sulfonylureas & meglitinides.

• Shortest acting sulfonylurea - Tolbutamide.
• Longest acting sulfonylurea - Chlorpropamide.
• All drugs can cause hypoglycemia (maximum with Chlorpropamide) & weight gain.
• Chlorpropamide - Cause dilutional hyponatremia (ADH like action), cholestatic jaundice &
disulfiram-like-reaction (alcohol intolerance).
• Gliclazide - Additional anti-platelet action.
• Glimepiride exerts beneficial effects with ischemic pre-conditioning.
• Due to lower potency & shorter duration of action.
• Tolbutamide & glipizide are relatively safe in elderly patients & renal disease.
• Insulinotropic potency - Maximum - Glyburide (Glibenclamide); Least – Tolbutamide.
• Glyburide effect persists beyond 24 hrs. Persistent effect due to,
• Production of active metabolite.
• Binding to membrane receptor.
• Gets sequestered within β-cells of pancreas - Distinguishing property of sulfonylurea.
• Among sulfonylureas, glimepiride decreases blood glucose at lowest dose.
• Meglitinides drugs included - Nateglinide & repaglinide.
• Uses - For treatment of postprandial hyperglycemia (due to rapid onset & short duration of action).
• Disadvantages - Result in hypoglycemic episodes & weight gain.
• Biguanides-
• Decreases blood glucose by activating AMPK (Adenosine Mono Phosphate-activated protein
kinase).
• Mode of action -
• Decreasing glucose production - By inhibiting gluconeogenesis & glycogenolysis.
• Increasing glucose utilization - By stimulation of glycolysis & tissue glucose uptake.
• Also inhibits intestinal glucose absorption.
• Reduced hepatic glucose production - By antagonizing glucagon’s ability to generate cAMP in
Hepatocytes.
• Phenformin -
• Lactic acidosis - More likely in presence of hepatic & renal impairment or alcohol ingestion.
• Metformin -
• Useful for polycystic ovarian disease (PCOD).
• Only oral agent demonstrating reduce macrovascular events in type-2 DM.
• First-line therapy for type 2 diabetes & cause maximum reduction in HbA1C levels.
• Disadvantages:
Megaloblastic anemia (due to vitamin B12 deficiency)
Interferes with calcium-dependent vitamin B12 absorption-intrinsic factor complex
in terminal ileum
3. Thiazolidinediones:
• Thiazolidinediones used to reverse insulin resistance in type II DM.

• Drugs - Troglitazone, pioglitazone & rosiglitazone.
• MOA: Acts as agonists of nuclear receptor (peroxisome proliferator-activated receptor gamma
(PPAR7).
• Disadvantages -
• Cause weight gain & edema.
• New onset or worsening of macular edema
• Increase in fracture risk in women
• Anemia
• Plasma volume expansion - Be avoided in CHF patients. (NYHA class III & IV).
• Troglitazone - Hepatotoxicity (More incidence).
• Rosiglitazone - Increases total & LDL cholesterol as well as HDL-cholesterol.
• Pioglitazone -
• Increases HDL cholesterol.
• Increased risk of bladder cancer on long-term use.
83. OPIOID ANTAGONIST
OPIOID ANTAGONISTS
• Naloxone, Naltrexone & Nalmefene are potent µ-receptor antagonist

• Methylnaltrexone, Alvimopan & Naloxegol are peripheral opioid antagonists
• Naloxone is ineffective orally & given parenterally.
• Nalmefene is given parenterally.
• Naltrexone is orally-effective.
• Opioid antagonist mainly reverses opioid effects on i.v. administration.
• Main uses of naloxone are drug of choice for acute opioid poisoning & neonatal resuscitation for
reversing opioid effects.
• Naloxone precipitates withdrawal symptoms.
• Naltrexone used as for maintenance drug for opioid poisoning, for preventing relapse, after opioid
de-addition & decreases craving in chronic alcoholics.
• Naltrexone along with bupropion for obesity treatment.
• Peripheral opioid antagonist indicated for opioid-induced constipation.
• For short duration/small doses of opioid addiction - Stoppage of drug attempted & treated with β-
blockers/clonidine/lofexidine.
• For long duration/large dosage addiction - Sudden withdrawal is dangerous & treated
with Methadone maintenance.
• For relapse prevention after de-addiction, Naltrexone is used.
• Naltrexone mainly prevents euphoric action by blocking µ receptors.
84. OPIOID DRUGS
OPIOID DRUGS
• Opioid drugs are substances obtained from crude extracts of Papaver somniferum (poppy plant).
• Main used as analgesic agents.
• Opioid receptors include, µ, κ and δ receptors.
• Pure
opioid includes Morphine, Methadone, Heroin, Hydromorphone, Oxymorphone, Pethidine, Codeine
, Hydrocodone & Oxycodone.
• Mixed agonist-antagonist drugs include Buprenorphine, Butorphanol, Nalbuphine, Pentazocine
& Tramadol.
• Opioid antagonists includes Naloxone, Naltrexone, Nalmefene & Naloxegol.
• Endogenous peptides include Endorphins, dynorphins, enkephalins & Nociceptin.
• Endorphins act on µ receptor; Dynorphins acts on κ receptor; Enkephalins acts on δ receptors.
• Morphine - Administered by oral, rectal, i.v., i.m., intrathecal or epidural routes.
• Fentanyl - Applied as transdermal patch; also administered by buccal transmucosal route.
• Butorphanol - Only opioid available in nasal formulation.
• Morphine acts on µ, κ and δ receptors.
• Morphine produce respiratory depression, cough suppression & miosis.
• Main feature for opioid poisoning diagnosis - Pinpoint pupil.
• Highly lipid soluble drugs include fentanyl, alfentanil & sufentanil.
• Fentanyl, alfentanil & sufentanil causes truncal rigidity on rapid i.v. infusion.
• Pure opioids peripherally cause increased heart rate, decreases BP & constipation.
• Alvimopan, a peripheral opioid antagonist, mainly used for paralytic ileus, because
of increased intrabiliary pressure, by constricting biliary smooth muscle.
• Morphine (i.v.) used in myocardial infarction, acute pulmonary edema & pre-anesthetic medication.
• Codeine, pholcodine, dextromethorphan & noscapine are effective cough suppressants.
• Loperamide & diphenoxylate used for non-infective diarrhea treatment.

• Highly lipid soluble drugs (fentanyl, alfentanil, sufentanil) are used as adjuncts to
other anaesthetic agents.
• Pethidine are used to reduce shivering after anaesthesia, due to its action on α2 receptor.
• Dextromethorphan is a drug devoid of constipating action.
• During pregnancy, prolonged opioid use --> Causes in-utero physical dependence of fetus &
precipitates severe withdrawal symptoms after birth.
• Morphine is absolutely contraindicated in head injury, due to increased intracranial tension,
respiratory depression & causes CO retention.
• Morphine mainly interferes with neurological function assessment & masks important pupillary
signs, resulting in miosis.
• Pethidine & pentazocine is contraindicated in MI.
• Methadone is a long-acting opioid analgesic, with potent agonistic actions at µ receptors.
• Methadone relieves neuropathic & cancer pain - Uncontrolled with morphine.
• Methadone useful for opioid abuse treatment & opioid rotation therapy - mainly due to its long t
1/2, development of dependence & very slow tolerance.
• Pethidine & pentazocine are relatively safer in biliary colic, due to anticholinergic properties.
• Accumulation of active metabolite of pethidine (norpethidine) can produce seizures.
• Propoxyphene is least potent & least efficacious analgesic agent.
• Diphenoxylate, difenoxin are useful for diarrhea.
• Nalbuphine shows ceiling effect to its respiratory depressant action.
• Buprenorphine dissociates slowly from µ receptors & is resistant to naloxone reversal.
• Butorphanol, pentazocine & dezocine have psychomimetic effects with κ-agonistic activity.
• Ziconotide are intrathecal analgesia, acts by blocking voltage-gated N-type Ca2+ channels.
• Tramadol are weak µ-receptor agonist.
• Tapentadol is a new drug with µ-receptor agonistic action & NA reuptake inhibiting action.
• Mixed agonists antagonist drugs included Buprenorphine, Nalbuphine, Pentazocine, Dezocine &
Butorphanol.
• Nalbuphine, pentazocine & dezocine are κ-agonists and µ-receptor antagonists.
• Buprenorphine are partial µ-receptor agonist with mild κ- and δ-antagonistic property.
• Butorphanol is predominant κ-agonist.
• Nalbuphine, pentazocine & dezocine produces psychomimetic effects with hallucinations,
nightmares & anxiety.
• Butorphanol is more sedative than morphine.
85. ERECTILE DYSFUNCTION
ERECTILE DYSFUNCTION
• Nitric oxide (NO) increases cGMP levels (This most important step is metabolized by
phosphodiesterase) --> smooth muscles relaxation of corpora cavernosa --> Penile erection.
• Primary & most common cause for ED is psychological.

• Secondary causes for ED include arteriosclerosis, hypertension, diabetes, smoking & alcohol
consumption.
• Diuretics have the maximum risk factor for causing ED.
• Alpha agonists (Phenylephrine), Beta blockers, CCB’s also cause erectile dysfunction.
• Phosphodiesterase (PDE) inhibitors are the mainstay for treating erectile dysfunction.
• PDE inhibitors include drugs like Sildenafil, vardenafil, udenafil, avanafil, tadalafil & Papaverine.
• Main mechanism behind PDE inhibitors is by blocking PDE enzyme, which
metabolizes cGMP formation by NO.
• Phosphodiesterase inhibitors are not to be prescribed for patients on nitrates, due to severe
hypotension risk.
• Sildenafil selectively inhibits PDE-5 & increases cGMP levels.
• Sildenafil causes color vision defect (blue vision), due to inhibition of PDE-6, present in retina.
• Tadalafil is the longest acting phosphodiesterase inhibitor.
• Avanafil is the new drug for ED.
• Papaverine is a non-selective PDE inhibitor used for treating ED.
• Apomorphine is a dopamine (D1) agonist, given sublingually for treating ED.
• Phentolamine is an α1 and α2 blocker (Non-selective), used for treating erectile dysfunction.
• Yohimbine is an α2 blocker, used for treating erectile dysfunction.
• L-arginine is a NO precursor used for treating ED.
• Trazodone is an anti-depressant used for treating ED.
• Combination of Trazodone (an antidepressant) & phentolamine (non-selective α blocker) is used for
treating ED.
• Intracavernosal injection therapy includes usage of PGE analogs, α-blockers, non-selective PDE
inhibitors & VIP analogs.
• Ketanserin (5-HT2) & alprostadil (α-receptor antagonist) combination is given intracavernosal for
treating ED.
• Papaverine is a non-selective PDE inhibitor used for treating ED.
• Thymoxamine & Phentolamine are given as intracavernosal injections, for treating ED.
• Thymoxamine is used for treating ED, mainly by acting as α-blocker with vaso-dilatory property.
• Alprostadil is a PGE1 analog, given directly in cavernosal tissue, for persons unresponsive to oral
sildenafil therapy during ED treatment.
86. ANTI-OBESITY DRUGS
ANTI-OBESITY DRUGS
• Arcuate nucleus in mediobasal hypothalamus is the main integrating center for feeding &
regulation of body weight.
• 5-HT2 activation causes weight loss.
• Drugs targeting 5-HT2 receptor includes mainly Lorcaserin, which is a selective
5HT2c agonist which decreases appetite.
• Orlistat is used as an anti-obesity drug, which mainly acts by inhibiting gastrointestinal lipases.

• Sibutramine is an appetite suppressant, acts by blocking pre-synaptic uptake of both nor-
epinephrine & serotonin.
• Rimonabant is used as an anti-obesity drug, which mainly acts
by antagonizing cannabinoid (CB1) receptor.
• Rimonabant mainly blocks orexigenic action of ghrelin, increases serotonin & dopamine levels,
ultimately resulting in appetite reduction.
• Rimonabant is an anti-obesity drug, which decreases BP.
• Combination of Phentermine + Topiramate is used for anti-obesity regime.
• Phentermine + Topiramate are teratogenic & contraindicated in pregnancy.
• Naltrexone + bupropion combination is recently approved for chronic weight management.
• Recently anti-obesity regime involves Neuropeptide Y (NP-Y) & Agouti-related peptide (AgRP)
antagonists, and Melanocyte-stimulating hormone (MSH) & CART (cocaine and amphetamine-
related transcript) agonists.
• Fenfluramine & dexfenfluramine were used as an anti-obesity drug but, banned due
to cardiotoxicity risk.
87. HEPARIN INDUCED THROMBOCYTOPENIA (HIT)
HEPARIN INDUCED THROMBOCYTOPENIA (HIT)
• Heparin-induced thrombocytopenia usually occurs 5-10 days after exposure to heparins.

• Type-1 HIT is a non-immune mediated reaction, resulting in decreased platelet count up to 10-
30,000/ml.
• In type-1 HIT, there is not any need for discontinuation of heparin.
• Type-2 HIT is an immune-mediated reaction, resulting in decreased platelet count up to 50%, or
less than 150,000.
• In type-2 HIT, heparin is discontinued & alternative anti-coagulant is started.
• Platelet transfusions, LMWH administration & warfarin usage particularly at initial stages, are all
contraindicated during HIT management.
• Direct thrombin inhibitors are mainstay therapy for HIT management.
• Drugs included in direct thrombin inhibitors are Lepirudin & Argatroban.
• Lepirudin & Argatroban are DOC for treating HIT.
• Lepirudin is safe in liver failure & used for indicated for HIT treatment even during hepatic
conditions.
• During HIT management, lepirudin continued till platelet count reaches 1,00,000/µL.
• Main goal aimed for lepirudin usage is achieving aPTT levels of 1.5-2.5x.
• Argatrobanused for HIT treatment nterferes at thrombin active site.
• During HIT management, only after direct thrombin inhibitors discontinuation (lepirudin
therapy), warfarin therapy is started.
• Main reason "hypercoagulability".
• Xa inhibitors like Fondaparinux & Rivaroxaban are used for HIT management.
• Heparin antibody used during management of HIT is "HIT antibodies"(IgG or PF4 or heparin).

88. ANTI-SMOKING DRUGS
ANTI-SMOKING DRUGS
• Nicotine replacement therapy is available in all forms like chewing gum, lozenges, patch, except
tablets.
• Bupropion (along with Varenicline & Nicotine replacement therapy) is a USFDA approved first-line
agent for pharmacotherapy in smoking cessation.
• Nicotine replacement therapy includes transdermal patch, gum, lozenges, oral inhaler & nasal
spray.
• Varenicline is a selective partial agonist at Alpha4-Beta2 Nicotinic A-Choline receptor, that is
believed to mediate nicotine dependence.
• Bupropion is a nicotinic receptor antagonist.
• Bupropion/amfebutamone is used both for atypical antidepressant & smoking cessation aid.
• Bupropion acts as a norepinephrine & dopamine reuptake inhibitor (NDRI), and alpha3 beta4-
nicotinic receptor antagonist.
• Bupropion is used in prophylaxis of nicotine addiction.
• Bupropion/Amfebutamone decreases nicotine craving.
• Bupropion/Amfebutamone shows increased efficacy when combined with nicotine patch.
• Mecamylamine is a nicotine antagonist, used as an anti-smoking drug.
• Nortryptyline is an active metabolite of amitriptyline, used as an anti-smoking drug.
89. BENIGN HYPERTROPHY OF PROSTATE (BHP)
BENIGN HYPERTROPHY OF PROSTATE (BHP)
• Drugs used for treating BHP include Selective α1-blockers & 5-α reductase inhibitors.
• α-adrenoceptor blockade results in smooth muscle relaxation in neck of urinary bladder & prostatic
urethra, reduces dynamic obstruction, increases urinary flow rate & causes complete bladder
emptying in BHP patients.
• Selective α1-blockers relieves dynamic obstruction & provides rapid symptomatic relief in BHP.
• Selective α1-blockers afford faster (within 2 weeks) & greater symptomatic relief (than finasteride).
• Selective α1-blockers relieves voiding symptoms (hesitancy, narrowing of stream, dribbling &
increased residual urine) effectively.
• Selective α1-blockers does not affect prostate size.
• Selective α1-blockers includes prazosin, terazosin, silodosin, doxazosin & alfuzosin.
• Selective α1-blockers are DOC for BHP.
• DOC for BHP cases with hypertension is Prazosin/Doxazosin.
• DOC for BHP cases without hypertension -Tamsulosin.
• Prazosin blocks α1 receptors in bladder trigone & prostatic smooth muscle --> Improves urine flow
& reduces residual urine in bladder.
• Tamsulosin & Silodosin acts by selectively inhibiting α1A receptor (α1 subtype) present in prostate.
• Tamsulosin & Silodosin has reduced propensity to cause postural hypotension, hence preferred for
treating BHP.
• 5-α reductase inhibitors like Finasteride & dutasteride.
• 5-α reductase enzyme converts DHT to testosterone.
• 5-α reductase inhibitors block 5-α reductase enzyme, conversion of dihydrotestosterone to
testosterone is blocked --> reduced DHT production --> Prostate gland growth is controlled.
• 5-α reductase inhibitors treats BHP by arresting growth/reducing prostate size.
• 5-α reductase inhibitors are used for relieving static component of urinary obstruction in BHP.
• Finasteride is 5α-reductase antagonist, mainly type II.
• Finasteride inhibits conversion of testosterone to dihydrotestosterone & reduces prostate volume.
• Finasteride reduces serum & prostatic concentrations of dihydrotestosterone --> prostatic volume
decrease & urine flow rate increases, hence useful for BHP treatment.
• Finasteride exhibits delayed action; hence, takes >3 months to exert its beneficial effect.
90. THALIDOMIDE
THALIDOMIDE
• Thalidomide tragedy is a serious adverse effect happened in the 1960s, on using the drug as a
sedative & anti-emetic drug for morning sickness.
• Thalidomide was banned due to teratogenic effects (phocomelia).
• Thalidomide has been re-introduced & marketed recently for anticancer drug in multiple myeloma
& melanoma.
• Though thalidomide has teratogenic effects, it also possesses anti-cancer properties,
immunomodulatory & anti-angiogenic characteristics.
• Thalidomide acts by inhibiting angiogenesis.
• Two enantiomers of thalidomide (R & S), are inter-convertible within body.
• Thalidomide are indicated for multiple myelomas at initial diagnosis,its relapsed/refractory states,
erythema nodosum leprosum & skin manifestations of SLE.
• Thalidomide is used in steroid-resistant type-2 lepra reaction.
• Daily dosage of thalidomide for controlling ENL is 200-300 mg.
• Major adverse effects of thalidomide includes, teratogenicity, peripheral neuropathy, sedation &
constipation in cancer patients.
• Thalidomide causes congenital abnormalities particularly phocomelia (defect in development of
long bones).
• Immunomodulatory derivatives of thalidomide are called IMiDs.
• Lenalidomide is an ImiD's, which is more potent & non-teratogenic derivative.
• Lenalidomide is approved as first-line therapy for multiple myeloma, combined
with dexamethasone & bortezomib.
• Lenalidomide is approved recently for mantle cell lymphoma.
• Lenalidomide can cause peripheral sensory neuropathy.

• Sel CID's are Selective Cytokine Inhibitory Drugs.
• Sel CID's are thalidomide analogs.
• Sel CID's are phosphodiesterase-4 (PDE-4) inhibitors with potent anti-TNFα activity.
• Pomalidomide is a SelCIDs (Selective Cytokine Inhibitory Drugs).
• Pomalidomide is used for treatment of relapsed & refractory multiple myeloma.
• Pomalidomide acts by directly inhibiting both tumor cell & vascular compartments of myeloma
cancers.
• Pomalidomide is more efficacious than thalidomide.
91. TRICYCLIC ANTIDEPRESSANTS
TRICYCLIC ANTIDEPRESSANTS
• Tricyclic antidepressants are drugs with low safety/therapeutic index.

• TCA acts by inhibiting serotonin & noradrenaline reuptake, particularly on
• On long-term administration of TCA, desensitization of pre-synaptic α2 & 5HT receptors occurs
resulting in enhanced transmission.
• Despite immediate inhibition of reuptake process, there is long latency (2-3 weeks) for anti-
depressant action of TCA & SSRIs, mainly due to desensitization of pre-synaptic α2 & 5-HT
receptors on long-term administration.
• Active metabolite of imipramine is desipramine.
• Active metabolite of amitriptyline is Nortriptyline.
• Bupropion acts by inhibits dopamine reuptake.
• Amoxapine acts by blocking D2-receptors & also, inhibits NA uptake.
• Amoxapine is a metabolite of antipsychotic drug “loxapine”.
• Imipramine is useful in nocturnal enuresis in children.
• Most TCA's have powerful anti-cholinergic characteristics, resulting in dry mouth, bad taste,
blurring of vision, epigastric distress, constipation, urinary hesitancy (especially in males with
enlarged prostate) & palpitation.
• Bupropion, clomipramine & maprotiline lowers seizure threshold.
• Amoxapine has antipsychotic property.
• TCA with least cardiotoxic property is Lofepramine.
• Tremors & insomnia are caused by TCA, due to inhibition of pre-synaptic NT uptake.
• TCA causes postural hypotension, due to α1 adrenergic blockade.
• There is risk of extrapyramidal symptoms & convulsion, mainly because of Amoxapine
• TCA causes conduction amitriptyline defects, arrhythmias & hypotension, due to inhibition of
cardiac fast Na+ channels.
• Among TCA drugs, amitriptyline causes arrhythmia, on toxic dosage.
• TCA drugs cause hyperthermia, flushing, mydriasis, paralytic ileus, urinary retention, sinus
tachycardia, due to inhibition of muscarinic ACh receptors.
• TCA drugs are sedative in nature, mainly due to H1 histamine receptor inhibition.
• TCA overdose manifestations are mainly anticholinergic.

92. TCA POISONING
TRICYCLIC ANTIDEPRESSANT POISONING (TCA POISONING)
• TCA overdose mainly causes cardiotoxicity, particularly cardiac (ventricular) arrhythmias.

• Arrhythmia in TCA poisoning is due to inhibition of cardiac fast Na+ channels.
• TCA poisoning mainly features anticholinergic signs like hyperthermia, flushing, dilated pupils,
mydriasis (pinpoint pupil).
• During TCA poisoning, metabolic acidosis with pH3< 24 mmol/L.
• Intravenous sodium bicarbonate is the single most effective intervention particularly
cardiovascular toxicity, in TCA poisoning.
• Lignocaine is DOC for TCA-induced ventricular dysrhythmias.
• Diazepam is DOC for management of acute-onset seizures, in TCA poisoning.
• Antidote for TCA poisoning used only in comatose/convulsion/arrhythmic patients, resistant to
standard therapy is Physostigmine.
93. UTERINE STIMULANTS & RELAXANTS
UTERINE STIMULANTS & RELAXANTS
• Uterine stimulants are also known as oxytocics/ecbolics.

• Substances causing uterine stimulation include oxytocin, ergot derivatives, prostaglandins
(particularly PGE2 & PGF2α).
• Functions of oxytocin as uterine stimulants:
• Oxytocin increases uterine contractions, increases contraction of upper segment of
uterus, relaxes lower segment facilitating fetus expulsion.
• Oxytocin is mainly used for labor induction in post-maturity & uterine inertia & for postpartum
hemorrhage treatment.
• Methylergometrine, an ergometrine derivative, is a most potent oxytocic substance.
• Ergometrine derived from Claviceps purpura.
• PGE2 & PGF2α- Powerful uterine stimulants.
• Dinoprostone (PGE2) intravaginally & Carboprost (PGF2α) intraamniotic injection is used for inducing
mid-trimester abortion.
• Misoprostol (PGE2α) along with methotrexate/mifepristone is used for abortion induction in 1st few
weeks of pregnancy.
• Uterine relaxants are also known as “tocolytics”.
• Uterine relaxants are mainly to delay labor, on premature contractions.
• Uterine relaxants include β-agonists (Ritodrine, isoxsuprine & terbutaline), Magnesium sulfate,
calcium channel blockers (Nifedipine & oxytocin antagonist ‘atosiban’), ethyl alcohol (i.v. infusion),
NSAIDs, progesterone, Halothane & Hydroxyprogesterone.
• Magnesium sulfate is used to control convulsions in eclampsia.
• Magnesium sulfate possesses tocolytic activity.
• Magnesium sulfate by i.v. or inhalational route is used for treatment of acute severe asthma.
• Nifedipine & oxytocin antagonist ‘atosiban’ used for delaying premature labor & also provide best
balance of successful delayed delivery with lesser risk to mother & baby.
• Halothane is an efficacious tocolytic agent.
• Hydroxyprogesterone prophylactically prevents pre-term labor.
94. DRUGS FOR MULTIPLE SCLEROSIS
DRUGS FOR MULTIPLE SCLEROSIS
• Main drugs used for treating multiple sclerosis include Interferon-β 1a

(DOC), Glatiramer, Natalizumab, Fingolimod, Mitoxantrone, Dimethyl fumarate, Teriflunomide, Clad
ribine & Dalfampridine.
• Baclofen & tizanidine reduces spasicity in multiple sclerosis.
• Dalfampridine helps is useful in cases with abnormal gait in multiple sclerosis.
• Modafinil improves fatigue in multiple sclerosis patients.
• Frequency of relapses in multiple sclerosis patient is decreased by beta-interferon/glatiramer.
• Newer drug approved for relapse in multiple sclerosis patients is Fingolimod.
• Teriflunomide is an active metabolite of leflunomide.
• Natalizumab is a monoclonal antibody against α4 subunit of α4β1 integrin on lymphocytes, useful
in treating multiple sclerosis.
• Glatiramer resembles myelin basic protein in relapsing-remitting MS.
95. JOINT NATIONAL COMMITTEE (JNC) GUIDELINES FOR HYPERTENSION
JOINT NATIONAL COMMITTEE (JNC) GUIDELINES FOR HYPERTENSION
• Revisions in JNC 8 guidelines include first-line drugs as Thiazide, ACE inhibitors, ARBs & calcium
channel blockers (CCBs).
• Beta-blockers are no longer considered as first-line drugs, according to JNC 8 guidelines for
hypertension.
• ACE inhibitors/ARBs are first choice drugs in patients with CKD irrespective of ethnic backgrounds.
• For African descent patients without CKD, calcium channel blockers or thiazides are preferred.
• Goal for all patients < 60 years, BP should be < 140/90 mmHg, irrespective of presence or absence
of diabetes (DM) or chronic kidney disease (CKD).
• Goal for elderly > 60 years without CKD or DM or both, BP is targeted at < 150/90 mm/Hg.
• Goal for elderly > 60 years with CKD or DM or both, BP is targeted at < 140/90 mmHg.

96. TREATMENT OF PULMONARY HYPERTENSION
TREATMENT OF PULMONARY HYPERTENSION
• First-line therapy for pulmonary hypertension treatment includes oral calcium channel
blockers (including amlodipine, diltiazem & nifedipine), only if patients respond to intravenous
vasodilators.
• First-line therapy for pulmonary hypertension treatment mainly depends upon function & patient's
status if patients don't respond to intravenous vasodilators.
• Patient with WHO Class 2 symptoms are treated using phosphodiesterase inhibitors
(Sildenafil/tadalafil) & Endothelin receptor blockers (Bosentan/ambrisentan).
• Patient with WHO Class 3 symptoms are treated using prostacyclin analogs particularly
epoprostenol intravenously, iloprost by inhalation & beraprost/treprostinil subcutaneously.
• Patient with WHO Class 4 symptoms are treated with epoprostenol or iloprost, as sole agent
therapies.
• Pulmonary transplantation has high operative mortality (around 20–25%).
• Bosentan & sitaxentan are useful in treating pulmonary hypertension, which is a non-specific
antagonist of endothelin receptors, both ETA & ETB.
• Phosphoramidon is a non-specific inhibitor of endothelin converting enzyme, which is useful for
treating pulmonary hypertension.
• PGI2 analogs, particularly with vasodilator action is preferred for treating pulmonary hypertension
like epoprostenol & longer acting PGI2 analog Treprostinil.
• Soluble guanylate cyclase (sGC) stimulator like Riociguat is specifically indicated
for persistent/recurrent chronic thromboembolic pulmonary hypertension.
97. ANTI-DYSLIPIDEMIC DRUGS
ANTI-DYSLIPIDEMIC DRUGS
• First line anti-dyslipidemic drugs are statins, bile acid binding resins & intestinal cholesterol
absorption inhibitors.
• Second line anti-dyslipidemic drugs are fibrates & niacin.
• Statins act by inhibiting HMG CoA reductase enzyme competitively.
• HMG CoA reductase catalyzes in cholesterol biosynthesis, mainly conversion of HMG CoA to
mevalonate.
• Rate-limiting step in cholesterol biosynthesis is conversion of HMG CoA to mevalonate, catalyzed
by HMG CoA reductase.
• Statins decrease cholesterol synthesis in liver, by inhibiting HMG CoA reductase enzyme.
• Statins decrease bile acids & steroid hormones synthesis.
• Statins are most powerful LDL lowering agents.
• Statins decrease TG, IDL & VLDL & increases HDL slightly.
• Statins have no effect on lipoprotein.
• Statins mainly pravastatin decreases plasma fibrinogen levels.
• Statins exhibit pleiotropic effects like antioxidant, anti-inflammatory & anti-proliferative properties.
• Pitavastatin, rosuvastatin, atorvastatin, fluvastatin & lovastatin are drugs included under statins.
• Pravastatin approved for children ≥ 8 years.
• Major adverse effect of statins includes Myopathy & hepatotoxicity.
• Pravastatin is safer with regard to causing myopathy.
• Statins are first-line drugs for type IIa, type IIb & secondary hyperlipoproteinemia.
• Long-acting statins are Rosuvastatin (t1/2 - 19 hours) & Atorvastatin (t1/2 - 14 hours).
• Rosuvastatin with t1/2 19 hours is the longest acting statin.
• Activity of HMG CoA reductase maximum at night, hence most statins are administered at night.
• Long-acting drugs like Rosuvastatin & Atorvastatin are administrated any time of day, due to their
longer half-life.
• All statins absorbed orally, maximum with fluvastatin.
• Lovastatin & simvastatin are administered as prodrugs & have extensive first-pass metabolism.
• Pravastatin, fluvastatin, atorvastatin & rosuvastatin are administered as active drugs.
• All statins are metabolized extensively by hepatic microsomal enzymes, except pravastatin.
• Pravastatin metabolized by sulfation (non-microsomal).
• Most potent statin is Pravastatin; Least potent statin is lovastatin.
• Ezetimibe is an intestinal cholesterol absorption inhibitor.
• Ezetimibe acts by inhibiting NPC1L1 transporter, involved in intestinal absorption of cholesterol.
• Intestinal cholesterol absorption inhibitor like Ezetimibe indicated in type IIa & IIb
hyperlipoproteinemia.
• Bile acid binding resins bind to bile acids in intestinal lumen Decreases its reabsorption results
in more excretion via feces.
• Bile acid binding resins are indicated only for type IIa disorder.
• Drugs included under bile acid binding resins cholestyramine, colestipol & colesevelam.
• Fibric acid derivatives act by activating LPL by activating nuclear receptor, PPARα (peroxisome
proliferator-activated receptor alpha).
• Fibric acid derivatives reduces TG (contained in VLDL), increases HDL & reduces plasma fibrinogen
level.
• Drugs included under fibric acid derivatives are Clofibrate, gemfibrozil, fenofibrate, bezafibrate.
• Fenofibrate is prodrug with longest half-life.
• Fenofibrate has maximum LDL cholesterol-lowering action & are uricosuric.
• DOC in hypertriglyceridemia (type III & IV) is Fenofibrate.
• Nicotinic acid acts by inhibiting lipolysis in adipose tissue.
• Main effects of nicotinic acid increase HDL cholesterol, decrease LDL cholesterol, VLDL
triglycerides, lipoprotein (a) & fibrinogen.
• Among all hypolipidemic drugs, nicotinic acid is maximum HDL increasing property.
• Due to maximum HDL increasing property, Nicotinic acid is useful in patients having increased risk
of CAD.
• Except for type-I disorders, nicotinic acid is useful in type IIb, III & IV disorders.
• Main limiting feature of nicotinic acid is cutaneous flushing & pruritis.
• Probucol is an anti-dyslipidemic drug useful for its antioxidant action.
• Probucol inhibits LDL oxidation resulting in reducing both HDL & LDL cholesterol levels.
• Gugulipid causes modest reduction of LDL & slight increase of HDL.

• Avasimibe is a new anti-dyslipidemic drug that acts by inhibiting ACAT-1 (acyl-coenzyme A:
cholesterol acyltransferase-1) enzyme.
• Torcetrapib & anacetrapib is an anti-dyslipidemic drug, which increases HDL
cholesterol, by inhibiting enzyme CETP (cholesterol ester triglyceride transport protein).
• Anti-dyslipidemic drug, Lomitapide acts by inhibiting MTP (microsomal triglyceride transfer
protein).
98. PLASMA EXPANDERS
PLASMA EXPANDERS
• Plasma expanders are high molecular weight substances.

• Plasma expanders are primarily used as plasma substitutes, mainly in burns (acute phase only),
hypovolemic, endotoxin shock, severe trauma & extensive tissue damage.
• Substances used as plasma expanders are Albumin, Dextran, Polygeline & Hetastarch.
• As a plasma expander albumin are used in hypovolemia, burns, shock & hypoalbuminemia.
• Dextran is the most commonly used plasma expander.
• Dextran reduces blood viscosity, decreases rouleau formation & improves microcirculation.
• Dextran-40 has thromboprophylactic (antithrombotic) effect.
• Polygeline is a degraded gelatin polymer, used as plasma expander.
• Polygeline exhibits hypersensitivity reactions like flushing, rigor, urticaria, wheezing & hypotension.
99. TREATMENT OF OSTEOPOROSIS
TREATMENT OF OSTEOPOROSIS
• Drugs used for treating osteoporosis are bisphosphonates, selective estrogen receptor modulators
(SERM), Teriparatide, Denosumab, Osteoprotegerin, Cinacalcet, Strontium
ranelate, Calcium, Gallium nitrate & Calcitonin.
• Bisphosphonates exhibit inhibitory effect on osteoclast-mediated bone resorption.
• Bisphosphonates cause osteoclast-mediated bone resorption, by accelerating osteoclastic
apoptosis & by suppressing differentiation of osteoclast precursors to mature osteoclasts.
• Least potent bisphosphonates are 1st generation drugs like medronate, clodronate & etidronate.
• Longest half-life of bisphosphonate in bone is with alendronate for almost 10 years.
• 3rd generation bisphosphonate drugs like risedronate & zoledronate are the most potent agents.
• Bisphosphonates are used in treatment of post-menopausal & steroid-induced osteoporosis.
• Pamidronate & zoledronate, by i.v route is preferred for treating hypercalcemia of malignancy.
• Distinctive toxicity of bisphosphonates is esophageal irritation & ulceration.
• Bisphosphonates are not taken by mouth & advised not to lie down, for at least half an hour.
• 1st generation bisphosphonate results in osteomalacia.

• On long-term bisphosphonate use, there is increased risk of atypical ‘chalkstick’ fracture of
femur (subtrochanteric or shaft).
• Estrogens inhibit bone resorption, directly by inhibiting osteoclast & indirectly by modulating
paracrine factors.
• Selective estrogen receptor modulators (SERM) increases anti-resorptive, suppresses pro-resorptive
factor synthesis by osteoblasts & increase bone formation.
• SERM is useful for treating postmenopausal osteoporosis.
• Estrogen deficiency in old age results in postmenopausal osteoporosis.
• Raloxifene, a SERM exhibits estrogen agonistic action on bone & antagonistic action on breast &
endometrium.
• Raloxifene, a SERM is a preferred drug for treatment & prevention of post-menopausal
osteoporosis.
• Bazedoxifene is a recently approved SERM for prevention of postmenopausal osteoporosis.
• Bazedoxifene also treats vasomotor symptoms of menopause.
• Teriparatide is a recombinant PTH1-34.
• Teriparatide & strontium ranelate stimulates osteoblast.
• Most osteoporotic drugs act by inhibiting osteoclast.
• PTH in low & pulsatile dose stimulates bone formation.
• PTH in excess causes bone resorption.
• Teriparatide stimulates new collagenous bone.
• Sufficient vitamin D intake & calcium is advised concurrently during teriparatide therapy.
• On administering Teriparatide 20 mcg/d subcutaneously for 2 years, dramatically improves bone
density in most bones, except distal radius.
• Teriparatide course is followed by bisphosphonates course mainly considered for retaining &
improving bone density.
• Teriparatide is used for healing of chalk stick fractures associated with bisphosphonate therapy.
• Denosumab is a monoclonal antibody against RANK ligand, useful for osteoporosis treatment.
• Osteoclasts have a surface receptor named ‘receptor for activated nuclear factor κ B (RANK), which
on stimulation by RANK ligand causes bone resorption.
• Osteoprotegerin acts as a decoy receptor for RANK ligand.
• Osteoprotegerin binds RANK receptors, preventing RANK-L binding to osteoclasts.
• Cinacalcet is a calcium-sensing receptor present on parathyroid gland.
• Cinacalcet acts as “calcimimetic drug”.
• Cinacalcet is approved for secondary hyperparathyroidism treatment.
• PTH secretion is decreased by Cinacalcet.
• Strontium ranelate inhibits bone resorption as well as stimulates bone formation.
• Calcium is a life-saving in extreme hyperkalemia (> 7 mEg/L).
• Calcium is approved for i.v.treatment of black widow spider envenomation & magnesium toxicity.
• Calcitonin inhibits bone resorption.
100. FIBRINOLYTIC DRUGS
FIBRINOLYTIC DRUGS
• Fibrinolytic drugs are also referred as “thrombolytics”.
• Fibrinolytic drugs are drugs activating plasminogen to form plasmin & helping thrombus lysis.
• Plasmin is generated from plasminogen, by tissue plasminogen activator (tPA).
• tPA selectively activates fibrin-bound plasminogen in thrombus.
• Bleeding is the major adverse effect of fibrinolytic, mainly due to lysis of physiological thrombi &
excessive circulating plasmin.
• Fibrinolytic drugs are indicated for treatment of acute myocardial infarction (Stemi) - Administered
i.v. within 12 hours preferably within 1st 3-6 hours.
• Absolute contraindications for fibrinolytic drugs include,
• History of non-hemorrhagic stroke within the past year/at any time,
• Marked hypertension (systolic >180 and/or diastolic > 110mm Hg),
• Active internal bleeding (excluding menses).
• Relative contraindications for fibrinolytic drugs include,
• Current use of anticoagulants (INR≥ 2),
• Recent (>2weeks) invasive or surgical procedure,
• Prolonged (> 10 min.) cardiopulmonary resuscitation,
• Known bleeding diathesis,
• Pregnancy,
• Hemorrhagic diabetic retinopathy,
• Active peptic ulcer disease,
• History of severe hypertension.
• Specific antidotes for fibrinolytic drug overdose are Epsilon aminocaproic acid (EACA) &
tranexaemic acid.
• Streptokinase, anistreplase urokinase, alteplase, reteplase & tenecteplase are some of the
important fibrinolytic drugs.
• Streptokinase, anistreplase & urokinase activate bound fibrin as well as circulating plasminogen.
• Reteplase, alteplase & tenecteplase are fibrin-specific drugs.
• Streptokinase activates fibrin-bound as well as circulating plasminogen.
• Unlike other plasminogen activators, streptokinase does not directly convert plasminogen to
plasmin instead forms complex with plasminogen.
• Streptokinase is antigenic in nature, causing allergic reactions.
• Anistreplase is formed by combining streptokinase with Lys-plasminogen.
• Urokinase directly converts plasminogen to plasmin.
• Streptokinase & Urokinase are contraindicated in intracranial malignancy.
• Fibrinolytic drug affecting both free & circulating plasmin is urokinase.
• Alteplase, reteplase & tenecteplase are recombinant tPA.
• Recombinant tPA is more efficacious than streptokinase.
• Reteplase & tenecteplase are longest acting tPA & are referred as "bolus fibrinolytic”.
101. POTASSIUM CHANNEL OPENERS
POTASSIUM CHANNEL OPENERS

• Potassium channel openers are mainly vasodilators (mainly arterioles) by opening potassium
channels.
• Important potsssium channel openers include, Hydralazine, minoxidil, diazoxide, nicorandil &
dalfampridine.
• Hydralazine acts both by vasodilatation & also by releasing nitric oxide (NO) from intact
endothelium.
• On prolonged hydralazine administration, causes drug-induced lupus erythematosus.
• Minoxidil is a prodrug activated in liver forming "minoxidil sulfate".
• Minoxidil sulfate opens potassium channels.
• Minoxidil is a safer anti-hypertensive drug for chronic renal failure cases.
• Minoxidil is useful as an anti-hypertensive drug & for alopecia treatment in males.
• By causing abnormal hair growth as an adverse effect in females (hirsutism), minoxidil is utilized
for alopecia treatment (Alopecia areata) in males.
• Combination of Minoxidil & hydralazine is given orally for severe hypertension.
• Diazoxide as rapid i.v injection is useful during hypertensive emergencies.
• Nicorandil is a cardioprotective potassium channel opener, by ischemic preconditioning & coronary
dilation.
• Nicorandil activates myocardial ATP sensitive K+ channels & result in coronary dilation.
• Dalfampridine is an oral potassium channel opener which helps improve walking ability in people
with multiple sclerosis.
102. CALCIUM CHANNEL BLOCKERS
CALCIUM CHANNEL BLOCKERS
• Calcium channel blockers block L-type of voltage-gated calcium channels present in blood vessels &
heart.
• CCB's causes vasodilation by inhibits calcium channels & reduces frequency of Ca+ channels
opening.
• CCB’s reduces cardiac activity including heart rate, AV conduction & contractility.
• Dihydropyridine (DHP) group of CCB drugs are referred to as peripherally acting CCB's.
• Strong cardio-depressant activity is mainly exhibited by verapamil & diltiazem (verapamil >
diltiazem).
• CCB's are indicated for both classical & variant angina, mainly verapamil, diltiazem & long acting
DHPs.
• DOC for hypertensive patients with migraine is calcium channel blocker.
• Flunarizine is weak CCB used for prophylaxis of migraine.
• CCB's are used in hypertensive patients with PVD (Raynaud’s phenomena).
• CCB's are contraindicated in sick sinus syndrome, as it causes reflex tachycardia.
• Short-acting DHPs like nifedipine accentuates angina symptoms, by causing tachycardia
& precipitates acute anginal attack.
• Nifedipine causes hyperglycemia by decreasing insulin release.
• CCB’s along with β-blockers are contraindicated.
• Nifedipine shows marked tachycardia.
• Long-acting CCB's like Amlodipine will show less tachycardiac effects.
• CCB's causes urinary bladder relaxation, resulting in voiding difficulty in elderly.
• CCB's increases plasma digoxin concentration, by decreasing its excretion.
• Verapamil shows maximum cardio-depressant action.
• Verapamil exhibits maximum effect on cardiac conduction.
• Verapamil increases PR interval.
• CCB with maximum plasma protein-bound nature is verapamil.
• Verapamil has racemic mixture of two enantiomers with different pharmacokinetic &
pharmacodynamic properties.
• Verapamil is used for treatment of angina, PSVT, hypertension & hypertrophic obstructive
cardiomyopathy (HOCM).
• Among CCB's, dihydropyridine drugs are safer in pregnancy.
• Nifedipine has predominant peripheral action.
• Nifedipine by increases angina risk by increasing heart rate & thus cardiac work.
• Nifedipine interferes with anesthesia.
• Mostly Nifedipine & beta-blocker are given together, to overcome nifedipine's increased
sympathetic activity.
• Nifedipine is banned for sublingual usage for hypertensive emergencies, due to increased risk of MI
& mortality.
• Nifedipine is also used for achalasia cardia.
• Longest acting parenteral CCB is Nicardipine.
• DOC for hypertensive emergencies is Nicardipine.
• Nimodipine is shortest acting CCB's with relatively cerebro-selective vasodilating nature.
• Nimodipine is used for reversal of compensatory vasoconstriction after subarachnoid hemorrhage.
• Clevidipine is an ultrashort-acting DHP.
• Clevidipine is recently approved for hypertensive emergencies.
• Amlodipine is DOC for managing asthmatic patient with hypertension.
• Rebound hypertension is seen with Amlodipine.
103. ANTI-PLATELET DRUGS
ANTI-PLATELET DRUGS
• Aspirin is a TXA2 synthesis inhibitor, used as anti-platelet drugs.

• Clopidogrel & ticlopidine are irreversible antagonists of P2 Y12 receptors of ADP, used as anti-
platelet drugs.
• Abciximab, tirofiban, eptifibatide are Gp IIb/IIIa antagonists used as anti-platelet drugs.
• For all anti-platelet drugs, bleeding is due to prolonged bleeding time, which is most common
adverse effect.
• Most serious adverse effect of antiplatelet drugs is Thrombocytopenia.
• Aspirin is most commonly used for prophylaxis of MI & stroke, mainly prevents arterial thrombosis.
• For CVS diseases & in artificial heart valves, Dipyridamole + warfarin preferred.
• Antiplatelet action of aspirin is exhibited only at its low doses (40-325mg).
• Aspirin irreversibly inhibits COX enzyme, thus inhibits COX, resulting in inhibition of TXA2 &
PGI2 synthesis.
• Aspirin has nil effect on platelet survival time.
• Aspirin inhibits only thromboxane synthesis but does not inhibit enzyme thromboxane synthetase.
• Dazoxiben is a thromboxane synthetase enzyme inhibitor.
• Irreversible antagonists of P2 Y12 receptors of ADP interfere with platelet activation by ADP &
fibrinogen.
• Drugs like ticlopidine, clopidogrel & prasugrel increase platelet survival time.
• Ticlopidine causes severe neutropenia with absolute neutrophil count <
500/mL & thrombocytopenia.
• Clopidogrel better tolerated than ticlopidine.
• Ticlopidine & clopidogrel are prodrugs, activated by CYP2C19 enzyme in liver.
• Prasugrel is a strong antiplatelet drug, which is faster acting than clopidogrel.
• Gp IIb/IIIa antagonists like Abciximab, eptifibatide & tirofiban are strongest antiplatelet drugs.
• Abciximab is a non-antigenic monoclonal antibody, which is an anti-platelet drug inhibiting Gp
IIb/IIIa receptor.
• Abciximab also inhibits αvβ3 receptor & αMβ2 receptor.
• αvβ3 receptor binds vitronectin.
• αMβ2 receptor is a leucocyte integrin.
• Abciximab is used in PTCA & cardiac transplants.
• Phosphodiesterase-3 inhibitors includes dipyridamole & cilastazole.
• Dipyridamole acts by inhibiting phosphodiesterase, increasing cAMP & potentiating anti-
aggregation factor like prostacyclin.
• Cilostazol is useful in treatment of intermittent claudication.
• Direct-acting & reversible P2 Y12 receptor antagonists like Ticagrelor & cangrelor are used as
antiplatelet drugs.
• Ticagrelor is orally effective antiplatelet drug.
• Ticagrelor & cangrelor are more rapid onset & offset of action, provides greater & more predictable
antiplatelet action.
• Ticagrelor & cangrelor are the 1st new antiplatelet drug demonstrating greater reduction in CVS
death in patients with acute coronary syndromes.
• PAR-1 inhibitors act by inhibiting thrombin receptors on platelets called protease-activated
receptor 1 (PAR-1).
• Vorapaxar is a PAR-1 inhibitor used as an antiplatelet drug.
Forensic Medicine
1. Criminal Procedure Codes
• A married woman died in unnatural conditions within 5 years of her marriage. Her parents
complained of frequent demand of dowry. Her autopsy will be conducted under Sec. 176 CrPC.
• Under section 53 CrPC, police can ask the doctor to examine without the accused person's consent.
• Sec. 176 CrPC is related to Magistrate inquest.
• Cognizable offence comes under 2(c) section of CrPC.
• Doctor suspects homicide poisoning. He needs to inform police under Section 39 CrPC.
• 412 CrPC is related to reasons to be recorded.
• A case of suspected homicide comes to a doctor. He is supposed to inform police under section 39
of CrPC.
2. Lead poisoning
• ‘Saturnism’ is seen in Chronic lead poisoning

• Facial pallor is the earliest sign of lead poisoning
• Lead poisoning shows abdominal colic, constipation, weakness of hand and anaemia
• Inhalation is the most common mode of lead poisoning
• International lead poisoning prevention week is celebrated in October
• Protoporphyrin levels >100 μg/dl indicate Lead poisoning
• Sideroblastic anaemia is caused by Lead poisoning
• The pathogenesis hypochromic anaemia in lead poisoning is due to Inhibition of enzymes involved
in heme biosynthesis
• Plumbism is caused by Lead poisoning
• Anaemia, punctate basophilia, constipation blue line and abdominal colic are characteristic of Lead
poisoning
• Least common complication of lead poisoning in adults Peripheral neuropathy
• Coproporphyrin is excreted typically in lead poisoning
• In case of chronic lead poisoning, the levels of 6-aminolevulinic acid
3. Postmortem Caloricity
• Postmortem caloricity is seen in Strychnine poisoning

• Postmortem caloricity is seen in death due to Sunstroke, Septicemia & Tetanus
• Postmortem caloricity is increased temp within 2 hours of death
4. IPC
• Cupable homicide not amounting to murder comes under 304 IPC

• Criminal responsibility under IPC is not present if age is below 7 years
• Article 377 of IPC deals with Unnatural sexual offence
• Dislocation or loss of a tooth,Nasal bone fracture, Loss of hearing of one ear, Emasculation & Any
hurt which endangers life come under section 320 of IPC
• The witness is liable to be prosecuted for perjury, and the imprisonment may extend upto seven
years falls under S.193 of I.P.C.
• Issuing or signing a false certificate is punishable under IPC 197
• A person is caught for destroying a document which would have been used as an evidence in the
court comes under Sec IPC 204
• Sec IPC 193 defines punishment for fabricating false evidence
• IPC 304 A is for Gross medical negligence
• Dying declaration comes under
• Negligent act likely to spread infection of disease dangerous to life comes under S.269, IPC
• S. 351, I.P.C.: An assault is an offer or threat or attempt to apply force to body of another in a
hostile manner.
• Section 228 A IPC section makes the printing or publication of the identity of the rape victim
punishable
• Criminal responsibility in Indian constitution is included in IPC section 84
• 304-B IPC are concerned with dowry death
• Sec 300: Murder
• Sec 304 : Culpable homicide not amounting to murder
• Sec 307: Attempt to murder
• Husband/relative of husband cruel behavior towards wife comes under which IPC section 498 A
• Punishment under 304-A IPC 2 years
• Sec 44 IPC defines injury
• Sec. 320, Sec. 331, Sec. 326 of IPC are related to grievous hurt
• Miscarriage is punishable under which IPC Sec 312
• Punishment for rape is given under IPC Sec. 376
• Punishment for rape under Sec. 376(1) IPC is 7 years imprisonment + fine
• Sec. 377 IPC deals with sodomy
• To plead for insanity in a court of law, the IPC is Sec. 84
• 320 IPC includes vitriolage i.e. potential cause of permanent disfigurement of face
• IPC 319 deals with Definition of hurt
• IPC 321 deals with Voluntarily causing hurt
• Hostile witness is covered under IPC section 191
• IPC 314 deals with Death of patient caused by miscarriage
• The legal responsibilities of an intoxicated person is given under Section of IPC 85
• Section 53 IPC is An accused can be examined by a medical practitioner at request of police, even
without his consent or by force
5. INQUEST
• In Death due to police firing, inquest is done by District magistrate

• In India, magistrate inquest is not done in Murder cases
• After postmortem body is handed over to The authority who has conducted inquest in that
particular case
• In Police inquest Senior head constable can investigate
• Police inquest is Most common inquest
• In Police inquest Panchnama has to be signed by IC
• The enquiry into the circumstances of death is called Inquest report
• A lady died due to unnatural death within seven years after her marriage. The inquest in this case
will be done by Sub-divisional Magistrate
• In case of death in lock up, the inquest is held by Magistrate
• Police inquest is required in Sucide, Accidental death , Murder, Homicidal death, Death by animals
• Inquest of Dowry death is done by Magistrate
• Inquest for custodial death is held by Magistrate
• Inquest not present in India are Medical examiner system & Coroner's inquest
• Before conducting the inquest, police should inform Executive Magistrate
• Magistrate's inquest is conducted by District, Executive or Sub-Divisional Magistrate
• Sec. 176 CrPC is related to Magistrate inquest
• Magistrate inquest not needed in Homicide
• Magistrate inquest is done in case of Death in psychiatry hospital
6. CONSENT
• Explaining to the patient the nature of his disease, the proposed treatment or procedure, the
alternative procedure, the risks and benefits involved in both the proposed and alternative
procedure, the relative chances of success or failure of both procedures
• In cases of emergency consent is not necessary
• In criminal cases, the victim cannot be examined without his/her consent
• The minimum age for giving consent for medical termination of pregnancy is 18 years
• Assistant surgeon working in a CHC and a rape convict is brought to him by the police constable.
The constable has a letter from the sub inspector of police from the concerned area requesting you
to do a potency test and forensic examination of the accused. The accused refused to give consent
for the examination and any further tests. A reasonable amount of force should be used if needed
and examine the accused.
• A person who has been arrested on charges of rape is brought to you. No requests for potency
test/forensic examination has been produced by the police constable but the arrested person asks
you to examine him and take evidences as he is innocent then Examining the person and collecting
informations and samples after getting the consent is the best scenario
• If the government has made it compulsory for any vaccination of an epidemic strainof infection at
the earliest so as to check the spread of the disease then vaccination mustbe done even if the
person refuses & threats to sue the doctor
• Minimum age for giving consent for organ donation in India is 18 years
• Form of acceptable consent include Informing the patient the nature of his disease, the proposed
treatment or procedure, the alternative procedure, the risks and benefits involved in both the
proposed and alternative procedure, the relative chances of success or failure of both procedures
• Form of acceptable consent includes information that In cases of emergency consent is not
necessary
• Form of acceptable consent include information that In criminal cases, the victim cannot be
examined without his/her consent.
• A school teacher gives consent for treating a child who becomes sick during a picnic away from
home town. This type of consent is known as Loco Parentis
• Consent can only be valid if it is given by a person who is sane and has attained maturity, ie. age of
18 yrs
• For sterilization of a married person, consent of both spouse, i.e. husband and wife is required
• In criminal cases, the victim cannot be examined without his/her consent.
• Informed consent includes All information should be given about treatment options
• Informed consent includes Any treatment option better than the treatment being provided should
be told
• Informed consent includes All disclosure should be done in a language that the patient can
understand
• A patient of head injury, has no relatives & requires urgent cranial decompression; Doctor
should Operate without formal consent
• 20 years old young female comes to a male gynaecologist for pelvic examination Implied consent is
used
• For MTP consent is taken from Wife only
• Consent from guardian/husband for MTP is required if Female is below 17 years of age
• Termination of pregnancy up to 20 weeks can be done by medical practitioner without consulting
specialist
• Female can give consent for sex if she is above 16 years
• Examining the patient without consent amounts to Assault
• Consent for examination in a psychiatric patient is given by Guardian
• A doctor while examining the patient without consent in an emergency is protected underSec. 92
IPC
• A doctor has to do an urgent operation on an unconscious patient to save his life. But there are no
relatives to take consent. He goes ahead without obtaining consent from anyone; he is using the
principle of Doctrine of implied consent
• Consent is required for Pathological autopsy
• Blanket consent is consent taken At the time of admission to do any surgery
• Minimum age to give consent for organ donation for therapeutic purposes is 18 yrs
• A valid consent is Obtained in presence of two witnesses
• A valid consent Should not be obtained with force, fear or fraud
• True information to be given freely in A valid consent

• Minimum age at which female can give consent for sex by 15 year if the female is the wife of the
male counterpart.
• Legal age of consent is 12 years
• Punishment for criminal abortion for the women who gives consent and the performer are covered
under IPC section 312
• Under which section, police can arrest a person and ask medical officer to examine him without
victims consentSec 53 IPC
• Blanket consent is consent taken at the time of admission to do any surgery
7. The Transplantation of Human Organs Act - 1994
• Transplantation of Human Organs Act was passed by Government of India in 1994

• According to the transplantation of Human organs act 1994, what is the punishment for a doctor
found guilty is 2 to 5 years
• Bone marrow Transplantation is outside the purview of Transplantation of Human Organs Act
• Brainstem death certification under the Transplantation of Human Organs Act include The doctor,
in-charge of hospital in which the brain-stem death occurred
• Brainstem death certification under the Transplantation of Human Organs Act includes A
neurologist or a neurosurgeon, nominated by the in-charge, from the panel
• Brainstem death certification under the Transplantation of Human Organs Act includes The doctor
treating the person whose brainstem death has occurr
8. PROFESSIONAL NEGLIGENCE (MALPRAXIS)
• Contributory negligence is by the part of Both Doctor & Patient

• After the unexpected death of a 17 year old boy on the ward the relatives claimed that it is due to
the negligence of doctor. According to recent ruling of supreme court he is punishable under IPC
304 A only if there is Gross medical negligence
• Professional negligence means malpraxis
• Conditions of defence available to a doctor against allegation of negligence are Medical
maloccurrence, Therapeutic misadventure & Res Judicata
• According to a recent Supreme Court judgement, doctor can be charged for Medical Negligence
under section 304-A, only in Gross negligence
• If death of a patient occurs during surgery due to the negligence of the surgeon, then he can be
charged under 304-A IPC
• In civil negligence cases against the doctor, the onus of the proof lies with Patient
• Contributory negligence is related with Avoidable consequence rule
• Medical negligence in which the patient contributed to the injury complained of Contributory
negligence
• Contributory negligence is negligence due to Both doctor and patient
• Contributory negligence is a defense in Civil negligence
• Apex body dealing with medical negligence cases National Consumer Commission
• Doctor liable to get sued by patient till what time limit from alleged negligence 2 years
• A person undergone appendisectomy. On post op day 10 he died, postmortem patholigst found
gossypiboma. It is a case of Criminal negligence
9. FUNCTIONS OF INDIAN AND STATE MEDICAL COUNCILS
• According to MCI act, medical education granted by Indian universities comes under Schedule I of
MCI act
• Medical qualifications awarded by institutions outside India and recognized by MCI are registered
in Second schedule of Indian Medical Council Act 1956
• Disciplinary control over Registered Medical Practitioners is under State Medical Council
• Indian council of medical research is presided over by Union health minister
• Professional death sentence is given by State Medical Council
• As per MCI, minimum period for which a doctor should preserve his patient's record 3 years
• Schedule-3 of MCI includes Diploma of CPS
10. Consumer Protection Act, (CPA/COPRA) - 1986
• Consumer protection act was passed in 1986

• Consumer protection act includes Decision within 3-6 months & Right to safety act
• Consumer protection act applies to all goods and services
• Maximum amount that can be received under the Consumer Protection Act is > 100 lakhs
11. EUTHANASIA
• Passive euthanasia is legal in India

• Physician assisted suicide is legal in some States of the US
• Active euthanasia is legal in Netherlands and Belgium
• A physician decides to discontinue or not to use extraordinary life sustaining measures to prolong
his patients life. It is known as Passive euthanasia
12. EXHUMATION
• Ideal time to start exhumation is Early morning

• Time limit of exhumation in India is No limit
• In India exhumation is ordered by Magistrate
• An order for exhumation can be given by District collector, Additional district magistrate or Sub-
collector
• Exhumation is done in All ages
• For exhumation the order should be passed by Executive magistrate
• Exhumation is usually done in conditions like Homicide, Death as a result of criminal abortion,
& Death due to criminal negligence
13. CORPUS DELICTI
• Corpus delicti means Proof of occurrence of crime or Essence of crime or body of offence
14. Drowning
Typical Drowning/Wet Drowning
1.Fresh water drowning:
• Large quantities of water cross the alveolar membrane into circulation

• Causing hypervolemia and hemodilution
• RBCs imbibe water and burst (hemolysis) with liberation of potossium
• Heart is exposed to volume overload, potassium excess, sodium deficit.(hyponatremia), and anoxia.
• Anoxia and hyperkalemia cause ventricular fibrillation and death in 4-5 minutes.
2. Salt water drowning :
• Seawater is hypertonic (3% NaCl)

• Water is withdrawn by osmosis from the plasma into alveolar spaces in the lungs.
• Giving rise to fulminating pulmonary edema
• With progressive hypovolaemia, circulatary shock, and eventually cardiac standstill(asystole)
• HB increases
• Death in 8-12 minutes.
Atypical drowning
1. Dry drowning:
• On contact with water, especially cold water, there results intense laryngospasm
• So that water does not enter the lungs.
• Death is due to asphyxia because of laryngospasm
2. Immersion syndrome (hydrocution/submersion inhibition/vagal inhibition) :

• Due to vagal inhibition sudden death
• Sudden impact with cold water
3. Near drowning (secondary drowning syndrome/post-immersion syndrome) :
• Hyperventilation before drowning can cause secondary drowning.
Cases of Drowning in India
• Most of the cases of drowning (2/3) in India are accidental.

• Rest 1/3 being suicidal
• Homicidal drowning is less common in India.
• Suicidal drowning is indicated by:
• Absence of signs of struggle or assault (e.g. torn clothes, injury marks).
• A determined suicide may tie his hands and legs together or attach weights to his body or take
poison or cut throat before immersion.
• In homicidal drowning,
• Signs of struggle and violence (assault) (e.g. head injury, signs of strangulation, or throttling).
• Head and feet may be tied, heavy weight may be attached to body or body may be tied up inside a
gunny bag.
Causes of death in drowning
• Asphyxia.
• Myocardial anoxia.
• Ventricular fibrillation.
• Vagal inhibition.
• Laryngeal spasm.
• Exhaustion.
• Secondary injuries.( for eg., head injuries)
15. Drowning-Autopsy findings
Cutis anserina or goose fleshings
• Occurs due to contraction of the erector pillae muscles.
Eyes
• The eyes are half opened with dilated pupil

• Conjunctivae may be congested with subconjunctival ecchymosis present
SKIN
• Washer woman’s hands and feet are seen after 48 to 72 hours
• Where the skin of the palms and soles becomes beached, wrinkled and saddened.
• Weeds, grass, plants, mud or stones in tightly clenched hand
• Due to cadaveric spasm
• Strongly suggest that the person was alive when drowned, as it indicates the struggle of person for
life
Froth:
• This froth is pathognomonic of drowning, the best indicator of antemortem drowning.

• When pressure is exuded upon the chest, then copious froth exudes.
Lungs
Fresh Water drowning
• Paltauf’s hemorrhage.
• The lungs show large subpleural haemorrhages
• Produced due to rupture of the intra alveolar partitions beneath the pleura.
• More prominent over the lower lobes and interlobar surfaces.
• The lungs are ballooned up, edematous, heavy and boggy.
• Emphysema aquosum
• On cut section crepitus like feeling is present due to entrapment of water.
Salt Water Drowning
• In saltwater drowning, lungs are much more edematous than fresh water drowning and appear
purple.
• Soft jelly like
• No crepitus
Ear
• Water may also be detected from middle ear resulting from violent respiratory
excursions( conclusion post mortem finding .
16. Drowning- Test
Diatom Test
• Most samples of the water contain microscopic unicellular algae or plankton called diatoms.
• These diatoms possess silicaceous cell membranes and vary from size 10 to 80 microns.

• Their presence in the victim’s body and the same set of diatoms present in the water, concludes the
case to be antemortem drowning.
• So, presence of diatoms in brain and bone marrow indicates death due to drowning.
• For detection of diatoms, bone marrow of long bones, e.g. femur, tibia, humerus or sternum is
highly suitable and reliable.
• As diatoms resist acid digestion, to extract them acid digestion technique is used.
Gettler Test
• This is also known as Chloride test.
17. Types of firearm
• Caliber of a rifled gun is calculated by distance between two diagonally opposite lands
• Cartridge case of shotgun has percussion (detonator) cap at the base of rim and top wad (retaining
cardboard) at top.
• Wad is responsible for separation, sealing, optimal pressurization & lubrication but not for fatal
injuries
• The killing range of a military rifle is about is 300 yards.
• Choking is the constricting device present at the muzzle end of the shotgun
• Air rifle & air pistol release shots or pellets (skirted) which are propelled by compressed air /gas
• The effective range of shot gun is 30 -40 yards
• The spread of pellets from a fully choked barrel is given below:
• 10 meter - 25 cm
• 15 meter - 35 cm
• 20 meter - 45 cm
• 30 meter - 75 cm
• Shotgun does not contain use bullet.
18. Bullet and Gunpowder
• Destructive power of bullet is determined by velocity of bullet.

• A pair of bullets are said to travel in tandem if the nose of one is in contact with the base of the
other.
• In tandem bullet, number of bullets coming out of the gun are 2
• A bullet travelling in an irregular fashion instead of straight line is known as yawning bullet.
• Dum-dum bullet
• Also called expanding bullet
• Produce larger diameter wounds of limited penetration.
• Souvenir bullet: A bullet left in body for long time and is surrounded by fibrous tissue.
• Tracer bullet:
• Leaves a visible mark in its flight
• Frangible bullets
• These bullets are designed to fragment upon impact.
• Smokeless gun powder is composed of nitrocellulose.
• Double based smokeless gun powder consists of Nitrocellulose plus nitroglycerine.
• Black powder contains PCS°
• Potassium nitrate (75%)°
• Charcoal (15%)°
• Sulphur (10°/0)°
19. Firearm wounds
• In a firearm injury, there is burning, blackening, tattooing around the wound, along with the cherry
red colour of the surrounding tissues and is cruciate in shape, the injury is close shot injury.
• Stellate wound is produced with firearm in contact shot.
• In a firearm injury, blackening seen around the entry wound is due to smoke
• Tattooing in entry wound of a firearm injury is due to gunpowder.
• The skull was burst open, charring and cherry red colouration in the track inside. Range of the shot
is contact shot.
• 'Rat hole' appearance of entry wound of firearm is seen in near range of shotgun.
• In firearm entry wound, arrangement of abrasion collar, dirt collar and tattooing from inside to
outside: Dirt collar, abrasion collar, tattooing
• Abrasion collar is seen in entry wound
• Bullet entry wound, for bullet entering at acute angle is identified by oval shape of abrasion collar
• Harrison-Gilroy test can detect gunshot residue
• Bullet entry wound in skull
• Punched in hole in outer table
• Inner table shows bevelling surface
• Wound is funnel-shaped with the funnel opening in the direction in which the bullet is travelling
• exit wound of a bullet
• Bevelled
• Everted
• No COHb
20. Firearm:Tests, Phenomenons and Suicide VS Homicide
• DERMAL NITRATE TEST ( PARAFFIN TEST ) and helps to detect gunpowder residue from suspects
hand.
• The Harrison & Gilroy test can also be used
• Kennedy Phenomenon: Medico-legal evaluation of firearm injury made difficult by surgical suturing
or alteration.
21. Firearm: Identification of Weapon
• Firearm detection determined by -

• Primary and secondary marking.
• The appearance of the wound.
• Presence of spiral grooves in the barrel of weapon is referred to as Rifling
• Empty cartridge case is ejected after firing in pistol.
• Compressed air is used to fire lead slugs in air rifle
22. Fingerprint
• Dactylography is the surest sign of identification

• The system of Dactylography to identify individuals was first started in India
• The first ever Finger Print Bureau of the world was established at Writer's Building at Calcutta in the
year 1897
• Characteristics
• Loop- 65%
• Whorl- 25%
• Arch- 7%
• Composite- 2-3%
• Permanent impairment of the fingerprint pattern occurs in leprosy
23. Laceration
• Normally, pus formation occurs in about 48 hours, but in a lacerated wound it occurs slightly
earlier.(24-48 hours)
• Lacerated wound appears as incised wound in which of the following sites-scalp, Tibial shin,
iliac crest, Zygomatic bone and forehead.
• Spilt laceration resembles Incised wound.
• Laceration is an open wound, tearing of the skin and subcutaneous tissue
• "Lacerated" wound has irregular margin
• Tissue bridges are seen in laceration
• In a lacerated wound, the hair bulb is crushed
• Lacerations produced without excessive skin crushing may have relatively regular sharp margins.
• Split" laceration is seen in blunt perpendicular impact
• Flaying is seen in avulsion type of lacerated wound
24. Organophosphates Poisoning

ORGANOPHOSPHORUS POISONS
• ALKYL PHOSPHATES
• ARYL PHOSPHATES
Alkyl phosphates are:
• HETP
• TEPP (Tetron)
• OMPA
• Dimefox
• Isopestox
• Malathion (Kill bug; Bugsolin)
• Sulfotepp
• Demeton
• Trichlorfon
Aryl phosphates are:
• Parathion (nitrostigmine) (Follodol; Kill phos; Ekato)

• Paraoxon
• Methyl-parathion (Metacide)
• Chlorthion
• Diazinon (Diazion; Tik 20)
Pathophysiology
• The organophosphates irreversibly inhibit acetylcholinesterase, resulting in an overabundance of

acetylcholine at synapses & the myoneural junction.
MUSCARINIC MANIFESTATIONS
• Salivation
• Lacrimation
• Urination
• Defaecation
• Distress
• Emesis
• Diaphoresis, diarrhoea,
• Miosis
• Bronchorrhea, bronchospasm
• C.V.S: Bradycardia, hypotension
• Ciliary Body: Blurred vision
• Bladder : Urinary incontinence

CNS MANIFESTATIONS
• Restlessness, emotional lability, headache, tremor, drowsiness, confusion, slurred speech, ataxia,
generalised weakness, coma, convulsion, depression of respiration and CVS centres
Severe poisoning:
• Porphyrinemia resulting in CHROMOLACHRYORRHOEA (shedding of red tears) due to accumulation

of porphyrin in the lacrimal glands is seen very rarely
Paralysis due to organophosphate (OP) poisoning can be three types
Type I (cholinergic phase) Involves acute paralysis secondary to persistent

depolarization at the neuromuscular junction
caused by persistent stimulation by excessive Ach.
Treatment- Atropine with or without oximes

Type II(intermediate syndrome.) It develops 1-4 days after resolution of acute
cholinergic symptoms.
It is manifested as paralysis and respiratory distress.
Atropine is ineffective, symptomatic treatment is given

Type III(OP-induced delayed It occurs 1-3 weeks after exposure and is associated
polyneuropathy (OPIDN)) with demyelination of axons.
DIAGNOSIS
• The cholinesterase activity of blood and plasma fall by 22 to 88%..
TREATMENT
• Activated Charcoal one gm/kg

• Atropine sulphate arrests the muscarinic and CNS symptoms. It has no effects on the nicotinic
symptoms
• 2-4 mg of atropine is given i.v as a test dose
• If no effect this dose is doubled every 5-10 min until secretions are controlled, the skin is dr./
and there is sinus tachycardia.
• Atropine is the mainstay of treatment (antidote of choice).
• Pralidoxime is most commonly used oxime.
25. Mercury poisoning

MERCURY
• The most poisonous Mercury salt is chloride
Nonoccupational Exposure
• Button batteries,Compact fluorescent lamp,Incandescent bulb,Fluorescent lamp
Mechanism of Action
• Binds to sulfhydryl groups as well as to phosphoryl, carboxyl, amide, and amine functional groups.
Chronic Exposure
• Classical triad of Gingivostomatitis, Tremor, Neuropsychiatric illness

• Tremors
• Resting and intentional( MAD HATTER SHAKE )
• rethismOphthalmic- Brown light reflex from anterior capsule of the lens vascular changes at the
corneoscleral junction
• Neuropsychiatric symptoms,
Acrodynia(Pink disease/Feer's disease)
• Chronic mercury exposure that occurs in infants and children
General symptoms
• Excessive sweating,tachycardia,irritability,anorexia,photophobia
• insomnia
• Tremors
• Paresthesias, decreased tendon reflex and weakness
• Skin
• Painful pinkish red discoloration of the extremities
• Rash may be urticarial, vesicular and hemorrhagic
• Hyperkeratotic induration of palms soles and face
Acute ingestion(Inorganic salts)
• Target organs are GIT and kidney(PCT)), nervous system
Chronic Intoxication(Organic Mercury)
• GI SYMPTOMS- colitis that resembles diptheritic colitis

• COARSE TREMORS

Treatment
Chelation
• Disodium EDTA is used as an antidote

• Chelating agent for copper, mercury, lead which is given by oral route is Penicillamine
• BAL (Dimercaprol)
26. Sex Determination-Nuclear Sexing
Nuclear Sexing
• The sex can be determined by studying the presence of:

• Barr bodies
• Davidson’s bodies and
• ‘Y’ chromosomes.
Barr bodies (Sex Chromatin)
• First detected in brain.

• In females more than 40% of nuclei of buccal mucosa contain chromatin body (chromatin positive),
• In males only less than 10% of nuclei contain chromatin body (chromatin negative).
Davidson Bodies
• This is absent in males
Y- Chromosomes
• The ‘Y’ Chromosomes present in males are fluroscent for the dye Quinacrine dihydrochloride.
Intersex States
Gonadal dysgenesis
a. Klinefelter’s syndrome
• Anatomical structure in male, but the nuclear sexing is female (chromatin positive).
• Barr bodies present
• The chromosomal pattern is 47XXY
• Testes are small & firm in consistency, aspermia, No semen, Hyalinised testis (histologically).
b.Turner’s syndrome
• Anatomical structure is female nuclear sexing is male (chromatin negative).
• Barr bodies absent
• The chromosomal pattern is 45 XO
True hermaphroditism
• A rare condition,wherein external genitalia may be of both sexes, but internally there is presence of
both testes & ovaries and ovotestes
Pseudohermaphroditism
• External characteristics of one sex, with gonads of opposite sex
a.Male pseudohermaphroditism:
• Nuclear sex XY, sex organs & sexual characteristic of female form
b.Female pseudohermaphroditism:
• Nuclear sex XX, sex organs & sexual characteristic of male form
Medico-Legal Importance of sex
• Marriage, divorce, Nullity of marriage, inheritance, rape, maternity, paternity, employment,

contesting for election & other civil rights.
27. Sex Determination by Skeleton
Important bones used for sex determination are:
• Pelvis(most common), skull, mandible, vertebra, femur, and scapula
ACCURACY OF SEXING….KROGMAN
ENTIRE SKELETON… 100%
PELVIS & SKULL…….98%
PELVIS………………..95%
SKULL…………………90%
LONG BONES………..80%

PELVIS
Male Female
Pelvic brim or inlet-Heart shaped Circular/elliptical
Ilio-Pectineal line- well marked Round and smooth
Suprapubic arch narrow (<70) >90
Obturator foramina ovoid Triangular
Greater sciatic notch narrow Wide
Preauricularsulcus(attachment of More frequent broad and deep

anterior sacroiliac ligament) not
frequent,noarrow and shallow.
• Skull
Male Female
Orbits Square, rounded margins Rounded, sharp margins
Zygomatic arch More Prominent Less prominent
Frontal & Parietal Small Large

eminences
Occipital area Prominent Not prominent
Capacity 1500 - 1550 cc. 1350 - 1400 cc.
• Mandible:
• Seen in female mandible i.e., ramus with smaller breath, angle of body of mandible obtuse, ramus
inverted,and chin (symphysis mentis) rounded
Vertebral Column
Male Female

Corporobasal index of sacrum 40.5
Breadth of first sacral vertebra/Breadth of base of

sacrum*100=45
28. Determination of Age- Introduction and Medico-legal Importance
Age determination from Height and Weight
Height of a children:
• At birth 50cm,at 6months 60cm,at 1year 70cm, at 2years 8Ocm,at 3years 90cm,and at 4 years 100
cm.
• At 4 years height becomes double than birth.(100 cm)
Medico-Legal importance of Age
Criminal responsibility
• Sec 82 IPC- child < 7 yrs, no criminal responsibility
Judicial punishment
• Juvenile offender-
• BELOW 18 yrs
Consent
• Sec 87 IPC- child < 18 yrs cannot give valid consent( implied or expressed) to suffer any harm which
may result from an act not intended or not known to cause death or grievous hurt. E.g. wrestling
contest
Rape
• Sec 375 IPC – girl below 16 yrs

• Wife below 15 yrs
Attainment of majority
• 18 yrs
Employment

• AMENDMENT: any child below the age of 14yrs cannot work
Infanticide
• The killing of an infant (child below 1 yr)
29. AGE IDENTIFICATION FROM BONES
The following data is used for radiologically age determination.
Region selected for Age

Girls Boys
X Ray
Elbow 13 -14 15 -17
Wrist 16 - 17 18 - 19
Shoulder 17-18 19-20
Crest of Ilium 18 -19 20 - 21
Ischial Tuberosity 21 - 220 23 - 24
• Average age of iliac crest fusion in Indian females is 19 yrs

• The metopic suture is usually closed by about 6 years of age,
• Below 2 years of age no ossific centre in the wrist.
30. Age determination of Fetus
Rule of Hasse
• Rule of Hasse is used to determine the age of fetus from crown to heel length in cm.
• During first five months, Length in cm = (Age in months)2
• After age of >5 months, Age in months = (Length in cm)/5
• The lack of cartilage and the easy foldability (lack of recoil are evident in the ear of premature
infant at 26 weeks.
• Prominence of the labia minora in a premature female infant represents the gestational age of
aprox 28 weeks.
• Heart is fully developed at 3 month age of intrauterine life
31. Age Determination- Teeth
The Gustafson’s criteria for age determination includes:
• Attrition
• Periodontosis
• Secondary dentin
• Cementum apposition
• Root resorption
• Root transparency
• Among the criteria transparency of the root is considered to be the single most important one in
age determination.
Eruption of temporary teeth will be completed by 2 - 2 n half years
Primary (temporary) dentition begins 6 weeks.
Secondary (permanent) dentition begins 6 years.
32. Postmortem changes -Immediate
Criteria for Brain Death/Brainstem death
• Absent Pupillary Light reflex (CN II, III)

• Dilated fixed pupil not responding to light surest sign of brain stem death
• Absent Central Motor Response to Pain (CN V, VII) (No response to deep somatic stimulation).
• A positive apnea test
After disconnection of ventilator.
• Complete Cessation of Circulatory Function

• Magnus’s test:Fingers fail to show congestion and swelling to a ligature applied at their base.
• Finger nail test:blanching and filling of blood on applying pressure and release of pressure.
• Diaphanous test(transilluminationtest):Fallure to show redness in finger web spaces on
transillumination from behind.
• Icard’s Fluorescein test:Failure to produce yellowish green discoloration of skin on injection of
fluorescrin dye.
Entire and permanent cessation of respiratory function
• Mirror test:Mirror held in front of nose does not show vapors and blurring
Suspended Animation
• It is a condition in which the vital functions of the body are at such a low level that they cannot be
appreciated by clinical examination
Apparent death
• This may last few seconds to minutes.

• Voluntary- by yogis
• Involuntary – drowning, electrocution, heat stroke, typhoid fever etc.
33. Postmortem changes - Early
Early changes
• Changes in the eye

• Changes in the skin
• Cooling of the body/Algor mortis
• Post-mortem lividity/Hypostasis
• Rigor mortis/Cadaveric rigidity
Changes In Eye
• Brownish discolouration of the sclera due to cellular debris and dust-Tache noire
Changes in Skin
• Wounds caused during life will retain their characteristic features
Cooling Of Body/Algor Mortis
• Imbalance between heat production and heat loss.

• Tetanus and strychnine poisoning, due to increase in heat production in the muscle.
• Acute bacterial or viral infection, lobar pneumonia, typhoid fever, encephalitis, etc.
Postmortem Lividity
• Post mortem staining/Hypostasis/Suggilation/ Vibices/ Livour mortis.- 1- 3 hr. Starts

• Purple coloration of dependent parts, except in areas of contact pressure, appearing within 30
minutes to 2 hours after death, as a result of gravitational movement of deoxygenated blood within
the vessels.
• If the body is lying in moving water, due to constant movement of the body postmortem lividity
may not develop.
Colour of post mortem lividity (hypostasis)
• Normal – Bluish pink which later turns into bluish purple

• Hypothermic- Bright Pink
• Carbon monoxide – Bright cherry red
• Cyanide – Pink
• Phosphorous – Dark brown
• Nitrates – Reddish brown
• Chlorates – Chocolate brown
• Hydrogen sulphide – Bluish Green
• Aniline – Deep blue
• Opiates – Black
Medicolegal Importance of Postmortem Lividity
• It gives the information about the position of the body at the time of death
• Time since death can be estimated
34. Rigor mortis
Rigor mortis (Cadaveric Rigidity or Death Stiffening)
• It is defined as contraction, stiffening, shortening and opacity of muscles after death.
Time of Onset :
• Temperate climates – 3-6 hours

• Tropical climates – 1-2 hours
Duration
• Temperate climate – lasts for 2-3 days.

• Tropical climate – 24 – 48 hours in winter,18 - 36 hours in summer
Pattern
• First appear in involuntary muscles

• However, it does not start in all muscles simultaneously (nysten's rule).
• Involuntary muscles (heart) are involved first than voluntary muscles.

• Sequence of muscles involvement is as follows : Heart> upper eyelid> neck >jaw > face > chest >
upper limb > abdomen > lower limb > finger and toes.
• It passes off in the same order in which it has appeared.
Factors affecting rigor mortis
• Rigor mortis is not seen : Fetus < 7 months

• Appears early and passes off quickly : Chronic diseases (TB, cancer, typhoid, cholera), Convulsive
disorders (strychnine poisoning ),Violent deaths (cut throat, electrocution, lightening).
• Early onset and last longer : Drowning and strychnine poisoning
• Early onset : Organophosphate poisoning, cholera, heat stroke and fatigue/exhaustion before death
• Delayed onset :Asphyxia, apoplexy, severe haemorrhage, pneumonia and paralysis of muscles.
• Lasts longer or delayed disappearance : CO poisoning and Arsenic poisoning
• Early disappearance : Widespread bacterial infection, e.g., gas gangrene.
35. Late Postmortem changes - Putrefaction
Late Changes
• Decomposition / Putrefaction.
BACTERIAL ACTION
• Action of bacterial enzymes on tissue components(lecithinase — Cl. welchii)
CHARACTERISTIC FEATURES
COLOUR CHANGES
• First external sign of putrefaction in a dead body

• Greenish discolouration of skin over caecum and flanks after death appears 18-24 hrs.
• Greenish to black discolouration- ‘Sulphmethahaemoglobin’ formed by H2S due to microorganisms
in the large intestine.
PRESSURE EFFECTS OF PUTREFACTIVE GASES
• Displaces the diaphragm upwards

• Discoloured fluid and liquefied tissue mixes with gases producing froth.
• Shifting of the area of hypostasis.
• Extrusion of fluid from the mouth and nose.(Post-mortem purge)
APPEARANCE OF MAGGOTS
• Maggots are seen on the dead body after 2-3 days
• 2-4 days in rainy season
INTERNALLY
Order of appearance of putrefaction from earliest to last is
• Larynx, trachea > stomach, intestine > spleen, liver> brain, lungs > heart > kidney, bladder >
uterus/prostate > bone
• Amongst the soft tissues uterus in female and prostate in males are last to undergo putrefaction, as
uterus and prostate resist putrefaction. Otherwise bones are last to undergo putrefaction, overall
LIVER
• Softens and flabby

• Becomes spongy ‘Foamy liver’
• Honeycombing
Factors causing delay of putrefaction
• Temperature 48° C (very high temperature).

• Dry weather and/or decreased air velocity.
• More than 2 meter deep grave.
• Tight clothing.
• Body in dry soil, and body packed in coffin.
• Infant not fed.
• Wasting diseases like anemia.
• Poisoning: Carbolic acid, ZnC12, strychnine (nux vomica), and heavy metals (arsenic, antimony).
• In water slower than in air (casper's dictum)
• .Caspers dictum.
• Rate of decomposition in soil water and air- 1:2:8.
• “According to an old rule of thumb (Casper's dictum) one week of. putrefaction in air is equivalent
to two weeks in water, which is equivalent to eight. weeks buried in soil, given the same
environmental temperature”
Factors facilitating putrefaction
• Free access of air

• Moisture
• Optimum warmth (10°C - 45° C).
• Thus decomposition is fast in shallow damp, marshy shallow graves, in bodies without clothes and
coffin.

36. Late Postmortem changes - Adipocere
• Adipocere is most commonly seen in the body immersed in water or in damp, warm environment
with lack of air.
• It is also called saponification
• Modification of putrefaction
• Body has an offensive sweet smell
• Hydrolisation of fatty tissue into fatty acids.
• Bacterial fat splitting enzymes and moisture are essential – Lecithinase.
• Cl. welchii bacteria helpful in adipocere formation
• It is usually formed first in the subcutaneous tissues of cheeks, breasts, buttocks, and abdomen.
37. Late Postmortem changes - Mummification
• Mummification is characterized by desiccation or drying of the dead body.

• Occurs when there is excess air and warmth but no moisture (humidity), i.e. hot dry and windy
climate, mummification takes place in place of normal putrefaction.
• Thus mummification occurs in deserts, especially in summer and also in bodies buried in shallow
grave in sandy soil.
• Body features and appearances are preserved but face is greatly distorted
• Time since death can be estimated.
38. Summon
SUBPOENA (SUMMONS)
• Sub- under; Poena- penalty)

• Also known as Duces tecum
Section
• Section 61 - 69 CrPC deal with summons
DEFINITION
• Subpoena is defined as a legal document compelling the attendance of a witness on a particular day
and time in the court of law under penalty.
• No conduct money is paid to the doctor in criminal cases
• Conduct money is paid to expert witness with summons from civil court
39. Medical Evidence
Types of Medical Evidence
Documentary
• Medical certificate
• Medico-legal reports
• Dying declaration
Medical Certificates:
• Documentary evidence
• Issuing false medical certificate is punishable under section 197IPC.
Dying declaration:
• It is a written or oral statement of a person, who is dying as a result of some unlawful act, relating
to the material facts of cause of his death.
• Magistrate should be called to record the declaration (if there is time).
• Doctor should certify his mental state and consciousness before recording(compos mentis).
Dying Deposition
• It is the statement of a person on oath, recorded by the magistrate in the presence of the accused
or his lawyer, who is allowed to cross-examine the witness.
• More importance in court then dying declaration
40. Witnesses and Recording Of Evidence
Witnesses
• A person who gives evidences regarding facts.
Types
• Common witness
• Expert witness

Expert witness:
• doctor, fingerprint expert, ballistic expert.

• Volunteering a statement can be done by doctor
Hostile witness:
• One who is supposed to have some interest or motive for concealing part of the truth, or for giving
completely false evidence.
• IPC -191
Perjury
• Willful false evidence

• Whoever, being legally bound by an oath or by an express provision of law to state the truth , or
being bound by law to make a declaration upon any subject , makes any statement which is false
, and which he either knows or believe to be false ,is said to give false evidence(sections 191 ,192
IPC and 344 CrPC).
• Punishment of up to 7 years(section 193 IPC)
Record of Evidence
• Oath is declaration required by law, which is compulsory and hold the witness responsible for the
consequences of his evidence.
Cross-Examination
• Witness is questioned by the lawyer for the opposite party.

• The defense witness is cross examined by the public prosecutor.
• Leading questions are allowed.
Conduct money
• It is money paid in some legal systems to a person under the compulsion of a summons to witness/
subpoena to pay for their expenses to attend in court.
• Conduct money is paid to expert witness with summons from civil court
• In civil cases, conduct money is decided by judge
41. Embalming
• The usual constituents of embalming fluids are:

1. Formalin 10% and
2. Methanol 55% as preservatives
3. Glycerine 20% as wetting agent
4. Phenol 5% as germicide
5. Water 10% as vehicle
6. Function of sodium borate in embalming fluid is buffer
7. Emblamings may be arterial emblaming and cavity emblaming.
• In a medicolegal case, conducing embalming before autopsy invites liability under section 201 IPC
42. Contusion/Bruise-Types
Types of contusion
1. Petechial haemorrhages
2. Intradermal bruises
• A 'negative image' of the profile of the impacting instrument is produced i.e. a 'patterned injury
• E.g tyre marks in a road traffic collision
3.Tramline bruises
• Appears as a pale linear central area lined on either side by linear bruising
4. Fingertip/pad bruises
• Where an assailant has forcefully gripped a person, for example around the neck (e.g. during
attempted manual strangulation) or arms etc, one may see small discoid or ovoid bruises in a
cluster.
6.Migratory or Ectopic or Percolated contusions: injury at one site, contusion at a remote site due to
gravitation of blood
• Fracture of floor of anterior cranial fossa - bruising around eye (black eye or spectacle hematoma)
• Battle’s sign (named after William Henry Battle) – bruising visible behind and below the ear at the
mastoid process, caused by the gravitational accumulation of blood from a basilar skull fracture
• ‘Racoon/ panda eyes’ – Bruising of the lax soft tissues around the eyes caused by skull base
fractures
43. Contusion/Bruise-Factors and Color changes
Colour Changes of Bruise:

Time Color change Pigment
At first Red Hemoglobin
Few hrs to 3 days Blue Reduced Hb
4th day Bluish black to brown, Hemosiderin
5-6 days Green Hematoidin
7-12 days Yellow Bilirubin
2 weeks Normal ---
• A contusion can be differentiated from postmortem staining by doing Incision test.

• Postmortem staining is easliy washable.
Feature of artificial bruising :
1) Seen on exposed easily accessible parts

2) Dark brown in colour
3) Well defined wound covered with vesicles
4) Inflammation around the surrounding site
5) Itching
6) Vesicles on the fingertip and other parts of the body due to scratching
Note: Artificial bruises can be caused by juice of marking nut, calotropis or plumbago rosea
44. Abrasion
Types of abrasions
1.Scratch abrasion
• Synonym: linear abrasion

• E.g. thorn, fingernails(Crescent shaped abrasion ), tip of knife
2.Graze abrasion
• Synonyms: grinding or sliding abrasions, brush burns

• Most common type - Commonly seen in road traffic accidents
• Mimics burn
3. Pressure abrasion

• Synonym: crushing abrasion
• E.g. Ligature mark in hanging and strangulation
4. Impact abrasions
• Synonym: Contact abrasion or Imprint abrasion
Patterned abrasion
• lmpact abrasion or pressure abrasion, which show pattern of the object (causing injury) are called
patterned abrasion.
• Examples are pattern of cycle chain, pattern of whip, pattern of teeth ond nails,Pattern of tyre,
pattern of string in hanging and strangulation (ligature mark), pattern of head
light/bumper/radiator in vehicles occident, and pottern of porallel lines in (railwoy line pattern)
blow with a stick.
Antemortem Abrasions
• Reddish brown colour.

• Margins are blurred due to vital reactions.
• Antemortem Abrasions can be confused with ant bite marks
45. Incised wounds
Incised wounds
• Its produced by sharp cutting instruments-knife,razor,blade,swords,chopper,axe etc.
Features:
• Edges are regular,clear cut, retracted and averted.

• Length is greater than the breadth.
• Gaping is more when the skin is cut across the Langer's line.
• Drawing cuts-Deeper at start,gradually become shallow and at the end only skin is cut with scratch
“Tailing of the wound”
• Sawing cuts-Multiple at the beginning and only one deep cut wound called “Tentative or Hesitation
cuts”
• Bevelling cuts-When weapon is used oblique or tangential way over the body.
Medico-Legal importance
Homicidal

• Any part of the body, commonly on the neck, head and trunk, also be found on the inner side of
forearm or hand of victim while defending or protecting. ‘Defence Wounds’.
• Slash cuts/chop wound
• Incised wound on nose, ear and genital are usually homicidal
46. Explosion injury
• In blast injury, tympanic membrane is the first organ to be damaged.

• The structures injured by the primary blast wave, in order of prevalence, are the middle ear, the
lungs and the bowel
• Organ is least vulnerable to the blast wave is liver
• Most common organ affected in underwater blast is intestine
• Primary Injury : It is due to shock wave which causes injury to hollow organs. e.g. ears, lungs, eyes,
GIT
• Secondary Injury: These are due to flying debris (missiles).
• Tertiary injuries: Displacement of air by the explosion creates a blast wind that can throw victims
against solid objects.
47. Motor Vehicle injuries
• Sparrow foot marks are multiple punctate lacerations on face, produced due to shattering of
windscreen glass
• Whiplash injury:
• Acute hyperflexion followed by hyperextension of neck due to violent acceleration or
deceleration force applied to (front seat) passenger
• Fracture not common
• Paresthesia and chronic pain
• Seat belt injury is chance fracture, causes laceration of mesenteries and rupture of small intestine.
• Ladder tear Multiple transverse intimal tears in aorta, adjacent to main rupture
• Motorcyclist fracture: Hinge fracture of base of skull, dividing it into anterior and posterior half
• Ring fracture of skull base separating the rim of foramen magnum from rest of the base.
48. Pedestrian Injury
1) Primary impact injuries:
• Overall, the most common site is leg 85%, followed by head (50-80%) > arms > pelvis > chest
orabdomen > neck and spine
Bumper fracture

• Bumper's fracture is the comminuted, depressed fracture of the lateral tibial condyle.
• Anterior cruciate ligament may be injured.
2) Secondary impact injuries:
• After the primary impact, the victim is then again thrown back over the vehicle, causing further
injuries.
3) Secondary injuries:
• Injuries due to contact with ground include abrasion and bruises over the face, hand, hips and legs,
and laceration over the bony prominence
4.) Rolling/Runover (degloving injuries) : Caused by wheel of vehicle or rolling over the victim. Children
are oftenly involved.
49. Regional Injuries
Contre coup injury
• Contrecoup means that the lesion is present in an area opposite the side of impact.
• It is caused when moving head is suddenly decelerated by hitting a firm surface
Fractures of vault of skull
Skull fractures may be classified by their appearance
1.Linear (fissure/crack fracture)
• Straight or curved fracture lines, which may radiate from a depressed region
• ‘Hinge’ fractures occur when the linear fracture passes across the middle cranial fossa, separating
the skull base into 2 halves, and may be caused by a heavy blow to the side of the head (e.g. in
motorcycle accidents).
2. Ring
3. Pond (indented fracture)
• Shallow depressed fracture, more common in infants.
4. Communited fracture/Mosaic (‘spider’s web’)
• Comminuted depressed fracture with radiating fissures.

5. Depressed – (signature fracture or fracture-ala signature)
• Caused by force applied in a ‘focussed’ area e.g. by a hammer.
6. Elevated fracture
7. Radiating fracture (stellate fracture)
• When there is branching or radiations lrom the main fracture line.
8.Gutter fracture
• When a part thickness of bone is removed (fracture involves only the outer table of skull), e.g.
glancing (oblique) bullet wounds in firearm injury
50. Injuries: Medicolegal Aspects
• The doctor who is certifying an injury report should keep in mind the Penal provisions (as below)
required by police to book the case.
• Â Simple injury: IPC Section 323.
• Â Simple injury caused by dangerous weapons: IPC Section 324.
• Â Grievous injury: IPC Section 325.
• Â Grievous injury caused by dangerous weapons: IPC Section 326.
• Â Dangerous injury: IPC Section 307.
• Â Injury likely to cause death: IPC Section 304.
• Â Injury sufficient to cause death: IPC Section 302.
• Â Causing hurt by means of poison: IPC Section 328.
Sec 302 IPC Punishment for murder (upto death sentence/life imprisonment with fine)
Sec 304 IPC Punishment for culpible homicide not amounting murder.
Sec 304-A IPC: Causing death by negligence (Sec 304-8 IPC is related to dowry death)
sec 319. Hurt: Whoever causes bodily pain, disease or infirmity to any person is said to cause hurt.
Section 320 of The Indian Penal Code – Grievous hurt, it has 8 categories.
51. Physical Torture

• TELEFONO consists of repeated slapping of the sides of the head[over the ears] by open palms of
the assailant .this may cause rupture of ear drums.
• FALANGA (also known as falaka or bastinado) In this canes/rods are used to beat on the soles of the
feet , which is very painful and debilitating. Aseptic necrosis may occur. also hyper pigmentation is
seen along lines of injury.
• SUBMARINO [also known as latina] Victim suffers forced immersion of head in water often
contaminated with feces/urine until suffocation.
• DRY SUBMARINO is tying a plastic bag over the head up to the point of suffocation.
• SAW HORSE forced straddling of a bar, forcing the victim to sit on a Rod like one sits on horse back,
leading to perineal/scrotal hematoma.
• CATTLE PROD [electric shock] especially over the genitals , Here a magnetic device delivering high
voltage may be used in which burns may not be found on skin, but it causes severe pain.
• BLACK SLAVE here a heated metal spear like object, is inserted into anus causing rectal/ perinea
burns.
• Parrot’s perch: head down from a horizontal pole placed under the knees with wrists bound to
ankle
• Chapuwa: the legs and thighs are tied very tightly with bamboo sticks to induce severe pain.
(practiced on Bhutanese refugees in Nepal).
• Ghotna: rolling a wooden log over the things up and down, while the long is weighed by one or two
policemen standing on it
• Sham execution: victim is blind folded and asked to stand before a wall and then threatened that a
vehicle is going to hit him. He hears the sound of a vehicle very near to him, causing fear and shock
• Dunking: victim is immersed into water, taken out after some time and given chance to confess.
• Pharmacological torture: Here psychotropic and/or other chemicals are used to induce pain and
agony. Likewise victim is forcibly injected with addictive drugs so much so that he becomes
addicted to it only to be denied to the drug and forced to go through withdrawal symptoms, unless
they comply with the demands of torturer, drug will not be given to them. Strong acids/alkalis are
used to cause burns
52. Inquest
1. POLICE INQUEST:
• Conducted by an officer in charge of a police station. It’s usually conducted by an officer of the rank of sub
inspector of police. The police officer making the inquest is known as investigating officer (I.O.).
• Police inquest is conducted under S.174 of Cr PC if the police officer in charge receives information that a
person has committed suicide, or has been killed by another or by an animal or by machinery or by an
accident, or has died under circumstances raising a reasonable suspicion that some other person has
committed an offence.
• Before the inquest is done by police it should be informed to the executive magistrate of the area. The
inquest report prepared by the police is known as Panchnama.
• In case of any doubt regarding the cause of death or in case of any unnatural the body of deceased is sent by
investigating officer for autopsy to the concerned medical officer with the inquest report.
• On refusing to give answer questions, person can be punished under Sec. 179 IPC with imprisonment upto 6
months and/ or fine of Rs. 1000/.

2. MAGISTRATE INQUEST
• This is empowered by a district magistrate, sub- divisional magistrate or any executive magistrate especially
empowered by the state government such as collector, deputy collector or Tahsildar.
• In case of any death a magistrate may conduct an inquest instead of or in addition to the police inquest
(S.176, Cr.P.C.).
• Magistrate inquest is conducted in case of
1. Death in prison
2. Death in police custody
3. while under police interrogation
4. Death due to police firing
5. Death in a psychiatric hospital
6. Dowry deaths
7. Exhumation (S.174(4) and 176, S.CrP.C)
53. Medical negligence
• Section 304-A of the Indian Penal Code, 1860 [IPC] prescribes punishment for death/ 2 years of
imprisonment with fine or both due to rash or negligent conduct of a person. It is under this section that
doctors or other medical practitioners have generally been proceeded against under criminal law.
• "Section 304-A deals with criminal negligence. Criminal negligence occurs when the doctor shows gross lack
of competence or inaction, gross recklessness or wanton indifference to the patient's safety, or gross
negligence in the selection and application of remedies. It involves an extreme departure from the ordinary
standard of care."
sections 52, 80, 81, 83, 88, 90, 91, 92 304-A, 337 and 338 contain the law of medical malpractice in India.
Sec. 88 in the Chapter on General Exceptions provides exemption for acts not intended to cause death,
done by consent in good faith for person's benefit.
Sec. 92 provides for exemption for acts done in good faith for the benefit of a person without his consent
though the acts cause harm to a person and that person has not consented to suffer such harm.
Sec. 93 saves from criminality certain communications made in good faith.
54. Professional secrecy and Privileged communication
• In India, Sections 126 to 129 of the Indian Evidence Act, 1872 deal with privileged that is attached to
professional communication between a legal adviser and the client
• Section 126 and 128 mention circumstances under which the legal adviser can give evidence of such
professional communication
• Section 127 provides that interpreters, clerks or servants of legal adviser are restrained similarly.
• Section 129 says when a legal adviser can be compelled to disclose the confidential communication which
has taken place between him and his client..
• Section 126 states that no barrister, attorney, pleader or Vakil shall at any time be permitted to
• exception to the general rule of professional secrecy between doctor and patient. Example are:-
1. In court of law: When asked by judge
2. As compulsor duty: Every doctor has to give details of birth, death and communicable disease.
3. As a social duty: Ifhealth ofa patient can cause danger to society, e.g
• Railway engine driver being colour blind

• Bus driver being epileptic, drug addict or hypertensive.
• Pilot having refractive errors.
• Hotel waitor suffering from TB or being typhoid carrier.
• Swimming pool user suffering from STD (e.g. syphilis) or infectious disease.
• Person suffering from STD or HIV infection likely to marry.
4. Cases of food poisoining, Water pollution.
5. In cases of suspected crime
6. ln self interesf, both in civil and criminal suits by patient.
55. Race Determination
Race determination of skeleton:
• The three key factors required to identify skeletal remains are age, sex and race
• The cranium is the only reliable bone and, even then, can only tell general category as below:
• Mongoloid: wider cheekbones, square shaped skull, rounded apertures, concave incisors, width between
eyes greatest
• Negro: Narrow elongated skull, squared orbit, rounded nasal aperture, more prominent ridges, wider nasal
opening
• Caucasian: Rounded skull, elongated nasal aperture, triangular palate
• Cephalic index: Cephalic index is defined as the index of breadth of skull
• CI = width ÷ length x 100 or CI = (Left/Right) ÷ (Front/Back) x 100.
• Dolico-cephalic: 70-75.(aryans, negroes).
• Mesati-cephalic: 75-80. (europe, chinese).
• Brachy-cephalic: 80-85. (mongoloids).
• Four carpal bones are present at age 4
56. Superimposition and Tattoo Mark

• Superimposition helps determine that the skull is that of person in the photograph, by adjusting
magnification till inter-pupillary distances correspond' It is done by following steps
• video superimposition mounted skull and photograph are videographed using a color camera and the
video signals are fed into a color camera. This digital image manipulation technique is better.
• Tatoo marks are designs made in skin by multiple small puncture wounds with needles or electric
vibrator dipped in colouring matter' The dyes commonly used are lndian ink), Carbon, indigo, cobalt,
prussion blue ,ultramarine, and vermilion or cinnabar.
• Tattoo mark is permanent when dye penetrates the dermis Infrared photography makes old tattoos
readly dsible. A faded tattoo mark becomes visible by use of utraviolet lamp or rubbing the part and
examining with magnifying lens.
• Latent tattoo marks are faded marks and they can be visualized by
• Use of ultraviolet light
• Infrared photograpy(Blackening and tattooing of skin and clothing can be best demonstrated).
• Rubbing the part and examining under magnifying glass
• If tattoo marks are obscured by decomposition they can be visualized by treating with 3 % H2O2.
• Tatto marks can be developed by treating the skin by 0.5% caustic potash.
• Histopathology of local lymph nodes for pigment:- sometimes Patient's relative gives a history of tattoo,
however it is not found during autopsy then Lymph node are dissected to find it.
57. Somatic ,molecular and Sudden Death.
• Somatic death (svstemic death or clinical death)

• It is the complete and irreversible stoppage of the circulation, respiration and brain functions
(bishop's tripod of life).
• Somatic death is associated with immediate signs of death :-i) Permanent and complete
cessation of function of brain and flat electric EEG(PGI03) with no response to external brain
death.
• Somatic death is due to stopped aerobic processes. However, anaerobic enzymatic processes
are still continuing, hence : Muscles still respond to mechanical, elecfiical and thermal stimuli.
• Absent of brainstem reflexes : Pupillary reflex, oculovestibular reflex, corneol reflex,
pharyngeal and tracheal reflexes.
Molecular death (cellular death)
• It occurs after somatic death. lt refers to death of all individual cells.

• It occurs when even anaerobic processes stop, due to non availability of ATP.
• Early signs : Changes in skin and eye, cooling of the body, post-mortem lividity, changes in
muscles (e.g. primary relaxation, rigor mortis).
Hydrocution or immersion syndrome refers to sudden death in water due to vagal inhibition as a result of:
58. PRESERVATION OF ORGANS

• In decomposed bodies, In Spot death in burns ,When an investigating officer requests so.
• The body should be stored averagely at 40C.
• The body should be never undressed before the forensic doctor has seen it.
• The body can be stored at 200C to preserve it for long duration.
• Brain- Neurotoxic poisons, alkaloids, volatile organic poisons. Preservation of brain is not required
in Heavy metal poisoning.
• Bile- Narcotic drugs, cocaine, methadone, Glutathione, Barbiturates, Tranquilizers, Opiates
• Vitreous Humour- Alcohol, Chloroform. (Vitreous Humour is preserved by keeping at 4ºC for 48
hours; normally preservative is of no value. Though could be preserved with sodium fluoride).
• Saturated sodium chloride: In all cases ofpoisoning excluding corrosive acids, except carbolic
acids (phenol), alkalis, corrosive sublimate and aconite.
• 30 mg potassium oxalate (anticoagulant) and 10 ml sodium fluoride (enzyme inhibitor): Blood
in suspected poisoning including alcohol but excluding oxalic acid, ethylene glycol, fluoride,
carbon monoxid.
• Rectified spirit : All except in cases of poisoning by phenol, phosphorus, paraldehyde, kerosene,
formaldehyde, formic acid, alcohol, acetic acid, chloroform, chloral hydrate, ether.
• Glycerine : Specimen for virological examination.
• I0 mg/ml Na/K, fluride and 3 mg K-oxalate: For preserving blood; fluride is also added to CSR
vitreous humor, and urine if alcohol estimation is required; and also in analysis of cocaine,
cyanide and carbon monoxide.
59. Asphyxial Death
• Asphyxial death is diagnosed by triad of the following

1. Cyanosis
2. Congestion : Due to increased venous pressure.
3. Petechial hemorrhages (tardieu's spots) : Present above the level of obstruction like scalp,
eyebrows, face in hanging or strangulation and above the level of compression in traumatic
asphyxia.
• Asphyxial death is diagnosed by triad of the following
1. Cyanosis
2. Congestion : Due to increased venous pressure.
3. Petechial hemorrhages (tardieu's spots) : Present above the level of obstruction like scalp,
eyebrows, face in hanging or strangulation and above the level of compression in traumatic
asphyxia.
• They are generally Found in those parts where capillaries are least supported, e.g. face,
conjunctivae, epiglottis, serous surface of heart and lungs, meninges and thymus.
• A method of homicidal smothering and traumatic asphyxia is known is Burking
(To execute (someone) by suffocation so as to leave the body intact and suitable for dissection.)
• Tardieu's spots are not pathiganic of asphlxia, as they are also found in bleeding disorders
(scurvy, leukemia);
• coronary thrombosis; electrocution; poisoning, anticoagulant therapy anil blood dyscrasia
(thrombocytopenia).
• Tardieu's spots are not found in some form of asphlxia, e.g. drowning.
mechanical causes of asphyxia which can cause violent asphyxial death. These mechanicai causes
can be divided into
• hanging,
• strangulation,
• suffocation,
• drowning
60. Hanging: Introduction,classification, causes of death
Complete hanging:
• When the whole body is suspended from the ligature material and no portion of the body is
touching the ground.
Partial hanging:
• As the name suggests, the body is partially suspended, the toe or feet or either part of the body
touching the ground.
• The deceased may be in kneeling down position, sitting position etc.
• the weight of the head is where the constricting force comes from.
Depending on position of the knot:
Typical hanging:
• Where the ligature runs from the midline, above the thyroid cartilage.
• symmetrically upwards on both sides of the neck(judicial hanging), to the occipital region.
• The knot is placed over the central part of the back of neck.
Atypical hanging: The knot is anywhere other than the central part of the back of neck.
Death may occur from :
• Cerebral ischemia and anoxia due to compression of carotid artery.

• It require 3-5 kg weight of suspension-
• Tear in intima of carotid artery is known as Amussat's sign.
• Cerebral congestion due to compression of jugular veins. It requires only 2 kg weight.
• Asphyxia due to compression of airways (larynx and trachea). It requires 15 kg weight.
• Neurogenic shock/vagal inhibition (due to pressure on vagus nerve or carotid sinuses)
• Fracture dislocation of upper cervical vertebrae with damage to spinal cord and brainstem : especially
in judicial hanging.

• Any combination of the above.
Combined asphyxia and cerebral venous congestion is the most common cause of death.
61. Hanging: Postmortem findings,Strangulation,Medico-legal aspects of hanging.
• Hanging. This is due to irritation of submandibular and parotid glands by ligature.

• There may be intimal tear of carotid arteries.
• In case of pressure of ligature on cervical sympathetic ganglia, the eye on that side is found open (La
facie sympathique) .
• Fracture of hyoid is usually not seen (may be seen only in l0%). Fracture of thyroid cartilage
• (20-30 % cases) and fracture of tracheal rings (5-l0 %) may be seen
• Lynching is a form of homicidal hanging where an accused of murder or rape is hanged in a public square
by a mob as a part of carrying out justice.
• Judicial hanging: In some countries, including India, hanging is the mode of carrying out capital punishment
or legal execution of death sentence. The rope is allowed to drop 5 to 7 metres according to the height and
weight of the person. Bilateral fracture of the pedicle of the second-third or third-fourth cervical vertebrae
occurs which is called hangman’s fracture.
• Sudden stop causes fracture dislocation usually at level of C2-C3 or C3-C4 vertebra, and injury to spinal cord
and brainstem (pons and medulla).
• the dislocation of the atlanto occipital joint or the odontoid process of the axis vertebra causes pulping of
the spinal cord and transaction of the cervical cord. There even can be rupture of the brain stem with proper
judicial hanging.
• Postmortem hanging: Sometimes the victim may be murdered by some other means and then hanged
postmortem in order to mislead the police. thorough and meticulous postmortem examination, the original
cause of death can also be established.
62. Lynchinq and Sexual asphyxia (autoerotic hanging).
Introduction
Lynching
It is homicidal hanging in which a suspect, accused or eneffiy is hanged by a rope from a tree by
the mob. Name is derived from William Lynch, a white captain in USA, who used to order hanging of
blacks (negroes) on the spot without trial..
It was practiced in tribal part of India and some southern states of America for sexual crimes or to
take revenge.
Sexual asphyxia (autoerotic hanging)

It is a peculiar type of hanging where the victims are usually young males with some form of
abnormal sexual behavior, usually masochism and transvestism.
Masochism:
• Masochism is the practice of seeking pain because it is pleasurable.

• Behaviors associated with Sexual Masochism Disorder can be acted out alone (e.g., binding, self-
sticking pins, self-administration of electric shock, or self-mutilation)
• Behaviors associated with a partner e.g., physical restraint, blindfolding, paddling, spanking,
whipping, beating, electric shock.
• cutting, pinning and piercing, and humiliation such as by being urinated or defecated upon, being
forced to crawl and bark like a dog, or being subjected to verbal abuse.
• Behaviors sometimes include being forced to cross-dress or being treated like an infant
Transvestism.
• Transvestism is the practice of dressing and acting in a style or manner traditionally associated with
the opposite sex.
• In some cultures, transvestism is practiced for religious, traditional or ceremonial reasons.
• Partial asphyxia causes cerebral distrubances with feeling of sexual gratification.
• The impaired consciousness caused by pressure on carotid vessels or partial obstruction of air
passages may lead to hallucinations of an erotic nature.
63. Suffocation
Smothering:
• Asphlxia is caused by mechanical occlusion of external air passage, i.e. entry of air to lungs is
prevented by closure of nose and mouth.
• Lips, gums, tongue, inner side of nose may show bruising or lacerations.
• Asphyxial signs (congestion, cyanosis, petechiae) are severe except when the head and face is
enclosed in plastic bag.
Chocking:
• Asphyxia caused by mechanical occlusion of internal air passage, i.e. obstruction of respiratory
passages (glottis, larynx, trachea, bronchi etc.)
Gagging:
• It is chocking by preventing air entry through mouth and nostril by filling piece of cloth in the
mouth.

Traumatic asphyxia:
• It is a form of asphyxia which is caused from respiratory atest due to mechanical

• fixation of chesf resulting from blunt trauma to chest or external pressure on the chest,
abdomen or back which prevents normal respiratory movements of the chest wall
Burking:
• It is combination of smothering and traumatic asphyxia.

• It was the method used by Burk and Hare. Burk used to sit on chest covering with one hand
the mouth and nostril and pushing up the jaw with other hand and Hare used to pull him
around teh room by feet.
64. Burns(Thermal injury): Degree of burns
• It is defined as tissue injury due to application of heat in any form to the external or internal body
surfaces.
• Section 324 & 326 I.P.C. specifies any ‘hurt’ or ‘grievous hurt’ which is caused by ‘fire or any heated
substance’ or ‘corrosive’ or ‘explosive substance’ is punishable more severely in comparison to
unspecified means.
Dupuytren classified burns into six degrees, which can be merged into three degree by Wilson.
(A) Wilson’s Classification (merged) : can be categorized into 3 types depending upon body layer involved.
1) Epidermal: (first-and second-degree dupuytren)
• The affected part is erythematous (red) and blister formation, there is capillary dilatation and
transudation of fluid into the tissue causing swelling.
• Repair is complete without scar formation. These are painful burns'.
2) Dermo epidermal : (third and fourth degrees dupultren)
• Whole thickness of skin is destroyed with destruction of dermal appendages.

• These burns appear as shriveled, depressed areas of coagulated tissue, bordered by reddish
blistered skin.
• Pain and shock are greater than in first-degree burns.
3) Deep: (fifth and sixth degrees)
• When deeper tissues below skin are involved viz. subcutaneous tissues, muscles and bones etc.
• These are relatively less painful owing to destruction of nerve endings and heal with scar and
contracture formation.
• Disfigurement and loss of function chiefly when near a joint.
65. Burns(Thermal injury): Extend of burns.
Introduction,
• It is most important parameter which affects the prognosis in case if burn injury. To estimate the
body surface area involved,
• Rule of Nines” given by Alexander Wallace is practiced clinically for calculating the amount of fluid
i.e. “ration” to be given to injured adult.
1 Head and neck 9% 7 Left upper limb 9%
2 Front of chest 9% 8 Front of right lower limb 9%
3 Back of chest 9% 9 Back of right lower limb 9%
4 Front of abdomen 9% 10 Front of left lower limb 9%
5 Back of abdomen 9% 11 Back of left lower limb 9%
6 Right upper limb 9% 12 Perineal area/Pudendal area 1%
• TOTAL= 100%
• Rule of five’’ may be more appropriate. For calculating percentage of body surface area involved in
children in practice.
1. Head & neck -20% (5%x4)
2. Abdomen -20% (5%x4)

3. Chest -20% (5%x4)
4. Upper Limb -20% (5%x4)
5. Lower Limb -20% (5%x4)
• For calculating percentage in case of scattered burn injuries ‘Palm rule’ has been found handy.
According to it the surface area of the palm of victim is approximately 1% of total body surface area
• Genitals constitute 0% up to 9 years of age and head forms the largest area in children.
• Area of palm (palmar surface), as a general rule, constitutes about l% of surface area both
in adult and children.

• In burnt area >l5% in adults and >10% in a child, the loss of circulatory blood volume must be
replaced, otherwise it will cause irreversible shock.
• Burns on head, neck, trunk and genitals are said to be more dangerous than on other parts
of the body.
• Infants, young children and elderly are particularly vulnerable to initial shock and subsequent
complications
66. Burns:Cause of death & Important postmortem findings
• The nasal and oral cavities may show presence of carbon soot and are inflamed.
• There is increased carbory-hemoglobin which gives cherry red colour to post mortem lividity.
• Presence of carbon particles (soot) in respiratory passages and elevated level of carboxy-
hemoglobin confirms that victim was alive when the burn occurred, i.e. ant-mortem burn.
• Laryngeal edema which is caused by passage of hot gases into respiratory tract.
• Raised carboxyhaemoglobin level in the blood; exceeding 10%. Chain smokers may develop blood
level upto 8%-10%; therefore it needs careful interpretation in such cases.
• Various levels of cyanide is found in blood depending upon the materials burning in fire. But
the levels are less than 0.3% mg (normal is zero.
• Presence of intact nerves, blood vessels and connective tissue in the floor of rupture.
• Absence of bleeding in the wound, Irregular matgins, Absence of bruising or other vital
reactions in margin.
67. Thermal injuries: chemical, electric and Lightening burns.
• Chemical burns are produced by corrosive acids and alkalis.

• Acids with a pH less than 2 precipitate proteins causing coagulation necrosis.
• Nitric acid gives a yellow-brown scab, sulphuric (vitriol) a black-brown scab,
• Hydrochloric acid (spirit of salt) a white to grey scab, and carbolic acid (phenol or Lysol) gives a light
grey to light brown scab.
• Alkalis with a pH above 11.5 cause more tissue damage than acids because they induce liquefactive
necrosis, which facilitates ever deeper penetration of the alkali.
• The caustic alkalis, such as sodium hydroxide (caustic soda or lye) and ammonium hydroxide, leave
a grey-white mucoid burn.
• Vesicles and blisters, Charring (soot) and singeing are absent, except in cases of mineral acids
where they are present.
• The most serious alkali burns of the eye are produced by: Strong liquid ammonia.
• High tension electrical burns from overhead electric lines can cause Myoglobinuria and Acute renal
failure.
• Electric burns are at times, also referred to as joule burns.
• Regarding high-voltage electrical burns to an extremity. Evaluation for fracture of the other
extremities and visceral injury is indicated.
• Ulceration is present, Coagulative necrosis is seen at the site of contact except for hydrogen
fluoride which chelate calcium.
• Calcium phosphate of bones may also melt and is radiologically seen as bone pearls (wax
dripping), Muscles show Zenker's degeneration.
• commonest cause of death in electric injury is ventricular fibrillation.
• The skin may get coloured due to metallic pigment :- green (in brass electrode), black (in iron
electrode), blue (in copper electrode) and grey (in aluminium electrode).
• In high-voltage (more than 1,000 volts) electrical burns the contact injury of exit often appears as a
blow-out type of wound.
• Alternating current (AC) is more dangerous than direct current (DC)
68. Seminal stains.
A) Chemical tests :These tests are divided into :
1) Microchemical tests :
Florence test:
• This test was discovered by Dr.Florence in the year 1886.

• When Florence reagent (PotassiumIodide+Iodine+Water) is applied to the slide it produces
rhomboidal shape dark crystals of choline periodide.
• choline can be detected if swab is collected within one day of sexual act,
Barberio's test:
• Invented by Barberio in the year 1905.

• When the questioned stain is allowed to react with picric acid it leads to the formation of yellow
needle shaped spermine picrate crystals.
2) Enzyme tests: Since spermatozoa contain gram positive protein, the presence of spermatozoa will be
confirmed by microscopic appearance of purple bodies
Acid phosphatase & specific glycoproteins:-
• This test is adopted because of high acid phosphatase activity of semen.

• Stability of acid phosphatase activity in seminal stain depends on temperature
3) Ammonium molybdate test: lt gives deep yellow colour, due to presence of phosphorus.
B) Microscopic examination : It is done to demonstrate the presence of spermatozoa in the vaginal

fluid or in stain.

C) Biological examination:
• Precipitin test : To know the species to which semen belongs.

• Blood group can be known from semen
D) UV light:
• Invisible, softened and dry semen stains of the clothes can be rendered distinct by the
filtered UV light which produces bluish fluorescence.
69. Hair: Examination, Importance, & difference between Human Hair Vs. Animal Hair
Hair Examination Importance
1) Identification: Identification of individual which may be accused, mutilated

body etc.
2) Source: Source of origin, whether animal or human.
3) Sexual offences: Rape and unnatural sexual offences.
4) Crimes: Hair or fibers found at the scene on weapons or clothes helps in identification of
accused.
5) Hit and run case: When specimens of hair removed from various parts of the motor car are sent
by authorities for comparison with victim's hair.
6) Chronic poisoning by metals: Arsenic, antimony radium and thallium.
70. FORENSIC PSYCHIATRY: INSANITY
INTRODUCTION:
• Insanity is an old term used loosely to denote any mental disorder or mental illness. The Indian Penal Code
employs the term unsoundness of mind while referring to insanity.
• Lucid interval is the period of sanity (sound mind) in an insane person, i.e. period in course of mental
illness when there is complete cessation of manifestations of insanity.
• During this period he is quite normal and can make valid will, sell/purchase property, give valid
evidence and is legally responsible for his deeds.
• Patient is kept under observation for l0 days which can be extended upto maximum 30 days.
Civil responsibilities of insane:

Management of property, Contract, Marriage, Competency as witness, Validity of consent, Civil rights,
Guardianship, Testamentary capacity (capacity of a person to make valid will).
Criminal responsibility of insane
In law, criminal responsibility means liability to punishment for the crimes committed.
Also that a person who is proved to be insane is not responsible for his actions, as he is devoid of free will,
intelligence and knowledge in relation to his acts.
The criminal responsibility of an insane is judged by rules:
1) MC Naughten rule ( legal test or right or wrong test).
It states that an accused person is not legally responsible, if it is clearly proved that at the time of
committing the crime, person was suffering from such a defect of reason from abnormality of mind that he
didn’t know the nature and quality of act he was doing or that what he was doing was wrong i.e. a person is
not responsible if he is not of sound mind (section 84 IPC).
2) Doctrine of partial responsibility: suffering from some weakness or aberration of mind (though not
completely insane).
3) Durhan rule: Accused is not responsible for the act, if his act resulted from mental disease or defect.
4) Currens rule: A person is not responsible if at the time of committing the crime, he did
not have the capacity to regulate his conduct according to the requirments of law as a result of his mental
disease or defect.
71. Dowry Death
Introduction
In some cases newly married girls are abused, harassed, cruelly treated and tortured by the
husband, in-laws and their relatives for or in connection with any demand for dowry. In extreme
cases, the woman is killed by burning or some other method. Law in relation to dowry death are:
IPC Section 304 - B deals with dowry death:
• Whoever commits dowry death shall be punished with imprisonment for a term ten years which
may extend to imprisonment for life.
Law prescribing punishment for causing cruelty to a married women (Sec.498A, IPC).
• Husband or (his any) relative will be tried under section 498A, IPC for causing cruelty to a
married woman.
• Punishment includes imprisonment which may extend upto 3 years and fine.
Section 174 (3) CrPC : Autopsy is compulsory in all cases of unnatural death of a female within 7
years of marriage (i.e.dowry death) or if she is less than 30 years of age (Note : Section 174 CrPC
allows police inquest for any case).
Section 176, CrPC: Authorize magistrate inquest for investigation of dowry death.
Section 113 A' IEA : Deals with presumption as to abetment (encouragement) of suicide by a married
woman due to cruelty by husband or his relatives.
Section 113 B, IEA: Deals with presumption as to dowry death.
Dowry Prohibition act, if any person gives or takes or abets the giving or taking dowry is
punishable with imprisonment for a term which shall not be less than 5 years and with a fine which
shall not be less than 15000 rupees or the amount of the value of such dowry, whichever is more.
Pathology
1. Pulmonary Tuberculosis
• The most common hematologic finding associated with pulmonary tuberculosis is Mild anemia,
leukocytosis,thrombocytosis with slightly elevated ESR
• Reactivation tuberculosis is almost exclusively a disease of the lungs
• Epitheloid cells in tuberculosis act as Secretory cells
• Pleural effusion is seen in two-thirds of cases of primary pulmonary tuberculosis
• Fibrocasseous lesion is seen in primary pulmonary tuberculosis
• Phlyctenular conjunctivitis is seen in primary pulmonary tuberculosis
• Primary pulmonary tuberculosis Shows Consolidation & pulmonary fibrosis
• Primary Tuberculosis most commonly involves Lungs
• Most commonly involved organ in congenital tuberculosis is lung
• A man presents with fever, wt loss and cough; Mantoux reads an induration of 17 x 19 mm: Sputum
cytology is negative for AFB shows pulmonary tuberculosis infection
• Secondary pulmonary tuberculosis usually involves Apex of lungs
• Ghon's focus is seen in primary pulmonary tuberculosis
• Paratracheal lymphadenopathy is seen in primary pulmonary tuberculosis
• Primary pulmonary tuberculosis Heal spontaneously by fibrosis
• Reactivation of pulmonary tuberculosis always occur at Apex of the upper lobe
• Cavitation of the lungs is a feature of secondary pulmonary tuberculosis

• Bilateral upper lobe fibrosis & Mediastinal enlarged necrotic nodes with peripheral rim
enhancement in chest CT is suggestive of tuberculosis
• Definition of relapse in TB is A pateint who returns sputum positive which was cured by previous
treatment
2. Genital Tuberculosis
• Mycobacterium can be grown from menstrual blood in TB patient showing pelvic inflammation
• In patient with infertility hysterosalpingography reveals 'Bead – like' fallopian tube & clubbing of
ampulla is suggestive of genital tuberculosis
• Most common site of genital tuberculosis is Fallopian tube
• Perforation of the uterus while doing endometrial biopsy in a case of suspeccted genital
tuberculosis can be treated by Laparascopy & Immediate laparotomy
• The commonest type of genital tuberculosis is Endosalpingitis
• Blood stream is the commonest method of spread of genital tuberculosis
• Primary focus is most often in the lung
• The commonest complication of pregnancy after complete treatment of genital tuberculosis
is Ectopic pregnancy
3. Genitourinary Tuberculosis
• Investigation of choice for advanced renal tuberculosis is CT

• Intravenous urography is the most sensitive imaging modality to detect early renal tuberculosis
• Sterile Pyuria is characteristically seen in Renal Tuberculosis
• Most common route of infection in kidney tuberculosis is hematogenous
• Earliest and often the only presentation of TB kidney is Increased frequency
• Cobblestone mucosa,Thimble bladder,Golf hole ureter are the Cystoscopic findings in TB bladder
• Most common site of genitourinary tuberculosis is kidney
• Renal tuberculosis originates in the Renal pyramid
4. Gastrointestinal Tuberculosis
• Ileocecal tuberculosis presents with Rapid emptying of narrowed terminal ileum

• Ileocecal tuberculosis shows Inverted umbrella sign
• Stellate ulcer with elevated margins is seen in Ileocecal tuberculosis
• Hyperplastic tuberculosis is Mass in rt iliac fossa
• Ileo caecal region is the Common site for Hyperplastic tuberculosis
• In Hyperplastic tuberculosis x-ray shows indrawing of caecum from ileum
• Ileocecal tuberculosis is associated with megaloblastic anemia
• Small intestinal tuberculosis can cause Diarrhoea & stricture
• Commonest site of tuberculosis of the intestines is illeum
• Most common site of tuberculosis in gastrointestinal tract is Ileocecal junction
• Pulled up cecum ,Obliteration of angle between ileum and cecum ,Narrowing of distal end of cecum
are seen in ileocaecal tuberculosis
5. Skeletal Tuberculosis
• Earliest sign in X-ray in TB spine is Narrowing of disc space

• Pott's spine is commonest at Thoracolumbar spine
• Old age,Long standing cases, Sphincter involvement, sudden onset are the indicators of poor
prognosis of tuberculosis of spine
• Most common cause of cold abscess of chest wall is Pott's spine
• Chronic retropharyngeal abscess is associated with tuberculosis of spine
• Triple deformity of the knee is a complication of tuberculosis of knee
• Commonest presenting symptom of Pott's spine is back pain
• In spinal tuberculosis, the commoner route of spread is blood
• Tuberculosis in Pott's disease involves spine
• Large paravertebral abscess ,Marked collapse of vertebra & Deceased joint space are radiological
features of tuberculosis of spine
• Progression to kyphosis deformity is least with lumbar lesions in children
• Spine is the most common skeletal tuberculosis site
• Investigation of choice for spinal TB is MRI
6. TUBERCULOUS MENINGITIS
• Loss of appetite cough followed by neck rigidity with increased protein level of CSF than normal &
lymphocytosis is suggestive of TB meningitis.
• Chronic headaches accompanied by chronic mild nuchal rigidity with Cerebrospinal fluid sampling
showing a chronic inflammatory infiltrate with lymphocytes, plasma cells, macrophages, and
fibroblasts is suggestive of Mycobacterium Tuberculosis infection
• Raised intracranial tension in the form of vomiting and altered sensorium & CT scan showing basal
exudates and hydrocephalus is suggestive of TB meningitis
• CSF findings in tubercular meningitis include:
• Elevated opening pressure
• High leukocyte count ( 1000/microl) predominantly lymphocytes
• Increased protein (100 - 800/mg/dl)
• Low glucose
• AFB seen on direct smear of CSF
• In tuberculous meningitis, the exudates tends to be most severe At the base of the brain
• C.S.F. cell count in tubercular meningitis varies between 100-1000
• Hemiplegia, quadriplegia, monoplegia, Cranial nerve palsies, Cerebral infarction, Ptosis,
Decerebrate Rigidity, Tremors, Decorticate Rigidity, Midline cerebellar syndromes, Cerebellar
Hemispheric Lesions are the neurological complications of tuberculosis meningitis
• Most common cause of adrenal insufficiency in India is Tuberculosis
• Characteristic finding in CT scan of patient with tubercular meningitis is Exudates seen in basal
cistern
7. TUBERCULOSIS OF SKIN
• A farmer with a single warty lesion on leg may be suggestive of Tuberculosis verrucosa cutis.
• Tuberculids are seen in Lichen scrofulososum.
• Lichen scrofulosorum is an extending eruption of small follicular papules characterized by
involvement of the sweat glands and hair follicles by causing noncaseating epithelioid
granulomas in young persons with underlying TB.
• Anatomist's warts/ Prosector's warts/ Verruca necrogenica are the synonyms of tuberculosis
verrucosa cutis.
• In miliary TB the granulomas are of size 1-2 mm.
• Cryptic type miliary TB usually affects elderly patients.
• Choroid tubercles are the pathognomonic finding in miliary TB.
• Miliary TB & Tuberculosis verrucosa cutis is a form of Post-primary TB infection.
• Lupus vulgari is the most common type of cutaneous T.B.
• Apple Jelly nodule at root of nose is the characteristic finding of Lupus vulgaris.
• Gradually progressive plaque on a buttock with of 15 cm in diameter, annular in shape, with
crusting and induration at the periphery and scarring at the center, is suggestive of lupus vulgaris.
• Miliary Tuberculosis occur following primary infection and secondary reactivation
• Sputum microscopy is usually negative & Montoux test is negative in 20-30% in Miliary
Tuberculosis
• Systemic miliary TB occurs when spread occurs via Arterial.
8. DIAGNOSTIC TECHNIQUES OF TUBERCULOSIS
• Tuberculin positive means Patient is infected with Mycobacterium

• 3000 infectious nuclei per cough are likely to be seen in sputum examination
• Mycobacterium tuberculosis is differentiated from other atypical mycobacteria by niacin test & Aryl
sulphatase test
• The most appropriate test to assess the prevalence of tuberculosis infection in a community is
tuberculin /Mantoux test
• False-negative tuberculin test is seen in Miliary tuberculosis, Convalescence from some viral
infections like Measles, Lymphoreticular malignancy, Sarcoidosis, Severe malnutrition,
Immunosuppressive therapy, Defective cell-mediated immunity
• Characteristic finding in CT in a TB case is Exudate seen in basal cistern
• Confirmatory test for tuberculosis is AFB
• Fastest method for diagnosis of TB Gene expert
• Sputum smears are usually positive in patients with laryngeal TB, endobronchial TB, and cavitary
pulmonary TB
• Radiometric BACTEC detect growth of M tuberculosis in 2-3 week
• Malachite green in LJ media Inhibits growth of other bacteria
• As per RNTCP guidelines first do in TB suspect case is sputum microscopy
• A rapid test used by WHO for tuberculosis is Sputum AFB
• Gene expert used for getting diagnosis of TB in 1-2 hrs
• L j medium is used for growth of M. tuberculosis
9. TYPHOID
• Healthy carriers in typhoid emerge from subclinical cases

• In typhoid fever, the urinary carrier is more dangers than an intestinal carrier
• Carriers of avirulent organisms in typhoid are called pseudo-carriers
• Typhoid is Most common among males
• IP: 7 - 14 days, but ranges from 3 days to 3 weeks
• Chronic case of typhoid carrier is a risk factor for cholangiocarcinoma
• To prevent the spread of infection, the patients are kept in isolation till three bacteriologically
negative stools and urine reports, are obtained on three separate days.
• Widal test is the investigation of choice in 3rd week.
• Step ladder pyrexia, Rose spots on trunk & pea-soup diarrhea are the common findings of typhoid
fever
• Chronic carrier state is associated with presence of bacilli in gall bladder
• Convalescent carriers excrete the organism for 3 – 8 weeks
• Chronic carriers excrete bacilli for many years
• Splenomegaly , neutropenia & positive urine & stool culture after 2weeks of infection may be seen
in Typhoid in children
• Vi antibody can be used for detecting carrier
• Blood culture (gold standard) - 90% positive in the first week
• H-antigen titre remains positive for several months after infection
• Person with prior infection or immunization may show anamnestic response
• Infection acquired by ingestion of faecally contaminated food or water
• Culture of feces, Bile, urine is useful in detection of carrier state in Typhoid
• Man is the only known reservoir
• Multiple ulcer found in terminal ileum
• Perforation in typhoid ulcer occurs in 3rd week
• Intestinal Perforation in typhoid is less common in children below 5yrs
• Erythrophagia and Mononuclear cell infiltration ulcers are seen in typhoid ulcer
• Perforation,Haemorrhage,Sepsis are the complications of typhoid ulcers
• In breast fed infant less chance of enteric infection is due to Ig & nutrients in breast milk

• Perforation appears clinically as Pyrexia for greater than ten days ,acute pain in periumblical region
spreading all over the abdomen.
• Typhoid perforation is diagnosed by Plain X-ray of abdomen in erect posture
• Enteric Fever is caused by salmonella typhi & paratyphi
• Enteric fever diagnosis in 2nd week is best made by widal test
• Most immunogenic in typhoid is H antigen
• Rose spots are bacterial emboli to the skin and occur in 1/3 of cases of typhoid fever
10. TUMOR PROTEIN 53 (TP53)
• p53 encodes 53k Da protein

• p53 is located on Chr. 17
• p53 arrests cell cycle at GI phase
• Half-life of p53 protein in normal cells is 20 minutes
• "Policemen gene’ or ‘Guardian gene’ is the name given to P53
• P53 is the most common oncogene mutation causing malignancy in humans
11. APOPTOSIS
• Inflammation is absent in Apoptosis.

• Annexin V is a marker of Apoptosis.
• Cell shrinkage, Chromosomal breakage, Clumping of chromatin, nuclear condensation and
fragmentation, Intact cell membrane, Cytoplasmic eosiophilia is seen in Apoptosis
• Councilman Bodies, Graft versus host disease, Menstrual cycle, Pathological atrophy following duct
obstruction are examples of apoptosis.
• Cytochrome C has a direct role in Apoptosis.
• Memory cells doesn't undergo apoptosis due to presence of Nerve growth factor.
• Organelle that plays a pivotal role in apoptosis is mitochondria.
• Apoptosis is inhibited by bcl-2.
• In apoptosis, Apaf-1 is activated by release of Cytochrome c from mitochondria.
• The most characteristic feature of apoptosis is condensation of nuclear chromatin which
corresponds to nuclear compaction (pyknosis) on light microscopy.
• Intact cell membrane is also a characteristic feature of Apoptosis .
• Cysteinyl aspartate specific proteases (Caspases) is involved in Apoptosis.
• Considerable apoptosis may occur in tissues before it becomes apparent in histology.
• Apoptotic cells appear round mass of the intensely eosinophilic cytoplasm with dense nuclear
chromatin fragments.
• Macrophages phagocytose the apoptotic cells and degrade them.
• The normal cellular counterparts of oncogenes are important for inhibition of Apoptosis.
• Peripheral aggregation of chromatin characterizes Apoptosis.
• Chemotherapeutic drugs can cause both necrosis and apoptosis.
• CD 95 is a marker of extrinsic pathway of Apoptosis.
• Caspases is activated for nuclear fragmentation in apoptosis.
• Ladder pattern of DNA electrophoresis in apoptosis is caused by the action of endonuclease
enzyme.
• Internucleosomal cleavage of DNA is characteristic of Apoptosis.
• Phosphatidyl serine has important role in Apoptosis.
• Starting point of apoptosis for programme cell death is activation of caspases.
• Apoptosis is self-initiated.
• Apoptosis is the hallmark of programmed cell death.
• CD 95 induces apoptosis when it engaged by fas ligand system.
• BCL-2 is the gene for apoptosis.
• The lymphocytopenia seen a few hours after administration of a large dose of prednisone to a
patient with lymphocytic leukemia is due to massive lymphocytic Apoptosis.
• Ubiquitin is required for Apoptosis.
• Inducers of apoptosis are growth factor withdrawal, detachment from matrix, glucocorticoids,
cytotoxic drugs & immune cytolysis.
• The earliest change seen in apoptosis is Cell shrinkage.
• Execution caspases of apoptosis are Caspase 3 & 7.
12. SICKLE CELL ANEMIA
• Parvovirus B19 has been associated with transient aplastic crises in persons with sickle cell disease.
• Target cells, Jaundice, Reticulocytosis, Sickle cells, Howell Jolly bodies are seen in Sickle cell Anemia.
• Sickle cell anemia leads to resistance towards P.Falciparum.
• In Sickle cell disease, single nucleotide change results in change of Glutamine to Valine.
• Sticky patch in sickle cell disease results from replacement of a polar residue (Glutamate) with a
non-polar residue (Valine) at the 6th position of the beta chain.
• RFLP results from a single base change in Sickle cell disease.
• HbS confers resistance against malaria in heterozygotes in Sickle cell disease.
• Hydroxyurea is used in sickle cell anemia.
• IV regional anesthesia is contraindicated in a young boy with sickle cell trait.
• Sickle cell disease is inherited as Autosomal recessive.
• In Sickle Cell Anaemia defect is in beta chain.
• Replacement of glutamate by valine in β-chain of HbA is the primary defect which leads to sickle
cell anemia.
• Sickle cell trait patient does not have manifestations as that of Sickle cell disease, because 50% HbS
is required for occurrence of sickling.
• 0 and 100% is the chances of having children with sickle cell disease and sickle cell trait respectively
in a mother diagnosed to have sickle cell disease, her husband is normal.
• If both parents are sickle cell anemia patients then the likelyhood of offsprings having the disease
is 100%.
• The decrease in size of the spleen is most likely related to infarction in a 6-month-old child with
sickle cell anemia having a chronically enlarged spleen and by 5 years of age, the child's spleen is no
longer palpable.
• Polymerase chain reaction with allele-specific oligonucleotide hybridization, Southern blot
analysis, DNA sequencing can be used to detect the point mutation in the beta globin gene that
causes sickle cell anemia.
• Decreased Solubility is the cause of sickling of RBC in sickle cell disease.
• Recrrrent infections - Most common cause of death in Sickle cell anemia.
• There is a positive correlation between HBS and polymerization of HBS in Sickle cell anemia.
• Patients require frequent blood transfusions in Sickle cell anemia.
• Patients usually presents after the age of 6 months in Sickle cell Anemia.
• In sickle cell anemia hemoglobin electrophoresis shows HbF, HbS, HbA2.
• PAH, Fish vertebra, Leukocytosis, Cardiomegaly is seen in Sickle cell anemia.
• The mechanism of increased susceptibility of Pneumococcal infection in patients with sickle cell
anemia is Splenic dysfunction.
• In sickle cell anaemia, the defect can be explained as having arisen from base substitution in DNA.
• Sickle cell anemia is the clinical manifestation of homozygous genes for an abnormal haemoglobin
molecule.
• The event responsible for the mutation in the B chain in Sickle cell anemia is Point mutation.
• Condom or Diaphragm is the safest contraceptive method for a woman with sickle-cell anaemia .
• Sickle cell anemia is commonly seen in black and R.B.C. size is altered.
• HbS concentration, HbA, pH are the factors affecting Sickling.
• Number of bands found in sickle cell trait is 2.
• Autosplenectomy in sickle cell anaemia is due thrombosis and infarction.
• Crew haircut appearance in X-ray skull and Gandy gamma bodies are seen in sickle-cell anaemia .
• Sickle cell disease causes extravascular hemolysis.
• Bone pain is the commonest presentation of sickle cell anemia.
• Salmonellosis is most common in sickle cell anemia.
• Vertebra plana, Bone infarct, Marrow hyperplasia, 'H' shaped vertebra are radiological features of
Sickle cell anemia.
• Splenectomy is indicated in Sickle cell anemia.
• Dactylitis, Pulmonary hypertension, Decreased osmotic fragility, Necrotizing pappilitis, pituitary
apoplexy, Persistent priapism is seen in Sickle cell anemia.
• 'Sea-Fan' retina is seen in SLE and Sickle cell disease.
• Splenomegaly may be a feature of Sickle cell anemia but Hepatosplenomegaly is not a feature.
• Sickle cell anemia is a non-metabolic cause of abdominal pain.
• Missense mutation occurs in Sickle cell disease.
13. LANGERHANS CELL HISTIOCYTOSIS (LCH)
• Peak incidence is less than 3 years of age in Letterer Siwe disease type of Langerhans cell
histiocytosis.
• Langerhans cell histiocytosis is radiosensitive.
• Diffuse form of Langerhans cell histiocytosis is known as Letterer Siwe disease.
• Langerhans cell histiocytosis produces a seborrheic dermatitis-like lesion in an infant.
• CD 1a is a marker of Langerhans cell histiocytosis.
• The nuclei of Langerhans giants' cells are arranged around the periphery.
• Localised Langerhans cells histiocytosis affecting head & neck is called Eosinophilic Granuloma.
• X-bodies called Birbeck granules are characteristically seen in Langerhan's cell granulomatosis.
• The histologic hallmark of Langerhans cells is Birbeck granules.
• Langerhans histiocytosis can be associated with diabetes insipidus.
• Hand Schuller Christian disease, Eosinophilic granuloma, Letterer Siwe disease are the types of
Langerhan's cell histiocytosis.
• Langerhans cells belong to Antigen presenting cells.
14. Transforming growth factor Beta
• During angiogenesis recruitment of pericytes and periendothelial cells is due to Angiopoietins, TGF
& PDGF.
• Fibrosis is due to TGF Beta.
• Actions of TGF: Anti-inflammatory ,Proliferation of fibrous tissue , Inhibition of metalloproteinases .
• Anaphylaxis is not an action of TGF.
15. ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY (ANCA)
• Hepatitis B is associated with an immune-mediated vasculitis characterized by p-ANCA antibodies.

• C-ANCA positivity indicates, antibody formed against Proteinase 3.
• Proteinase-3, in neutrophil azurophilic granules, is the major cANCA antigen.
• The major target for pANCA is the enzyme myeloperoxidase.
• There are two major categories of ANCA.
• pANCA pattern of staining has been associated with non-vasculitic entities such as rheumatic and
nonrheumatic autoimmune diseases.
• ANCA associated with Wegner's granulomatosis is c-ANCA.
• pANCA is sensitive and specified for Idiopathic crescentic glomerulonephritis.
• ANCA positive vasculitis is Wegener's Granulomatosis, Churg-Strauss syndrome, Microscopic PAN
• Goodpasture syndrome is positive for pANCA.
• The most likely diagnosis in a patient presenting with respiratory symptoms i.e. cough, hemoptysis
and glomerulonephritis and CANCA levels in serum found to be raised is Wegener's granulomatosis.
• ANCA associated with crescentic glomerulonephritis is seen in Wegener's granulomatosis,
microscopic polyangiitis.
• The most likely diagnosis in a 20-year-old male presenting with mucus and repeated
gastrointestinal bleeding and positive for ANCA is Ulcerative Colitis.
• Likely diagnosis in a patient presenting with hemoptysis and hematuria few weeks after a
respiratory tract infection with the presence of ANCA antibodies is Goodpasture's syndrome.
• cANCA Positivity is specific for Wegener's granulomatosis.
• p-ANCA is characteristic for Microscopic Polyangitis.
• c-ANCAs are present in up to 95% of cases of Wegener's granulomatosis.
16. GRANULOCYTE STIMULATING FACTOR (G-CSF)
• Drug of choice for Neutropenia due to cancer chemotherapy is Filgrastim.

• G-CSF stimulates production of a wider variety of hematopoietic stem cells.
• Filgrastim is used in treatment of Neutropenia.
• Treatment in a child with recurrent severe bacterial infections and diagnosed of having Kostmann's
syndrome is G-CSF.
17. HEMPHILIA
• Increased total body iron concentration within liver.

• Biopsy showing large amounts of granular golden- brown pigment which stains blue with Prussian
blue stain is suggestive of haemophilia.
• Haemophilia causes an overgrowth of epiphyses.
• Prenatal diagnosis of Hemophilia is best done by PCR
• Prolong APTT with normal PT, BT & platelets with postpartum haemorrhage is suggestive
of acquired haemophilia A.
• Normal platelets, Deficient factor VIII & IX are suggestive findings of hemophilia
• Hemophilia is associated with X chromosome
• Hemophilia B is due to deficiency of clotting Factor IX
• Patients with hemophilia A have bleeding disorder because of lack of reaction accelerator during
activation of factor X in coagulation cascade.
• DDAVP is the drug used in mild hemophilia.
• A child who bleeds from gums and has swollen knee - probably due to hemophilia
• Spontaneous muscle bleeding is typically seen in hemophilia
• Bleeding time may be used to differentiate hemophilia A from von Willebrand disease
• Recurrent Spontaneous Hemarthrosis is commonly seen in patients with Hemophilia when
factor VIII levels are <5%.
• The most common manifestation of moderate /severe Hemophilia A is Recurrent Hemarthrosis.
• The most common cause of fracture in a patient with Hemophilia is Osteoporosis and Restricted
Joint Movement.
• Females are mostly carriers and all males are affected in hemophilia.
• In Hemophilia with Rheumatoid arthritis, analgesic of choice is Acetaminophen.
18. APLASTIC ANEMIA

• A patient aged 65 years, is diagnosed to have severe aplastic anemia with HLA compatible sibling is
best treated with Antithymocyte globulin followed by cyclosporine
• Carbamazepine may lead to aplastic anemia.
• Parvovirus causes aplastic anemia in chronic hemolytic diseases
• Pancytopenia is caused by Aplastic anemia
• Reticulocytopenia is caused by Aplastic anemia
• Aplastic anemia can progress to AML,Myelodysplastic anemia,Paroxysmal nocturnal
hemoglobinuria
• Splenectomy done in Aplastic anemia.
• Aplastic anemia is seen in PNH,Chloramphenicol,HIV- I, Pregnancy (rare), Gold salts.
• Fever, weakness, splenomegaly, low hemoglobin & pancytopenia are features seen in aplastic
anemia.
• Most common cause of aplastic anemia is Exposure to drugs.
19. THALASSEMIA
• Oral deferiprone is the most appropriate drug used for chelation therapy in beta-thalassemia
major.
• Splenomegaly, target cells on peripheral smear, microcytic hypochromic anaemia are seen
in thalassemia major.
• Hb-A2 estimation will be diagnostically helpful in a case of beta thalassemia trait.
• Hb-H disease is a form of alpha thalassemia.
• Intracorpuscular hemolytic anemia is seen in Thalassemia
• Defect leading to thalassemia lies in Haemoglobin.
• Thalassemia occurs due to Splicing mutation.
• In Beta thalassemia, there is decrease in beta chain & increase in alpha chain.
• A2 concentration in thalassemia trait is >3.5
• The investigation done to establish the diagnosis of thalassemia is Hb-electrophoresis.
• NESTROFT test is used in screening of Thalassemia.
• In α-thalassemia, there is no α-chain
• Thalassemia gives protection against malaria.
• Bone marrow iron is increased in Thalassemia.
• Decrease in osmotic fragility cause hemolysis in Thalassemia.
• Test for beta-thalassemia trait is HbA2
• Hair on end appearance is seen in X-ray skull in Thalassemia.
• Hepatosplenomegaly and edema all over body of new born leading to death is diagnosed to have α-
thalassemia
• Splenectomy is least useful in Thalasemia major
• Normal levels of free Erythrocyte Protoporphyrin with hypochromic microcytic anemia, seen
in Thalassemia
• Haptaglobin levels are decreased in Thalasemia
• Thalassemia is inherited as Autosomal recessive
• In alpha-thalassemia trait,electrophoresis shows Normal HbF and normal HbA2
• Defect in Snurps causes thalassemia
20. PARANEOPLASTIC SYNDROME
• Paraneoplastic Syndrome seen in RCC is Acanthosis nigricans, Hypertension, Hypercalcemia,

Amyloidosis and Polycythemia.
• Two important causes of paraneoplastic syndrome among the cancers are Small cell carcinoma lung
and carcinoid
• Cushing syndrome as paraneoplastic syndrome is seen with Bronchial carcinoid, Thymus, Medullary
carcinoma thyroid
• Paraneoplastic syndrome is associated with Renal Ca & Breast Ca
• Parathyroid-related peptide causes lung carcinoma & increased PTH
• ACTH, ADH and Carcinoid syndrome are the paraneoplastic syndromes seen with small cell ca lung.
• The paraneoplastic syndrome associated with Hodgkin's disease is Cerebellar degenerative disease.
21. SEBACEOUS CYST
• Sebaceous cysts are mostly found on the face, neck, back, scrotum, or torso.
• Cocks peculiar tumor is actually a complication of sebaceous cyst.
• Chalazion is a sebaceous cyst.
22. PULMONARY EMBOLISM
• Best investigation when there is clinical suspicion of pulmonary embolism in a patient is Multi
detector CT angiography
• Hampton's hump is seen in chest X-ray in Pulmonary embolism.
• Test results that confirm or exclude pulmonary embolism are Perfusion scan & CT pulmonary
angiogram
• Hampton's hump, Westermark sign & Fleischner sign are radiological sign present in a young lady
with symptoms suggestive of pulmonary embolism.
• The anticoagulant effect of heparin in pulmonary embolism would be most appropriately assessed
by Activated partial thromboplastin time.
• Treatment of choice for acute pulmonary embolism with right ventricular hypokinesis and
compromised cardiac output but normal blood pressure is Thrombolytic agent.
• Obesity, Malignancy & Protein S deficiency may predispose to pulmonary embolism
• In acute pulmonary embolism, Sinus tachycardia is the most frequent ECG finding
• Activation of juxtapulmonary-capillary receptors during pulmonary embolism causes Tachypnea
• The most common source of pulmonary embolism is Large veins of lower limb.
• D-dimer is the most sensitive test for Pulmonary embolism
• In pulmonary embolism, findings in perfusion scan are perfusion segmental defect with normal lung
scan & radiography.
• Best method to diagnose pulmonary embolism Pulmonary angiography
• Gold standard for diagnosing pulmonary embolism Ventilation-perfusion scan
• The sequence of symptoms in pulmonary embolism is Dyspnea, pain, haemoptysis
• In pulmonary embolism, fibrinolytic therapy is responsible for risk of haemorrhage
• A patient undergoing surgery suddenly develops hypotension, the monitor shows that end-tidal
CO2 has decreased abruptly by 155 mm Hg. Diagnosis - Pulmonary embolism
• The most common cause of preventable Hospital Death is Pulmonary embolism
• ECG pattern seen in pulmonary embolism is S1Q3T3.
23. Primary hyperaldosteronism
• Diastolic hypertension, Polyuria and Hypokalemia are seen in primary hyperaldosteronism

• Class,Triad of Biochemical Criteria for diagnosis of Primary Hyperaldoteronism
• Hypokalemia with inappropriate kaliuresis (Metabolic alkalosis)
• Suppressed plasma renin activity
• Elevated Aldosterone levels that do not fall appropriately in response to volume expansion or
sodium load
• Primary hyperaldosteronism lead to Hypernatremia,Hydrogen depletion and metablic
alkalosis, Hypertension
24. Wilson's disease
• Advatage of Zinc treatment in wilson disease is that it's Nontoxic, Produces a negative copper
balance by blocking intestinal absorption of copper, induces hepatic metallothionein synthesis,
which sequesters additional toxic copper
• In wilson disease patients with hepatic decompensation the disease severity is assessed using Nazer
prognostic index.
• DOC in Wilson disease with Neurologic/Psychiatric manifestation is Tetrathiomolybdate and zinc
• Low ceruloplasmin is the diagnostic feature of wilson's disease
• Siblings of the diagnosed patient with Wilson disease will be having 25% risk of Wilson disease
• Free copper level is increased in the body however Serum copper level is usually lower than normal
in wilsons disease
• Due to the large amount of copper released into blood stream in wilson disease anemia occurs
• Kayser-Fleischer ring will be present in Almost 100 % proportion of patients with neurologic
manifestations of wilson disease
• The gold standard for the diagnosis of Wilson disease is Liver biopsy with quantitative copper assay
• In a patient with wilson disease related compensated cirrhosis, without evidence of neurologic or
psychiatric symptoms the best treatment option is Zinc

• During treatment for Wilson disease with trientine and penicillamine, free serum copper should be
kept below 25mcg/dl
• Intestinal absorption is increased in Wilson disease
• Gene responsible for Wilson disease is situated on chromosome no 13
25. Systemic Lupus Erythematous
• Commonest cutaneous eruption in Systemic Lupus Erythmatosus is Erythema of light exposed area
• Criteria for diagnosis of systemic lupus erythematosus includes Photosensitivity, Malar rash ,Discoid
rash
• 22% of patients with disseminated discoid lupus erythematosus develops SLE
• Anti Ro autoantibodies is most suggestive of subacute cutaneous lupus erythematosus
• High titers of Anti dsDNA are considered to be highly specific for Systemic lupus erythematosus
• Neonatal lupus erythematosus (NLE) is characterized by Cutaneous lesions, Heart block
& Thrombocytopenia
• Libman-Sacks endocarditis may develop with systemic lupus erythematosus
• Woman with systemic lupus erythematosus (SLE) and chronic renal failure develops anemia
because of IgG directed against red blood cells
• There may be an increase in spontaneous abortions and prematurity in patient with SLE planning
for pregnancy
• Diffuse proliferative is the most common histological type of nephritis seen in systemic lupus
erythematosus (SLE)
• Children born to mothers with systemic lupus erythematosis are likely to have Complete heart
block
• Characteristic feature of SLE is Polyserositis
• Autoimmune Hematolytic Anemia & Anti-ds DNA are seen in SLE
• In SLE, characteristic kidney lesion is Wire loop lesions
• Indications of steroids in SLE are Endocarditis
• SLE is Type III hypersensitivity reaction
• Onion skin spleen is seen in SLE
• Normal CRP with elevated ESR seen in SLE
• Skin biopsy of SLE patient using RTC labeled human IgG antiserum shows deposition of irregular
particles at dermoepidermal junction. This means there is presence of Immune complex deposits
• SLE is can cause both cicatricial as well as noncicatrical alopecia
• Band test is done in SLE
• According to WHO, membranous glomerulonephritis seen in SLE, is Class V

26. CYSTIC FIBROSIS
• Cystic fibrosis can cause diarrhea

• Staphylococcus aureus, Hemophilus influenzae, and Pseudomonas aeruginosa are common causes
of respiratory infections in cystic fibrosis
• Rhinosinustis is a common finding in CF
• The most common cause of pulmonary abscesses in Cystic Fibrosis is Pseudomonas aeruginosa
• Cystic fibrosis affects Respiratory, Hepatobiliary & Genitourinary systems
• Most common organism associated with cystic fibrosis is Pseudomonas aeruginosa
• Meconium ileus is associated with Cystic fibrosis
• Sweat chlorides are increased in Cystic fibrosis
• Cystic fibrosis (CF) is an Autosomal Recessive Disorder
• Cirrhosis is an established complication of CF
• The earliest chest X-ray change in cystic fibrosis is Hyperinflation
• Steatorrhoea, Hypochloremia, Recurrent pneumonias are seen in a patient with cystic fibrosis
• The most common inherited disorder of cholangiocyte injury is Cystic fibrosis
• Intracanalicular hepatic apparatus is affected by Cystic fibrosis
• Cystic fibrosis is Associated with CFTR gene
• Cystic fibrosis is associated with Infertility, Azoospermia, Nasal polyps
• Chromosome defective in cystic fibrosis is Chromosome 7
• 3 episodes of chest infection and passage of foul smelling stools is diagnosed with Cystic Fibrosis
• Cause of thick pancreatic secretions in cystic fibrosis Defect in chloride channel leading to water
reabsorption
• Most common pathogen causing, pulmonary infection in cystic fibrosis in infants & young children
is Staphylococcus Aureus
• Xerophthalmia is caused by cystic fibrosis
• Exocrine pancreatic insufficiency is caused by cystic fibrosis
• Central bronchiectasis is seen with Cystic fibrosis
• Sweat gland ducts are not obstructed in cystic fibrosis
• Chance of having cystic fibrosis if only one parent is affected and other is normal is 50%
27. Cellular adaptation
• Hypertrophy is an increase in the size of cells resulting in increase in the size of the organ and there
is no change in the number of cells.
• Hypertrophy examples- Physiologic -
a) Enlarged size of uterus in pregnancy, breast tissue in puberty & pregnancy is an example of hypertrophy
as well as hyperplasia.
• Hyperplasia- Hyperplasia is an increase in the number of cells but there is no change in the size of
tissue.

• Hyperplasia examples- Physiologic (Hormonal)- female breast at puberty, pregnancy and pregnant
uterus.
• Metaplasia- Vitamin A deficiency (in respiratory epithelium) or excess leads to metaplasia.
• Metaplasia can be two types-
Epithelial-
a) Squamous- Uterine endocervix in prolapsed uterus & old age, Bronchus in chronic smoker.
b) Columnar- Columnar metaplasia in Barrett’s oesophagus (intestinal metaplasia).
Mesenchymal example is myositis ossificans
• Mechanism of atrophy is by Ubiquitin proteasome pathway.
28. Reversible cell injury
• Hypoxia is the most common cause of cell injury which is caused due to ischemia.
• ATP depletion to 5- 10 % of normal levels will induce cell injury.
• Decreased generation of cellular ATP— it occurs in both reversible & irreversible cell injury.
• Intracellular lactic acidosis results in nuclear clumping as there is decrease intracellular pH and
glycogen by anaerobic glycolysis.
• Failure of sodium- potassium pump (Na+- K+ ATPase) resulting in cell swelling (Hydropic swelling).
• Failure of calcium pump by increased sodium level where excess of calcium will move into the cell
resulting in deposition of phospholipase & cell swelling.
• Due to hypoxia, ribosomes detach from endoplasmic reticulum & golgi apparatus which degrades
into monosomes leading to decrease in protein synthesis.
• Plasma membrane alterations in the form of blebbing & loss of microvilli.
• Myelin figures derived from damage of the membranes (whorls of lamellate phospholipid and
calcium)
• Mitochondrial swelling & small amorphous densities within mitochondria.
29. Irreversible cell injury
• Irreversible cell injury has two phenomenon consistently- Inability to reverse mitochondria
dysfunction.
• Mitochondria damage results in formation of large flocculent mitochondrial densities.
• Increased calcium influx activates phospholipase cell membrane damage.
• Karyolysis- decreased basophilia due to dissolution of nucleus.
• Lysosomal membranes are damaged lysosomal hydrolytic enzymes leakage.

30. Necrosis
• Coagulative necrosis-
• It effects- heart, kidney, spleen (except brain).
• Underlying tissue architecture is preserved.
• Coagulative necrosis is characteristics of infarcts in all solid organs (mainly heart).
• Hallmark of coagulative necrosis is conversion of normal cells into their tombstones.
• The cell injury causes denaturation of protein.
• Liquefactive necrosis- Examples are- Infarct brain and abscess cavity.
• Caseous necrosis- It is found in the centre of foci of tuberculous infections & histoplasmosis.
• It has features of both coagulative & liquefactive necrosis.
• Fat necrosis- Mesentric fat necrosis due to acute pancreatitis as there is liberation of pancreatitic
lipases resulting in necrosis of pancreas & peritoneal cavity.
• Traumatic fat necrosis of the breast.
• The released fatty acids combined with calcium gives a chalky white appearance.
• Fibrinoid necrosis- Fibrinoid necrosis is a special form of necrosis in immune reactions in which
antigen and antibodies are deposited on the walls of arteries.
• It is seen in vasculitis & malignant hypertension.
• Seen in sarcoidosis.
31. Necroptosis
• Necroptosis- It is a programmed cell death without caspase (cysteine- aspartic proteases) activation.
• Pyroptosis- It is a caspase (caspase 1 & 11) dependent programmed cell death.
• Free radical occurs by- Oxidation- reduction reactions- examples are
a) Fenton reaction- iron is oxidised from ferrous to ferric form.
• Antioxidant mechanism-
• Two categories-
a) Non- Enzymatic-
i) Vitamin A (not antioxidant in vitreous eye), C and E
ii) Tissue proteins (transferrin, ceruloplasmin)
b) Enzymatic- they are peroxisomal enzymes
i) Catalase
ii) Superoxide dismutase (SOD)- SOD1 protects brain causing amytrophic lateral sclerosis.
iii) Glutathione peroxidase

32. Autophagy
• Autophagy refers self eating (lysosomal digestion) of cell’s own components during nutrient deprivation.
• Macrophage- specific deletion of Atgs- 5 (autophagy related genes- Ag) increases susceptibiltiy to
Tuberculosis.
33. Intracellular accumulations
1. Fatty change (Steatosis)

Abnormal accumulation of triglycerides within parenchymal cells is fatty change (steatosis).
Seen in liver (most common), heart, skeletal muscle, and kidney.
2. Protein-
Disorder associated with misfolded/ unfolded proteins are alzeheimer’s disease, Huntington disease and
parkinson’s disease.
3. Water
Intracellular water accumulations are known as cloudy swelling.
4. Pigment
a) Lipofuschin-
Also known as wear and tear pigment/ aging pigment.
It is perinuclear brown pigment.
• b) Melanin-
Detected by Fontana masson staining.
• c) Hemosiderin-
Detected by Perl’s Prussian blue staining.
• Color of hemosiderin is brown
34. Pathological clacification
• Pathological calcification starts in mitochondria or microsomal vesicles except for kidney where it starts at
basement membrane.
• Dystrophic calcification- Deposition of calcium salts in dead and degenerated tissues and has normal calcium
level.
• Calcification in degenerated tissues- Artheromas
• Metastatic calcification- Deposition of calcium salts in normal tissues associated with deranged calcium
metabolism & hypercalcaemia.
• Mestatic calcification- Excessive absorption of calcium from gut-
i) Hypervitaminosis D
ii) Williams syndrome
iii) Vitamin A toxicity
• Site of metastatic calcification are- lungs (most common), kidney, stomach, blood vessels, cornea
35. Cellular ageing
• Most widely accepted theory for ageing is – “free radical mediated damage”.
Changes seen during ageing are-
• Increased cross linking of collagen

• Increased somatic mutations
• Telomere shortening
• Decreased cellular replication-
• Werner syndrome- premature ageing due to defective DNA helicase.
• With progressive cell division telomeres will be shortened & induce cellular senescene due to
chromosal damage.
• Environmental stresses like Sirtuin – where calorie restriction will induce sirtuin. Sirtuin plays key
role in ageing, diabetes mellitus and cancers.
36. ACUTE INFLAMMATION- Vascular events
• Four cardinal signs of inflammation by Celsus-

• Rubor (redness)
• Tumour (swelling)
• Calor (heat)
• Dolor (pain)
• Fifth sign is function laesa (loss of function) by Virchow.
• Vascular events- includes 2 changes
a) Vasodilation
b) Increased vascular permeability

• Transient vasoconstriction vasodilation elevation of local hydrostatic pressure increase
vascular permeability slowing or stasis leucocyte migration.
LEWIS TRIPLE RESPONSE
• Red line- capillary vasodilation

• Flare- bright reddish appearance (arteriole dilation)
• Wheal- exudation swelling
• Mechanism of increased vascular permeability-
• Endothelial cell contraction
• Contraction or Mild endothelial injury
• Direct endothelial cell injury
• Leucocyte mediated endothelial injury
• Neovascularisation
• Increased vascular permeability mediated by histamine, bradykinin, IL-1 , TNF- α.
• Immediate transient response types takes place in venules.
37. Acute inflammation- cellular events
Transmigration-
• Occurs mainly in post- capillary venules except in lungs (capillaries)

• Cytokines activates leukocyte & endothelial cell to induce PECAM- 1 or CD 31.
• Diapedesis- is transportation of leucocytes through endothelial gap.
• PECAM- 1 is most important adhesion molecule for diapedesis.

Chemotaxis-
• Leucocyte moving towards sites of infection or injury along a chemical gradient by a process called
chemotaxis (unidirectional).
• Agents can be-
a) LTB4
b) IL8
c) C5a & C3a
Phagocytosis
• Normal human cells are protected from phagocytosis due to presence f N- acetylgalactosamine or
terminal sialic acid.
• Opsonisation is when phagocytosis is enhanced as microorganisms are coated with specific proteins
ie. Opsonins from the serum.
• Main opsonins present are-
a) IgG opsonin- naturally occurring antibody
b) C3b opsonin
c) Lectins
Engulfment-
• Opsonised microbes are ready to be engulfed by formation of cytoplasmic pseudopods.

• Both phagocytosis & chemotaxis requires polymerization of actin filament.

38. Cell derived inflammatory mediators
I) Vasoactive amines-
II) Arachidonic acid metabolites (Eicosanoids)
• A) Via cyclooxygenase pathway- includes

III) Lysosomal components
1. Primary granules (azurophil granules)
• Develop at promyelocytic stage.

• More destructive
• These are-
i) Myeloperoxidase (MPO)
ii) Cathepsin
iii) Non- specific collagenase
2. Secondary granules (specific granules)
• i) Lactoferrin
• ii) Lysozyme
• iii) Type IV collagenase
• iv) Vitamin B12 binding proteins
3. Tertiary granules (C- particles)
• Involved in chemotaxis
• Contains gelatinase
IV) Platelet activating factor (PAF)

V) Cytokines
• They are soluble polypeptide.

• Source- lymphocytes & monocytes.
• They are highly specific.
• Important cytokines are-
a) Interleukines
i) IL1- fever
ii) IL4- anti-inflammatory
iii) IL6- synthesis of acute phase proteins
b) Tumour necrosis factor (TNF)
TNF- α- acute inflammatory, septic & shock, systemic inflammatory response syndrome & cachexia.
c) INF- γ- granuloma formation
VI) Chemokines
• Action- leukocyte movement, chemotaxis
a) Alpha chemokines (C-X-C)- IL-8
b) Beta- chemokines- Ecotaxin, RANTES, MIP1- alpha
c) Gamma- chemokines- lymphotactin
VII) Nitric oxide-
• Now synthsized from arginine amino acid

• Action- Vasodilation, anti platelet aggregation, microbicidal action

39. Plasma derived inflammatory mediator
1. Complement system-
a) Classic pathway- activated by both IgM & IgG
b) Alternate pathway- activated by antibody
• Complement system functions- C3a, C5a, C4a (anaphylatoxins) activates mast cells & basophils
which releases histamine. (inflammation)
• Actions-
• C3b is an opsonin (opsonisation)
• C5a is chemotactic for leukocytes.
• Membrane attack complex (MAC) (C5b- C9) is a lipid dissolving agent (cell lysis)
2. Kinin system
• Activated by factor XIIa generate bradykinin (Hageman factor)
3. Clotting system
• Factor XIIa initiates the cascade of clotting system resulting in fibrinogen formation.
• Clotting activates fibrinolytic system.

4. Fibrinolytic system-
• Activated by plasminogen activator.

• Lately fibrinopeptides or fibrin is formed.
40. Chronic inflammation

Characteristics of Chronic inflammation-
• Infiltration with mononuclear cells includes- macrophages (most important), lymphocytes and
plasma cells.
• Tissue destruction or necrosis- Hallmark of chronic inflammation by activated macrophages.
• Repair- healing by fibrous & collagen takes place.
System effects of chronic inflammation-
• Fever
• Leucocytosis
41. Granulomatous inflammation
• Formation of granuloma is a Type IV granulomatous hypersensitivity reaction.
Pathogenesis-
Composition of granuloma-
• Epitheloid cells
• Multinucelated giant cells
• Lymphoid cells
Types of granuloma-
• Immunological granuloma

• Non- immunological granuloma- silicosis, foreign body pneumonia
Special forms of granuloma-
1. Stellate granuloma- Cat scratch disease
2. Durck’s granuloma- celebral malaria
3. Eosinophillic granuloma- Churg- strauss syndrome

4. Naked granuloma- Sarcoidosis
Systemic effects-
• Fever- IL-1 (most important pyrogens)

• Most important cytokine for synthesis of acute phase protein is IL-6.
Examples of granulomatous chronic inflammation-
42. Wound healing & repair
Repair- results in fibrosis & scarring.
Granulation tissue growth consist of triad-
• Neovascularization (angiogenesis)
• Fibrogenesis
• Non specific inflammation
• Scar tissue & adult skin - Type I collagen
• Early granulation tissue- Type I & III collagen
Types of cells-
43. Stem cells
Stem cells has major 2 properties-
• Self renewal
• Asymmetric replication (stochastic differentiation)
Embryogenic stem cells (ES cells)-
• They are pluripotent (generate all cell lineages)
Adult stem cells
• Also called as tissue stem cells.

• Adult stem cells are-
a) Liver stem cells-
• At canals of Hering
• Forms bipotent progenitor called oval cells.
b) Skin stem cells-
• Forms bulge stem cells.
c) Small intestinal crypt epithelium-

• Located above Paneth cells.
d) Skeletal muscle
• Located at basal lamina of myotubules.

• Called as satellite cells.
e) Cornea
• Located limbal stem cells.
f) Bone marrow
• Pluripotent
• Marrow stromal cells
g) Brain
• Located at dentate gyrus

• When stem cells transforms to form cells characteristic of other tissues, the process is called
as trans differentiation.
44. Healing of Skin wounds
• Secondary intention-
• Initial hemorrhage
• Inflammatory phase
• Epithelial changes
• Granulation tissue
• Wound contraction- is most prominent seen in wound healing.
• Presence of infection

45. WOUND HEALING- Complications, Factors & Strength
Complications of Wound Healing-
• Infection
• Deficient scar formation
• Hypertrophied scar
• Keloid formation
Wound Strength-
• Wound contraction- completed by 14th day

• At the end of 3rd month 70- 80% of normal skin (maximum strength)
• Fibroblasts in healing wound are derived from local mesenchyme.
• Vitamin C promotes wound healing.
• Vitamin E inhibits wound healing
46. Healing of specialised tissue (fracture healing)
• Healing of any fracture takes place by-

• Primary union of fracture
• Secondary union (more common)- it is described under 3 heading-
a) Procallus formation- it is as follows
i) Hematoma formation

ii) Local inflammatory response- fragments of necrosed bone are scavenged by macrophages &
osteoclasts
iii) Ingrowth of granulation tissue- soft tissue callus formed
iv) Callus composed of woven bone & cartilage
b) Osseous callus formation-
• Callus formation takes place- 4 to 12 weeks
c) Remodelling
• Osteoblast & osteoclast removes necrotic content, which results in remodelling of the united bone
end into compact bone.
47. Hyperemia & Congestion
• Passive hyperaemia or venous congestion is impaired venous drainage.
CVC lung- Alveoli contains hemosiderin laden macrophages (heart failure cells)
CVC liver-
• Central section shows characteristics nutmeg appearance.

• The changes are more seen in Centrilobular zone.
• It has dilated blood vessels.
CVC spleen-
• Hyperplasia of reticuloendothelial cells.
• Gamna gandy bodies are seen.
48. Edema- basics
• Edema is an accumulation of interstitial fluid within tissues (5-6 litres)

• Edema develops when plasma protein is below 5 gm/dl.
• Decreased plasma oncotic pressure- E.g. a) Oedema in renal diseases- nephritic & nephritic
syndrome
• Lymphatic obstruction-
• It results in lymohoedema.
• E.g. inflammation of lymphatics seen in filariasis results in lymphoedema of scrotum & legs.
• Milroy’s disease or hereditary lymphoedema
• Sodium & water retention-
• Oedema of renal disease- nephritic disease & nephritic syndrome
49. Amyloidosis- introduction
• Amyloidosis is a group of diseases characterised by extracellular deposition of fibrillar insoluble

proteinaceous substance called amyloid.
• The term amyloid was coined by Lister.
• Amyloidosis is basically a disorder of protein misfolding.
• Etiology of amyloidosis is unknown.
Physical & Chemical properties of Amyloid-
• Amyloid is composed of 2 main types of complex proteins-

1. Fibril protein- 95% of amyloid
2. Non- fibrilar component- P component & 5% amyloid.
• Amyloid is formed of 4-6 fibrils of 7.5- 10 nm diameter.
• Dye congo red binds to fibrils & forms v
• By X- ray crystallography & infra red spectroscopy – cross β pleated sheet produce 1000
A0 periodicity.

50. Forms of Amyloid
1. AL protein derived from immunoglobulin light chain.
• AL fibril protein is derived from lambda (λ) light chain (twice more common) than kappa (κ).
• Seen in plasma cell dyscrasias & primarily systemic amyloidosis.
2. AA protein-
• It is deriived from reticuloendothelial system.
3. Aβ amyloid-
• Formed in the cerebral lesions of Alzheimer disease.
4. Aβ2M (Aβ2- microglobulin)-
• Seen in long term hemodialysis.

• It has predilection for bones & joints.
II) Non- fibrillar components-
• Amyloid P component
51. Amyloidosis- pathogenesis

52. Amyloidosis- Classification & Diagnosis
• A/c to clinicopathological classification, amyloidosis can be divided into 2 types mainly-
I) Systemic (generalised) amyloidosis-
1. Primary amyloidosis
• Biochemical type- AL type

• Associated disorders- Plasma cell dyscarias, multiple myeloma
2. Secondary amyloidosis (Reactive systemic amyloidosis)
• Biochemical type- AA type

• Associated disorder- Chronic inflammation
• Precursor proteins- SAA
3. Hemodialysis associated ayloidosis-
• Biochemical type- Aβ2M

• Associated disorder- dialysis associated amyloidosis
• Precursor proteins- β2 microglobulin
4. Hereditary Amyloidosis-
a) Familial Mediterranean fever-
• Biochemical type- AA type

• Precursor proteins- SAA
b) Familial amyloidotic neuropathies-
• Biochemical type- ATTR type
c) Rare hereditary forms
• Biochemical type- AFib, TTR

• Associated disorder- familial systemic/ visceral amyloidosis, familial amyloid polyneuropathy.
II) Localised amyloidosis-
1. Senile cardiac
• Biochemical type- ATTR
• Associated disorder- senility (senile cardiac amyloidosis)
• Precursor proteins- Transthyretin
2. Senile cerebral
• Biochemical type- Aβ type

• Associated disorder- Alzheimer syndrome, Dutch.
• Precursor proteins- APP
3. Endocrine
• Biochemical type- Procalcitonin, proinsulin (AIAPP)

• Associated disorder- medullary carcinoma, Type II DM
• Precursor proteins- Calcitonin, Islet of langerhans.
DIAGNOSIS OF AMYLOIDOSIS-
• Most common & best site for biopsy is abdominal fat aspiration.
• Congo red staining-
a) Ordinary light- pink or red amyloid (non diagnostic)
b) Polarized microscopy- apple green birefringence

53. MORPHOLOGICAL FEATURES OF AMYLOIDOSIS OF ORGANS
1. Amyloidosis of kidneys-
• It is the most common & most serious feature of renal disease.

• Deposits in the kidney mostly in secondary amyloidosis.
• Amyloidosis deposition occurs primarily in glomeruli.
• Glomerulus develops focal deposits within mesengial matrix & diffuses the basement membranes
of capillary loops.
• It results in proteinuria & nephrotic syndrome.
2. Amyloidosis of spleen-
• It has 2 patterns-
a) Sago pattern-
• Cut surface shows characteristics tapioca- like granules (sago spleen).
b) Lardaceous spleen-
• Amyloidosis involving splenic sinuses, extending to splenic pulp with formation of large, sheet like
deposits.
3. Amyloidosis of Liver-
• It may cause mastium enlargement.

• Histologically, amyloid deposits first appear in the space of Disse.
4. Amyloidosis of Heart-
• It may produce arrhythmias due to deposition in conduction system.

• Amyloid first deposits in subendocardial areas of atrium.
• Most common cause of death is cardiac failure.
• AL amyloid binds & inactivates factor X causes bleeding disorder.
54. Haematopoiesis
• Haematopoiesis takes place in bone marrow.

• Liver & spleen are the main sites for blood cell formation.
• 2 methods-
i) Aspiration- Salah bone marrow aspiration needle.

ii) Trephine biopsy- jamshidid trephine needle.
• Romanowsky technique used for staining & a stain for iron assess the reticuloendothelial stores of
iron.
• Most common site for bone marrow biopsy-
a) Infants- tibia (anterior medial area)
b) Adults & children- posterior iliac crest
c) Obese- anterior superior iliac crest
Normal bone marrow counts (myelogram)
• Fat cells : erythroid ratio – 4: 1

• Fat : cell ratio- 1 : 1
• Pleuripotent HSC is CD34 cells.
Sites of Haemotopoeisis-
• Site of haemotopoiesis is seen on 19th day (3 weeks) in embryonic life.

• First cell formed is erythrocytes.
• 1 month till birth in liver.
• HSC progenitors originate in bone marrow.
55. Erythropoiesis
• Eryhthropoiesis occurs in flat bones.

• Predominant site for erythropoiesis during gestational phase is liver.
Erythroid series-

Reticulocytes-
• It is non- nucleated.
• Reticulocytes counted by vital staining from new methylene blue or brilliant cresyl blue.
• Reticulocytes- 1- 2 days in marrow.
• 1-2 days circulate in the peripheral blood before maturing in the spleen.
56. Iron deficiency anaemia
• Hypochromic anemia can be due to iron deficiency.

• Commonest nutritional deficiency disorder throughout the world is iron deficiency.
• Storage form of iron is serum ferritin (Fe+3) in liver, spleen, bone marrow.
IRON METABOLISM
• Heme iron enters mucosal cells and non heme iron is first reduced to ferrous iron and then
absorbed in duodenum.
• Then, it is transported inside enterocytes via apical transport called DMT1 (divalent metal
transporter 1).
• Absorbed iron transported to basememnt membrane which requires ferroprotein & Hephaestin for
conversion of ferrous to ferric form.
• Finally ferric iron will be utilized for maturation of erythroid precursors.
• DMT1 also facilitates uptake of cadium & lead.
Iron excretion-
• Amount of iron lost per day- 0.5 – 1 mg.
Clinical Features-
• Weakness, fatigue, pallor of skin

• Plummer Vinson syndrome
• Plummer Vinson syndrome
Lab findings-
• Anaemia- iron level indicated by reticulocytosis

• Haemoglobin decreased
• RBC- hypochromic & microcytic
• Anisocytosis & poikilocytosis
• Reticulocytes count is normal.
• MCV, MCH, MCHC- reduced.
• WBC count is normal.
• Platelets count normal.
• Bone marrow findings-
a) Marrow cellularity increased
b) Erythropoiesis- micronormoblasts
c) Iron staining on bone marrow aspirate shows decrease iron stores (Prussian blue reaction)
• Biochemical findings-
a) Serum level decrease
b) TIBC increase
c) Serum ferrritin decrease
d) Red cell protoporphyrin decrease
e) Serum transferring receptors protein increased. (STFR to log of ferritin)
TREATMENT
a) Oral iron salts (0-3 months)- 100- 150 mg

b) Parentral therapy- Iron dextran may be given IM or IV.
57. Sideroblastic anaemia
• Sideroblastic anaemia is a group of disorder in which erythroid precursor in the bone marrow show
characteristic ‘ringed sideroblastic’.
• Siderocytes are erythrocytes & sideroblasts are normoblasts.
• Siderocytes contains granules of non- heme iron.
• Granules are positive with Prussian blue reaction & Romanowsky dyes called Pappenheimer bodies.
TYPES OF SIDEROBLAST ANAEMIAS-
• Herediatry sideroblastic anaemia

• Rare X- linked disorder associated with defective enzyme aminolevulinic acid (ALA) synthetase for
haem synthesis.
2. Acquired sideroblastic anaemia-
a) Secondary- Drugs, chemical & toxins (Isoniazid- antituberculous drugs & pyridoxine antagonist).
b) Alcohol & lead.
Lab findings-
• Blood picture- hypochromic, microcytic.

• MCV, MCH, MCHC decrease in hereditary type.
• MCV increase in acquired type.
• Bone marrow examination- macronormoblastic erythropoiesis.
• Marrow iron stores increase.
• Pathognomonic ring sideroblasts present serum ferritin increase.
• Serum iron increase.
• Iron deposition increase.
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58. Hereditary spherocytosis
Hereditary spherocytosis-
• It is a common autosomal dominant inheritance disorder in which red cell membrane is abnormal.
• RBC lifespan is decreased to 10- 20 days.
• Decreased reticulocyte count is a feature aplastic crisis caused by parvovirus B-19 infection.
Pathogenesis-
1. Spectrin deficiency- can be α- spectrin & β- spectrin.
• Deficiency in the structural protein of red cells membrane, spectrin.
2. Ankyrin abnormality (most common mutation)
Clinical Features-
• Splenomegaly
• Jaundice
• Pigment gallstone
Lab findings-
• Reticulocytosis
• Abnormality of erythrocytes formed microspherocytes.
• MCHC increased
• Osmotic fragility increased (main diagnostic test)
• Autohemolysis test increases & corrected by glucose.
• Direct Coomb’s test is negative.
• Spherocytosis.
59. Glucose-6 -phosphate dehydrogenase deficiency (G6PD)
• Hereditary disorders of red cell interior are of 2 types-

• Red cell enzyme defects (enzymopathies)
• Defective red cell metabolism involves 2 pathways-
a) Defect in hexose monophosphate shunt- E.g. G6PD deficiency.
• G6PD gene is located on the X- chromosome & its deficiency.

• Sex- linked trait affecting males and femal are carriers.
• A- type G6PD variant protects against malaria.
• Abnormal protein folding leads to G6PD loss.
• Haemolytic attacks due to oxidant stress-
a) Drugs- antimalarial (Pyrimaquine), sulphonamides, vitamin K.
b) Ingestion of Fava beans (favaism)

c) Infections
Pathogenesis-
• In G6PD deficient cells oxidant will denature globin of haemoglobin to form Heinz bodies.
• To detect Heinz bodies stain, crystal violet is used.
Clinical features-
• Acute haemolytic anaemia

• Acute renal failure
Lab findings-
• During period of acute haemolysis,

• Rapid fall in haematocrit value.
• Formation of Heinz bodies is visualized by crystal violet called Heinz body haemolytic anaemia.
ENT
1. CSF Rhinorrhoea
• Discharge is clear, watery, appears suddenly in a gush of drops when bending forward (tea pot sign)
or straining
• Uncontrollable and cannot be sniffed back
• Glucose content > 30mg/dI (nasal discharge - < 10 mg/dl)
• β2 transferrin is specific for CSF (absent in nasal discharge)
• Olfactory slit – cribriform plate of Ethmoid Bone (most common site)In traumatic CSF leak, CSF and
blood are mixed – double ring sign or target sign
• Immediate Management - Antibiotics and Observation
• Persistent Case Treated surgically by nasal endoscopy or intracranial route
• CSF Rhinorrhea Occurs in fracture of maxilla in Le Fort type II and type III. (as cribriform plate is
injured here) and also in nasal fracture class Ill
2. Malignant Otitis Externa (ENT)
• Caused by Pseudomonas aeruginosa infection

• Diabetes is the major predisposing factor
• Can occur in Immuno-compromised Patients
• Severe pain worsening at night
• Presence of granulations at bony cartilaginous junction (Also in Floor of External Auditory Canal)
• Biopsy and radical surgery to be avoided
• Multiple cranial nerve palsies can occur – Most Common – Facial Nerve Palsy
3. EXTERNAL EAR- Pinna / Auricle
• The entire pinna (except its lobule and outer part of external acoustic canal) is made up of a
framework of a single piece of yellow elastic cartilage
• Pinna develops from the cleft of 1st and 2nd pharyngeal arch
• Ear pinna develops from Ectoderm
• Skin over the pinna is closely adherent to the perichondrium on the lateral surface while it is loosely
attached on the medial surface.
• Greater auricular nerve(C2C3)-Supplies Major Part of Pinna
• Sensory nerve supply of pinna is Mandibular nerve
• Cauliflower ear (boxer's ear, wrestler's ear)
• Is an acquired deformity of the outer ear.
• In this injury, the ear can shrivel up and fold in on itself and appear pale, giving it a cauliflower-like
appearance, hence the term cauliflower ear.
• Wrestlers, boxers and martial artists in particular are susceptible to this type of injury.
• When the ear is struck and a blood clot develops under the skin, or the skin is sheared from the
cartilage, the connection of the skin to the cartilage is disrupted.
4. Otosclerosis / Otospongiosis
• Most often the otosclerotic focus involves stapes, leading to stapes fixation and CHL
• Family history present, Autosomal dominant
• Age 20-30 yrs
• Females affected twice more than males.
• Stapedial otosclerosis causing stapes fixation and CHL is the most common variety
• Cochlear otosclerosis – causes SNHL, Otosclerosis tinnitus
• Fissula ante fenestrum - in front of oval window is the site of predilection (anterior focus)
• Hearing loss – painless progressive bilateral CHL
• Paracusis willisi - hears better in noisy surroundings
• Membrane – normal and mobile
• Schwartz sign – reddish hue seen on the promontory through TM, which indicates active focus
• TFTs- negative Rinne, Weber lateralized to the ear with greater hearing loss
• The tympanogram is Type AS
• In some cases a dip in the bone conduction curve appear at 2000Hz which disappears after
successful stapedectomy (Carhart's notch)
• Gene’s test and Gelle's test identifies Otosclerosis
• The prosthesis used in the surgical treatment are Teflon (M/C used)
5. Septoplasty
Clinical indications of septoplasty:
• Deviation of the nasal septum with partial or complete unilateral or bilateral obstruction of airflow
• Persistent or recurrent epistaxis
• Evidence of sinusitis secondary to septal deviation
• Headaches secondary to septal deviation and contact points
• Anatomic obstruction that makes indicated sinus procedure difficult to perform efficiently
• Obstructive sleep apnea
• As an approach to transseptal transsphenoidal approach to pituitary fossa
Used as an alternative for Sub Mucosal Resection(SMR)
Tissue sparing procedure where septa' deviation is corrected by minimal resection of cartilage and bone
6. Atrophic rhinitis / Ozaena
Klebsiella ozanae causes Primary Atrophic rhinitis
Secondary Atrophic rhinitis are due to Specific infections, such as syphilis, lupus,
leprosy, and rhinoscleroma.
• Can also result from long standing purulent sinusitis ,

• radiotherapy of nose,
• excessive surgical removal of the turbinate and
• as complication of DNS on the root side of nose.
Clinical features of atrophic rhinitis:
• The disease is mostly seen in females and tends to appear during puberty.
• There is foul smell from the nose making the patient a social outcast though patient himself is
unaware of the smell due to marked anosmia (merciful anosmia).
Surgically treated with Young's operation
7. Vasomotor Rhinitis
VASOMOTOR RHINITIS
• Non allergic rhinitis

• Symptoms:
• Paroxysmal sneezing – bouts of sneezing just after getting out of bed in the morning
• Surgical treatment: vidian neurectomy
8. Meniere's disease
• Meniere’s disease is characterized by Vertigo,tinnitus,sensation of aural fullness and fluctuating

hearing loss.
• Endolymphatic Hydrops is seen in Menier's Disease.
• In meniere’s disease there will be marked bulging of the reissner’s membrane.
• Salt restricted diet is advised in Menier's Disease.
• Permanent Hearing loss is the most common morbidity associated with Meniere's disease.
• Menier's Disease and Perilymph fistula present with positive Hennebert sign.
• Electrocochleography is the gold standard investigation for diagnosis of Menier's Disease.
• Recruitment test is positive in Menier's Disease.
• Meniere's disease is associated with Cochlear deafness .
• Hyperacusis may be seen in Menier's Disease.
• Glycerol test is used for diagnosis of Menier's Disease.
• Fick's operation and Cody Tack's procedure is for Menier's Disease.
9. Acoustic Neuroma / Vestibular Schwannoma / Neurilemmoma / 8th Nerve tumor
Origin
• in the internal auditory canal from the inferior or superior portion of the vestibular nerve
• 80% of all Cerebello-pontine angle tumors
• 10% of all intracranial tumors
• Benign encapsulated, extremely slow growing tumors
• Bilateral tumors seen in neurofibromatosis type 2 (NF2), a syndrome resulting from a chromosome
22 mutation.
• Tumors almost always arise from the Schwann cells of the vestibular division of VIII nerve
Classification based on size
• Intracanalicular (confined to internal auditory canal)

• Small size (< 1.5 cm)
• Medium size (1.5 — 4 cm)
• Large size (> 4 cm)
• Age group: 40-60 years
• No sex predilection
Cochleovestibular symptoms
• Earliest symptoms -Unilateral sensorineural deafness

• The three most common presenting symptoms include insidious hearing loss, high-pitched tinnitus,
and disequilibrium
• Difficulty in understanding speech out of proportion of pure tone hearing loss (characteristic of
AN)
Cranial nerves
• 5th nerve earliest to be involved

• Reduced corneal sensitivity, numbness and paresthesia of face
• Superior division of vestibular nerve – most common site of AN
Facial nerve involvement
• Hitzelberger's sign (hypoaesthesia of posterior meatal wall

• Loss of taste
• Decreased lacrimation
Investigations
• Pure tone audiometry — SNHL more marked in higher frequencies

• Speech audiometry - Poor speech discrimination and Roll over phenomenon
• Recruitment absent
• Short Increment Sensitivity Index (SISI) shows a score of 0-20%
• Threshold tone decay — retrocochlear type of lesion
• Diminished or no response to calorie tests.
• Gold standard for diagnosis: MRI with gadolinium enhancement
Treatment -
• surgical removal, gamma knife or Cyber knife surgery

• Auditory brainstem implant (ABI) – ideal intervention for bilateral acoustic neuromas
10. Rhinoscleroma
Cause:
• Chronic granulomatous disease caused by Gram negative bacillus called Klebsiella rhinoscleromatis
(Frisch bacillus)
Clinical and Histologic features:
• Rhinoscleroma may be found in all age groups, but typically young adults 20–30 years old are most
frequently affected.
• Airborne transmission combined with poor hygiene, crowded living conditions, and poor nutrition
contributes to its spread.
• Subdermal infiltration of the lower part of external nose and upper lip giving a woody feel
• Miculicz' cells (macrophages containing large amounts of bacteria-filled vacuoles)
and Russell bodies (spherical structures found in the cytoplasm of plasma cells and also seen in
multiple myeloma)
Treatment: streptomycin + tetracycline for 4-6 weeks
11. Choanal atresia
Clinical symptoms:
Persistence of bucconasal membrane associated with CHARGE syndrome:
• Coloboma of the eye

• Heart malformations
• Choanal Atresia
• Retarded growth, development, or both
• Genital hypoplasia
• Ear malformations, deafness, or both
Bilateral atresia type presents with respiratory obstruction
Diagnosed by:
• Absence of air bubbles in the nasal discharge

• Failure to pass a catheter from nose to pharynx(posterior rhinoscopy)
Investigated using CT scan
12. Frenzel Glasses
• Illuminated frenzel glasses are used in detecting Nystagmus.

13. Cauliflower Ear
• Cauliflower ear is Perichondritis in Boxer's.

• Cauliflower ear is associated with Hematoma of Auricle.
14. Otoslerosis
Otosclerosis is characterized by abnormal removal of mature dense otic capsule bone by osteoclasts, and
replacement with the woven bone of greater thickness, cellularity, and vascularity.
When disease involves the annular ligament of the oval window and stapes footplate, a conductive hearing
loss (CHL) occurs which is slowly progressive, usually bilateral and asymmetric.
The hallmark of bone conduction thresholds in otosclerosis is the Carhart notch which is as a result from
the disruption of normal ossicular resonance, approximately at 2000 Hz. One of the earliest signs of
otosclerosis is an abnormal acoustic reflex.
Carharts notch
• Bone conduction is normal in otosclerosis.

• In some cases there is a dip in bone conduction curve which is maximum at 2000 Hz / 2 KHZ called
as Carharts notch.
• Carharts notch is seen only in bone conduction curve.
• It disappears after successful stapedectomy/stapedotomy.
• Hormonal influences during pregnancy might cause a more rapid progression in women, bringing
them to clinical attention.
• While otosclerosis may potentially involve any part of the bony labyrinth, it carries a distinct
predilection for the region near the anterior border of the oval window (fissula ante fenestram).
Otosclerosis is caused by immobility of the stapes.
• Its most distinctive feature is conductive hearing loss, but sensorineural hearing loss and vertigo are
also common;
• tinnitus is infrequent due to Cochlear Otosclerosis,increased vascularity in lesion or conductive
deafness
• Paracusis Willis refers to improved hearing with background noise. It is seen in patients with
otosclerosis.
• Otosclerosis is suggested by a positive family history(50% have family history)
• a tendency toward onset at an earlier age,
• the presence of conductive hearing loss, or
• bilateral symmetric auditory impairment.
• Females are more commonly affected than males.
• Whites are affected more than negroes.
• Age = most common between 20-30 years and is rare before 10 and after 40 years.
• Deafness is increased by pregnancy, menopause, trauma and major operations.
• Viruses like measles virus have also been associated with it.
• Stapes footplate—Shows a rice grain / biscuit type appearance
• Blue mantles are seen histopathologically.
Gene's Test
This test was earlier done to confirm the presence of otospongiosis.
In this test, BC (bone conduction) is tested and at the same time Siegle's speculum compresses the air in
the meatus.
In normal individuals hearing is reduced after this; i.e. Gelles test is positive; but in stapes fixation,
sound is not affected. i.e Gelles test is negative.
FINDINGS IN OTOSCLEROSIS
Symptoms of otosclerosis
• Hearing loss :- Bilateral conductive deafness which is painless and progressive with insidious onset.
In cochlear otosclerosis sensorineural hearing loss also occurs along with conductive deafness.
• Paracusis willissii :- An otosclerotic patient hears better in noisy than quiet surroundings.
• Tinnitus :- More common in cochlear otosclerosis.
• Speech :- Monotonous, well modulated soft speech.
• Vertigo :- is uncommon.
Signs in otosclerosis
• Tympanic membrane is quite normal and mobile.

• In 10% of cases flamingo - pink blush is seen through the tympanic membrane called as Schwartz
sign. It indicates active focus with increased vascularity.
Tuning fork tests in otosclerosis
• As otosclerotic patients have conductive deafness, the tuning fork tests results will be as follows :?
• Rinnes :- Negative
• Webers :- Lateralized to the ear with greater conductive loss.
• Absolute bone conduction (ABC) :- Normal (can be decreased in cochlear otosclerosis).
• Gelles test :- No change in the hearing through bone conduction when air pressure of ear canal is
increased by Siegle's speculum.
Audiometry in otosclerosis

• Audiometry is one of the important tools in evaluation of a patient of otosclerosis.Various
audiometric tests are :?
1) Pure tone audiometry
• Shows loss of air conduction, more for lower frequencies with characteristic rising pattern. Bone
conduction is normal. However in some cases, there is a dip in bone conduction curve which is
maximum at 2000 Hz (2 KHz) and is called the Carhart's notch.
2) Impedance audiometry
• Impedance audiometry shows :-
i) Tympanometry
• Patient with early disease may show type A tympanogram (because middle ear areation is not
affected) Progressive stapes fixation results in classical As type tympanogram.
ii) Acoustic (stapedial reflex)
• It is one of the earliest sign of otosclerosis and precedes the development of airbone gap. In early
stage, diphasic on-off pattern is seen in which there is a brief increase in compliance at the onset
and at the termination, stimulus occurs. This is pathognomonic of otosclerosis. In later stage the
reflex is absent.
• Treatment with a combination of sodium fluoride, calcium gluconate, and vitamin D may be
effective. If not, surgical stapedectomy/stapedotomy/fenestration should be considered.
15. Menier's Disease
• Meniere’s disease is characterized by Vertigo,tinnitus,sensation of aural fullness and fluctuating

hearing loss.
• Endolymphatic Hydrops is seen in Menier's Disease.
• In meniere’s disease there will be marked bulging of the reissner’s membrane.
• Salt restricted diet is advised in Menier's Disease.
• Permanent Hearing loss is the most common morbidity associated with Meniere's disease.
• Menier's Disease and Perilymph fistula present with positive Hennebert sign.
• Electrocochleography is the gold standard investigation for diagnosis of Menier's Disease.
• Recruitment test is positive in Menier's Disease.
• Meniere's disease is associated with Cochlear deafness .
• Hyperacusis may be seen in Menier's Disease.
• Glycerol test is used for diagnosis of Menier's Disease.
• Fick's operation and Cody Tack's procedure is for Menier's Disease.

16. Otitis externa
• Otomycosis is most commonly caused by Aspergillus Fungus and then Candida fungus.
• Patients with diabetes are susceptible to otitis externa.
• Findings of Otits externa:ear pain, pruritus, and discharge. On examination, the ear canal is
erythematous and edematous. Tenderness to manipulation of the external ear present.
• Exacerbating factors of Otits externa include: Warm humid climates, swimming, frequent hair
washing (especially if in the bath), and insertion of foreign bodies can introduce bacterial infection
and cause local trauma to the ear canal, making infection more likely. Prolonged use of hearing aids
may also predispose to infection.
• Most common cause of otitis externa is Pseudomonas Aeruginosa ans Staphylococcus Aureus.
• External otitis/Diffuse otitis externa is also known as Telephonists ear.
• Otitis externa haemorrhagica is most commonly caused by influenza virus and is characterised by
formation of haemorrhagic bullae on the tympanic membrane.
17. Pinna
• Keratocanthoma-Flesh-colored, dome-shaped, on the ear lobe with central keratin-filled crater

and surrounded by proliferating squamous epithelium. This lesion regresses over/ the next
month and then disappears.
• Malignant Otitis externa-Ear pain and drainage in an elderly diabetic patient must raise concern
about malignant external otitis.It is associated with tenderness in the pinna and swelling and
inflammation of the external auditory meatus.This infection is almost always caused by P.
aeruginosa.
• Ear pinna develops from Ecdoderm.
• Ramsay Hunt Syndrome-A clinical condition characterised by a facial palsy and often associated
with facial pain and the appearance of vesicles on the canal and pinna.Vertigo and sensor neural
hearing loss (VIIIth nerve) may occur.
• Pinna is formed at birth.
• The entire pinna (except its lobule and outer part of external acoustic canal) is made up of a
framework of a single piece of yellow elastic cartilage.
• Pinna develops from the cleft of Ist arch.
• Auriculotemporal nerve-Mandibular branch of trigeminal nerve is one of the sensory nerve
supplying the pinna.
• Major part of the skin of Pinna is supplied by Greater Auricular nerve.
• Pinna is supplied by Greater Auricular Nerve,Auriculotemporal nerve,Lesser Occipital
Nerve,Auricular Branch of Vagus Nerve and Facial Nerve.
• Skin over the pinna is closely adherent to the perichondrium on the lateral surface while it is loosely
attached on the medial surface.
• Boil can occur on Pinna.
• The auricle starts to develop when 6 hillocks appear around the first pharyngeal groove(cleft),
which lies between the first and the second branchial arches.

• Acute mastoiditis is characterized by Clouding of Mastoid Air cells,Deafness and Outward and
downward deviation of the pinna.
• Darwin's tubercle (or auricular tubercle) is a congenital earcondition which often presents as a
thickening on the helix at the junction of the upper and middle thirds.
• Incisura terminalis is the area between the tragus and crus of helix.
• Boxer's ear is Hematoma of Auricle
18. External Auditory Canal
• Malignant Otitis externa-Ear pain and drainage in an elderly diabetic patient must raise concern
about malignant external otitis.It is associated with tenderness in the pinna and swelling and
inflammation of the external auditory meatus.Granulation tissue may be present in the external
auditory canal.This infection is almost always caused by P. aeruginosa.
• Other features -Facial palsy, not responding to antibiotics, increased uptake on technetium bone
scan.
• Severe Hearing Loss is absent.ESR is used for follow-up.
• Antibiotic of Choice-Antipseudomonal penicillin or cephalosporin (3rd generation piperacillin or
ceftazidime) with an aminoglycoside/fluoroquinolone
• Length of external auditory canal is 24 mm.
• Use of Isotretinoin may lead to teratogenic effects like Cleft lip,Cleft Palate and Agenesis of the
External ear canal.
• Corrective surgery for a new born with microtia is usually performed at 5-7 years of age.
• Mechanical stimulation of ear canal while cleansing it can cause stimulation of the auricular
branch of vagus nerve and may induce cough.
• The cartilaginous part of external auditory canal has 2 deficiencies - the "fissures of
santorini" through which infections can pass from external ear to parotid and vice versa.
• Mac Even's Triangle is formed by Posterosuperior segment of bony external auditory
canal,Temporal line(Suprameatal crest) and Tangent drawn to the external auditory meatus to
Suprameatal Crest.
• External Auditory canal is formed from first pharyngeal groove/Cleft.
• Keratosis Obturans occurs due to defective epithelial migration from the tympanic membrane to
posterior meatal wall, which results in collection of pearly white desquamated epithelial debris with
cholesterol in deep meatus.
• Lateral wall of Mastoid Antrum is related to External Auditory Canal.
• Exostosis of External Auditory canal occurs due to recurrent proplonged cold water exposure.
19. Tympanic Membrane
• Most common site of perforation of tympanic membrane in ASOM is Anterior inferior quadrant.
• Rupture of an ear drum may occur at the noise level above 160 dB.
• Use of nitrous oxide is contraindicated during Tympanic Membrane Grafting Surgery.
• The torture method involving simultaneous beating of both ears with palms of hand, resulting in
rupture of tympanic membrane is called Telefono.
• Uses of of Siegel's Speculum during Ear Examination are Magnification ,Assessment of movement
of the tympanic membrane, As applicator for the powdered antibiotic of ear and to suck out middle
ear secretions in patients with chronic serous ottitis media.
• In a case of conductive hearing loss of 55 db with normal cochlera reserve,due to accident,with
normal tympanic membrane,the tympanogram would show Ad type of Curve.It occurs due to
Ossicular Discontinuity.
• Maximum hearing loss occur when there is ossicular interruption with intact tympanic membrane
(54dB).
• Glomus Tumor-Otoscopy shows a red reflex through intact tympanic membrane. “Pulsation sign” is
positive, progressive deafness and pulsatile tinnitus
• Handle of Malleus is attached to the center of the tympanic membrane.
• The presence of conductive type of hearing loss, dull tympanic membrane and type B
tympanogram suggests the presence of fluid in middle ear cavity or serous otitis media.
• Serous otitis media in an older individual should raise the suspicion of nasopharyngeal malignancy.
The presence of enlarged lymph nodes adds to the suspicion.
• Tympanic membrane develops from all the three germinal layers-represents all the 3 components
of the embryonic disc.
• Auriculotemporal nerve is one of the nerves providing sensation to the tympanic membrane.
• The treatment of traumatic rupture of tympanic membrane is no active treatment.
• Normal consciousness and blood in the tympanic membrane may be found in a case of Basilar
fracture due to head injury.
• Normal colour of tympanic membrane is pearly white.
• The most mobile part of the tympanic membrane is peripheral part.
• Pars flaccida of the tympanic membrane is also called Shrapnell's membrane.
mm.
• Surface area of tympanic membrane is 90 mm2.
• The effective diameter of the tympanic membrane is 45 mm2.
• Lever ratio of tympanic membrane is 1.3-1.
• The hearing loss after rupture of tympanic membrane is 10-40 db.
• Chalky white tympanic membrane is seen in Tympanosclerosis.
• Features of moderately retracted tympanic membrane : Handle of malleus appearance
foreshortened ,Cone of light is absent or interrupted , Lateral process of malleus becomes more
prominent,Non prominent Umbo.
• Bluish tympanic membrane is seen in Glue ear(Secretory Otitis Media).
• Myringoplasty is plastic repair of Tympanic membrane,done with Operating Microscope.
• Procedure of surgical opening in Tympanic Membrane is Myringotomy.
• Tympanoplasty is eradication of middle ear disease with reconstruction of tympanic membrane &
ossicles.
• Thin painless otorrhoea, multiple perforations of the tympanic membrane and failure to respond to
antimicrobial treatment is characteristic of Tubercular Otitis Media.
• Areas of spontaneously healed tympanic membrane are called Dimeric.

20. Middle ear Anatomy
• Referred pain from tonsil to middle ear is due to Glossopharyngeal Nerve.

• Nitrous Oxide should be avoided during Middle ear Surgery.
• The structure injured by the primary blast wave, in order of prevalence, are the middle ear, the
lung, and the bowel.
• The joints between ossicles are synovial.
• The chorda tympani nerve is related to the lateral wall of Middle ear.
• The Eustachian tube(auditory tube )connects the nasopharynx with the anterior wall of Middle ear.
• Middle ear structures which are of adult size at the time of Birth are all three ossicles,the middle
ear cavity, the oval window, round window.
• The facial nerve passes in a canal situated in the posterior and medial walls of the middle ear.
• Teunissen's classification is used in classification of congenital anomalies of Middle ear.
• The conclusion post mortem finding of death by drowning is presence of water in the middle ear.
• Floor of middle ear cavity is in relation with bulb of the internal jugular vein
mm.
• Sensory nerve supply of middle ear cavity is provided by Glossopharyngeal Nerve.
• Tegmen seperates middle ear from the middle cranial fossa containing temporal lobe of brain by
roof of the Middle ear.
• Narrowest part of middle ear is Mesotympanum.
• Promontory seen in the middle ear is the Basal turn of Cochlea.
• Eustachian Tube opens in the Middle ear cavity at the Anterior wall.
• Lateral wall of middle ear is formed by Tympanic Membrane.
• Bones of middle ear are responsible for reduction of impedance to sound transmission and and
conduct sound energy from the tympanic membrane to the oval window and then to the inner ear
fluid.
• Scutum is present in Lateral Wall of Middle ear.
• Treatment of middle ear papilloma is Tympanomastoidectomy.
• Contents of Middle ear Cleft include Eustachian Tube,Middle ear,Aditus which leads to Mastoid
Antrum and Air cells.
• Most common bony tumour of middle ear is Squamous Cell Carcinoma.
• Treatment of carcinoma of middle ear includes Surgery consisting of radical mastoidectomy /
subtotal or total petrosectomy.
• Tendon of Stapedius muscle passes through the pyramid in middle ear
21. Auditory Ossicles
• Ear Ossicles attains adult size before birth.

• Synovial type of joint exists between the ossicles of the ear.
• Malleus and incus are derived from 1st Arch.
• Fossa incudis contains short process of Incus.
• Austin's classification for ossicular chain defects depends on Malleus handle and stapes
suprastructure.
• Function of Ossicles is to conduct sound energy from the tympanic membrane to the oval window
and then to the inner ear fluid and Reduction of impedance to sound transmission.
• Ossicle M/C involved in CSOM is Long process of incus.
• Features of ossicles in moderately retracted tympanic membrane are Handle of malleus
appearance foreshortened and Lateral process of malleus becomes more prominent.
• Ossicular disruption with intact tympanic membrane causes maximum hearing loss.
• Body of incus lies in Epitympanum.
• Cone of light is due to Handle of malleus.
• Superior malleolar ligament connects Head of malleus to roof of epitympanum.
• Otosclerosis mostly affects Stapes.
• Incus and head of malleus removed in modified radical mastoidectomy .
• Handle of Malleus is attached to the center of the tympanic membrane.
22. Eustachian Tube (ENT)
Auditory tube formed of Elastic cartilage.
• The auditory tube connects the nasopharynx with the anterior wall of the Middle ear.
• Tests for Eustachian Tube Patency are Valsalva test,Methylene blue test,Sonotubometry,Politzer
test,Toynbee test,Frenzel maneuver,Catheterization,Inflation - Deflation test.
• Cholesteatoma invading Eustachian tube is an indication for Radical Mastoidectomy.
• Eustachian tube opens behind the level of inferior turbinate.
• Cartilaginous part of auditory tube is inferior to Sphenopetrosal Synchondrosis.
• The length of Eustachian tube is 36 mm.
• Inner 2/3rd part is Cartilaginous and outer 1/3rd part is Bony of the Eustachian Tube.
• Tensor Veli Palatini and Levator veli palatini muscle causes opening of Eustachian Tube during
Swallowing,yawning,sneezing.
• Higher elastin content in adults in Eustachian Tube.
• Eustachian Tube develops from the first and second pharyngeal arch.
• Otoscopic findings of Eustachian tube dysfunction are Malleus is easily visible,Lusterless tympanic
membrane,No movement of the tympanic membrane on siegel's method,distorted light image on
the anterior quadrant of tympanic membrane.
• Common cause of eustachian diseases is Adenoids.
• Throat infection causes Ear infection through Eustachian Tube.
• Patency of Eustachian Tube is closed and communication of middle ear with ET is obliterated during
Radical Mastoidectomy.
• Eustachian tube gets blocked if pressure difference is more than 90 mm.
• Structures seen on posterior Rhinoscopy are Both choanae ,Posterior end of nasal septum ,Opening
of Eustachian Tube,Posterior end of superior/tube middle and inferior turbinates,Fossa of
Rosenmuller,Torus Tubarius, Adenoids ,Roof and posterior wall and nasopharynx.
• Ostmann's pad of fat- helps the Eustachian tube closed at pharyngeal end.
23. Labyrinth
• Infection of CNS spreads in inner ear through Cochlear aqueduct.

• Endolymph in the inner ear is secreted by Stria vascularis.
• Internal ear derives its blood supply from labyrinthine (internal auditory) artery which is usually a
branch of anterior inferior cerebellar artery or sometimes of basilar artery.
• Endolymph has high concentration of K+ and low concentration of Na+.
• Inner ear is present in Petrous part of temporal bone .
• Inner ear bony labyrinth is an example of cartilaginous bone (i.e. a bone which ossification
cartilage).
• The commonest genetic defect of inner ear causing deafness is Scheibe aplasia.
• Trautmann's triangle is bounded by the bony labyrinth anteriorly, sigmoid sinus posteriorly and the
dura or superior petrosal sinus superiorly.
• Labyrinthis can occur due to extracranial complication of CSOM.
• Fluctuating recurring variable sensorineural deafness is seen in Perilabyrinthine fistula .
• Positive Fistula Test is seen in:
• Perilabyrinthine Fistula due to erosion of horizontal semicircular canal (Cholesteatoma or
fenestration operation)
• Abnormal opening in oval window (post stapedectomy fistula) or round window (rupture of round
window).
• A positive fistula test also implies that the labyrinth is still functioning.
• In destructive lesions of labyrinth, the nystagmus is towards the opposite side
24. Sensorineural Hearing loss
• Paget's Disease may present with abnormality at upper tibia,Hip and Back pain,Sensorineural
Hearing loss,Elevated Alkaline Phosphatase,Ivory Vertebra and Cotton Wool Spots in Skull X Ray.
• Basilar Migraine presents with intermittent headache in association with tinnitus,vertigo and
hearing loss.
• Ramsay Hunt Syndrome may present with facial palsy ,facial pain ,vesicles on the canal and
pinna,vertigo and sensor neural hearing loss .
• Exposure to noise above 160dB can cause permanent loss of hearing.
• The diagnosis of classic alport syndrome is based on X-linked inheritance of hematuria,
sensorineural hearing loss, and lenticonus
• Psycho-acoustic index of loudness is indicated by the term 'Phon'.
• In chidren suffering from meningitis,sensorineural hearing loss may occur despite prompt initiation
of appropriate antimicrobial therapy.

• Alport Syndrome,Nail-patella syndrome,Pendred's syndrome,Treacher-Collins syndrome,Noonan
Syndrome,Bartter syndrome and distal renal tubular acidosis may be associated with Sensorineural
Deafness.
• Air Conduction is more than Bone Conduction in case of Sensorineural Deafness.
• Late features of kernicterus include upward gaze palsy,sensorineural deafness,choreoathetosis.
• Prolonged exposure to noise levels greater 100 dB can impair hearing permanently.
• Measles,Mumps and Rubella can cause Sensorineural Hearing loss.
• Fluctuating recurring variable sensorineural deafness is seen in PeriLabyrinthine Fistula.
• Congenital malformations of the cochlea are not contraindications to cochlear implantation.
• Aminoglycoside class of drugs causes hearing loss by damaging Outer hair cells of basal turn.
• Threshhold for moderate hearing loss is 41-55dB.
• The earliest symptom of acoustic nerve tumor is Sensorineural hearing loss.
• Presbycusis is Hearing loss due to aging.
• The acceptable noise level that can be tolerated without any damage to hearing is 85 dB.
• Menier's Disease is characterised by Episodic vertigo, fluctuating hearing loss, tinnitus and sense of
fullness or pressure in the involved ear.
• Irreversible hearing loss is caused by Gentamycin.
• In Severe hearing loss, the patient fails to understand normal speech, but can understand shouted
or amplified speech.
25. Conductive Hearing Loss
• Ossicular disruption with intact tymnpanic membrane causes maximum hearing loss.
• After rupture of tympanic membrane, the hearing loss is 10-40 dB.
• Permanent privation of the hearing of either ear comes under grievous injury .
• Commonest cause of hearing loss in children is Chronic secretory otitis media.
• The hearing loss when the patient fails to understand normal speech, but can understand shouted
or amplified speech would be severe hearing loss.
• Cause of unilateral conductive hearing loss in a patient with history of head injury with tympanic
membrane normal and mobile would be Ossicular Chain Discontinuity.
• Otosclerosis-Family history positive,Bilateral hearing loss,type As Tympanogram,PTA -bone
conduction hearing loss with an apparent bone conduction hearing loss at 2000 Hz,hearing might
worsen during pregnancy
26. Cochlear versus Retrocochlear hearing loss
• Recruitment phenomenon is seen in Presbyaccusis,Meniere's Disease(Cochlear lesion)

• To distinguish between cochlear and post cochlear damage, test done is Brainsterm evoked
response audiometry.
• Stapedial Reflex Decay is absent in 8th nerve lesion.(suggestive of Retrocochlear lesion)

27. Tuning Fork Tests
• Tuning fork frequency used most commonly in the ENT clinic is of 512Hz.
• Weber’s test best elicited by placing tuning fork on the middle of the patient’s forehead and he is
asked to say in which ear he hears the sound better.
• Tuning fork tests used to differentiate hearing loss are:Rinne’s test,Weber test,Absolute bone
conduction (ABC) test,Schwabach’s test,Bing test,Gelle’s test.
• False Negative Rinne's Test:
• When a patient has unilateral sensori-neural deafness in the test ear, the bone conduction stimulus
may be perceived by the opposite ear. Hence it can be interpreted as Rinne's Negative.
• In such cases,Weber's test will be lateralised to the normal ear thus confirming false negative
Rinne's result. The above can also be avoided by giving a masking sound to the non-test ear.
• Frequency of tuning fork commonly used for performing Rinne's test is 512Hz.
• The most preferred and commonly used is 512 Hz frequency tuning fork because it is better felt.
• Negative Rinne's test for 256 Hz tuning fork indicates a minimum air-bone gap of 15dB.
28. Audiometry
• Pure Tone Audiometry is a subjective type of Audiometry Test

• High frequency audiometry used to monitor hearing loss due to Ototoxicity.
• In Non-organic hearing loss continuous tracing above pulsed tracing is used in Bekesy audiometry.
• Pure tone audiogram with a dip at 2000 Hz(Carhart's Notch) is characteristic of Otosclerosis.
29. Impedance Audiometry
• Type of Tympanogram in a patient with conductive hearing loss of 55 dB due to head trauma is
Type-Ad(as it occurs in Ossicular Discontiniuty).
• Impedance Audiometry is done by pressure changes in Middle ear.
• Type of Tympanogram in a patient with Otosclerosis is Type As.
• Secretory otitis media is diagnosed by Impedance Audiometry.
• Impedance denotes disease of Ossicles.
• Most common cause of Type B tympanogram in an old aged patient with neck nodes is
Nasopharyngeal Carcinoma.
30. Tympanoplasty
• Myringoplasty is plastic repair of Tympanic membrane.

• Myringoplasty is generally done using Temporalis Fascia or Perichondrium.
• In Myringoplasty,underlay graft is placed medial to the annulus.
• Columella effect is seen in Tympanoplasty.
• Tympanoplasty is mainly done in mostly in cases of CSOM.
• Tympanoplasty is eradication of middle ear disease with reconstruction of tympanic membrane &
ossicles.
31. Malignant Otitis Externa
MALIGNANT (NECROTISING) OTITIS EXTERNA:
• It is an inflammatory condition caused by pseudomonas infection usually in the elderly diabetics, or

in those on immunosuppressive drugs.
• Its early manifestations resemble diffuse otitis externa but there is excruciating pain and
appearance of granulations in the meatus. Facial paralysis is common. Infection may spread to the
skull base and jugular foramen causing multiple cranial nerve palsies. Anteriorly, infection spreads
to temporomandibular fossa, posteriorly to the mastoid and medially into the middle ear and
petrous bone.
• CT scan is useful, to know the extent of disease.
• Treatment consists of high doses of i.v. antibiotics directed against pseudomonas (tobramycin,
ticarcillin or third generation cephalosporins). Antibiotics are given for 6-8 weeks or longer.
Diabetes should be controlled. Surgical debridement of devitalised tissue and bone should be done
judiciously.
32. BERA
• Investigation of choice for audiometric evaluation of an infant is BERA.

• Best screening test to evaluate hearing in a neonate is Otoacoustic Emission.
• Wave II in BERA originates from Proximal eighth nerve.
33. Acoustic reflex
• Stapedial reflex is a protective reflex against loud sounds.

• Stapedial reflex is mediated by 7th and 8th Cranial Nerves.
• Acoustic/Stapedial reflex decay test is positive in lesion of Eighth nerve

34. Vertigo
• Intermittent brief vertigo with occasional drop attacks, ataxia, visual loss, double vision and
confusion: Vertebrobasilar insufficiency.
• Vertigo is defined as subjective sense of imbalance
• Epley's Maneuvre is used in the treatment of BPPV.
• Most likely diagnosis in an adolescent female with a positive family history having occipital
headache which is intermittent in episode and associated with tinnitus, vertigo,ataxia and hearing
loss is Basilar Migraine.
• Vertigo with sensorineural hearing loss, facial weakness,appearance of vesicles on the canal and
pinna and loss of taste sensation:Ramsay hunt syndrome.
• Vertigo, tinnitus, headache and visual disturbances due to hyperviscosity,Systolic
hypertension,Aquagenic pruritus:Polycythemia rubra vera.
• Most possible diagnosis in a patient on total parenteral nutrition for 20 days presenting with
weakness, vertigo and convulsions is Hypomagnesemia.
• Postitional vertigo is due to stimulation of Posterior Semicircular Canal.
• Vestibular Exercises is the treatment for Benign Positional vertigo
• In BPPV,patients display nystagmus and the symptoms that can be reproduced by head movement.
• In addition, the symptoms show latency, fatigability and habituation.
• Ocular features like Chronic granulomatous anterior uveitis, posterior uveitis ,etc,Neurological
lesions like meningism, encephalopathy, tinnitis, vertigo and deafness and Cutaneous lesions
likealopecia, poliosis and vitiligo may be present in Vogt-Koyanagi Harada syndrome.
• Antiemetic Phenothiazine with labrynthine suppressant activity used for vertigo is
Prochlorperazine.
• Tullio phenomenon is a condition where the subject gets attack of vertigo/dizziness by loud sounds.
35. Nystagmus
• Nystagmus that occurs when the patient looks straight is Optokinetic Nystagmus.
• Nystagmus is absent in a brain stem dead patient.
• A patient has a right homonymous hemian-opia with saccadic pursuit movements and defective
optokinetic nystagmus.The lesion is most likely to be in the Parietal lobe.
• Cerebellar hemisphere is the site of lesion in unilateral past pointing nystagmus.
• In caloric test,Cold stimulation causes nystagmus towards opposite side while warm stimulation
causes Nystagmus towards same side.
• Spontaneous vertical nystagmus is seen in the lesion of Midbrain/Medulla.
• Central Nystagmus changes the direction,with no fatiguability,no latency and does not disappears
on visaul fixation.
• Peripheral Nystagmus has fixed direction,latency and fatiguability present and disappears on Visual
Fixation.
• Cochlear problems is associated with hearing loss and not nystagmus.
• In destructive lesions eg. trauma to labyrinth, the nystagmus is towards the opposite side.
• Stimulation of posterior semicircular canal produces Torsional vertical nystagmus.
• Miners nystagmus is of Rotatory type.
• Illuminated frenzel galsses are useful for abolishing fixation and thus revealing peripheral vestibular
nystagmus
36. Cochlear Implant
• Cochlear malformation is a surgical challenge but not a contraindication for cochlear implantation.
• Use of nitrous oxide is contraindicated in Cochlear Implant Surgery.
• In Cochlear implants, the electrodes are most commonly placed at Cochlea.
• Auditory Nerve should be intact for Cochlear Implantation.
• Patients of profound binaural SNHL-PTA of 70 dB or more(with non functional cochlear hair cells)
who have intact auditory nerve functions and show little or no benefit from hearing aids are the
candidate for Cochlear Implant surgery.
• Facial recess is a suprapyramidal recess,middle ear can be approached through it and important in
Cochlear Implant Surgery.
• Minimum age for Cochlear Implant Surgery is 1 year
• Electrode is kept in Scala Tympani in Cochlear Implant surgery.
• In cochlear implants, electrodes are most commonly placed through Round window.
• Switch on of Cochlear Implant is done after 3 weeks.
• Pre-op investigation before a Cochlear Implant is placed:HRCT Temporal Bone and Complete
Audiological Examination.MRI may be needed.
• Receiver/Stimulator and Electrode array are the part of internal component of cochlear implant,
which are fitted inside the body.
37. Mastoidectomy
• Operation of choice for a patient having Attic cholesteatoma of ear with lateral sinus
thrombophlebitis is Canal Wall Down Mastoidectomy.
• Iatrogenic traumatic facial nerve palsy is most commonly caused during Mastoidectomy.
• Schwartz operation is Cortical Mastoidectomy.
• Radical mastoidectomy is done for Attico-Antral Cholesteatoma.
• Coalescent Mastoiditis is an indication for cortical mastoidectomy.
• Incus and head of malleus,lateral attic wall ,posterior meatal wall are removed in a Modified
Radical Mastoidectomy in a patient with Cholesteatoma.
• Cholesteatoma invading eustachian tube is an indication for Radical Mastoidectomy.
• The treatment of choice for atticoantral variety of chronic suppurative otitis media is Modified
radical Mastoidectomy.
• Treatment of choice for Perforation in pars flaccida of the tympanic membrane with cholesteatoma
is Modified Radical Mastoidectomy.
• Treatment of cholesteatoma with facial paresis in child is Immediate Mastoidectomy
• Communication between middle ear and Eustachian tube is obliterated in Radical mastoidectomy.
• Treatment of middle ear malignancy includes Excision of petrous part of temporal bone
and Modified radical mastoidectomy.
• Treatment of middle ear papilloma is Tympanomastoidectomy.
• Treatment for postauricular subperiosteal abscess is Antibiotics along with drainage of abscess and
cortical mastoidectomy.
38. Eustachian Tube
• Eustachian tube opens at the level of inferior turbinate

• Eustachian tube opens into middle ear cavity at Medial wall
• The length of Eustachian tube is 36mm
• Inner 2/3rds of eustachian tube is cartilaginous
• Eustachian tube Opens during swallowing
• Levator veli palatine causes opening of Eustachian tube
• Higher elastin content in adult's Eustachian tube
• Eustachian tube develops from 1st & 2nd pharyngeal pouch
• Muscle which helps to open Eustachian tube while sneezing Tensor veli palatini & Levator veli
palatini
• Length of the cartilaginous part of Eustachian tube is 25mm
• Eustachian tube gets blocked if pressure difference is more than 90 mm Hg
• Tests for Eustachian tube patency are Valsalva, Methylene blue ,Sonotubometry, Politzer ,Toynbee
,Frenzel maneuver, Catheterization & Inflation - Deflation test
• Ostmann fat pad is related to eustachian tube
39. Otits Media with Effusion
• In chronic secretory otitis media(also known as Glue ear), the treatment of choice is Myringotomy
with ventilation tube insertion
• Glue ear is a painless condition.
• Glue ear is also known as Chronic Secretory Otits Media.
• During follow up of a case of acute otitis media, a 6 year old child found to have glue ear with no
symptoms.
• Commonest cause of hearing loss in children is Chronic secretory otitis media.
• Cause of U/L secretory otitis media in an adult is Nasopharyngeal Carcinoma.
• Acute non suppurative otitis media in adults is due to Malignancy.
• Secretory otitis media is diagnosed by Impedance Audiometry.
• Bluish tympanic membrane is seen in Glue ear.
• Effusion is sterile in Otits media with effusion.
• Type-B Tympanogram is seen in Otits media with effusion.
• Otitis media with effusion is also known as Serous Otitis Media or Mucoid Otitis Media.
• Patients with Wegener's Granulomatosis may present with Secretory Otitis Media
• Characteristic triad of Wegener's granutomatosis is vasculitis of the upper respiratory tract (serious
otitis media and epistaxis), vasculitis of the lower respiratory tract (hemoptysis) and vasculitis of
the kidney (proteinuria).
• Watchful waiting is recommended without immediate use of antibiotics for children with
uncomplicated otitis media with effusion.
• Conducting hearing loss with intact tympanic membrane occurs in Glue Ear.
• Treatment of choice in a patient presenting with mouth breathing, recurrent serous otitis media
and adenoid facies is Adenoidectomy.
40. Acute Suppurative Otits Media
• Most common site of perforation of tympanic membrane in ASOM is Anterior inferior quadrant.
• Most common extra-cranial complication of ASOM is Subperiosteal abscess.
• 95% of all cases of invasive disease (epiglottitis, meningitis) due to H. influenzae are caused by type
b organisms that possess a polyribitol phosphate capsule. Otitis media is generally not caused by
type b organisms.
• Streptococcus Pneumoniae is the most common cause of Acute otitis media in children.
• Infection of middle ear can spread to CNS through Cochlear Aqueduct.
• The quadrant for a myringotomy in a case of acute suppurative otitis media is Postero-inferior as it
is easily accessible,damage to ossicular chain does not occur and damage to chorda tympani is
avoided
• Most frequently ASOM resolves without sequelae.
• Cart Wheel sign is seen in ASOM.
• Acute suppurative otitis media is treated using Erythromycin,Penicillin or Cephalosporin.
• Pulsatile otorrhoea is seen in ASOM.
• Light house sign is seen in ASOM.
• Inadequate antibiotic treatment of acute suppurative otitis media may lead to Secretory Otitis
Media.
• Most common complication of acute otitis media in children is Mastoiditis.
• Incomplete resolution despite antibiotics when drum remains full and bulging is an indication for
Myringotomy in a case of ASOM.
• Light house sign in seen in ASOM in stage of Suppuration.
41. CSOM
• Most common organism cultured in CSOM is Pseudomonas seruginosa.

• Treatment of choice in a patient of CSOM has choleastatoma and presenting with vertigo or Facial
Palsy is immediate Mastoid Exploration.
• Perforation of pars flaccida is associated with cholesteatoma.
• Perforation of tympanic membrane with destruction of tympanic annulus is called Marginal
perforation.
• Treatment of choice for Perforation in pars flaccida of the tympanic membrane with cholesteatoma
is Modified Radical Mastoidectomy.
• Cholesteotoma is seen in Attico-antral CSOM.
• Ossicle M/C involved in CSOM is Long process of Incus.
• CSOM is caused by multiple bacteria.
• Conservative management is the treatment of choice in central,safe tympanic membrane
perforation.
• Treatment of choice in case of Attico-antral Cholesteatoma is Modified radical
Mastoidectomy/Tympano-mastoid exploration.
• Cholesteatoma is associated with scanty,foul smelling,painless discharge.
• 7 th cranial nerve is most commonly involved in CSOM.
42. Complications of Otits Media
• Commonest complication of CSOM is Mastoiditis.

• Gradenigo's syndrome involves V, VI cranial nerves.
• Features of Gradenigo Syndrome include Diplopia,retro-orbital pain (due to involvement of the
Cranial nerves VI and V),persistent ear discharge.
• Extracranial complications of CSOM:Mastoiditis, Mastoid
Abscess(Subperiosteal,Zygomatic,Bezold's,Citelli's,Luc's Abscess), Petrositis, Facial paralysis
,Labyrinthitis
• Acute mastoiditis is characterized by Clouding of air cells ,Deafness and Outward and downward
deviation of the pinna.
• Essential radiological feature of acute mastoiditis is Clouding of air cells of Mastoid.
• In Mastoiditis ,tenderness present at tip.
• Gradenigo's Syndrome is caused by abscess over the apex of Petrous bone.
• Most common nerve to be damaged in CSOM is Facial Nerve.
• In a patient with CSOM, labrynthine fistula most commnonly involves Lateral SCC.
43. Lateral Sinus Thrombophlebitis
• Presence of delta sign on contrast enhanced CT SCAN suggests presence of Lateral Sinus
thrombophlebitis.
• Operation of choice in a patient with Attic cholesteatoma of ear with lateral sinus thromboplebitis
would be Canal Wall Down Mastoidectomy.
• Griesinger's sign is seen in Lateral Sinus Thrombosis.
• Lateral sinus thrombosis is associated Greisinger sign, Lily-Crowe sign and positive Tobey Ayer test.
44. Atrophic Rhinitis
• Atrophic laryngitis or Laryngitis sicca is characterized by atrophy of laryngeal mucosa and crust
formation,often seen in women and is associated with atrophic rhinitis and pharyngitis.
• Etiology in a patient with long standing nasal obstruction to develop secondary atrophic rhinitis can
be long standing purulent Sinusitis.
• Atrophic rhinitis may occur due to Chronic sinusitis ,Nasal deformity ,Strong hereditary factors.
• Merciful anosmia is seen in Atrophic Rhinitis.
• Cause of nasal obstruction in Atrophic rhinitis is Crusting.
• Organisms is known to cause Atrophic Rhinitis are Coccobacillus ozaena, Diphtheroid bacillus,
Kiebsiella ozaenae,Bordettela bronchiseptica,Pasteurella multocida, P. vulgaris, E. coli
,Staphylococcus ,Streptococcus.
• Atrophic rhinitis is not associated with the chronic use of nasal drops and is uncommon in males
and not associated with Diabetes.
• Young's operation is done for Atrophic Rhinitis.
45. Allergic Rhinitis
• Immediate hypersensitivity skin test is most useful in diagnosis of allergic rhinitis.

• When small-vessel vasculitis is associated with peripheral eosinophilia, cutaneous purpura,
mononeuritis, asthma, and allergic rhinitis, a diagnosis of Churg-Strauss syndrome is considered.
• Rhinolalia Clausa may be associated with Allergic Rhinitis.
• Early mediators of allergic rhinitis are Leukotriene,IL-4 ,IL-5.
• In Allergic rhinitis nasal mucosa is Pale and swollen.
• Surgical procedure like Radiofrequency ablation/Laser ablation of the inferior turbinate or Inferior
turbinectomy may be done in a case of Allergic Rhinitis.
• Treatment of Allergic Rhinits includes avoiding allergen,corticosteroids,surgery.
• Allergic Rhinitis does not leads to Epistaxis.
• Most common cause of Nasal Discharge is Allergic Rhinitis.
• Histamine is a preformed toxin involved in mechanism of allergic rhinitis.
• Allergic rhinitis is a type 1 hypersensitivity reaction.
• Allergic salute is seen in Allergic Rhinitis.
46. Acute Sinusitis
• Most common sinus involved in infant and children is Ethmoid sinus.

• Frontal Sinusitis- Pain shows periodicity,Tenderness is present just above the medial canthus of
eye,Pain is referred to as office headache.
• Pathognomonic feature of Maxillary sinusitis is Mucopus in the middle meatus.
• Most definitive diagnosis of sinusitis is Sinoscopy.
• Sphenoid sinusitis pain is referred most commonly to Occiput.
• Common organisms causing sinusitis:S. pneumoniae and nontypable Haemophilus influenzae are
the most common pathogens, accounting for 50-60% of cases. Moraxella catarrhalis causes disease
in a signigicant percentage (20%) of children but less often in adults.
• Sinus least involved in sinusitis is Sphenoid.
• Probable diagnosis in a male patient presenting with recurrent sinusitis ,recurrent chest infections
,infertility and Chest X-ray revealing dextrocardia and situs invertus is Kartagener's syndrome.
• Caldwell view of the X-ray is the best to show frontal sinus in a patient with recurrent frontal
sinusitis.
• Trephination is indicated for frontal sinustis because of persistence or exacerbation of pain or
pyrexia in spite of medical treatment for 48 hours.
47. Complications of Sinusitis
• Pott’s puffy tumor is a complication of frontal sinusitis due to osteomyelitis of frontal bone .
• The probable diagnosis in a patient with history of running nose and pain over medial aspect of the
eye presenting with sudden onset of high grade fever, prostration, chemosis, proptosis and diplopia
on lateral gaze with congestion of the optic disc would be Cavernous Sinus Thrombosis.
• Complications of acute sinusitis are Orbital cellulitis,Pott's puffy tumor and Conjunctival chemosis.
• Orbital cellulitis may occur as a complication of Parasinusitis, Faciomaxillary trauma,Endoscopic
sinus surgery.
• Frontal lobe abscess may be associated with fever,papilloedema,Personality changes and headache.
48. Fungal Sinusits
• The diagnostic criteria for allergic fungal sinusitis (AFS) are the presence of characteristic allergic
mucin, type I hypersensitivity (eosinophilic-lymphocytic inflammation), absence of fungal invasion,
immuno-compromised individuals and radiological confirmation (areas of high attenuation on CT
scan).
• Type 1 and Type 3 Allergic reaction is seen in patients with Allergic fungal sinusitis.
• Causative organism in a diabetic with orbital cellulitis and maxillary sinusitis showing hyaline,
narrow, septate and irregular branching hyphae with invasion of the blood vessels on microscopy
would be Aspergillus.
• Mucormycosis has a predilection for vascular invasion.
• Orbital mucormycosis may occur as a complication of Diabetic Ketoacidosis.
• Amphoterecin B IV is used for invasive fungal sinusitis.

49. Acute Tonsilitis
• During Tonsillitis, pain in the ear is due to involvement of Glossopharyngeal Nerve.

• Splenic Rupture in the most likely complication in a patient suffering from exudative
tonsillitis,palatal petechiae, cervical lymphadenopathy,tender hepatosplenomegaly,complete blood
count revealing mild anemia, lymphocytosis with about 30% of the lymphocytes exhibiting atypical
features, and a mild thrombocytopenia and Coombs' test is positive suggestive of infectious
mononucleosis.
• Pathognomonic enlarged, grayish yellow or orange tonsils are seen in Tangier disease.
• Commonest causative organism for acute tonsillitis is Group A beta Hemolytic Streptococcus.
• Fever, cervical lymphadenopathy and grey membrane on the tonsil extending to anterior pillar is
suggestive of diphtherial infection. For rapid growth the specimen is inoculated on Loeffler's serum
slope.
• but diagnosis is best made by culture in Tellurite medium
50. Tonsillectomy
• Coblation intracapsular tonsillectomy utilizes a thin layer of ionized sodium to ablate tissues.
• Tonsillectomy is contraindicated in Polio Epidemic.
• Tonsillectomy is recommended if number of acute infections in a year exceed 3 years.
• Recurrent throat infections, peritonsillar abcess, tonsillitis causing febrile seizures, hypertrophy of
tonsils causing sleep apnoea or speech interference and any suspicion of malignancy are absolute
indications for tonsillectomy.
• Secondary Haemorrhage after tonsillectomy usually presents between the 5th to 10th
postoperative day.
• Torrential bleed during tonsillectomy is due to Paratonsillar vein.
51. Quinsy
• There is collection of pus in the peritonsillar space in quinsy.

• Quinsy is also known as Peritonsillar Abscess.
• Swelling between tonsillar area and superior constrictor muscle is known as Quinsy.
• Quincy tonsillectomy is done in Tonsillitis.
• Tonsillectomy following peritonsillar abscess is done after 6-8 weeks .
• Quinsy is collection of pus outside the capsule (not in capsule) in peritonsillar area.
• Quinsy is usually unilateral.
• Penicillin is used in treatment of Quinsy.
• The best treatment in a child with peritonsillar abscess presenting with trismus is Systemic
antibiotics up to 48 hours then drainage.
52. Adenoid
• Adenoidectomy with grommet insertion is treatment of choice for Serous otitis media in children .
• Best line of management in a patient presenting with mouth breathing, recurrent serous otitis
media and adenoid facies is Adenoidectomy.
• Treatment of a child with recurrent URTI with mouth breathing and failure to grow with high
arched palate and impaired hearing is Grommet insertion with Adenoidectomy and tonsillectomy
(to remove the causative factor).
• Common cause of eustachian diseases is due to Adenoids.
• Next step of management in a child has adenoidectomy done but has effusion in middle ear is
Grommet insertion.
• Regarding adenoids ,there is failure to thrive,high arched palate and mouth breathing is seen.
• The inner Waldeyer's group of lymph nodes constitutes of Tonsils, Lingual tonsils ,Adenoids.
• Indication for Adenoidectomy in children include Recurrent respiratory tract infections, Chronic
serous otitis media and Multiple adenoids.
• Torticollis can occur as a complication of adenoidectomy due to ligamentous laxity secondary to
inflammatory process following adenoidectomy.
• In a patient with hypertrophied adenoids, the voice abnormality that is seen is Rhinolalia Clausa.
• Complications of adenoidectomy include Retro pharyngeal abscess,Velopharyngeal insufficiency
and Grisel syndrome.
• Adenoidectomy results in hypernasality of speech.
• CT scan is not routinely preferred to assess Adenoid size.
53. Ludwig's Angina
• Ludwig's angina is infection of submandibular space.

• Ludwig's angina involves both submandibular and sublingual spaces and most common cause is
dental infection.
• Ludwigs angina is cellulitis of floor of mouth,infection can spread to retropharyngeal space and
usually caused by both aerobic and anaerobic organisms.
54. Epistaxis
• In ulcerative form of nasopharyngeal carcinoma, epistaxis is the common symptom.

• Ethmoidal artery is responsible for epistaxis after ligation of external carotid artery..
• Management of Septal Hematoma in a child presenting with recurrent epistaxis after fall injury is
Incision and Drainage

• Squamous cell carcinoma is the commonest nasopharyngeal malignancy in a middle aged man
presenting with epistaxis, serous otitis media with hearing loss,otalgia and a history of infectious
mononucleosis few weeks earlier.
• Epistaxis can be a manifestation of Vitamin C deficiency.
• Epistaxis can be a feature of Henoch Schonlein Purpura along with tetrad of palpable purpura,
arthritis, glomerulonephritis and abdominal pain.
• Aminocaproic acid would be recommended for a hemophilic child with Epistaxis and oral bleeding.
• M/C cause of epistaxis in 3 years old child is Upper respiratory catarrh.
• Recurrent epistaxis in a 15-year-old female, the most common cause is Hematopoietic Disorder.
• Epistaxis in elderly person is common in Hypertension.
• Systemic causes of epistaxis are Hypertension ,Anticoagulant treatment and Hereditary
telangiectasia.
• If posterior epistaxis cannot be controlled, Sphenopalatine artery artery is ligated.
• In case of uncontrolled epistaxis, ligation of internal maxillary artery is to be done in
the Pterygopalatine fossa.
• Treatment of choice in recurrent epistaxis in a patient with hereditary hemotelangiectasis is Septal
dermatoplasty.
• Allergic rhinitis does not cause epistaxis.
• Posterior epistaxis is commonly seen in Hypertension.
• Posterior epistaxis occurs from Woodruff's plexus.
• Diagnosis in a 15 year old child with unilateral nasal obstruction along with a mass in cheek and
profuse and recurrent epistaxis is Juvenile Nasopharyngeal Angiofibroma.
• Sphenopalatine Artery is known as artery of epistaxis.
• Wegener's Granulomatosis is characterized by vasculitis of the upper respiratory tract (serious
otitis media and epistaxis), vasculitis of the lower respiratory tract (hemoptysis) and vasculitis of
the kidney (proteinuria) ,with or without presence of ANCA and rheumatoid factor .
• Rhinolith can cause Epistaxis.
55. Tracheostomy
• Advantages of a double lumen tracheostomy tube are easy to remove,clean and replace inner
cannula.
• In emergency tracheostomy the following structures are damaged: Isthmus of the thyroid,Thyroid
ima and Inferior thyroid vein.
• High tracheostomy is indicated in Carcinoma of Larynx.
• Cardiac tamponade,Uncomplicated Bronchial Asthma,Pneumothorax is not an indication for
tracheostomy.
• Mid tracheostomy is done over 3rd and 4th tracheal rings.
• In Pediatric tracheostomy,most common early complication is subcutaneous emphysema and 3rd &
4th tracheal rings are incised.
• Indications of Tracheostomy are Flail chest,Head injury,Tetanus,Tracheal stenosis,Bilateral vocal
cord palsy,Foreign body larynx,Emphysema,Bronchiectosis,Atelectasis.

• A new born with a goiter large enough to cause dyspnoea may be treated with
Tracheostomy.(Partial thyroidectomy is preferred over tracheostomy).
• Interstitial Emphysema may be found in Tracheostomy.
• A cricoid hook is used particularly in Tracheostomy.
• Immediate management in a patient of carcinoma larynx with stridor presents in casualty is
Immediate Tracheostomy.
• Maintenance of airway during laryngectomy in a patient with carcinoma of larynx is best done by
Tracheostomy.
• The most common indication for tracheostomy is Foreign body aspiration.
• Tracheostomy tube(Jackson's tube) is a double tube,made of titanium silver alloy and Cuffed tube
for IPPV and to prevent aspiration of pharyngeal secretion.
• Tracheoesophageal fistula ,Tracheocutaenous fistula and Surgical emphysema are common
complications of tracheostomy .
• "Gold standard" surgical procedure for prevention of aspiration is Tracheal division and permanent
tracheostome
• Trachea can't be easily palpated during tracheostomy in infants and children.
• Complication commonly occurring in tracheostomy in children is difficult decannulation.
• Hemorrhage is one of the most important complication of tracheostomy .
• Emergency tracheostomy is the method to establish a safer airway in a patient with neck trauma,
cricoid fracture with possibility of a difficult airway.
• Mini tracheostomy is performed through Cricothyroid membrane.
56. Laryngo-tracheo-bronchial foreign bodies
• For foreign body causing sudden choking, most appropriate first line of management is Heimlich
maneuver.
• Heimlich manoeuver is done to remove upper airway obstruction by foreign body.
• Advantage of fibreoptic bronchoscopy over rigid bronchoscopy is Good View.
• The treatment of choice for airway foreign bodies is prompt endoscopic removal with a
Bronchoscope
• In child, foreign body in lung is removed by rigid bronchoscopy.
• Commonest sign of intrabronchial foreign body in children is Cough.
• A 4-year child presents with a history of hoarseness, croupy cough and aphonia, the child has
dyspnoea with wheezing. The most probable diagnosis is Laryngeal foreign body.
• In erect posture commonest site of foreign body is in Right posterior basal bronchus.
• Foreign body aspiration in supine position commonly affects Apical part of right lower lobe.
• A foreign body completely obstructing the right main bronchus causes decreased Ventilation-
perfusion ratio.
• Palpatory thud audible slap is seen in Tracheal foreign body.
• During autopsy, foreign body is found in respiratory tract; manner of death is Accident.

57. CSF Rhinorrhea
• CSF rhinorrhea immediate management is wait & watch for 7 days + antibiotics.
• CSF Rhinorrhea is usually due to fracture of cribriform plate which is a part of Ethmoid.
• CSF will separate from blood when the mixture is placed on filter paper resulting in a central area of
blood with an outer ring or halo. Blood alone does not produce a ring.
• CSF examination produces clinically detectable signs of the ring sign, double-ring sign or halo sign in
CSF Rhinorrhea.
• Most probable diagnosis in a patient brought to the emergency department following head trauma
who is conscious and complaining of fluid coming out of his nostrils without having running nose
before the traumais CSF Rhinorrhea.
• Nasal intubation is contra indicated in CSF Rhinorrhea.
• CSF rhinorrhea is seen in Le Fort II and Le Fort III Maxillary fracture and Nasoethmoid fracture.
• CSF rhinorrhea occurs due to break in cribriform plate and contains glucose.
• CSF rhinorrhea is diagnosed by Beta-2 transferrin.
• Management of persistent cases of CSF rhinorrhea is Endoscopic repair.
• CSF rhinorrhea is diagnosed by Glucose estimation,Halo sign,Immunoelectrophoresis.
58. Nasopharyngeal Angiofibroma
• Nasopharyngeal angiofibromas are most frequently seen in the second decade.

• Hypotensive Anesthesia in nasopharyngeal angiofibroma is/are given by Propofol and
Phentolamine.
• Nasopharyngeal fibroma is the most common benign tumor of nasopharynx.
• Clinical features of nasopharyngeal angiofibroma are Adolescent male and Epistaxis and nasal
obstruction is the cardinal symptom.
• A 14 years boy presented with repeated epistaxis, and a swelling in cheek.Diagnosis is
nasopharyngeal angiofibroma and Contrast CT scan should be done to see the extent.
• Surgery is treatment of choice in juvenile Nasopharyngeal Angiofibroma.
• The most probable diagnosis in a 14-year old boy presenting with history of frequent nasal bleeding
and Hb found to be 6.4 g/dL and peripheral smear showing normocytic hypochromic
anemia is Juvenile nasopharyngeal angiofibroma.
• Most probable diagnosis in a child with unilateral nasal obstruction along with a mass in cheek and
profuse and recurrent epistaxis is Nasopharyngeal Angiofibroma.
• Hormonal etiology in implicated in Nasopharyngeal Angiofibroma.
• Radiotherapy may be given in Nasopharyngeal Angiofibroma.
59. Snoring and Obstructive Sleep Apnea

• The most probable diagnosis in a 45 year old male patient complaining of frequent tiredness and
headache,loud snoring and physical examination revealing leg edema,hypertension, and cardiac
arrhythmia is Obstructive sleep apnea.
• Modafinil is an FDA approved drug in the treatment of obstructive sleep apnea, shift work disorder
and narcolepsy.
• Snoring is treated by laser-assisted uvulopalatoplasty.
• OSA is associated with >5 episodes of apnea per hour.
• OSA is commonly associated with Hypertension.
• OSA is more common in males as compared to females.
• OSA is commonly found in patients with receding jaw,Obesity and Acromegaly.
• Next line of management in a 36 years old obese man who is a known smoker suffering from
hypertension and snoring with > 5 apnea/hyperapneas episodes per hour found in sleep test and
given antihypertensives and advised to quit smoking is Weight reduction and diet plan.
60. Acute Epigottitis
• Most common cause of acute epiglottitis in children is Hemophilus influenzae type B.

• Thumb sign is seen in Acute epiglottitis.
• Acute laryngeal spasm during indirect laryngoscopy is seen in Acute epiglottitis.
• Most cases of invasive disease (epiglottitis, meningitis) due to H. influenzae are caused by type b
organisms that possess a polyribitol phosphate capsule. Otitis media is generally not caused by type
b organisms.
• In acute epiglottitis, common cause of death is Respiratory obstruction.
• The antibiotic of choice in acute epiglottitis pending culture sensitivity report is Ampicillin or 3rd
generation Cephalosporin like Ceftriaxone.
61. Acute Layngo-tracheo-bronchitis
• Laryngotracheobronchitis is the most probable diagnosis in a 4 year old boy, with three days history
of upper respiratory tract infection presenting with stridor, which decreases on lying down.
• Laryngotracheobronchitis is caused most commonly by Parainflueza Virus.
• Seal barking like croupy cough is a feature of laryngotracheobronchitis .
• Management of Croup includes Oxygen inhalation and Hydration.
• Steeple sign is seen in Croup.
62. Fracture of Hyoid Bone
• On postmortem examination, contusion of neck muscles is seen along with fracture of hyoid bone.
The most probable cause of death is Throttling.
• Fracture of hyoid bone is indicative of Hanging or Strangulation or Throttling
• Hyoid bone fracture does not occur in Choking.
• Outward displacement of fractured hyoid bone is seen in Hanging.
• Hyoid bone fracture most common occurs in Manual strangulation(Throttling)
63. Fracture of Temporal bone
• CSF otorrhoea is caused by Fracture of petrous temporal bone.

• Transverse fractures of the petrous bone will cause facial nerve palsy.
• Treatment of choice for mastoid fracture with facial nerve palsy is Nerve decompression.
• Middle meningeal artery is usually torn in temporal bone fracture.
• Best investigation for temporal bone fracture is CT scan.
• The type of temporal bone fracture in a patient who was punched over his face,he was conscious
and blood was trickling from right ear which got controlled and Audiometry showing conductive
type of hearing loss would be Longitudinal fracture of Temporal bone.
64. Fracture of the facial bones-Nose,Maxilla,Mandible,Zygomatic
• Le Forte II facial fracture implies Fracture running through zygomatic process of the maxilla, floor of
orbit, root of nose on both the sides.
• Craniofacial dissociation is seen in Le Fort 3 fracture.
• CSF Rhinorrhea Occurs in fracture of maxilla in Le Fort type II and type III (as cribriform plate is
injured here) and also in naso-ethmoid fracture
• Bone commonly fractured in facial injuries is Nasal Bones.
• Most common site for fracture mandible is Condyle.
• LeFort's fracture would include Maxilla,Zygoma and Nasal Bones,
• Tripod fracture is the name given for Zygomatic fracture.
• Pyramidal fracture of maxilla is Le Fort-2
65. Glomus Jugulare
• Most probable diagnosis in a patient presenting with Browns sign and a Mass in ear on touch
bleeding heavily is Glomus jugulare tumour
• Pulsatile Tinnitus in ear is due to Glomus jugulare tumour
• Rising sun sign is seen in Glomus juglare
• 9th and 10th cranial nerve may be involved in Glomus juglare.
• Probable diagnosis in a middle aged female presenting with progressive deafness(conductive in
nature) and tinnitus and Otoscopy shows a red reflex through intact tympanic membrane with
Pulsation sign”positive is Glomus Jugulare Tumor.
• Glomus Jugulare is the most common benign neoplasm of middle ear.
• Glomus tumor is a benign tumor, therefore lymph node metastats is not present.
• Glomus cells may be seen in Carotid body tumor.

• Pulsation sign: When ear canal pressure is raised with Siegle’s speculum tumor pulsates vigorously
and then blanches and the reverse happens when the pressure is released.
• Probable diagnosis in a patient presenting with pulsatile tinnitus and hearing loss and a vascular
mass is seen behind the tympanic membrane is Glomus Jugulare
• Fisch classification is used for classifying -Glomus Jugulare tumor.
• The usual location of Glomus jugular tumor is Hypotympanum.
• Earliest symptom of glomus tumor is Pulsatile tinnitus
• Glomus jugulare tumor arises from non-chromaffin cells.
• Glomus jugulare tumor is more common in females.
• Glomus jugulare tumor included in a group of tumors referred to as paragangliomas.
• Sensorineural hearing loss may be seen in Glomus Jugulare tumor.
• Glomus Jugulare invades labyrinth, petrous pyramid and mastoid.
• Glomus Jugulare is not a disease of infancy.It is seen in patients with 5th-6th decade of life.
66. Layngomalacia
• Omega shaped epiglottis is seen in Laryngomalacia.

• Most likely cause in a 3 month old child presenting with intermittent stridor is Laryngomalacia.
• Most common cause of stridor shortly after birth is Laryngomalacia.
• Laryngomalacia is the commonest cause of stridor in a newborn who is born at term, infants and
young children.
• Treatment of choice in a newborn presented with stridor due to laryngomalacia is only
observation.No active treatment.
• Reassuarance of the patient is the treatment of choice in Laryngomalacia.
• Most likely cause for a 2-month old infant having inspiratory stridor since the first month of life,
otherwise well, Physical examination shows moderate inspiratory stridor and retractions which are
worse when the infant is supine or agitated and better when he is prone and quiet is
Laryngomalacia.
• Most common congenital anomaly of larynx is Laryngomalacia.
• Inspiratory Stridor is seen in Laryngomalacia.
• Surgical management is not the preferred initial treatment in Laryngomalacia.
• Laryngomalacia is self-limiting by 2-3 years of age.
• Most common neonatal respiratory lesion is Laryngomalacia.
• Laryngomalacia is first noticed in the first few weeks of life by inspiratory stridor
67. Carcinoma of Tongue
• A patient has carcinoma of right tongue on its lateral border of anterior 2/3rd, with lymph node of
size 4 cm in level 3 on left side of the neck, stage of disease is N2.
• In carcinoma base of tongue pain is refered to the ear through Glossopharyngeal nerve.
• A patient with carcinoma of tongue is found to have lymph nodes in the lower neck. The treatment
of choice for the lymph nodes is Radical neck dissection.
• Radiotherapy is used for which stage-I cancer -Anterior 2/3rd of Tongue.
• A patient presented with a 1 x 1.5 cms growth on the lateral border of the tongue. The treatment
indicated would be Laser ablation.
• Carcinomatous ulcers are painless but may become painful in advanced stages, with extension into
surrounding tissues.
• Commonest site of carcinoma tongue is Anterior 2/3 of Lateral borders
• Carcinoma tongue less than 2 cm is treated by Excision
• Tobacco chewing is a risk factor for Tongue Carcinoma.
• Lymph node invovlement occurs in case of Tongue Carcinoma.
• 60 year old man presents with an ulcer on lateral margin of tongue also complains of ear pain, most
probable diagnosis is Carcinomatous Ulcer.
• Tongue carcinoma is usually Radio-sensitive.
• Posterior tongue most commonly metastasizes to cervical lymph nodes.
• Referred pain in the ear is commonly from Carcinoma of Tongue.
• Most common histological type of carcinoma of tongue is Squamous cell carcinoma.
68. Carcinoma of Larynx
• Referred otalgia can be due to Carcinoma larynx.

• Treatment of choice in a patient presenting with carcinoma of the larynx involving the left false
cords, left arytenoid and the left aryepiglottic folds with bilateral mobile true cords is Horizontal
partial hemilaryngectomy.
• T3 N1 Mo stage of Carcinoma larynx is treated by Surgery and radiotherapy.
• Smoking increase the risk of Larynx cancer.
• Management in a 50 year old male chronic smoker complaining of hoarseness of voice for the past
4 months and Microlaryngoscopic biopsy showing it to be keratosis of the larynx is Stop
smoking,Laser vaporizer or Stripping of vocal cord.
• Ca Larynx has poor prognosis.
• Ca Larynx is commonly seen in males.
• Method of speech communications after laryngectomy include: Electrolarynx ,Oesophageal speech
,Tracheo-oesophageal speech.
• Treatment of choice in a case of carcinoma larynx with the involvement of anterior commissure and
right vocal cord and perichondritis of thyroid cartilage is laryngectomy and then post-operative
radiotherapy.
• Best treatment modality for a middle aged man diagnosed of having T3N1M0 stage of carcinoma of
larynx is Organ preservation treatment with combined chemotherapy and radiation therapy .
• Elevating the point of the shoulder (shrugging) would be the most likely difficulty in a patient with
squamous cell carcinoma of the larynx who has undergone radical neck dissection to remove the
tumor and regional lymph nodes and the spinal accessory nerve is severed.
• Treatment for stage I of cancer larynx (glottic cancer) is either microlaryngoscopic surgery or
Radiotherapy.
• Laryngeal carcinoma is commonly seen after 40 years of age.
• The most common cause of laryngeal stridor in a 60-year old male is Carcinoma larynx.
• Reflux laryngitis produces Subglottic stenosis and Ca larynx.
• Premalignant conditions for carcinoma larynx would include: Leukoplakia, Papillomas,Keratosis of
larynx
• Infraglottic carcinoma of larynx commonly spreads to mediastinal nodes.
• Treatment of choice for carcinoma larynx in stage III is Radiotherapy and Surgery.
• A patient of carcinoma larynx with stridor presents in casualty, immediate management is
Tracheostomy.
• Maintenance of airway during laryngectomy in a patient with carcinoma of larynx is best done by
Tracheostomy.
• Glottic Ca is the most common in Ca larynx.
• The preferred treatment of verrucous carcinoma of the larynx is Endoscopic removal.
• Treatment of choice for laryngeal carcinoma of glottis extending to supraglottic region with vocal
cord fixation with papable solitary ipsilateral lymph node is total laryngectomy with radical neck
dissection.
69. Carcinoma of Oral Cavity
• Referred otalgia can be due to Carcinoma oral cavity.

• In Hard palate cancers lymph node metastasis is least common.
• Probable diagnosis in a patient chewing tobacco for the past 50 years presenting with a six months
history of a large, fungating, soft papillary lesions in the oral cavity penetrating into the
mandible,Lymph nodes not palpable and biopsy showing benign appearing papillomatosis with
hyperkeratosis and acanthosis infiltrating the subjacent tissues is Verrucous carcinoma.
• Alveobuccal complex is the commonest site of oral cancer among Indian population.
• Abbey-Estlander flap is used in the reconstruction of Lip.
• Malignant potential for erythroplakia is 17 times higher than in leukoplakia.
• Erythroplakia is a red patch or plaque on the mucosal surface. The red colour is due to decreased
keratinization.
• The most common pre-malignant condition of oral carcinoma is Leukoplakia.
• Erythroplakia,Leukoplakia, Submucosal fibrosis predisposes to oral cancer.
• Lichen Planus does not predispose to Oral Carcinoma.
• Oral Carcinoma:Systemic Metastasis is un-common and responds to Radiotherapy.
• Predisposing factors for development of oral carcinoma are Smoking,Alcohol, Syphilis.
• Commonest cancer of the oral cavity is Squamous cell carcinoma.
• Trismus in oral cancer patients is severe in those treated with Surgery and Radiotherapy.
• Ca. Lip. has best prognosis.
• Second primary tumor of head and neck is most commonly seen in malignancy of Oral cavity.
• Base of tongue and soft palate is not included in oral cavity carcinoma.
• 3 cm oral cavity tumor with single ipsilateral 5 cm lymph node with no distant metastases; stage of
tumor is T2N2aM0.
• Most common cancer in males in India is Ca oral cavity.

70. Maxillary Carcinoma
• Ohngren's line that divides maxillary sinus into superolateral and inferomedial zone is related
to Maxillary cancer.
• Early maxillary carcinoma presents as Bleeding per nose.
• First lymph node involved in maxillary carcinoma is Submandibular.
• In Maxillary carcinoma of a 60 year old patient involving anterolateral part of maxilla, the preferred
treatment is Radiotherapy followed by total/extended maxillectomy.
71. Nasopharyngeal Carcinoma
• Treatment of choice of Nasopharyngeal Carcinoma is Radiotherapy.

• Radiotherapy is the treatment of choice for Nasopharyngeal carcinoma T3N I.
• Nasopharyngeal carcinoma is mostly Squamous cell carcinoma.
• Trotter's triad is seen in Nasopharyngeal carcinoma.
• Commonest site of Nasopharyngeal carcinoma is fossa of rosenmuller in lateral wall of
nasopharynx.
• Nasopharyngeal Carcinoma is associated with Epstein-Barr virus infection.IgA antibody to EBV is
observed
• Role of smoking and development of nasopharyngeal carcinoma is still not clear.
• Concomitant chemoradiotherapy is indicated in T1 N2 M0 Nasopharyngeal Cancer.
• In ulcerative form of nasopharyngeal carcinoma, epistaxis is the common symptom.
• Nasopharyngeal cancer can cause conductive deafness (Eustachian tube blockage), ipsilateral (not
contralateral) temporoparietal neuralgia (involvement of cranial nerve V) and palatal paralysis (CN
X)- collectively called Trotter’s triad.
• Nasopharyngeal carcinoma most commonly found in China.
• Radiotherapy is the treatment of choice for nasopharyngeal carcinoma and not
Nasopharyngectomy.
• Bimodal age distribution is seen in Nasopharyngeal Carcinoma.
• Secondaries in the neck with no obvious primary malignancy is most often due to Ca. Nasopharynx.
• Most common tumor to produce metastasis to cervical lymph nodes is Nasopharyngeal carcinoma.
• Cause of U/L secretory otitis media in an adult might be Nasopharyngeal carcinoma.
• Nasopharyngeal Ca involves Nasal cavity.
• Most common presentation in nasopharyngeal carcinoma is with Cervical lymphadenopathy.
• Probable diagnosis in a 70-year-old male presenting with neck nodes,examination revealing a dull
tympanic membrance, deafness and tinnitus and Audiometry showing Curve B is Nasopharyngeal
carcinoma.
• Nasopharyngeal Ca causes deafness by Serous effusion.
• Nasopharyngeal carcinoma can cause Horner's syndrome due to involvement of cervical
sympathetic chain.
• Unilateral serous otitis media is seen in Nasopharyngeal Carcinoma.
• Nasopharyngectomy and lymph node dissection is not the mainstay of treatment in
Nasopharyngeal Carcinoma.
• Nasopharyngeal Carcinoma can be a cause in a 70-years-old man presenting with cervical
lymphadenopathy.
• Patient with nasopharyngeal carcinoma can present with Homer's syndrome,Epistaxis and
proptosis, Trismus.
• Nasopharyngeal Carcinoma does not lead to Sensorineural Hearing loss.
• Keratinizing squamous cell carcinoma of nasopharynx is Type I.
72. Retropharyngeal and Parapharyngeal Abscess
• The most likely diagnosis in a patient having lower third molar extracted due to dental caries and
then developed high fever and pain and on examination, tonsil deviated medially and there was
swelling in upper one-third of sternocleidomastoid muscle is Parapharyngeal Abscess.
• Retropharyngeal abscess is confined to one side of the midline and presents with dysphagia &
difficulty in breathing.
• Retropharyngeal abscess can be palpable per orally by pressing the finger on posterior pharyngeal
wall.
• Retropharyngeal Abscess may present with High fever and hoarseness of voice.
• Post-styloid space of parapharyngeal space contains cranial nerve IX ,XII and Lymph nodes.
• Retropharyngeal abscess lies anterior to the prevertebral fascia.
• Parapharyngeal space is also known as Lateral pharyngeal space.
• The medial bulging of pharynx is seen in Pharyngomaxillary abscess.
• Trismus in parapharyngeal abscess is due to spasm of Medial Pterygoid muscle.
• Most common cause of chronic retropharyngeal abscess is caries of cervical spine.
• Chronic retropharyngeal abscess is associated with tuberculosis of spine and suppuration of
Rouviere lymph node.
• Retropharyngeal abscess may present with swelling on posterolateral wall of the pharynx.
73. Laryngeal Paralysis
• Cadaveric position of vocal cords is seen in Bilateral recurrent and superior laryngeal nerve palsy.
• The voice is not affected in unilateral abductor palsy.
• Recurrent laryngeal nerve palsy and External branch of superior laryngeal nerve palsy may occur as
a complication of hemithyroidectomy surgery.
• In complete bilateral palsy of recurrent laryngeal nerves,there is preservation of speech with severe
stridor and dyspnea.
• Twenty-four hours following partial thyroidectomy where the inferior thyroid artery was also
ligated (tied off), the patient now spoke with a hoarse voice (whisper), and had difficulty in
breathing.Recurrent Laryngeal Nerve is injured in this case.
• Recurrent Laryngeal Nerve injury most commonly leads to vocal cord paralysis.
• Damage to the internal laryngeal nerve results in anaesthesia of the larynx.
• Thyroid Ca causes laryngeal paralysis due to Recurrent Laryngeal nerve palsy.
• Vocal cord palsy in thyroid surgery is due to injury to Recurrent Laryngeal nerve.
• Bilateral Recurrent laryngeal nerve injury may lead to respiratory distress after Thyroid Surgery.
• Hoarseness secondary to bronchogenic carcinoma is usually due to extension of the tumour into
Left Recurrent laryngeal nerve.
• Posterior crioarytenoid , Lateral cricoarytenoid ,Thyroarytenoid. muscles of larynx are affected in a
casr of Recurrent Laryngeal nerve palsy.
• Laryngeal carcinoma especially glottic can cause U/L or B/L Vocal Cord paralysis .
• Vocal nodule does not cause vocal cord palsy.
• Thyroid surgery ,Thyroid malignancy,Cancer cervical oesophagus are the causes of Bilateral
Recurrent laryngeal nerve palsy.
• Throid surgery is the most common cause of B/L recurrent laryngeal paralysis.
• Most dangerous lesion of vocal cords is bilateral abductor paralysis (Bilateral RLN palsy).
• Injury to superior laryngeal nerve causes Loss of timbre of voice.
• Paralysis of recurrent laryngeal nerve is common on Left side
74. Laryngeal Nerve Supply
• Cricothyroid muscle is supplied by external laryngeal nerve.

• The nerve supply of the muscles:Lateral cricoarytenoid ,Posterior cricoarytenoid ,Thyroepiglotticus
is by Recurrent laryngeal nerve.
• Nerve supply of the mucosa of larynx is by Internal and recurrent laryngeal nerve.
• Recurrent laryngeal nerve is in close association with Inferior thyroid artery.
• External Laryngeal Nerve is the most common nerve injured in ligation of superior thyroid artery.
• Galen's anastomosis is between Recurrent laryngeal nerve and internal laryngeal nerve.
75. Tubercular Laryngitis
• Mammilated appearance , Mouse nibbled appearance,Turban epiglottis is seen in TB of larynx.

• TB,Sarcoidosis,Syphilis may affect the Anterior Larynx.
• Paralysis of Vocal cord does not occurs in TB Larynx.
• TB Larynx may present with ulceration of Arytenoid and Odynophagia.
• Tubercular laryngitis affects primarily Posterior commissure of larynx.
76. Neonatal Airway
• A child able to breathe and suckle at the same time due to high placed larynx.

• Infant airway compared to adult airway is relatively large size of the tongue ,Epiglottis is omega
shaped , Larynx is funnel shaped.
• The narrowest part of trachea in a newborn is at the level of cricoidl cartilage.
• In administering anesthesia in infants, this may lead to Trauma to the subglottic region ,Post
operative stridor,Laryngeal oedema.
• Larynx extends from C2 to C4 in neonates.
• Subglottic region is the narrowest part of infantile larynx.
77. Laryngeal involvement in miscellaneous causes.
• 29-year-old male with episodic abdominal pain and stress-induced edema of the lips, the tongue,
and occasionally the larynx is likely to have low functional or absolute levels of C1 esterase
inhibitor.
• The most probable diagnosis in a man taking peanut and developing stridor, neck swelling, tongue
swelling and hoarseness of voice is Angioneurotic Edema.
• C1 esterase inhibitor deficiency is causative in a patient presenting with history of episodic painful
edema of face and larynx.
• Laryngopharyngeal reflux is the cause of pseudosulcus in the larynx in an alcoholic presenting with
globus sensation in throat, cough and hoarseness.
• Scleroma of larynx is caused by Klebsiella,Subglottic stenosis is a common complication,Treatment
may include steroids.
• Larynx is the most common site in respiratory tract for amyloidosis.
• Epiglottis is the most common site in larynx for sarcoidosis.
• Reflux laryngitis produces subglottic stenosis and Ca larynx.
• A patient with burns die within 24 hours. Physical burn injury to the airways above the larynx could
be the most probable cause.
78. Subglottic Stenosis
• The Myer-Cotton grading system is used for Subglottic stenosis

• A 38 year old man presents with stridor following a respiratory infection. Cotton's grading is used to
classify the pathology.Subglottic stenosis is the diagnosis in this case.
• Subglottic stenosis in term infants is a subglottic diameter of less than 4 mm
79. Recurrent Laryngeal Papillomatosis
• Recurrent Laryngeal Papillomatosis is caused by Human Papilloma Virus (HPV).

• HPV6 and HPV11 are most commonly implicated.
• Transmission to neonate occurs through contact with mother during vaginal delivery.
• The disease associated with HPV-11 is more severe than with HPV-6.
• Multiple Paillomatosis is the most common manifestation of HPV infection in children.
• Adult onset papilloma usually arise from the anterior half of the vocal cord or anterior commissure.
• CO2 laser resection is done in a casr of multilpe laryngeal Papillomatosis.
80. Benign Lesions of Larynx
• Vocal nodule is also known as screamer's node and occur at junction of ant. 1/3rd and post. 2/3rd
of vocal cords.
• Reinke's space is situated in edges of True vocal cord.
• Chronic irritation of vocal cords due to misuse of voice, heavy smoking, chronic sinusitis and
laryngopharyngeal reflux are likely to be associated in Reinke's Edema.
• In Reinke’s edema hoarseness is the common symptom.
• In Reinke's edema, bilateral symmetrical swelling of the membranous part of the vocal cords is
present.
• In Reinke's edema,Polypoid degeneration of vocal cords is due to oedema of the subepithelial
space.
• The most important cause for contact ulcer in vocal cords is Voice abuse.
• Contact ulcer can be caused by intubation injury, adductor dysphonia.
• Contact ulcer can be caused/aggravated by acid reflux
• Vocal process is the site for contact ulcer formation.
• Kiss ulcer of larynx is due to Vocal Abuse.
81. Voice Disorders
• Rhinolalia clausa is associated with Allergic rhinitis , Adenoids, Nasal polyps.

• Rhinolalia clausa is associated with Palatal paralysis.
• In dysphonia plica ventricularis, sound is produced by False vocal cords.
• Functional Aphonia is seen commonly in females.
• Functional aphonia is not due to vocal cord paralysis.
• In a case of functional aphonia,the patient is able to cough.
• Habitual dysphonia is characterized by poor voice in normal environment .
• Treatment of Habitual Dysphonia is Vocal exercise and reassurance.
• Young man whose voice has not broken is called Puberphonia.
• Patient with the adductor type of Spasmodic dysphonia have strained and strangled voice.
• Botulinum toxin is the standard treatment for Spasmodic dysphonia.
• Spasmodic dysphonia may be associated with other focal dysphonia.
• Type -III Thyroplasty is the surgical treatment of Puperphonia.

82. Ethmoidal Polyp
• Ethmoidal polyp can cause bilateral nasal obstruction and loss of taste.
• Rhinorrhea may be present with Ethmoidal polyp.
• Ethmoidal polyp may be associated with Cystic Fibrosis.
• All polypi should be subjected to histology,especially in old age patient as a simple nasal poylp in an
old patient may masquerade a malignancy underneath.
• On examination, smooth, glistening, grape-like masses which are pale in color are seen in case of
Ethmoidal polyp.
• A patient with Ethmoidal polyp may present with is a history of asthma and allergies.
• Ethmoidal polyp is not associated with epistaxis.
• Ethmoidal polyp typically occurs in middle aged individuals and not in the first decade of life.
• Recurrent polyps are seen in Ethmoidal polyp.
• Epinephrine,Corticosteroids and Antihistamines is the medical treatment of multiple ,bilateral nasal
polyp.
• Extranasal ethmoidectomy should be done in a patient who presents with an Ethmoidal polyp,6
months later after undergoing polypectomy for Ethmoidal polyp.
• "Bernoulli's theorem" explains Nasal Polyp.
• Multiple nasal polyp in children should guide the clinician to search for underlying Mucoviscidosis.
• Aspirin-sensitive asthma is associated with Nasal Polyp.
• Most common nasal mass is polyp.
• Nasal Steroids may be given post-operatively to prevent recurrence in a case of Ethmoidal polyp.
83. Antrochoanal Polyp
• Antrochoanal polyp is unilateral and single.

• Antrochoanal polyp grows backwards to the choana.
• Antrochoanal polyp is common in children.
• Endoscopic sinus surgery is the treatment of choice in Antrochoanal polyp(not Avulsion).
• Intranasal Polypectomy is the most appropriate management for Antrochoanal polyp in children.
• Antrochoanal polyp does not bleeds on touch.
• Antrochoanal polyp arises from Maxillary antrum.
• Killian term is used for Antrochoanal polyp.
• Antrochoanal Polyp is not pre-malignant in nature.
• FESS is treatment for recurrent atrochoanal polyp.
• FESS is the current treatment of choice for a large antrochoanal polyp in a 10 year old .
• "Bernoulli's theorem" explains Nasal polyp.
• Topical steroids are not recommended post-surgery for Antrochoanal Polyp .
• A patient presents with antrochoanal polyp arising from the medial wall of the maxilla. FESS with
polypectomy would be the best management for the patient.
• Antrochoanal polyp is associated most commonly with middle meatus.
• Xray showing air column between soft tissue mass and posterior wall of nasopharynx is suggestive
of Antrochoanal polyp.
84. Thyroplasty
• In thyroplasty type 2, vocal cord is lateralized.

• Vocal cord medialization is the indication of type-I thyroplasty.
• Type III Thyroplasty is the surgical treatment of Puberphonia.
• U/L vocal cord palsy treatment includes Isshiki type I thyroplasty
85. Laryngocele
• Laryngocele arises from herniation through Thyrohyoid Membrane.

• Laryngocele arises from Saccule of the Ventricle.
• External laryngocele is a herniation that arises from Thyrohyoid Membrane.
• An old man presented with hoarseness, cough, dysphagia, and foreign body sensation in the throat.
Laryngocele was suspected which arises from herniation through Thyrohyoid Membrane.
86. Rhinosleroma
• Mikulicz cells and Russell bodies are seen in Rhinoscleroma.

• A roomy nasal cavity and atrophic dry nasal mucosa with thick crust formation and woody hard
external nose is seen in Rhinoscleroma.
• Rhinoscleroma is caused by Klebsiella Rhinoscleromatis.
• Rhinoscleroma is a slowly progressing granulomatous disease.
• Rhinoscleroma is most common in young adults 20–30 years old.
• Poor nutrition contributes to the spread of Rhinosleroma.
• Drug of choice in Rhinoscleromatosis is Tetracycline.
• Frish bacillus causes Rhinoscleroma.
87. Rhinosporidiosis
• Rhinosporidiosis presents as a nasal polypoidal mass.

• Rhinosporidiosis presnts as a fungal granuloma.
• The etiologic agent of rhinosporidiosis, R seeberi, has traditionally been considered a fungus.
• Recent RNA gene analysis has placed R seeberi into a novel group of aquatic parasites .
• Surgery is the treatment in a case of Rhinosporidiosis.
88. FESS

• Maxillary Sinus is preserved in FESS Surgery.
• FESS surgery is not contraindicated below 12 years of age.
• FESS is the treatment in all cases of Atrochoanal polyp.
• FESS is the best surgical treatment for chronic maxillary sinusitis.
• FESS means Functional endoscopic sinus surgery.
• Orbital cellulitis can occur as a complication of FESS.
• Endoscopic nasal surgery is indicated in Chronic sinusitis,Epistaxis,Inverted papilloma,Orbital
abscess,Nasal polyposis.
• Endoscopic repair is the management of persistent cases of CSF rhinorrhea.
89. Physiology of hearing (ENT)
• Function of Stapedius is Protects the ear from loud frequency sound.

• Exposure to noise above 160 dB causes permanent loss of hearing.
• Permanent privation of the hearing of either ear ,even though correctable by surgery,comes under
Greivous injury.
• Psycho-acoustic index of loudness is indicated by the term 'Phon'.
• Sense gravity and Linear acceleration is associated with ‘otolith organs’.
• The limit of loudness expressed as decibels that people can tolerate without substantial damage to
their hearing is 85 dB.
• Foetus starts hearing by what time in intrauterine life by 20 weeks.
• Sense organ for hearing is Organ of Corti.
• Bones of middle ear are responsible for Reduction of impedance to sound transmission.
• Impedance matching occurs at Difference of surface are of tympanic membrane and foot plate.
• Primary receptor cells of hearing is Hair cell
90. Special Hearing Tests
• In Electrocochleography,action potentional is produced by outer hair cells.

• Electrocochleography is mostly used in monitoring the Meniers disease.
• Electrocochleography is the gold standard investigation for diagnosis of Meniers disease.
• In Electrocochleograpgy,the electrode must be kept close to source of amplitude.
• Otoacoustic emissions arise from Outer hair cells.
• Recruitment phenomenon is seen in Presbyacusis.
• Otoacoustic Emissions is the best screening test to evaluate hearing in a neonate.
• Brainstem Evoked Response Audiometry(BERA)
• Electrocochleography is a method of recording auditory evoked response taken from cochlea and
auditory nerve is the investigation of choice in assessing hearing loss in neonates.
• Auditory screening is required in children under following conditions:Before doing exchage
transfusion for hyperbilirubinemia, In premature babies , Before starting aminoglycoside therapy
• To distinguish between cochlear and post cochlear damage, test done is BERA.
• In Electrocochleography,Outer hair cells are mainly responsible for cochlear microphonics and
summation potential.
• Recruitment test is positive in Meniere's disease.
• Best time for hearing assessment in an infant is 1st month of life
91. Auditory Pathway
• Medial geniculate body is related to Hearing.

• Damage to one of the auditory cortex causes no noticable deficit at all as there is overlap of cortex.
• Higher auditory centre determines Sound localization.
• Cranial nerve VIII lesion affects Position sense and equilibrium.
• Auditory cortex is present in area Area 41.
• Auditory transmission is via Lateral lemniscus.
• Genu of internal capsule is not associated with the Auditory pathway.
• Trapezoid body,Medial geniculate body ,Lateral leminiscus are concerned with the Auditory
pathway.
• Primary auditory area is Superior temporal gyrus.
• Auditory processing of spoken language is done by Temporal lobe
Ophthalmology
1. ACANTHAMOEBA KERATITIS
• Acanthamoeba does NOT depend upon a human host for the completion of its life-cycle.
• Acanthamoeba keratitis is Seen in contact lenses users.
2. INTERSTITIAL KERATITIS
• Salmon patch appearance of cornea seen in Interstitial Keratitis.

• Interstitial keratitis is commonly seen in Congenital syphilis.
3. Calcific degeneration / Band shaped keratopathy
• Band shaped keratopathy seen in JRA.

• Band shaped keratopathy is caused by Calcium.
• Sarcoidosis is associated with Band shaped keratopathy.
4. KERATOPLASTY
• Cornea should be removed from cadaveric donors within 6 hrs after death (Golden Period).
• Short term storage (upto 48 hours) – whole globe is stored at 4°C in a moist chamber.
• Intermediate storage (upto 2 weeks) - in Mc Carey Kaufmann medium.
• Long term storage (upto 35 days) – organ culture method or cryopreservation at minus 70°C.
• The cornea graft with graft diameter b/w 7 & 8.5 mm has more chances of survival.
• Deep anterior lamellar keratoplasty is indicated in Superficial corneal opacities.
• Endothelial cell loss in donor tissue of Descemet stripping endothelial keratolplasty is nearly 36%.
5. STAPHYLOMA
• Staphyloma is lined internally by uveal tissue (iris or ciliary body or choroid) .

• Staphyloma involvement is Iris with Cornea.
• Most common type of staphyloma in myopia is Posterior.
• Most common cause of anterior staphyloma Corneal ulcer.
• Most common cause of posterior staphyloma Myopia.
• Posterior staphyloma is most commonly seen in Degenerative myopia.
• Ciliary staphyloma is a complication of Scleritis.
6. RETINITIS PIGMENTOSA
• Combination of retinitis pigmentosa and ichthyosis is seen in Refsum's syndrome.

• Retinal neovacularization is seen in Retinitis pigmentosa.
• Most characteristic finding of retinitis pigmentosa is Ring scotoma
• In diagnosis of retinitis pigmentosa ERG is Less sensitive than the EOG.
• Most common mode of inheritance for retinitis pigmentosa is Autosomal recessive.
• Jet-black spots in the retina are seen in Retinitis pigmentosa.
• Refsum's syndrome is associated with Retinitis pigmentosa
• Waxy pallor of optic disc is seen in Retinitis pigmentosa
7. KERATOCONUS
• Non-inflammatory bilateral ecstatic condition of cornea with Protrusion of anterior cornea and
characterized paraxia/stromal thinning
• Progressive myopia, regular and irregular astigmatism
• Munson's sign – bulging of lower lid on downward gaze
• Placido disc – irregular circles
• Fleischer's ring at the base of cone due to iron deposition
• Acute corneal hydrops due to rupture of Descemet's membrane (especially in Down syndrome)
• Spectacles, rigid gas permeable contact lenses, intacs (intracorneal ring segments)
• Late stages – Deep anterior lamellar keratoplasty or Penetrating keratoplasty

8. CONJUNCTIVA
• Epithelial lining of conjunctiva is stratified non- keratinized epithelium

• Fusion of palpebral and bulbar conjunctiva is Symblepharon.
• Maximum number of goblet cells are present in Nasal conjunctiva.
• Normal conjunctival flora is Coagulase negative staphylococci.
9. Sympathetic ophthalmitis
• Giant cells located within the choroid ,T lymphocytes & Eosinophils are the histopathologic features
of sympathetic ophthalmia
• Dalen Fuch's nodules are seen in Sympathetic ophthalmia
• If a person shows impaired vision of eye after few weeks of gun shot injury to another eye this is
suggestive of Sympathetic ophthalmia
• Sympathetic ophthalmitis affects both eye because Uveal pigment act as allergen which inturn
induce plastic uveitis in the sound eye.
• Common features between sympathetic ophthalmitis and Vogt Kanayagi Harada syndrome
is Autoimmune etiology & Uveitis
• In sympathetic ophthalmitis first sign is Presence of KP's.
• The earliest symptom of sympathetic ophthalmitis is Photophobia
• Sympathetic ophthalmitis develops 3 wks-12 wks after trauma
• Structure commonly involved in sympathetic ophthalmia is Iris and ciliary body
• Sympathetic ophthalmitis or ophthalmia almost always results from a penetrating wound
• Clinically in the non-injured eye, sympathetic ophthalmitis may manifest as Acute plastic
iridocyclitis,Neuroretinitis,Choroiditis
10. OPHTHALMIA NEONATORUM
• Ophthalmia neonatorum is a common causes of childhood blindness

• Systemic treatment of erythromycin, gentamycin and bacitracin are used for the treatment
• N gonorrhoeae is the likely organism causing ophthalmia neonatorum on the 3rd day of birth
• Chlamydial infection is causative organism of Ophthalmia neonatorum
• Ophthalmia neonatorum is most commonly caused by Chlamydia trachomatis, Neisseria
gonorrhea
• Ophthalmia neonatorum is Inflammation of the conjunctiva occurring in an infant less than 30 days
old
• Herpes Simplex Virus II is responsible for causing ophthalmia neonatorum on 5-7th day after birth
11. CRVO & CRAO

• Cattle track appearance in fundoscopy is due to CRAO
• Sudden loss of vision is seen in CRAO & CRVO
• Central Retinal Venous Occlusion (CRVO) from Ocular Ischemic Syndrome can be differentiated on
the basis of Tortuous Retinal Vein,Retinal Artery Pressure, Ophthalmodynamometry
• Cherry red spot on the macula in Fundus examination of a patient presenting with loss of vision is
seen in CRAO
• Rubeosis iridis is seen in CRVO
• CRAO may be seen in Orbital mucormycosis
• Neovascular glaucoma can occur in both CRAO & CRVO
• Vitreous haemorrhage is seen in CRVO
• Hundred day glaucoma is associated with CRVO
• CRVO & CRAO ' blood & thunder ' appearance of retina
12. REFSUM DISEASE
• Refsum's disease is a rare genetic disorder due to deficiency of phytanate alpha oxidase.
• Combination of retinitis pigmentosa and ichthyosis is seen in Refsum's syndrome.
• Ichthysis is caused by Refsum's syndrome.
• Refsum's syndrome is associated with Retinitis pigmentosa.
13. GLAUCOMA
• Double arcuate or ring shaped scotoma in glucoma develops when two arcuate scotomas join.
• Most common cause of neovascular glaucoma Diabetes
• Pupil in acute congestive glaucoma Vertically oval & semidilated
• Patient with open angle glaucoma of myopia, complains of blurring of vision on administration of
pilocarpine due to Small pupil
• Pseudophakia is a cause of secondary angle closure glaucoma
• Hundred day glaucoma is associated with CRVO
• Neovascular glaucoma is caused by CRVO, CRAO, Diabetes mellitus
• Tears of the iris sphincter and ciliary body is seen in angle recession glaucoma
• Angle recession more than 180 degree in angle recession glaucoma
• Secondary open angle glaucoma can occur in angle recession glaucoma
• Frequent change in presbyopic correction is seen in open angle glaucoma
• open angle glaucoma is most common with Open anterior chamber angle
• In angle closure glaucoma Small cornea, shallower Anterior chamber & Short axial length of eyeball
are the anatomical changes seen
• Angle closure glaucoma may be associated with Hypermetropia
• Most common etiolopathogenetic cause of glaucoma is Decreased outflow
• Intractable secondary glaucoma is seen in Diffuse iris melanoma
• Congenital glaucoma presents as Photophobia
• First sign seen in open-angle glaucoma is Extension above blind spot
• The most reliable provocative test for angle-closure glaucoma is Dark room test
• In haemolytic glaucoma the mechanisms are Siderosis of trabeculae,Deposition of haemosiderin
& RBC clogging the trabecular
• Secondary glaucoma following corneal perforation is due to Peripheral anterior synechiae
• The earliest change in glaucoma is Baring of the blind spot
• In chronic simple glaucoma the most common field defect is Baring of blind spot
• Inverse glaucoma occurs in Spherophakia
14. EALES DISEASE
• Eales disease is Recurrent vitreous hemorrage

• Panretinal photocoagulation is done in Eales disease
• Eales disease is characterized by Recurrent retinal haemorrhage, Recurrent vitreous haemorrhage
& Neovascularization
• Retinal detachment seen in Eale's disease
• In a young patient presenting with recurrent vitreous hemorrhage, diagnosis is Eale's disease.
• A 25 year old male presents withpainless sudden loss of vision, ocular and systemic examination is
not contributory is diagnosed with Eale's disease.
• Eales disease is Recurrent periphelbitis retina.
• Eale's disease is Vitreous hemorrhage
• Eales' disease is best treated with Steroids
• Argon laser is used in Eales' disease
• Both soft and hard exudates are seen in Eale's disease
• Parachute lesions are seen in Eale's disease
15. THYROID OPTHALMOPATHY
• The walls of the orbit which are removed in the two wall decompression for proptosis of thyroid
ophthalmopathy include part of Orbital floor and medial wall
• Occurrence of diplopia, dysphagia, dysarthria, blurring of vision and muscle weakness could be due
to Botulism
• Muscle mostly affected in thyroid ophthalmopathy is Inferior rectus
• Earliest symptom of thyroid ophthalmopathy is Lid retraction
• Most common cause of proptosis in adults is Thyroid Ophthalmopathy
• Sign of thyroid ophthalmopathy are Van Graefe's sign , Dalrymple's sign & Joffroy's sing
• Most common ocular movement affected in thyroid ophthalmopathy Elevation
16. VITREOUS HEMORRHAGE

• The most common cause of vitreous hemorrhage in adults is Diabetes
• Causes of floaters in DM is vitreous hemorrhage
• In a young patient presenting with recurrent vitreous hemorrhage, diagnosis is Eale's disease
• Trauma is the most common cause of vitreous hemorrhage in young individuals
• Vitreous hemorrhage is caused commonly by Retinal vein occlusion
• No treatment is given immediately in vitreous hemorrhage in eye
• Vitreous hemorrhage produces Sudden painless loss of vision
• Most common complication after lens extraction persistent hyperplastic primary vitreous
is Vitreous hemorrhage
• A 40-year old male with diabetes presents with vitreous hemorrhage may be due
to Neovascularization at disc
17. DIABETIC RETINOPATHY
• Earliest feature of Diabetic Retinopathy is Microaneurysms

• HTN and DM with reduced vision showing central bleed on fundoscopy can be diagnosed
as Diabetic retinopathy
• Diabetic retinopathy is related to Duration of disease
• The screening strategy for prevention of blindness from diabetic retinopathy according to the NPCB
involves High Risk Screening
• Microaneurysms, Retinal hemorrhages & Neovascularisation are feature in diabetic retinopathy on
fundus examination
• Oxidative stress, VEGF (vascular endothelial growth factor) & Increased protein kinase-C
are implicated in the pathogenesis of macular oedema in diabetic retinopathy
• In maturity onset diabetes mellitus, screening for diabetic retinopathy should be done Immediately
• Cotton wool spots in diabetic retinopathy are due to Retinal edema
• ETDRS stands for Early treatment for diabetic retinopathy study
• Diabetic retinopathy, most likely present with NIDDM with 2 years duration
• Development of Diabetic retinopathy depends on Intensity of disease, Age of onset & Duration of
disease
• Diabetic retinopathy is characterized by Hard exudates, dot haemorrhages and microaneurysm
& Flame shaped haemorrhages, soft exudates
• Diabetic retinopathy is treated by Strict glycemic control, Panphotococagulation & Antihypertensive
• Diabetic retinopathy is essentially an angiopathy affecting retinal Precapillary arterioles, Capillaries
& Venules
• Spontaneous regression of proliferative retinopathy may occur in Diabetic retinopathy
• Visual loss in diabetic retinopathy is due to Cataract formation, Ischaemic maculopathy & Vitreous
hemorrhage
• Commonest cause of loss of vision in non-proliferative diabetic retinopathy is Macular edema
• Sudden loss of vision in patient with diabetic retinopathy is due to Vitreous defects
• Vitreous haemorrhage in diabetic retinopathy is Prolifertive diabetic retinopathy
• Panretinal photocoagulation is indicated in Prolifertive diabetic retinopathy
• Capillary microaneurysms is an earliest sign of Non-proliferative diabetic retinopathy
• Diabetic retinopathy is the most common cause of ruheosis iridis
18. ANATOMY OF SCLERA
• Thinnest portion of sclera→ Posterior to inserƟons of rectus muscle.

• Thickest portion of sclera→ Posterior pole
• Retrobulbar cellulitis is the only option which can present late after trauma to eye.
• Pneumo-orbit, Retrobulbar hematoma & carotico-cavernous fistula - all present early after trauma.
• Rupture of sclera m/c seen in Superonasal quadrant.
• Lamina cribrosa is the weakest part of sclera.
• Absence of lamina cribrosa is feature of Morning glory syndrome.
• SCLERA BUCKLING used for the treatment of Retinal detachment.
• Blue coloured sclera is frequently associated with Osteogenesis imperfecta.
• Non necrotising anterior scleritis is the most common types of scleritis.
19. HISTOLOGY OF CORNEA
• Metabolically active layer of cornea is Endothelium & Epithelium.

• Corneal epithelium composed of stratified squamous non-keratinized epithelial cells.
• Schwable's ring is seen in Descemet's membrane layer of cornea.
• Bowmann's membrane has no regeneration capacity.
• Corneal transparency is maintained by Endothelium.
• Corneal deturgescence is maintained by an active sodium-potassium pump situated in
endothelium.
• The cell density of endothelium is around 3000 cells/ mm2 in young adults.
• Corneal endothelium regenerates rapidly after injury.
20. ANATOMY OF CORNEA
• Avascular coat in eye is Cornea.

• Anterior surface of Cornea is elliptical, posterior surface is circular.
• Radius of curvature of anterior surface of Cornea is 7.8 mm
• Refractive power of cornea is about 43-44 D.
• Refractive index of Cornea is 1.376.
• Most of the refraction in eye occur at anterior surface of cornea (air-tear interface).
• The critical angel of cornea-air interface is 46°.
• Cornea gets its nourishment mainly from Aqueous humour.

21. MYOPIA
• In senile nuclear cataract Index myopia is seen.

• Maximum correction of myopia can be done by LASIK.
• Retinal detachment is the most common complication of high myopia.
• Haemorrhage at macular spot in high myopia is called Foster-Fuchs fleck.
• Radial keratotomy corrects myopia by causing Flattening of cornea.
• Posterior staphylomas are commonly seen in patients with high myopia.
• Refractive surgery most commonly performed for myopia is LASIK.
22. ASTIGMATISM
• Astigmatism is defined as refractory error wherein refraction varies along different meridians.
• Astigmatism is due to irregularity of curvature of cornea.
• Astigmatism is considered to be Spherical abberation.
• In simple astigmatism, foci of image formed on One on retina, other behind the retina.
• Regular stigmatism → Principal meridians are pendicular
• Irregular astigmatism → Principal meridians are not perpendicular.
• Lens used to treat astigmatism Cylindrical lens.
23. CONTACT LENSES
• Contact lens is best used in Irregular astigmatism.

• Soft contact lens is made of hydroxymethymethacrylate (HEMA)
• Non foldable lens is made of PMMA.
• Consistency of the gas permeable contact lenses is Hard.
• Most common infection in contact lens users is Pseudomonas.
• 2nd Commonest cause of keratitis in soft contact lens users is Acanthamoeba.
• Continous contact lens wear may lead to Giant papillary conjunctivitis.
24. APHAKIA
• The typical signs of aphakia are deep anterior chamber, iridodonesis (tremulousness of iris) and a
dark pupillary reflex.
• Most common cause of aphakia is surgical removal of cataractous lens.
• In aphakia purkinje images absent are 3rd & 4th.
• Treatment of choice for Aphakia is IOL.
• The ideal rehabilitation for aphakia is Posterior chamber intraocular lens.

25. EYEBALL
• Weight of an adult eyeball is 7gm.

• Volume of an adult eyeball is 6.5ml.
• Circumference of an adult eyeball is 75 mm.
• Anteroposterior diameter of normal adult eyeball is 24mm.
• vitreous humor is a constituent of posterior segment.
26. DEVELOPMENT OF EYE
• Uveal & conjunctival melanocytes are derived from neural crest.

• Sclera is derived from mesoderm.
• Crystalline lens, corneal epithelium & lacrimal gland are derived from surface ectoderm.
• Corneal stroma is made from Mesoderm.
• Most common site for coloboma is Inferonasal.
• The lens continues to grow throughout the lifetime.
• Eye of new born is usually hypermetropic by +2 to +3D.
• Normal level of visual acuity is attained by 3 yrs of age.
• Gaze fixation starts developing in the first month & is completed in 6 months.
27. CONJUNCTIVITIS
• Most common bacteria associated with conjunctivitis is Staphylococcus aureus.

• Adult inclusion conjunctivitis caused by serotypes D & K of Chlamydia trachomatis.
• Angular conjunctivitis is caused by Moraxella axenfeld (Moraxella lacunata).
• Vernal keratoconjunctivitis is associated with Corneal opacity.
• Acute hemorrhagic conjunctivitis is caused by Enterovirus 70.
• Ligneous conjunctivitis is caused by Membranous conjunctivitis.
• Unilateral conjunctivitis is commonly seen in Dacryocystitis.
• Pseudomembranous conjunctivitis is caused by Streptococcus.
• Acute haemorrhagic conjunctivitis is seen with Adenovirus.
• Swimming pool conjunctivitis is caused by Chlamydia trachomatis.
28. TRACHOMA
• Cicatrising trachoma is seen in Stage-3.

• Trachoma is characterized by Ectropion of upper eyelids.
• Cause of blindness in trachoma is Conjunctival Scarring.
• Single drug used for treatment of trachoma is Azithromycin.
• Drug of choice for chylamydial trachomatis is Azithromycin.
• Drug of choice of trachoma is Tetracycline.
• Chlamydia trachomatis infection causes Pneumonitis, Conjunctivitis & Urethritis.
• Chlamydia trachomatis infection commonly causes Infertility.
• In the grading of trachoma, trachomatous inflammation-follicular is defined as the presence of 5 or
more follicles in the upper tarsal conjunctiva.
• Pathognomic features of trachoma follicle are Presence of Leber's cells & Areas of necrosis.
29. VERNEAL KERATOCONJUNCTIVITIS (SPRING CATTARRH)
• Vernal keratoconjunctivitis is associated with Corneal opacity.

• Epidemic keratoconjunctivitis is caused by Adenovirus.
• Keratoconjunctivitis sicca refers to Aqueous tear deficiency dry eye.
• Features of vernal keratoconjunctivitis are Papillary hypertrophy, Shield's ulcer, Trantra's spot.
• Treatment of vernal keratoconjunctivitis includes Steroids, Chromoglycate, Olopatadine.
30. PINGUECULA & PTERYGIUM
PTERYGIUM
• Pterygium is Connective tissue proliferation.

• Cause of blindness in pterygium is Astigmatism.
• Drug used to avoid recurrence of pterygium is Mitomycin C.
• The histology of pterygium includes Elastotic degeneration.
• Lacy white lesion in mouth with pterygium is seen in Lichen planus.
PINGUECULA
• Degenerative condition of conjunctiva.

• Characterized by triangular yellowish white patch on the bulbar conjunctiva near the limbus.
31. BACTERIAL CORNEAL ULCER
• Most common bacterial cause of keratitis/corneal ulcer → Staphlococcus aureus

• Most common cause of keratitis/ corneal ulcer in a contact lens wearer → Pseudomonas
• Most common viral cause of keratitis/ corneal ulcer → HSV
32. CORNEAL DYSTROPHIES
• Corneal dystrophies are degenerations that are usually Primary and bilateral.
Anterior corneal Dystrophies Stromal corneal Dystrophies Posterior Corneal Dystrophies

Epithelium: Stroma: Endothelial dystrophy:
Meesamnn’s dystrophy Granular dystrophy Fuch’s endothelial

(Groenouw’s type 1) dystrophy
Epithelium Basement
membrane dystrophy Lattice dystrophy (Type I, Congenital hereditary
Type III, IIIA & IV) endothelial dystrophy
Bowmnann’s layer:
Macular dystrophy Posterior polymorphous
Reis- Bucklers dystrophy dystrophy
Gelatinous droplike
Anterior membrane dystrophy
dystrophy of Grayson-
Wilbrandt Fleck dystrophy
Honycomb dystrophy of Pre- Descement dystrophy

Thiel & Behnke
Avellino’s dystrophy
Subepithelial mucinous
corneal dystrophy Meretoja syndrome (Lattice
type II)
Marginal crystalline
dystrophy of Bietti
Epithelial basement Lattice dystrophy is the most Fuch’s Endothelial
membrane dystrophy is common Stromal Corneal Dystrophy is the most
the most common dystrophy. common
Anterior Corneal Posterior/Lattice
Dystrophy Lattice Type I is the Dystrophy
commonest type of
dystrophy.
Endothelial corneal
Dystrophy is the least
common of the classical
stromal dystrophies
33. BLOW-OUT FRACTURES
• Orbital blow-out fracture involves Medial wall and floor of orbit.

• Blow-out fracture of orbit is characterized by :
• Diplopia
• 'Tear drop" sign
• Positive forced duction test
• Blow out fracture of the orbit most commonly leads to fracture of Posteromedial floor of orbit.
• Orbital emphysema may result in a black eyebrow sign
• Inferior herniation of the intraorbital fat may result in a "teardrop" sign
34. LACRIMAL APPARATUS
LACRIMAL APPARATUS
• Consists of secretory & excretory systems.

• Secretory system consists of:
• Lacrimal gland & its duct
• Accessory lacrimal glands (Gland of Krause, Glands of Wolfring)
• Excretory system consists of:
• Lacrimal puncta
• Lacrimal canaliculi
• Lacrimal sac
• Nasolacrimal duct
TEAR
• Major function of lacrimal apparatus is to secrete & drain tear.

• Tear film consists of 3 layers:
1. Mucous / mucin layer (innermost)
2. Aqueous layer (intermediate)
3. Lipid layer (outermost):
• Secreted by the Meibomion, Zeis & Moll glands.
CAUSES OF TEAR DEFICIENCY (Dry Eye)
1. Aqueous deficiency (Keratoconjunctivitis sicca):

• Congenital alacrimia
• Sjogren's syndrome
• Riley Da syndrome
2. Mucin deficiency:
• Xeropthalmia
• conjunctival scarring (Stevens- Johnson syndrome, Trachoma)
3. Lipid deficiency:
• Congenital anhydrotic ectodermal dysplasia along with absence of meibomian gland

• Chroniv blepheritis
4. Chronic eyelid function:
• Bell's palsy
• Exposure keratitis
• Pterygium
35. HEMORRHAGE IN RETINA
• The superficial retinal hemorrhage is seen in Nerve fibre layer of retina.
CHERRY RED SPOT
• Central part of macula appears as a red spot, whenever there is retinal edema.
• This is because, vascular choroid shins through the very thin area of retina at this area.
Causes of cherry red spot

• GM2 gangliosidoses (Tay sachs & sandhoff)
• GM1 gangliosidoses
• Niemann- Pick’s disease
• Gaucher’s disease
• Metachromatic leukodystrophy
• Central retinal artery occlusion (CRAO)
• Trauma (Berlin’s edema/ commotion retinae)
• Farber’s disease
• Goldberg’s disease
• Hurler’s syndrome
• Mucopolysacharidosis VII
• Multiple sulfatase deficiency
• Poisoning-Carbon mono-oxide, methanol
• Rarely in Krabbe’s disease
36. CENTRAL SEROUS RETINOPATHY
• In central serous retinopathy, in the macular region Spontaneous detachment of neuro-sensory

retina.
CENTRAL SEROUS CHOROIDOPATHY
Idiopathic condition
• Affecting young or middle aged Caucasian man.

• Patient presents with a sudden onset of painless loss of vision.
Ophthalmoscopic findings:
• Mild elevation of macular area demarcated by a circular ring reflex.

• Foveal reflex is distorted or absent.
Diagnosis:
• Confirmed by fluorescein angiography.

• It shows focal leakage of fluorescein in following two patterns:
1. Ink-blot pattern or enlarging dot sign:
• A small hyperfluorescent spot which gradually increases in sign.
2. Smoke-stack pattern:

• Small hyperfluorescent spot which ascends vertically like a smoke stack.
• Gradually spreads laterally to take a mushroom or umbrella configuration.
TREATMENT
• When left alone, central serous retinopathy heals spontaneously within 4-12 weeks, with full
recovery of vision in 90% of patients.
• Reassurance is the only treatment required in majority of the cases.
37. RETINAL DETACHMENT
• Retinal detachment occurs in Sensory retina.

• Retinal detachment occurs between Neurosensory retina and pigment epithelium.
• Earliest manifestation of retinal detachment Photopsia.
• Commonest type of retinal detachment is Rheugmatogenous.
• Tractional retinal detachment is seen in DM retinopathy.
• Cause of exudative retinal detachment IS Harada's syndrome.
• Primary retinal detachment is seen in High myopia.
• Primary aim of retinal detachment surgery - Encirclage.
• A diabetic patient is at greatest risk of developing Traction type of retinal detachment.
38. DIABETIC RETINOPATHY
• Most common early feature of diabetic retinopathy Dot and blot hemorrhages.
• Earliest feature of Diabetic Retinopathy is Microaneurysms.
• Diabetic retinopathy is characterized by Hard exudates, dot haemorrhages , microaneurysm, Flame
shaped haemorrhages & soft exudates.
• Sudden loss of vision in patient with diabetic retinopathy is due to Vitreous defects.
• Commonest cause of loss of vision in non-proliferative diabetic retinopathy is Macular edema.
• Diabetic retinopathy is treated by Strict glycemic control, Panphotococagulation, Antihypertensive.
• Diabetic retinopathy, most likely present with NIDDM with 2 years duration.
• Cotton wool spots in diabetic retinopathy are due to Retinal edema.
• Diabetic retinopathy is related to Duration of disease.
39. PAPILLOEDEMA
• Earliest sign of papilloedema is Blurring of disc margin.

• Ipsilateral optic atrophy with contralateral papilloedema is a feature of Foster kennedy syndrome.
• Acute Papilloedema present with Severe loss of vision.
• Most severe papilloedema is caused by Posterior cranial fossa tumor.
40. OPTIC NEURITIS
CAUSES OF OPTIC NEURITIS
1. Demyelinating disorders
• Multiple sclerosis (most common)

• Neuromyelitis (Devic’s disease)
• Leucodystrophies (Schilder’s adrenoleucodystrophy, Krabbe’s galactocerbroside dystrophy,
Metachromatic sulfatase deficiency, Pelizaeus- Merzbacher disease).
2. Viral infection
• Measles
• Mumps
• Chicken pox
• Whooping cough
• Glandular fever
3. Metabolic/Nutritional deficiency:
• Vitamin B2, B12 deficiency

• Folic acid deficiency
• Thyroid dysfunction
• Diabetes
4. Toxic ambylopia
• Quinine
• Chloroquine
• Ethambutol
• Isoniazid
• Digitalis (digoxin)
• Methyl alcohol
CLINICAL FEATURES OF OPTIC NEURITIS
• Unilateral
• Profound vision loss (major symptom)
• Mononuclear sudden, progressive & profound loss of vision
• Pain behind the eyeball, particularly in retrobulbar neuritis which there is pain on eye movements.
• Visually evoked response (VER) shows reduced amplitude & delayed transmission time.
SIGNS
1. Clinical signs:
• Reduced visual acuity

• Impaired colour vision
• Pupillary reaction is sluggish & ill sustained
• There may be relative afferent pupillary defect (RAPD)
• Marcus Gunn pupil detected byswinging flash light test.
2. Visual field defect:
• Central or centrocaecal scotoma

• Paracentral, arcuate, sectorial & altitudinal field defects
TREATMENT
• Treatment hastens visual recovery & decreases the likelihood of recurrence

• Though the long-term visual outcome is no different
• i.v. Prednisolone followed by iral prednisolone for 11 days.
• Oral prednisolone therapy alone is contraindicated
• Intravenous vitamin C can also ne evaluated for treatment
• MRI of brain & orbit sholud be done begore starting treatment to see the extent of demyelination.
41. VISUAL PATHWAY
Parts of optic nerve
• Intraocular part: 1 mm
• Intraorbital part: 25 - 30 mm
• Intracanalicular part: 5 - 9 mm
• Intracranial part: 10 - 16 mm
Lesions of visual pathway

No Site of lesion Causes Features
1 - - Normal
2 Optic nerve Optic neuritis Complete blindness in affected eye
Optic atrophy Loss of light reflex on the affected side and
Sarcoidosis consensual reflex loss on the other side
LHON Near reflex present
Traumatic avulsion Central/paracentral scotoma

3 Central chiasma Pituitary tumors (MCC) Bitemporal hemianopia
Suprasellar aneurysm, Bitemporal hemianopic paralysis of
Craniopharyngioma, pupillary reflexes
Glioma of Ill ventricle
3a Lateral chiasma Distension of Binasal hemianopia Binasal hemianopic

3rd ventricle, Atheroma paralysis of papillary reflexes
of post. communicating
A
4 Optic tract Geniculate Syphilitic meningitis, Incongruous (contralateral) homonymous
body gumma, tuberculosis, hemianopia Contralateral Wernicke's
tumors of optic pupil (optic tract)
thalamus

5 Optic radiations in Superior quadrantic hemianopia (pie in
temporal lobe (inferior the sky) Normal pupillary reactions
fibres)
5a Optic radiations in Inferior quadrantic hemianopia (pie on the

floor)
parietal lobe
Normal pupillary reactions
(Superior fibres)
6 Optic radiations Homonymous hemianopia
7 Anterior occipital Occlusion of posterior Congruous homonymous hemianopia
(visual) cortex cerebral artery sparing macula
8 Tip of occipital cortex Congruous homonymous macular defect
• Optic atrophy (partial, descending) – occurs in lesions of chiasma, optic tract and geniculate body
• Optic atrophy does not occur in lesions of optic radiations and visual cortex
42. LESIONS OF VISUAL PATHWAY
Parts of optic nerve
• Intraocular part: 1 mm
• Intraorbital part: 25 - 30 mm
• Intracanalicular part: 5 - 9 mm
• Intracranial part: 10 - 16 mm
Lesions of visual pathway

No Site of lesion Causes Features
1 - - Normal
2 Optic nerve Optic neuritis Complete blindness in affected eye
Optic atrophy Loss of light reflex on the affected side and
Sarcoidosis consensual reflex loss on the other side
LHON Near reflex present
Traumatic avulsion Central/paracentral scotoma

3 Central chiasma Pituitary tumors (MCC) Bitemporal hemianopia
Suprasellar aneurysm, Bitemporal hemianopic paralysis of
Craniopharyngioma, pupillary reflexes
Glioma of Ill ventricle

3a Lateral chiasma Distension of Binasal hemianopia
3rd ventricle,
Binasal hemianopic paralysis of papillary
Atheroma of post. reflexes
communicating A
4 Optic tract Syphilitic meningitis, Incongruous (contralateral) homonymous
gumma, tuberculosis, hemianopia
Geniculate body tumors of optic thalamus
Contralateral Wernicke's pupil (optic tract)

5 Optic radiations in Superior quadrantic hemianopia (pie in the
temporal lobe sky)
(inferior fibres)
Normal pupillary reactions
5a Optic radiations in Inferior quadrantic hemianopia (pie on the
parietal lobe floor) Normal pupillary reactions
(Superior fibres)
6 Optic radiations Homonymous hemianopia
7 Anterior occipital Occlusion of posterior Congruous homonymous hemianopia

(visual) cortex cerebral artery sparing macula
8 Tip of occipital cortex Congruous homonymous macular defect
• Optic atrophy (partial, descending) – occurs in lesions of chiasma, optic tract and geniculate body
• Optic atrophy does not occur in lesions of optic radiations and visual cortex
43. OPTIC ATROPHY
• Optic atrophy can be caused by Methyl alcohol poisoning.

• In optic atrophy pallor of the disc is an index of Loss of vascularty of the disc.
44. COLOUR VISION & COLOUR BLINDNESS
Congenital colour blindness (Hereditary)
• M/c type of colour blindness.

• Sex linked & is inherited as X-linked recessive.
• More common in males (3-4%) than females (0.4%).
• Results due to absence of one group of colour cones.
• Person may be colour blind for any one primary colour.
• When Green cones are absent, person is green blind.
• The condition is c/d Deuteranopia. Person is c/d deutranope.
• When red cones are absent, the person is red blind.
• Condition is c/d Protanopia. Person is c/d pronatope.
• When blue cones are absent, the person is blue blind.
• The condition is c/d tritanopia. Person is c/d tritanope
• Patients can appreciate only 2 colours, this defect is c/d Dichromatic colour blindness.
• Person can appreciate all three primary colour but is defective for one or two of them.
• Therefore c/d trichromatic colour blindness.
• Three types of such anomalies are there:
• Red colour defective → Protanomaly
• Green color defective → Deuteranomaly
• Blue colour defective → Protanomaly
TESTS FOR COLOUR VISION
1. Pseudoisochromatic charts
• Ishihara plates mainly to screen congenital protan & deuterons (i.e red & green defects)
2. Edridge Green lantern test
3. City university test
4. Fansworth Munsell 100 hue test
• Most sensitive for both congenital & acquired colour defects.
5. Fansworth D 15 hue discrimination test
6. Nagel’s anomaloscope
7. Holmgren’s wool test
• Currently there is no treatment for colour blindness.
Preventive & Social Medicine
1. Cohort Study
• Cohort study is a type of analytical study.

• Cohort study is best to test the association between risk factor and disease.
• To test the association between risk factor and disease, the weakest study design is Ecological
Study.
• Proceeds from cause to effect(Also seen in RCT and ecological studies).
Cohort Studies are indicated when there is good evidence of an association between an exposure
and disease.
• It is a study is one in which the outcome (e.g. disease) has not yet occurred at the time the
investigation begins.
• Yields incidence rate, relative risk, attributable risk(except Odds Ratio-a measure of the strength of
the association between risk factor and outcome).
• Advantage of Case control studies over Cohort Study is that Odds ratio(estimate of Relative Risk)
can be measured and rare disease can be studied but Chances of bias are maximum in case-control
study.
• Can not study many causal factors at a time as in Case Control Study.
• Cohort study along with case control study and randomized control trials are based on the
comparative study of two groups.Natural history of a disease is best studied by cohort studies.
• Matching is not required in a case of Case report.
• Randomized control trials produce best evidence for evidence of causation
• Cohort Study is a Study of the group who do not have the disease of interest initially but develops
with time or not.
• Cohort study is best to test the association between risk factor and disease.
• To test the association between risk factor and disease, the weakest study design is Ecological
Study.
• Bias associated with Cohort's study are Selection,Confounding,Interviewer's and Attention
Bias(Hawthorne Effect)
• Relative Risk is a direct measure of strength of the association between the suspected cause and
effect.
• Attributable risk indicates to what extent the disease under study can be attributed to the
exposure.
• Example-In a cohort study nonsmokers were found to have carcinoma lung. This indicates that
Etiology for lung Ca is multifactorial.
• Several possible outcomes related to exposure can be studied simultaneously in a Cohort Study.
• Cohort Study is a Study of risk factor associated with multiple diseases.
• Cohort Study involves large number of people and is expensive.
• Cohort Study is unsuitable for investigating uncommon diseases or diseases with low incidence.
• Cohort Study takes a long time to complete the study and obtain results.
• Differential loss to follow up which can introduce bias is one of the major practical problem in a
cohort study.
• Outcome has not yet occurred when the study has begun: Only exposure has occurred-It is called
Prospective or Concurrent or Current Cohort Study.
• Framingham Heart study is a type of Cohort Study.
2. Asbestosis
• Asbestosis is asssociated with lung cancer and Ascites.

• Asbestosis is associated with extensive pleural thickening and calcification especially involving the
diaphragmatic pleura.
• Ferruginous bodies are commonly seen in Asbestosis.
• Asbestosis is associated with the following pulmonary manifestations: Mesotheliomas
,Pneumoconiosis,Calcified pleural plaques , Diffuse pulmonary interstitial fibrosis,Progression of
lesion even after stopping exposure to asbestos ,Honeycombing,Basal peribronchial fibrosis,
Asbestos bodies in sputum,Nodular lesions involving lower lobe.

• There are six types of asbestos; one is serpentine (chrysotile) and five are
fibrous amphiboles (amosite, crocidolite, anthophyllite, tremolite, and actinolite).
• The most likely diagnosis in a 35 year old roofer presenting with complain of dyspnea and chronic
dry cough and Chest x-ray revealing pulmonary hyperinflation with "honeycombing" and calcified
parietal pleural plaques is Asbestosis.
• The probable diagnosis in a 48 years old man, resident near a textile mill presenting with
respiratory symptoms, X Ray chest showing - fine reticular & nodular pattern in lower zone with
loss of clarity of diaphragm & cardiac shadows and the presence of small pleural effusion is
Asbestosis.
• Asbestosis does not usually appear until 5-10 years of exposure.
• Asbestosis may be associated with peritoneal Mesothelioma.
• Asbestosis and smoking act synergistically to cause lung cancer.
• Asbestosis is a notifiable disease under Factory's act 1948 in India.
• Asbestosis causes shaggy heart borders.
3. Odd's Ratio
• In a study done to establish Smoking as a risk factor for a disease, 30 out of 50 smokers developed
the disease while 10 out of 50 non-smokers developed the disease. Odd's ratio is 6
• Odds ratio is related to Relative risk
• Odds = Probability/(1-probability)
• Using case control study only odds ratio can be calculated.
• Association can be measured by odds ratio
• In a case control study, the most characteristic feature is odd's ratio
• Odds ration is designated as ad/bc
4. Biomedical waste management
• Human anatomical waste is disposed by Incineration.

• Human Anatomical Waste is disposed in a Yellow bag
• Contents from a Red bag may be a source of contamination
• Black bags are used for disposal of ash from incineration
• Hospital waste product accounts Plastic 10%,
• Amount of waste infectious produced in hospitals 45%
• Average hospital waste produced per bed per day in Government hospital 0.5-4 kg
• Biomedical waste(s) to he discarded in Yellow are Category I (Human anatomical
waste), Category 2 (Animal waste), Catagory 3 (Microbiology and Biotechnology waste), and
Catagory 6 (Solid waste).
• Best for Incineration of infectious waste is Double - chamber
• Halogenated plastic, Mercury,Radiological waste & waste sharp cannot be incinerated
• Disposal of expired & cytotoxic drugs is by Separate land fill disposal
• The majority of the waste produced by health-care providers is General waste
• Sharp instruments like needles, syringes, scalpels hospital waste products are thrown in Blue bag
• Human anatomical waste is the category I of biomedical waste in India
5. MILLENNIUM DEVELOPMENT GOALS
• Proportion of children underweight, Proportion of population using biomass fuel & Tuberculosis
morbity and mortality are part of MDG
• According to Millennium development goals Targets to be achieved by 2015
• In Millennium Development Goals (MDGs),3 out of 8 goals are health related
• Millennium development goals aim to reduce MMR by 3/4
• Eradication of extreme poverty, Global partnership for development, Sustainability of the
environment, Reducing child mortality comes under Millennium Development Goals (MDGs)
• Total number of goals in the Millennium Development Goals are 8
• MDG was adopted by UN 2000
• Reduce by 2/3" the tinder five mortality by year 1990-2015 MDG
• Number of children orphaned by HIV/AIDS, Prevalence and death rates of tuberculosis
& Prevalence and death rates of malaria comes under indicators of goal 6 of Millennium
Development Goal
• In Target 10 of Goal 7 of Millennium Development Goal, “access” to an improved water source
mean Availability of at least 20L water / person/ day from a source within 1 km of dwelling
• Millennium developmental goal for HIV/ AIDS is 6
6. Levels of Health Care
• Principles of primary health care Equitable distribution, Community participation, Intersectoral

coordination & Appropriate technology
• Provision of Essential Drugs, Immunization against major infectious diseases & Health education
are essential component of primary health care
• Community Participation is the current trend in Health Care
• Dependency ratio,Rate of population increase, Literacy rate, Level of unemployment, Family size,
Housing ,Per capita GNP are socio economic indicator of health care
• Alma - Ata Declaration is associated with the provision of Primary Health care
• Primary health care in India is a 3 tier structure
• A good indicator of the availability, utilization and effectiveness of health care services in a country
is DALY's
• Example of "deprofessionalization" of medicine widely seen in India as Primary health care
practices
• The degree to which a specific health care intervention achieves its objectives, w hen applied in a
given population, is termed as its Effectiveness
• Primary Health Care includes Treatment is done by a doctor
• Primary health care is Essential health care for all
• Primary health care is Placing people's health in people's hands
• Primary health care is Sectors like agriculture, animal husbandary. food, industry & communication
are involved
• Elements of primary health care include Adequate supply of safe water and basic
sanitation, Providing essential drug & Health Education
• Under the Primary health care, Multipurpose health workers are present at the subcentre level
• A primary health care center should provide Treatment of common diseases, Immunization
& Family planning services
• Alma-Ata declaration Was held in 1978
• Alma-Ata declaration emphasizes on the need for "individual and community participation"
• Alma-Ata declaration Health for all
• Highest level of health care system in India Tertiary health care
• Most basic level of Health Care System in India Primary health care
7. ICEBERG PHENOMENON
• Infectious disease showing iceberg phenomenon are Rubella, Influenza, Polio, Japanese
encephalitis, Mumps , Hepatitis A and B & Diphtheria
• An infectious disease shows iceberg phenomenon. That means it has More subclinical case
• Demarcation line in iceberg disease is between Apparent and inapparent cases
• According to the concept of iceberg phenomenon of disease It includes sub-clinical cases, carriers
& It constitutes undiagnosed reservoir of infection
• Iceberg phenomenon differentiates Apparent and inapparent
8. Vaccines and Vaccination
Meningococcal vaccine:
• The vaccine for meningococcal meningitis is ineffective in children < 2 years old .
• Vaccines are available for group A, C, Y and W-125. There is no group B vaccine available at present.
• Meningococcal vaccines should be stored at 2-8° C.
• Vaccine for meningococcal meningitis should be routinely given to young adolescents.
• Bivalent meningococcal vaccine is is AC.
Rabies:
• Recombinant glycoprotein vaccines (Subunit vaccines) for Rabies are still in experimental Stage.
• Following rabies vaccines are commercially available : Killed sheep brain vaccine, Human diploid cell
vaccine , Vero continous cell vaccine.
• Recommended vaccines for rabies is HDCV.
• Chick fibroblast anti-rabies vaccine has been recommended by WH.
• Neurological complications following Rabies vaccine is common with Semple Vaccine.
• Fixed virus is used to produe rabies vaccine.
• In rabies, human diploid cell culture vaccine for post-exposure vaccination is given on 0, 3, 7, 14, 28
then booster dose 90 days.
• Schedule of intradermal rabies vaccine is 8-0-4-0-1-1.
• Number of doses of HDCV vaccine required for preexposure prophylaxis is 3.
• Site for injection of cell culture rabies vaccine is Deltoid.
• It an cause adverse effects in persons with allergy to egg ,
Rota virus:
• Best vaccine for rotavirus infection is Genetic Reassortment.

• Contraindication of rota virus vaccine is SCID , Intussusception , Severe allergic raction
Hepatitis B:
• Risk of HIV transmission is not seen with plasma derived hepatitis B vaccine.
• Hepatitis B vaccine should be given as per which schedule at 0,1,6 months.
• Hepatitis B vaccine is a killed 'inactivated' vaccine
Live vaccines:
• Live Vaccines should be avoided in the long-term follow-up of a renal transplant recipient on
ciclosporin.
• Two live vaccines can be administered simultaneously..
• Booster doses are not required when live vaccines are administered.
• Single dose of live vaccine gives life long immunity.Live vaccine contains both major and minor
antigens.
• Live, attenuated virus and live bacterial vaccines generally are contraindicated during pregnancy.
• Minimum interval between 2 live vaccine immunization is 4 weeks.
Examples of Subunit vaccines are:
• Meningococcal vaccine from cell wall polysacchlaride

• Pneumococccal vaccine from Capsular polysaccharide
• Hepatitis B polypeptide vaccine
• Typhoid vaccine from Vi polysaccharide
• H. Influenza vaccine from capsular polysaccharide.
BCG vaccine :
• It is a live attenuated vaccine

• It has no preservative at all .
• WHO recommends Danish 1331 strain for vaccine production.
• BCG vaccine is diluted with normal saline.
Polio vaccines:
• Two types of vaccines are used throughout the world :?Inactivated (salk) polio vaccine (IPV)
and Oral (sabin) polio vaccine (OPV)
• In OPV, the vaccine potency is stabilized with molar magnesium chloride or sucrose..
• IPV:Given in 4 doses,Being an inactivated vaccine, it can be given to immunosuppressed individuals,
e.g. AIDS patients,Produces circulatory antibody,Does not require stringent refrigeration,Not
effective in an epidemic,Does not provide Immunity against paralytic and wild strains ,It prevents
paralysis,Easily transported,Oral polio can be given as booster.
• Trivalent oral polio vaccine contains:
i) Over 300,000 TCID 50 of type 1 poliovirus
ii) Over 100,000 TCID 50 of type 2 poliovirus
iii) Over 300,000 TCID 50 of type 3 poliovirus.
• OPV bivalent vaccine contains type 1 and 3 viruses.

• Being living viruses, the vaccine viruses, particularly type 3 do mutate in the course of their
multiplication in vaccinated children, and rare cases of vaccine associated paralytic polio have
occured in -Recipients of the vaccine and their contacts.
• Maintenance of cold chain.
• 5 doses of OPV given.
• Killed vaccine is effective in India.
• OPV:Stored at Sub-zero temprature,Intestinal & humoral immunity,Main problem is residual neuro-
virulenceoor growth in stable cell line of monkey kidney,
• OPV was discovered by Albert Sabin (Sabin vaccin). IPV was discovered by Jonas Salk (Salk
vaccine).
• As it prevents heat inactivation mgCl2 can be added to polio vaccine so that it can be stored at a
higher temperature.
• In a epidemic of poliomyelitis, the best way to stop spread is by OPV drops to all children.
• Reverse cold chain is used for Carrying stool samples of polio patients from MC to lab .
• The efficiency of cold chain system for oral polio vaccine as monitored by Vaccine Vial Monitor
(VVM) depends on Change in Colour of Monitor.
• Vaccine Vial Monitor:
• Colour of central square Lighter than ring --Can be used
• Colour of central square Same or darker than ring Discard.
DPT vaccine:
• Thiomersal is preservative in DPT vaccine.

• Aluminium salt has an adjuvant effect in DPT vaccine.
• Whole killed bacteria of Bordetella pertusis has an adjuvant effect in DPT vaccine.
• Presence of acellular pertusis component in DPT vaccine.
• DPT vaccine should not be given to a child suffering from convulsions.
• DPT vaccine must be stored in cool part of a freeze (at 4-8°C) but not in freezer.
• Exposure to direct sunlight should be avoided.
• Open multi-dose vials which have not been fully used should be discarded at the end of session.
• The adjuvant used is Al.
• The peripheral workers in a primary health centre return one day late; after an immunisation
session. The primary health centre is locked. The vaccine carrier still contains a few unopened vials
of DPT vaccine and sufficient ice. The workers are to retain the vaccine in the ice-box.
• Prevent development of carrier
Measles:
• Usually there is no preservative in measles vaccine, though it may contain very small amounts of
Kanamycin, neomycin or erythromycin..
• Measles vaccine given to contact of measles case exerts protective effect within 7 days.
• In measeles vaccine can be given within- 6 months.
• MMR is a type of live attenuated vaccine.
• Can cause TSS.
• Contraindicated in neomycin allergic patients.
• In epidemics measles vaccine is to be given within 3days of exposure.
• Encephalopathy can occur as complication
At PHC level vaccine storage is by IRL.
Chicken pox vaccine:
• It is a live vaccine.
• OKA strain is used to produce vaccine for Chicken Pox.
Rubella vaccine is given in 1-14 years age .
Newer Influenza vaccine are Split-virus vaccine & Neuraminidase.
Cholera Vaccine:
• It is WC-r BS.
• Oral cholera vaccine is effective for 3 years.
Typhoid:

• For a typhoid endemic country like India, the immunization of choice is Typhoral 21 A oral vaccine.
• Typhoid oral vaccine is given at 1,3,5 days.
The Vi polysaccharide vaccine can be co-administered with other vaccines relevant for international
travelers.
Yellow fever vaccine :
• In India is produced at- Central research institute,Kasauli.

• It is contraindicated in pregnancy.
• SA-14-14-2 Japanese Encephalitis vaccine - is a Cell culture derived live attenuated vacine.
• Pneumococcal vaccine is most effective when given preoperatively.
• German measles (rubella) need not be given to boys.
• After reconstitution, the vaccine must be stored in the dark at 2-8 degree C and used within: 6
hours.
• Term vaccine was coined by Louis Pasteur.
Refrigerator:
• Deep freezers are used for making ice packs and to store OPV and measles vaccines.
• Vaccines which must be stored in cold part but never allowed to freeze are: typhoid, DPT, Tetanus
toxoid, DT, BCG, and diluents.
• Polyvalent snake vaccines contains immunoglobins against : Naja naja , Daboia rusellii , Bungarus
caeruleus.
• Bivalent HPV vaccine contains types 16,18.
• Mumps vaacine efficacy is 95%..
• Hepatitis A:
• Both live and inactivated for Hepatitis A.
• Recomended at age of 12 months.
• 2 dose of killed vaccine 6 months apart.
• 1 dose of live vaccine
• Intramuscular is is the route of administration of avian influenza vaccine.
• Children should receive Influenza vaccine at 2 doses at one month interval with one booster dose
later.
• Fundamental aspects of disaster management include disaster mitigation, disaster preparedness,
and disaster response.
• Rehabilitation,reconstruction and response are is seen in recovery phase after disaster.
• Vaccines recommended in disasters
• Following vaccines are recommendedVaccination against typhoid and cholera is not recommended.
1) Children < 10 years :- DPT, inactivated polio (IPV), H.influenzae type b (Hib), hepatitis B, pneumococcal
conjugate vaccine (PCV), measles-mumps-rubella (MMR), varicella vaccine, influenza, hepatitis A and
rotavirus.

2) Children and adolescents (11-18 years):- Tetanus, diphtheria, pertussis, meningococcal conjugate
vaccine (MCV), Influenza.
3) Adults (>18 years):- Tetanus, diphtheria, pertussis, pneumococcal polysaccharide

vaccine (PPSV23), and influenza.
• Hydrological disasters (i.e. floods, tsunamis) are associated with causing maximum death toll.
• Control room is is the nodal centre for disaster management.
• Disease common in Post-disaster Phase
• Gastroenteritis (MC) ,Acute respiratory tract infections (Pneumonia) , Leptospirosis ,Rickettsiosis
,Rabies ,Equine encephalitis.
• The 4 triage categories (with corresponding color codes), in precedence, are:
• Black indicates dead,
• Red indicates that the patient needs immediate attention,
• Green indicates that a patient has only minor injuries.
• Yellow signals medium priority
• A natural disaster is a major adverse event resulting from natural processes of the Earth; examples
include floods, volcanic eruptions, earthquakes, tsunamis, and other geologic processes.
• Accidental radioactive gas leak from factory is most commonly a result of human or mechanical
error and thus not a natural disaster.
9. Disaster Management
• Fundamental aspects of disaster management include disaster mitigation, disaster preparedness,

and disaster response.
• Rehabilitation, reconstruction and response are is seen in recovery phase after disaster.
Vaccines recommended in disasters
• Following vaccines are recommendedVaccination against typhoid and cholera is not recommended.
• Children < 10 years:- DPT, inactivated polio (IPV), H.influenzae type b (Hib), hepatitis B,
pneumococcal conjugate vaccine (PCV), measles-mumps-rubella (MMR), varicella
vaccine, influenza, hepatitis A and rotavirus.
• Children and adolescents (11-18 years):- Tetanus, diphtheria, pertussis, meningococcal conjugate
vaccine (MCV), Influenza.
• Adults (>18 years):- Tetanus, diphtheria, pertussis, pneumococcal polysaccharide vaccine (PPSV23),
and influenza.
• Hydrological disasters (i.e. floods, tsunamis) are associated with causing maximum death toll.
• Control room is is the nodal centre for disaster management.
Disease common in Post-disaster Phase

• Gastroenteritis (MC) ,Acute respiratory tract infections (Pneumonia) , Leptospirosis ,Rickettsiosis
,Rabies ,Equine encephalitis.
The 4 triage categories (with corresponding color codes), in precedence, are:
• Black indicates dead,

• Red indicates that the patient needs immediate attention,
• Green indicates that a patient has only minor injuries.
• Yellow signals medium priority
• A natural disaster is a major adverse event resulting from natural processes of the Earth; examples
include floods, volcanic eruptions, earthquakes, tsunamis, and other geologic processes.
• Accidental radioactive gas leak from factory is most commonly a result of human or mechanical
error and thus not a natural disaster.
10. Incubation period
• Time interval between invasion of the infection agent and appearance of first sign or symptom is
Incubation period.
• Incubation period is useful for : -
• Tracing the source of infection and contacts.
• Period of surveillance or quarantine
• Immunization
• Identification of point source or propagated epidemics
• Estimating the prognosis of a disease.
• As a rule, infectious diseases are not communicable during the incubation period, but there are
exceptions, for example, measles, chickenpox, whooping cough (pertusis) and hepatitis A are
communicable during the later part of incubation period.
• Epidemiological studies is carried for a period of twice the incubation period.
• Characteristic of a point source epidemic is that all cases develop within one incubation period.
• Prognosis of a disease can be given by- Incubation Period.
• In control of communicable diseases, the period of quarantine in respect of a disease is determined
by Incubation period.
• Incubation period of new disease determined by?Generation time.
• Leprosy is not targeted for global eradication because of Long incubation period.
• Shortest incubation period is seen in: Influenza.
• Incubation period of influenza is 18-72 hours.
• Incubation period of swine flu is 1-3 days.
• Incubation period of rubella is 2-3 weeks.
• Incubation period of typhoid is 3-20 days.
• The incubation period of yellow fever is 3-6 days.
• Incubation period of Hepatitis A is 2 to 4 weeks.
• Incubation period of staphylococcus aurues food poisoning is 1-6 hours.
• Incubation period of Cholera: few hours upto 5 days
• Shortest incubation period is for food poisoning from Bacillus Cereus.
• Following are used as proxy measures for incubation period: Latent period ,Serial interval ,
Generation time.
• Incubation period of plasmodium vivax is 10-14 days.
• Incubation period of chancroid is < 7 days.
• Incubation period of Diptheria is 2-5 days.
• The usual incubation period of pertusis is 7-14 days.
• Incubation period of syphilis is 10-90 days.
• Incubation period of measles is 10 days.
• Average incubation period of AIDS is 10 years.
• Incubation period of gonorrhoea is 2-8 days.
• In leptospirosis, the incubation period ranges from 2 to 20 days.
• In rabies,Incubation period depends on the site of bite,number of bites,animal species.
• Incubation period of HBV is 45 to 180 days.
• There is long incubation period in prion disease.
• Incubation period of scabies is 4 weeks.
Incubation period for B.cereus:
• Incubation period of emetic type of food poisoning 1-5 hours

• Incubation period of diarrheal type of food poisoning 8-16 hours.
• The incubation period of gas gangrene depends upon the causative organism :
• Cl. Perfringens 10 - 48 hrs (1 to 2 days)
• Cl. septicum 2 - 3 days
• Cl. novyi 5 - 6 days.
Incubation period of Clostridium Tetani is 6-10 days.
Incubation period of salmonella typhi is 3-21 days.
• The limitation of movement of well persons or animals exposed to communicable diseases for a
period usually not longer than the longest incubation period is known as Quarantine.
11. International Health Agencies
Content of services of UNICEF:

• Child health
• Child nutrition
• Fanmily and child welfare
• Education (formal and non-formal)
UNICEF promotes GOBI campaign for a child health revolution.
It consists of:
• G: using growth charts for monitoring child development

• O: oral rehydration therapy to treat dehydration
• B: breastfeeding
• I: immunization
International Classification of Disease was devised by WHO.
As per the World Health Organisation guidelines, iodine deficiency disorders are endemic in a community if
the prevalence of goiter in school age children in more than 5 %. The world health organisation day is 7th
April.
United nations agencies (other than WHO)
• UNICEF (United nations international children's emergency fund).

• UNESCO
• FAO (Food & agriculture organization)
• UNDP (United nation development Programme)
• ILO (International labour organization)
• UNFPA (UN fund for population activity).
The headquarters of UNESCO is in Paris,WHO- Geneva. UNICEF- New york, FAO- Rome.
UNDP is an international agency which works for Development or human & natural resources in a country
.
World Bank :
• It gives loan for economic Growth.

• Assessment and aiding for development of funds for the National Blindness control Programme is
done by World Bank.
• The eye condition for which the World bank assistance was provided to the National Programme
for Control of Blindness is Cataract.
• The organization concerned with improving the working and living conditions of the working
population all over the world is ILO.
Regarding Baby-friendly UNICEF plan,

• Mother and child are left together 24 hours a day.
• Feeding on demand.
• No food/water given other than breast milk.
• Feeding is started within 1/2 hour of normal vaginal delivery and within 4 hours of Caesarean
section.
12. ESI act
• Sickness benefit under the ESI act consists of periodical cash payment to an insured person in case
of sickness. The benefit is payable for a maximum period of 91 days in any continuous period of 365
days, the daily rate being about 505 of daily wages.
• Under the ESI act, an insured woman is entitled to maternity benefit for 12 weeks in case of
confinement, 6 weeks for miscarriage, 30 days for sickness arising out of confinement.
• The Employees State Insurance (ESI) Act act passed in 1948
• Educational institutions are also included under ESI scope.But it is included only in some states and
there should be 20 or more employed persons
• ESI act does not cover railway
• The scheme is run by contribution by employees and employers and grants from central and state
governments?
• Employers contribution → 4.75% of total wages bills
• Employee contribution → 1.75% of total wages bills
• The state government's share of expenditure on medical care is '/8 of total cost of medical care.
13. Case Control Study
• Direction of Case control study is reverse but time is forward .

• Case control study is Retrospective.
• Recall bias is most commonly associated with case control study design.
• Bias associated with Case-control study:
• Selection
• Confounding
• Recall bias
• Berkesonian bias
• Interviewer's bias.
• Nested case control study is a type of prospective Study.
• As compared to a routine case control study, nested case control study avoids problems (in study
design) related to temporal association.
• Case control study is used for study of rare diseases.
• Using case control study only odds ratio can be calculated.
• Incidence rates, relative risk and attributable risk can be calculated using cohort study.

• Case control study is inexpensive, easy to carry out, used to investigate rare diseases, used to
identify risk factors, allows study of different etiological factors and is associated with minimal
ethical problems.
• Case control study proceeds from the effect to cause.
• Those with disease and not diseased compared in Case control study.
• In a case control study, the most characteristic feature is Odd's Ratio estimation.
• Risk in case control study is calculated by odds ratio (cross product ratio).
• In a case controlled study. It is found that the disease is more common in the group taking coffee as
compared to the control group. The significance of this is Caffeine is associated with occurrence of
disease.
Case-control study can only tell the association between cause and effect.
• In a case control study on smoking and lung cancer, out of 35 lung cancer patients, 33 are smokers.
Out of 82 controls, 27 are non smokers. The odds ratio is 8.1.
• Important risk factors and their outcomes/diseases which have been studied by case-control study
are :-
• Cigarette smoking and lung cancer.
• Maternal smoking and congenital malformation.
• Radiation and leukemia.
• OCP used and hepatocellular carcinoma.
• Herpes-simplex and Bells palsy.
• Artificial sweeteners and bladder cancer.
• DES exposure in fetal life and vaginal adenocarcinoma.
• OCP use and thromboembolic disease.
• Thalidomide use in pregnancy and teratogenicity.
• Matching is method to eliminate confounding bias. It is used in Case Control Study.
14. Randomized Controlled Trial
About Randomized Controlled trial:
• Baseline characteristics are comparable

• Bias can be eliminated by double blinding.
• Sample size depends on the type of study.
• Clinical trials.
• the essential purpose of randomization is to eliminate selection bias.
• Most important factor which decides the results of a randomized controlled trial is effective
randomization.
Types of randomized controlled trials:
• Clinical trials
• Risk factor trials
• Trial of etiological agents
• Preventive trials
• Cessation experiment
• Evaluation of health services
15. Human and Cow milk
In a neonate with inadequate breast milk intake the weight loss is more than 8-10%.
• Other signs of inadequate breast milk intake are: Less than six noticeably wet diapers per 24 h by
day 3–4 ,Less than four stools per day by day 3–4 ,Nursing less than eight times per 24 h.
•
• The protective effects of breast milk are known to be associated with IgA antibodies.
• Most common immunoglobulin secreted by mother in milk and colostrum is IgA.
• Para amino benzoic acid of breast milk prevent the infection of Plasmodium Vivax.
• Breast milk contains several antiinfective factors -
• Antibodies secretory IgA, IgM
• Lysozyme
• Antistaphylococcal factor
• Specific inhibitory substances against viral infections.
• Lactoferrin Inhibits growth of E. coli.
• Bile stimulated lipase kills entamoeba histolytica and Giardia lamblia.
• Bifidus factor -4 Inhibits growth of E. coli
• Para-amino-benzoic acid (PABA) - Provides protection against malaria
• Phagocytic macrophages and lymphoid cells
Under normal conditions breast milk production reaches a maximum when the baby is around 4 - 6
months.
Colostrum:
• Compared with mature milk, colostrum contains more minerals and amino acids. It also has more
protein, much of which is globulin, but less sugar and fat.
• It also contains antibodies, and its content of immunoglobulin A (IgA) offers the newborn
protection against enteric pathogens.
• Other host resistance factors found in colostrum and milk include complement, macrophages,
lymphocytes, lactoferrin, lactoperoxidase, and lysozymes.
Milk ejection occurs in response to a surge of oxytocin, which induces a contractile response in the smooth
muscle surrounding the gland ductules.
Fatty acid found exclusively in breast milk is Docosahexanoic acid.
Cow Milk:
• Whey protein constitutes 80% of the protein in human milk, while the main protein in cow's milk is
casein.
• Has more K+ and Na' than infant formula feeds.
• Has more protein than breast milk.
• Compared with Cow's milk, mothers milk has more lactose.
• Human milk has less fat, less protein, more carbohydrates and less calcium, in comparison to cow
milk .
• Cow's milk contains 3.2 % proteins.
• Percentage of lactose in human milk is 7.0 gm.
• Calcium in human milk is 35 mg/dl
• Hind milk is richer in fat.
Breast milk:
• Can be stored at room temperature For 8-10 hours

• In a refrigerator For 24 hours
• In a freezer -20°c for 3 months.
• Breast milk transmits (with definitive evidence) 1) HIV , 2) CMV
• Breast milk can rarely transmit 1) HTLV - type 1 ,2) Rubella virus ,3)HBV , 4) HSV.
• Premature milk contains less lactose in comparison to term milk.
• The coefficient of uptake of iron in breast milk is 70%.
• Calcium absorption of human milk is better that that of cow's milk.
• The milk of human contains the least amount of calcium.
• Human milk gives 67 kcal per 100 ml .
• Protein forms 8-10% of total energy.
• Carbohydrate forms 3 8-40% of total energy.
• Fat forms 50-52% of total energy.
• Breast milk protein is a reference protein.
• Vitamin K is absent in breast milk.
• Milk is a poor source of Vitamin C.
• Vitamin not present in breast milk is Vitamin B.
• According to WHO, exclusive breast milk is given upto 6 months.
• Fat content of milk: Buffalo > Goat > Cow > Human
• Protein content of milk: Buffalo > Goat > Cow > Human
• Lactose content of milk: Human > Buffalo > Goat > Cow
• Energy content of milk: Buffalo > Goat > Cow > Human.
• Clonazepam antiepileptic drug is least secreted in breast milk.
• Protein content in F-75 milk formula is 0.9 gm/100 ml.
• Average daily breast milk output during first 6 months is 500-600 ml.
16. Sampling

• Sampling error is classified as Alpha and Beta Error.
Simple random sampling:
• It is ideal for Homogeneous Population.

• In simple random sampling, the samples are taken completely at random from a given population.
• Every element in the population has an equal probability of being included.
• Haphazard collection of certain number for a sample
Stratified Sampling.
• The method in which the sample is taken from each predefined strata of society is called Stratified
Sampling.
Systemic sampling:
• samples are taken according to a predetermined periodicity.

• the units are picked up at regular intervals from the universe in Systematic random sampling.
• People are arranged alphabetically by their names and then every 3rd person is chosen for study.
The type of sampling is Systematic Random.
Random Sampling:
• In random sampling chance of being picked up is Same and known.

• If sample size is bigger in random sampling ,then it decreases standard error.
Types of random sampling are :
• Simple random sampling

• Systematic random sampling
• Stratified random sampling
• Cluster random sampling
• Multiphase random sampling
• Multistage random sampling.
Types of non-random sampling are.
• Quota sampling
• Volunteer sampling
• Convenience sampling
• Snowball sampling
In multistaged sampling,

• The researcher randomly selects elements from each cluster instead of using all the elements
contained in the selected clusters.
• For Randomized Control Trial (RCT) to assess dating in adolescent, a study was done by selecting
random schools, then random classes, then random sections and then random students.
Stratified Random Sampling.:
• For a survey a village is divided into 5 lanes then each lane is sampled randomly is an example of
Stratified Random Sampling.
• In stratified random sampling, the population is divided into strata.
• Type of sampling, if random sample is taken from a characteristic population, eg. Hindus, Muslims,
Christians etc
Cluster sampling:
• it is a two-stage sampling.
• it is cheaper than other methods of sampling
• it has the disadvantage of higher sampling error.
• Children surveyed in cluster sampling for coverage of national immunization programme is 30
cluster of 7 children.
• A region is divided into 50 villages for the purpose of a survey. 10 villages are then selected
randomly for the purpose of a study. This type of sampling is termed as Cluster Sampling.
• Cluster sampling is cost effective.
• Is a Rapid and simple method.
• It is a type of probability sample.
• The sample size may vary according to study design.
• Estimation of percentage of children immunized in community as per WHO is to be done by Cluster
Sampling.
• In the WHO recommended EPI Cluster sampling for assessing primary immunization coverage, the
age group of children to be surveyed is 12-23 months.
• Design Effect' is associated
• Snowball sampling is used for hidden population
17. ASHA
ASHA(Accredited Social Health Activist) is the central component of the National Rural Health Mission
(NRHM):
• One per 1000 rural population

• Mobiliser of antenatal care
• Female voluntary worker.
• The ASHA is employed in the rural area at the village level.

• Under Janani suraksha yojana Scheme, amount of financial incentive to ASHA per institutional
delivery in low performing state is 200 Rs.
• Angan-Wadi Workers (AWW) and Auxiliary Nurse Midwife (ANM) act as resource persons far
training of ASHA.
• Infant Mortality rate is the best indicator to assess the impact of ASHA.
• ASHA gets remuneration on: Institutional delivery, Recording birth weight, Birth registration.
• Informs about birth and deaths in her village to PHC.
• Local resident.
• Preferably in the age group of 25-45 years.
• Formal education up to eighth class
Monitoring and evaluation of ASHA's work
1. Process Indicators:
• Number of ASHAs selected by due process

• Number of ASHAs trained
• % of ASHAs attending review meeting after one year
2. Outcome Indicators:
• % of newborn who were weighed and families counselled

• % of children with diarrhoea who received ORS.
• % of deliveries with skilled assistance
• % of institutional deliveries
• % of JSY (Janani Suraksha Yojna) claims made to ASHA.
• % of completely immunized in 12-23 months of age group
• IMR% of unmet need for spacing contraception among BPL
• % of fever cases who received chloroquine within the first week in malaria detected area.
3. Impact Indicators:
• Child malnutrition rates

• Number of cases of TB /Leprosy detected as compared to previous year.
18. National Rural Health Mission And IMNCI
• The National Rural Health Mission (NRHM) was launched on 12th April 2005
• INcludes
• Reduction in IMR and MMR by 50% from existing levels in 7 years
• Integrating vertical Health and Family Welfare programmes at National, State, Block, and District
levels.
• Accredited Social Health Activists (ASHA)-Recruitment & training
• formulation of state and district health programme
• Promotion of Rogi Kalyan Samiti
• NRHM aims at mainstreaming the Indian systems of medicine to facilitate healthcare
• Including posting of anaesthetists in CHC
• Integrated Management of Neonatal and Childhood Illness (IMNCI) includes
• Diarrhea, Malaria, Malnutrition, ARI (Pneumonia, Otitis media), Measles.
19. Lathyrism
Lathyrism
• Neurolathyrism (NL) is a neurodegenerative disease that is caused by heavy consumption of grass

pea, Lathyrussativus.
Toxin
• The pulse contains the neurotoxin called b-N-oxalyl-a,b-diaminopropionic acid (b-ODAP).[Synonym

b-oxalylaminoalanine(BOAA)
20. Mortality rates
• In a certain population, there were 4050 births in the last one year. There were 50 still births. 50
infants died within 7 days whereas 150 died within the first 28 days. Neonatal mortality rate is 50.
• Perinatal conditions like low birth weight is the commonest cause of IMR (20%). It is followed by
acute respiratory infection (19%), Diarrhoea (15%). Underlying malnutrition is present in 46% in
India.
• The socioeconomic status of community is best indicated by IMR.
• Maternal mortality rate:
• The numerator of the rate includes the total number of female deaths due to complications of
pregnancy, childbirth or within 42 days of delivery from puerperal causes in a particular area during
a given year.
• The denominator includes the total number of live births in a particular area during a particular
year and not the number of stillbirths and abortions.
• Perinatal Mortality rate includes: still borns and death within 7 days of birth.
IMR in India : 57/1000 live births
U5MR in India : 74/1000 live births.

• A community has a population of 10,000 and a birth rate of 36 per 1000. 6 maternal deaths were
reported in the current year. The Maternal Mortality Rate (MMR) is 16.6.
• The comparison of mortality rates between two countries requires the application of direct
standardization. Age distribution parameters makes it necessary to have standardization.
• A good indicator of the availability, utilization and effectiveness of health care services in a country
is IMR.
• The simplest measure of mortality is the crude death rate.
• Proportional mortality rate is Number of death due to particular a cause.
• Crude Mortality rate should be adjusted for age to allow comparisons.
• Death rates of two countries are best compared by standardised mortality rate.
• Age standardised death rate is used to compare the death rates of two different populations.
• In a certain population, there were 4050 births in last one year. There were 50 still births. 50 infants
died within 7 days where as 150 died within 28 days.Neoonatal mortality rate is 50.
• Babies included for perinatal death statistics should have the following features :
a. birth weight above a minimum of 1000 gm.
b. If birth weight is not available a gestation period of at least 28 weeks
c. Where (a) and (b) are not available body length (crown-heel) at at last 35 cm . should be used.
• Almost 3/5' of infant mortality rate (IMR) occurs in neonatal period.

• Almost 3/4' of the under-five mortality occurs in the first year.
• Neonatal mortality is higher among female children as compared to males.
• Major cause of infant mortality rate in India is Immaturity.
• You were posted at a PHC catering to a population of 1,20,000. In the year 2006, a total number of
2500 liver born babies were delivered. Number of children dying under one year of age during 2006
was 150. The infant mortality rate of this population is 60.
• IMR is the best indicator to assess the impact of ASHA.
• Numerators in 'natal' death
• Perinatal death includes late foetal deaths (28 weeks of gestation and more) + early neonatal
deaths (1st week)
• Early neonatal death occurs between births to first 7 days of life
• Late neonatal death occurs between 7th days of life till 28th day of life
• Post-neonatal deaths occurs between 28th day of life till 1 year.
IMR = Number of deaths of children less than 1 year of age in a year X 1000/number of live births in the
same year.
• The maternal mortality rate is the number of maternal deaths due to childbearing per 100,000 live
births.
• The crude death rate is the total number of deaths per year per 1000 people
• Infant Mortality Rate for Japan is 3.
• Mortality rates are taken into account while calculating Net Reproduction Rate.
• For international comparisons, perinatal mortality rate is calculated as late fetal deaths (28 weeks
gestation or more) plus early neonatal deaths (first week) [weighing over 1 kg at birth] in a year
per 1,000 live births [weighing over 1 kg at birth].
• Least neonatal mortality is recorded in Kerala.
• Proportional Mortality rate:It is defined as "number of deaths due to a particular cause (or in
specific age group) per 100 total deaths".
• Best indicator for burden of disease is Proportional mortality rate.
• Positive mortality indicator is Life Expectancy.
• In MCH programme, best indicator for mother and child health is IMR.
21. Disease causation
• In 1873 he proposed the germ theory of disease

• Epidemiological triad
• Agent
• Host
• Environment
Multifactorial causation
• Suggested by Pettenkofer of Munich
Web of causation
• Mac Mohan and Pugh

• Web of causation considers all predisposing factors or risk factors and their interaction
BEINGS Model Of Disease causation
• Preventable causes of disease

• B: Biological factors and behavioural factors.
• E : Environmental factors.
• I : Immunological factors.
• N : Nutritional factors.
• G: Genetic factors.
• S : Services, social, spiritual factors.
22. LEVELS OF PREVENTION
Primordial Level of Prevention:

• It is the prevention of the emergence or development of risk factors in countries or population
groups in which they have not yet appeared.
• Modes of Intervention:
• Individual Education
• Mass Education
• Primordial Level is Best level of prevention for Non-communicable diseases.
• Examples
• Control of tobacco (discouragement from adopting a harmful lifestyle)
Primary Level of Prevention:
• It is the action taken prior to onset of disease, which removes the possibility that a disease will ever
occur.
• Health Promotion:
• Health Education, Environmental modifications, Nutritional interventions, Lifestyle & behavioural
changes
• Specific Protection:
• Example
• Immunization
• Installation of sanitary latrines
• Provision of safe water
• Use of mosquito net
• Health education (cancer education) and specific protection (radiation protection) are primary
levels of prevention..
• Wearing a seatbelt will not prevent the collision but may lessen its effects. Thus it is secondary level
of prevention.
Secondary Level of Prevention:
• Early Diagnosis
• Treatment
• It is an important level of prevention for diseases like Tuberculosis, Leprosy and STDs.
• Examples
• Breast self exam
• Total mastectomy for breast cancer
• Cervical pap smear checking
Tertiary Level of Prevention:
• Disability Limitation:
• It 'prevents the transition of disease from impairment to handicap'.
• Rehabilitation
• Examples
• Tendon transplant in leprosy
• Physiotherapy in residual polio myelitisProvision of spectacles for refractive errors
23. Humam Development Index
• HDI is a composite index combining indicators representing three dimensions -
i) Longevity (life expectancy at birth)
ii) Knowledge (expected years of schooling (Earlier Adult literacy rate) and mean years of schooling,
i.e. Gross enrolment ratio)
iii) Income GNI per capita (Earlier it was real GDP per capita in purchasing power parity in US
dollars)
• Calculation of each dimension index:

• Actual value - Minimum value/Maximum value - Minimum value
• HDI is Geometric mean of 3 dimension indices = Ilife1/3 * I education 1/3* Iincome1/3
• Ranges from 0-1
• As for the year 2016, HDI for India stood at 0.624.
24. Epidemic Dropsy
• Epidemic dropsy is a condition caused by consumption of mustard oil contaminated with argemone
oil
• Active component of Argemone Mexicana is Sanguinarine.
Clinical features:
• Sudden. non-inflammatory, bilateral swelling of legs

• Disc-edema
• Diarrhoea
• Dyspnea
• There is an occurrence of erythematous matting & raised hemangiomas on the skin & mucous
membrane
• Glaucoma
• Peri-retinal haemorrhage
• Tortuous-retinal vessels
• Heart failure – may lead to death (5-50% mortality rate)

25. Aflatoxicosis
• Aflatoxins are produced primarily by filamentous fungi Aspergillus flavus and

Aspergillus parasiticus.
• B1 aflatoxin(most potent liver carcinogen)
• Long-term consumption of small doses causes liver tumours as these are potent carcinogens.
26. Endemic ascites
• Endemic ascites is caused by a hepatotoxin - pyrrolizidine alkaloid found in weed seeds

of Crotolaria (Jhunjhunia).
• Kusmi block of Sarguja district of Madhya Pradesh during the years 1973 and 1976
27. The Factories Act, 1948
• A maximum of 48 hours per week. not exceeding 9 hours per day

• Maximum working hours including overtime per week: 60 hours
• Minimum 500 cubic feet space per worker
• Prohibition of employment of children below 14
28. Mental Health Act
• 1987: Mental Health act of 1987(Indian psychiatric society)

• Mental Health Care Bill proposed in 2013
Objectives of Mental health Act:
• To ensure availability and accessibility of minimum mental health care for all in the foreseeable
future, particularly to the most vulnerable and underprivileged sections of population
• To encourage application of mental health knowledge in general health care and in the social
development'.
• To promote community participation in the mental health services development7
• Provisions of voluntary admission and admission on the reception orders were retained.
• Role of Police and Magistrate to deal with cases of wandering mentally ill.
• Guardianship and Management of properties of mentally ill.
• Provisions of penalties in case of breach of provisions of the Act

29. Reproductive and Child health programme,Janani Suraksha Yojana
JSY
• JSY is an abbreviation for Janani Suraksha Yojana. It is a new initiative by the RCH - phase II
(Reproductive and Child Health programme) which began from 1st April, 2005.
• Under Janani suraksha yojana Scheme, amount of financial incentive to ASHA per institutional
delivery in low performing state is 200 Rs.
• Benefit is awarded upto 2 live births.
• Janani Suraksha Yojana is applicable to poor women of low performing states for all births.
• The practices for preventing neonatal tetanus under JSY include clean hands, clean delivery
surface, clean cord care i.e. clean blade for cutting cord, clean cord tie and no application on cord
stump.
Reproductive and, Child Health (RCH) Programme
Essential Components
• Essential and emergency obstetric services

• 24-hour delivery services,
• Medical termination of pregnancy
• Control of reproductive tract infections (RTI) and sexually transmitted diseases (STD)
• Immunization, drug and equipment kit
• Essential newborn care
• Oral rehydration therapy
• Acute respiratory disease control
• Prevention and control of vitamin A deficiency and anaemia in children.
Districts are divided on the basis of-
• Crude Birth Rate and Female Literacy Rate.
30. Herd Immunity
• A herd immunity of over 70% is considered necessary to prevent epidemic spread, but some believe
that the critical level may be as high as 90%.
• Herd immunity refers to group protection beyond what is afforded by the protection of immunized
individuals
• It is affected by :
• The presence and distribution of alternative animal hosts
• Depends on clinical and subclinical cases
• Influenced by immunization
• In the case of tetanus, it does not protect the individual
• Herd immunity can be achieved by immunizing a population with a vaccine that interrupts
transmission
• The live virus in the vaccine can replicate in the immunized person and spread to other members of
the population
• The vaccine must prevent transmission of the virus as well as prevent disease.
Disease Herd Immunity threshold
Diptheria 85%
Measles 92-94%
Mumps 75-86%
Pertussis 92-94%
Polio 80-86%
Rubella 80-85%
Small pox 83-85%
31. Isolation
• "Isolation separates those who are already ill or infected from those who are not for the period of
communicability".
• For which diseases isolation is beneficial?
• Isolation has a distinctive value in the control of some infectious diseases, e.g.,
• diphtheria, cholera, streptococcal respiratory disease, pneumonic plague.
• Isolation is strictly recommended for pneumonic plague
• In some diseases where there is a large component of subclinical infection and carrier state, even
the most rigid isolation will not prevent the spread of disease, e.g.
• polio, hepatitis and typhoid fever.
31. Isolation
• "Isolation separates those who are already ill or infected from those who are not for the period of
communicability".
• For which diseases isolation is beneficial?
• Isolation has a distinctive value in the control of some infectious diseases, e.g.,
• diphtheria, cholera, streptococcal respiratory disease, pneumonic plague.
• Isolation is strictly recommended for pneumonic plague

• In some diseases where there is a large component of subclinical infection and carrier state, even
the most rigid isolation will not prevent the spread of disease, e.g.
• polio, hepatitis and typhoid fever.
• Periods of isolation recommended
Disease Duration of isolation

Chickenpox Until all lesions cursted; usually about 6 days after onset of rash
Measles From the onset of catarrhal stage through 3rd day of rash
German None , except that women in the first trimester or sexually active, non-
measles immune women in childbearing years not using contraceptive measures
should not be exposed.
Cholera, 3 days after tetracyclines started, until 48 hours of antibiotics (or
diphtheria negative cultures after treatment)
Shigellosis Until 3 consecutive negative stool cultures.
Salmonellosis 3
Hepatitis 3 weeks
A
Influenza 3 days after onset
Polio 2 weeks adult, 6 weeks paediatric.
Tuberculosis Until 3 weeks of effective chemotherapy (sputum +)
Herpes zoster 6 days after onset of rash

Mumps Until swelling subsides
Pertussis 4 weeks or until paroxysms cease Meningococcal
meningitis Until the first 6 hours of effective
Streptococcal antibiotic therapy are completed Pharyngitis

32. Quarantine
• 'Quarantine' (meaning "40 Days') is the restriction of activities of apparently healthy persons who
have been exposed to a case of communicable disease during its period of communicability
• It applies to those who have been exposed to a contagious disease but who may or may not
become ill.
• Quarantine was first applied for plague
• Quarantine period for yellow fever: 6 days (maximum IP)
• Quarantine period of cholera 5 days
• Quarantine currently has been 'replaced with active surveillance
• Absolute quarantine
• Restriction of movement for maximum incubation period.
• Modified quarantine
• A selective partial limitation of freedom of movement, such as the exclusion of children from
school.
33. Epidemic
Definition:
• Epidemic refers to an increase, often sudden, in the number of cases of a disease above what is
normally expected in that population in that area.
Types Of Epidemic:
A. Common Source epidemic.
• Origin of an epidemic is a common source

• For example, water poisoning.
Point source epidemic:
• It is also known as "single exposure epidemic".

• All the resultant cases develop the disease within the incubation period of disease at the same
time.
• Epidemic curve, in this case, shows a sharp peak and sharp decline.
• Clustering of cases' in a narrow interval of time All cases develop within one incubation period' of
the diseasesExamples: Food poisoning, Measles, Chickenpoxholera, BHOPAL GAS TRAGEDY
• Common source, continuous or repeated exposure.
• In this case, epidemic reaches a sharp peak but tails off gradually over a longer period of time
although the sharp peak is attained after a longer time than a point source epidemic.
• This occurs because of prolonged and repeated exposures or when the source of infection is not
eliminated.
• Fall in no. of cases is interrupted by'Secondary wave/ Peaks
• Examples: Contaminated well in a village nationally distributed brand vaccine or food, a prostitute
in a gonorrhoea outbreak, LEGIONNAIRE'S DISEASE outbreak in Philadelphia (1975)
• For example, a prostitute may be a common source in a gonorrhoea outbreak but in this case,
epidemic curve will rise gradually as she infects her clients over a period of time. But in case of
waterborne cholera, the epidemic curve reaches a sharp peak but tails of gradually. These are the
two different models of common source continuous epidemic.
B. Propagated Epidemic.
• A propagated epidemic occurs due to transmission of the infectious agent either

• Person to Person
• Through Vectors (insects etc)
• Through animal reservoir
• The epidemic curve shows gradual rise and tails of over a much longer time as compared to
common source repeated exposure epidemic.
• Examples: HIV, tuberculosis
• Steps for Investigation of Epidemic :
• Verification of diagnosis :
• Is the first step in investigation of an epidemic'
• Confirmation of existence of an epidemic:
• Compare with disease frequencies during same period in previous years
• Searching for more cases: Search for new cases is carried out every day, till the area is declared free
of epidemic; this period is usually taken as 'twice the incubation period of the disease since the
occurrence of last case'
34. Sex Ratio
Sex ratio
• Sex ratio is defined as the number of females per 1000 males.
Sex Ratio (India): [Census 2001)
• Sex ratio (India):933(Highly Unfavourable )
Sex Ratio (India): [Census 2011]
• Sex ratio (India):940 (Highly Unfavourable )

• Favourable sex ratio in India:
• Kerala:1084
• Pondicherry:1038
Child Sex Ratio
• Child sex ratio is defined as females (0-6 years age) per 1000 males (0-6 years age).
• Sex ratio at birth in India is 914.
35. Literacy
Literacy and education
• It was decided in 1991 census to use the term literacy rate for the population > 7 years
• A person is deemed as literate if he or she can read and write with understanding in any language
Literacy rate India
• National effective literacy rate in India (2011) - 74.04

• Literacy rate in males: 82.14%; females: 65.46%
Mid-day meal programme/school lunch programme
• Was introduced in a large scale in 1960s under the chief ministership of K. Kamraj Nadar in Tamil
Nadu.
• The meal supply should provide at least one-third of the total energy requirement, and half of the
protein need.
Model Menu for School Lunch Program:
Food item g/day/child

Cereals and millets 75
Pulses 30
Oils and fats 8
Leafy vegetables 30
Nonleafy vegetables 30
36. Crude Birth Rate, Crude Death Rate And Growth Rate
• CRUDE means it include all causes and all ages - It is independent of age of population
Crude birth rate

• Is the natality or childbirth per 1,000 mid-year population
• It excludes the still births
• It is unaffected by age-distribution
• Crude birth rate = (Number of liver births in a year/ Estimated mid year population) x 100
• Is a measure of fertility
Crude death rate
• It is the simplest measure of mortality.

• A rate comprises the following elements
• Numerator
• Denominator
• Time specification
• Multiplier
Denominator
• Mid year population population estimated on first of July of an year
Growth rate
• The growth rate india 1.64%.
Annual GR % Yrs required

Stationary No growth -
Slow growth 0.5 >139
Moderate growth 0.5-1 139-70
Rapid growth 1-1.5 70-47
Very rapid growth 1.5-2 47-35
Explosive growth 2-2.5 35-28
Explosive growth 3-3.5 23-20
Explosive growth 3.5-4 20-18
Skin
1. Pityriasis Versicolor
• The skin patches often fluoresce an apple green in long-wave UVR (Wood's light).
• Ketoconazole shampoo to wash the affected areas once daily for 5 days
• Caused by yeast-like micro-organism Pityrosporum ovale (orbiculare) or Malessezia furfur
2. Tinea capitis
• Ringworm of the scalp occurs in children exclusively

• Mainly due to M. canis or Trichophyton tonsurans
• It invades the hair cuticle (ectothrix infection), causing pink, scaling patches on the scalp skin
• Scalp ringworm caused by T. schoenleini, invades the interior of the hair shaft (endothrix) and
causes intense inflammation on the scalp, with swelling, pus formation and scalp scarring.
3. Dermatitis herpetiformis
• Intensely itchy vesicles, papulovesicles and urticaria papules symmetrically distributed

over extensor surfaces (elbows, knees, buttocks, back, scalp, and posterior neck)
• Almost all have an associated, usually subclinical, gluten-sensitive enteropathy
• >90% express the HLA-B8/DRw3 and HLA-DQw2 haplotypes
• Biopsy of new lesions - vesicle forms subepidermally and develops from collections of inflammatory
cells in the papillary tips (the papillary tip abscess)
• Direct IF- presence of IgA in the papillary tips in the skin around the lesions
• Gluten-free diet
• Dapsone therapy
• Patients are at increased risk for development of gastrointestinal lymphoma
4. Acrodermatitis enteropathica
• Autosomal recessive
• Inherited form of zinc deficiency
• Triad of
• Acral dermatitis (face, hands, feet, anogenital area)
• Alopecia
• Diarrhea
• Treatment
• Requires lifelong zinc supplementation
5. Dermatomyositis
• Groton's sign is seen in Dermatomyositis
• Heliotrope rash is seen in Dermatomyositis
• Gottrens papules, Helitrope rash & Mechanics hand is seen in Dermatomyositis
• Perifascicular atropy of muscle fibres is seen in Dermatomyositis
• A 40 year old woman presented with a 8 month history of erythema and swelling of the periorbital
region & papules & plaques on the dorsolateral aspect of forearms & knuckles with ragged cuticles.
There was no muscle weakness is diagnosed to have dermatomyositis
6. ELECTROCONVULSIVE THERAPY
• ECT operates a modulation of serum Brain derived neurotrophic factor levels in drug resistant
depressed patients.
• There is no absolute contraindication for ECT
• Mainly used for the treatment of major depressive disorder
• Pheochromocytoma is a relative contraindication
7. Vitiligo
• In Vitiligo Genetic predisposition present

• In Vitiligo Narrow range UV-B is very effective
• In Vitiligo Topical steroid is used for localised lesion
• An increased incidence of vitiligo is found in Diabetes mellitus
• In a patch of vitiligo Melanocytes are absent
• Vitiligo vulvaris, best treatment is PUVA
• Vitiligo vulvaris is treated with PUVA, Steroids & Coaltar
• Woods lamp used in diagnosis of Vitiligo
• Psoralen - A is used in the treatment of Vitiligo
• The Uveitis associated with vitiligo & auditory defects occurs in Vogt-Koyanagi syndrome
• Defect seen in Vitiligo is Absent melanocytes
• Vitiligo is associated with Addison's disease, Men syndrome & Pernicious anemia
8. URTICARIA
• Solar urticaria Lesions subsides spontaneously on avoiding exposure within 24 hours

• In Solar urticaria Some cases may develop severe urticaria/bronchospasm.
• Almost all cases of Solar urticaria are idiopathic

• A 5 year old male child has multiple hyper pigmented macules over the trunk, on rubbing the lesion
with the rounded end of a pen. He developed urticarial wheal, confined to the border of the lesion.
The most likely diagnosis is Urticaria pigmentosa
• Urticaria pigmentosa is a disorder of mast cells
• Solar urticaria is characterized by Wheal formation
• Urticaria pigmentosa produce a positive Darier's sign
• Recurring urticaria are SLE associated rashes
• Recurrent episodes of flexural exzema contact urticaria is seen in Atopic dermatitis
• A patient gets reccurent urticaria while doing exercise and on exposure to sunlight
suggest Cholinergic Utricaria
• Investigation done for the diagnosis of itchy tense blisters on normal looking skin and urticarial rash
is Direct immunofluorescence
9. ERYTHEMA MULTIFORME
• The most clinically significant skin eruption associated with M. pneumoniae infection is Erythema
multiforme major
• After taking sulphonamide group of drugs, one patient developed certain oral lesions of Erythema
multiforme
• Erythema multiforme lesions consist of vesicles, ruptured to form ulcers covered with
pseudomembrane.
• While touching, the lesions of Erythema multiforme bleed easily with Hemorrhagic crusts on lips
and other skin .
• Commonest etiology among infection of erythema multiforme is Viral
• In Erythema multiforme Target lesions are seen
• Erythema multiforme Involves face and neck regions
• Erythema multiform shows Sign of internal malignancy
• Erythema multiforme is most commonly caused by idiopathy
10. Integumentary System
• The portion of the skin that serves as a barrier to water loss is the Epidermis
• Melanoblast cells appear in basal layer of epidermis during 3rd month of intrauterine life
• Lymphatics are found in Dermis of skin
• Stratum corneum is underdeveloped in the VLBW infants in the initial 7 days
• Normal turnover time of epidermis (skin doubling time) is 4 weeks
• Function of the epidermis layer of the skin provides a waterproof barrier and creates our skin tone.
• Haascheiben cells in epidermis are responsible for Touch
• Dead layer of epidermis is Stratum corneum
• Skin and facia of great toe drains into Vertical group of superficial inguinal lymph nodes
• It has been calculated that a human adult has about 1012 bacteria on the skin
• Density of bacterial population at most sites is between 100-1000 per square cm.
11. SKIN APPENDAGES
• Sebaceous gland is an example of Holocrine gland

• The ducts of Sweat gland consist of stratified cuboidal epithelium
• Halocrine secretion is seen in Sebaceous glands
• Fordyce spots are Ectopic sebaceous glands
• Apocrine gland are Modified sweat gland
• Apocrine sweat glands are found in axillary and anogenital areas
• Rate of growth of beard hair is 0.4 mm/day
• DNA can be taken as sample from Hair roots
• In humans, cortex of hair is usually 4-10 times broader than the medulla
• Hair follicles, Sebaceous glands & Mammary gland are derived from ectoderm
• Telogen phase of hair growth lasts for 100 days
12. IMPETIGO
• Impetigo contagiosa is caused by Group A beta hemolytic streptococci

• Commonest skin infection in children is Impetigo contagiosa
• Impetigo is a Contagious Bacterial skin infection
• Primary pyodermas are Impetigo contagiosa
• Treatment for impetigo includes either dicloxacillin or cephalexin can be given at a dose of 250 mg
four times daily for 10 days.
13. Epidermolysis Bullosa
• Mutation in collagen -VII is present in epidermolysis bullosa .

• In congenital dystrophic epidermolysis bullosa defect is seen in Collagen-7.
• Etiology of Epidermolysis bullosa is Genetic.
• The target antigen in dermolytic variant of epidermolysis bullosa is Collagen-7.
• A 5 year old girl presented with recurrent skin lesions over the body as shown in the
image following trivial trauma.The most possible diagnosis would be Epidermolysis bullosa.
• A 2 day old newborn girl born out of non-consanguinous marriage was evaluated for tense blister
and areas of denuded skin that had been present since birth. The child develops while mother
handles for bathing and feeding. The sibling of child also had h/o developing similar lesions.The
most possible diagnosis would be Congenital Epidermolysis bullosa.

• In a 8 day old child with no history of consanguinity in the parents. The mother reports blisters and
peeling off of skin at the site of handling and pressure. There was a similar history in previous child
which proved to be fatal. The most possible diagnosis would be Congenital Epidermolysis bullosa.
• U-serrated pattern in direct immunofluorescence is seen in Epidermolysis bullosa acquisita.
14. Xeroderma Pigmentosum
• Xeroderma pigmentation is caused due to a group of closely related abnormalities in Nucleotide

excision repair.
• Xeroderma pigmentosum is produced as a result of a defect in DNA Polymerase I and DNA ligase.
• The primary defect in Xeroderma pigmentosa is formation of Thymidine dimers.
• Xeroderma pigmentosum is a genodermal disease that can cause skin malignancy .
• Cells cultured from patients with this disorder exhibit low activity for the nucleotide excision repair
process. This autosomal recessive genetic disease includes marked sensitivity to sunlight (Ultra
voilet light) with subsequent formation of multiple skin cancers and premature death, the disorder
is Xeroderma pigmentosum.
• Defective DNA repair is a/w Xeroderma pigmentosum.
15. Icthyosis
• Pigmentation and icthyosis are side effects of Clofazimine.

• Icthyosis may be associated with Hodgkin's disease, AIDS, Hypothyroidism.
• A male child with cryptorchidism presents with large black scales on body flexures. Skin biopsy
showed hyper granulosis & steroid sulfatase deficiency. Probable diagnosis is X- linked icthyosis
nigra.
16. Tuberous Sclerosis
• Type of inheritance in Tuberous sclerosis is Autosomal Dominant.

• Color of tuberous sclerosis lesions on wood lamp examination is Blue-white.
• Giant cell astrocytoma,Subependymal nodule, White matter lesion, Shagreen patch, Depigmented
Naevi, Tubers, Renal Cortical Cyst, Pulmonary lymphangioleiomyomatosis may be seen in Tuberous
Sclerosis.
• Ependymoma is not seen in Tuberous Sclerosis.
• Tuberous Sclerosis presents with Vogt's triad of epilepsy, low intelligence/mental retardation/
delayed mile stones and adenoma sebaceum (arjgiofibroma of face)(Acronym-Epiloia)
• Tumor which may be associated with tuberous sclerosis are Renal angiomyoma, Subependymal
giant cell astrocytoma, Rhabdomyoma heart.
• Drug of choice for infantile spasms in a patient with tuberous scleosis is Vigabatrin.
• A couple has two children affected with tuberous selerosis. On detailed clinical and laboratory
evaluation (including molecular studies) both parents are normal. Germline mosaicism explains the
two affected children in this family.
• Asch leaf spot is the earliest feature of Tuberous sclerosis.
• Koenen's periungual fibromas are associated with Tuberous Sclerosis.
• Differential diagnosis of congenital disorders of pigmentation includes Tuberous Sclerosis along
with Waardenburg syndromes types 1-4 ,Tietz syndrome ,Piebaldism ,Woolf's syndrome,
Generalized vitiligo, Segmental vitiligo, Vogt-Koyanagi-Harada syndrome, Chemical leukoderma
Tuberous sclerosis, Ziprkowski-Margolis syndrome (X-linked albinism-deafness syndrome).
• Most probable diagnosis in a child with seizures, oval hypo-pigmented macules on the trunk, and
sub-normal IQ is Tuberous sclerosis.
• Honey comb appearance on X-ray may be seen in Tuberous Sclerosis.
17. (VON RECKLINGHAUSEN'S DISNEUROFIBROMATOSISEASE)
• Neurofibromatosis shows which of the Autosomal Dominant type of inheritance.

• Neurofibromatosis may be associated with Cataract, Scoliosis, Hypertrophy of limb and
Neurofibroma.
• Neurofibromatosis-1 is asociated with family history, Optic Glioma and Axillary Freckles.
• Optic Gliomas are the most common intracranial tumors of Neurofibromatosis 1.
• Neurofibromatosis type 2 is associated with Bilateral Acoustic Neuroma, Cafe-au-lait spots, Axillary
Freckling, Lisch Nodule, Meningioma
• Gene for NF-2 is located on chromosome 22.
• Neurofibroma are unencapsulated and needs to be resected along the nerve fibres.
• Neurofibromatosis presents as Elephantiasis neuromatodes, Plexiform neuroma,Von
Recklinghausen's disease.
• Plexiform neurofibromatosis commonly affects Trigeminal Nerve.
• Neurofibromatosis may be associated with Pheochromocytoma.
• The pathognomic sign of Neurofibromatosis is Axillary Freckling.
• Scoliosisis is the MOST common skeletal manifestation in Type-1 Neurofibromatosis.
• Juveile Myelomonocytic Leukemia is the most common tumour associated with Neurofibromatosis
-1 (NF-I) in a child.
• Rib notching,Pseudarthrosis may be seen in Neurofibromatosis.
• Wide neural foramina is associated with Neurofibromatosis.-I.
• Ependymomas are commonly associated with Neurofibromatosis-II.
• A 22-year-old patient, Sreeraj presents with multiple neural tumors, pigmented iris hamartomas,
and numerous tan macules on his skin. He informs the physician that his father, as well as one uncle
and his paternal grandfather, had a similar condition. This patient likely suffers
from Neurofibromatosis.-I.
18. Pellagra
• Pellagra is characterized by classical triad of 3Ds :-Diarrhea,Dermatitis,Dementia.
• Pellagra is due to deficiency of Niacin.
• In South India pellagra is reported in population eating Jowar.
• Pellagra in jowar eating population is due to excess of Leucine.
• Patient presenting with pellagra, parkinsonism, convulsions, anemia and kidney stones has
deficiency of Pyridoxal Phosphate.
• Development of pellagra like skin lesion in carcinoid syndrome is due to inadequate conversion of
Tryptophan to Niacin.
• A 10 year old child is suspected of having pellagra because of chronic symptoms including diarrhea,
a red scaly rash, and mild cerebellar ataxia. However, his diet is not deficient in protein and he
appears to be ingesting adequate amounts of niacin. A sister has a similar problem. Chemical
analysis of his urine demonstrates large amounts of free amino acids. Hartnup's Disease is the most
probable diagnosis.
• Consumption of maize may aggravate Pellagra. As some strains of maize contains excess of Leucine
which interferes in the conversion of Tryptophan into Niacin.
• Casal's paint necklace is caused by Pellagra.
• Photosensitive dermatitis are Psoriasis, Pellagra, Pemphigus, SLE, Congenital erythropoietic
porphyria
19. Chancroid
• Chancroid is caused by H.Ducreyi.

• DOC in chancroid is Erythromycin.
• Reliable test for chancroid detection is Grams stained smear.
• Chancroid may be caused by Herpes virus - hominis.
• Incubation period of chancroid is < 7 days.
• Syndromic Management of genital ulcer syndrome in India includes Chancroid, Primary Chancre
and herpes simplex
• Painful lymphadenopathy may be seen in Chancroid.Tender Bubos seen are used in the diagnosis of
Chancroid.
• A man having multiple, painful, indurated, undermined, sloughed edged glans which occurred 5
days after exposures; most likely diagnosis is Chancroid.
• Ito's test is used in the diagnosis of Chancroid
20. Granuloma Inguinale
• Donovan bodies are seen in Granuloma inguinale.

• Treatment of granuloma inguinale is tetracycline.
• A 25 year old male presents to the clinic with a lesion on his penis. On examination he was noted to
have a beefy red ulcer on the glans which bled when touched. Smear taken from the ulcer showed

gram-negative intracytoplasmic cysts filled with deeply staining bodies that had a safety-pin
appearance. He is most likely suffering from Granuloma Inguinale.
• The hard chancre is seen in Granuloma Inguinale.
• A 26 year male patient presented with a granulomatous penile ulcer. On Wright Giemsa staining,
tiny organisms of 2 microns are seen engulfed by macrophages. Calymmatobacterium granulomatis
is the causative organism.
• Donovanosis/granuloma venerum is caused by Calymatobacter granulomatis.
• Pseudolymphadenopathy is present in Donovanosis.
• Pseudo bubo is seen in Donovanosis.
21. Lymphogranuloma Venerum
• LGV (lymphogranuloma venerum) is caused by Chlamydia Trachomatis.

• Drug of choice for lymphogranuloma venerum is Tetracycline/Doxycycline.
• Most common diagnostic test in LGV is Cell culture.
• Groove sign of greenbalt is seen in LGV.
• Multiple fistula in ano commonly occurs in LGV and Tuberculosis.
• Frie test is done in LGV.
• Esthiomine is seen in LGV.
• Sign of Groove is found in LGV.
• Bubos with multiple sinuses discharging into inguinal lymph nodes are seen in LGV.
• Genital ulcer is not seen in LGV.
22. Leprosy
• Leprosy spreads by skin to skin contact and by droplet spread .

• Neurological involvement is pronounced in Tuberculoid type of leprosy .
• Single skin lesion is seen in TT type of leprosy.
• Long contact with tuberculoid leprosy can transmit the disease .
• Slit skin smear, Fine needle aspiration cytology, Skin biopsy are used for diagnosis of Leprosy.
• Lepromin test is not used for the diagnosis of Leprosy.
• In the management of leprosy, lepromin test is most useful for prognosis.
• Exacerbation of lesions in patients of borderline leprosy is seen in Lepra reaction type -I.
• Under leprosy eradication programme the managment of single lesion is Rifampicin, ofloxacin and
minocycline single dose.
• Subtype of leprosy with maximum number of TH -1 cells is TT.
• Lepra cells found in lepromatous leprosy are Macrophages.
• In Leprosy most common renal lesion seen is MGN.
• Fastest acting drug in leprosy is Rifampicin.
• Kanamycin is not used in the treatment of leprosy.
• Drug causing icthyosis and hyperpigmentation, when used in leprosy is Clofazimine.
• Most common type of leprosy in India is TT.
• Skin smear is negative in Neuritic,Tuberculoid,Intermediate leprosy.
• Characteristic feature of borderline leprosy is inverted saucer lesion.
• Vesicles are not seen in Leprosy.
• Erythematous Macule, Hypo pigmented patch, Flat & raised patches may be seen in Leprosy.
• Gynaecomastia, Madarosis, Saddle nose, Leonine facies, Loss of libido and impotence are features
of lepromatous leprosy.
• Commonest nerve involved in leprosy is Ulnar.
• In leprosy nerves commonly involved are high ulnar and low median.
• Abnormal EMG, voluntary muscle wasting, decreased response to tactile sensation may be seen in
Leprosy.
• Decreased Proprioception is not seen in Leprosy.
• Leprosy do not involve CNS, uterus.
• Tuberculoid leprosy is characterised by non-caseating granuloma in nerve.
• Presence of globi, subepidermal free zone, decreased cell mediated immunity can be seen in
Lepromatous Leprosy.
• Skin biopsy in leprosy is characterized by pariappendegial bacilli,pariappendegeal lymphocytosis,
perivascular lymphocytosis.
• Lepromin test is positive in Tuberculoid leprosy.
• A 27-year-old patient was diagnosed to have borderline leprosy and started on multibacillary multi-
drug therapy. Six weeks later, he developed pain in the nerves and redness and swelling of the skin
lesions. The management of his illness should include all of the following:Continue Anti-leprosy
Drugs,Costicosteroids, Analgesics, Rest to the limb.
• Best method of treatment of ulnar never abscess in case of leprosy is Incision and drainage.
• ENL is seen in LL form of leprosy.
• The first line antileprosy drugs include : Dapsone, Clofazimine, Rifampicin
• Side effect of clofazimine used in leprosy therapy is Hyperpigmentation and Discolouration of body
secretions.
• Control of TB and leprosy is by early diagnosis and treatment.
• WHO regime for paucibacillary leprosy:100 mg Dapsone daily + Rifampcin 600 mg monthly.
• Duration of treatment in pauci bacillary leprosy is 6 months.
• Average duration of treatment in multibacillary leprosy is 1 year.
• Prevalence of leprosy is decreasing in past decade in India.
• Insect can transmit Leprosy.
• Transplacental spread is not the mode of transmission of Leprosy.
• "Multibacillary" is a spectrum of disease, seen in Leprosy.
• Ridley jopling leprosy classification is a type of Clinical, bacteriological, immunological, histological
classification.
• Lepromin test is negative in most of the child in 1st 6 month of life.
• BCG vaccination converts lepra reaction from negative to positive.
• A patient with leprosy had slightly erythematous, anesthetic plaques on the trunk and upper limbs.
He was treated with paucibacillary multidrug therapy (PB-MDT) for 6 months. At the end of 6
months, he had persistent erythema and induration in the plaque. The next step of action

recommended by the World Health Organization (WHO) in such a patient is to stop anti-leprosy
treatment.
• Treatment of severe ulnar neuritis in borderline tuberculoid leprosy is MDT with steroids.
• For treatment of paucibacillary leprosy drugs used are Rifampicin and Dapsone.
• In multibacillary leprosy the follow up examination after adequate treatment should'be done yearly
for 5 years.
• 2 yrs duration in terms of leprosy is with regard to post Rx surveillance of paucibacillary leprosy.
• Immunoprophylaxis of leprosy includes BCG and ICRC bacillus.
• Strategies in National Leprosy control program are early detection of cases; short course multi drug
therapy;rehabilitation
• In leprosy eradication programme the multidrug therapy is not long term but short term therapy.
• Effective leprosy control programme may be indicated in : Decreased grade 2 disability,Low MDR
resistant, multibacillary cases ,High new case detection rate.
• Elimination of leprosy is defined as prevalance < 1 per 10000.
• As per WHO, leprosy is a public health problem if prevalence is 0.01%.
• SET centres are established if prevalence leprosy is 1-5.
• National Leprosy Eradication Programme was started in 1983.
• Special Action Project for Elimination of leprosy is for rural areas.
• Trophic ulcers may be caused by Leprosy.
• Leprosy may lead to secondary Amyloidosis, Depressed bridge of nose, Septal perforation of nose.
• 'Iris-pearls' are seen in Leprosy.
• Ocular lesions of leprosy include : Avascular keratitis ,Interstitial keratitis , Neuroparalytic keratitis.
• Hansen (1874) described leprosy bacillus.
• Thalidomide is useful in treatment of type II lepra reaction.
• Foamy histocytes, Epitheliod cells, Noncaseating granulomas can be seen in histological
examination in a case of Leprosy.
• Very numerous, symmetrically distributed, erythematous or copper coloured shiny macules/papule
are feature of LL.
• More than 5 lesions on skin smears seen in Multibacillary Leprosy.
• Clofazimine is an important drug to be given in Multibacillary Leprosy.
• Asmmetrical several nerves thickening with several hypoesthetic macules on skin indicates
Borderline borderline stage of leprosy.
• Most important in establishing diagnosis of leprosy is Slit smear for AFB.
• Innumerable, small, normoesthetic and symmetrical skin lesions are present in Lepromatous type
of leprosy.
• The fingerprint pattern may be impaired permanently in case of Leprosy.
• Globi in leprosy consist of AFB with macrophages.
• Leprosy is not targeted for global eradication because of long incubation period.
• Multiple hypoaesthetic, hypopigmented macules on right lateral forearm with numerous acid fast
bacilli is indicative of Borderline Leprosy.
• Patient with leprosy, smear sample taken show 10 - 100 bacilli in one field. Bacterial index is 4+.
• Ulceronecrotic nodule is seen in Lucio Leprosy.
• Nerves are not involved in Indeterminate Leprosy.
• If a claw hand develops in a patient with Leprosy, the deformity is Grade II.

• Most sensitive index of transmission in leprosy is Incidence.
23. Cutaneous Tuberculosis
• Tuberculosis verrucosa cutis is a form of Postprimary tuberculosis with good resistance.

• Tuberculosis of skin is called as Lupus Vulgaris.
• Cutaneous (skin) Tuberculosis secondary to underlying tissue eg lymph node is
called as Scrofuloderma..
• Cutaneous manifestation of tuberculosis:Lupus vulgaris, Scrofuloderma, Exanthematous lesion.
• Apple jelly nodules on the nasal septum are found in cases of Lupus Vulgaris.
24. Toxic Epidermal Necrolysis
• Skin involvement in toxic epidermal necrolysis?> 30%.

• Lesions are similar in appearance to partial thickness bums in toxic epidermal necrolysis.
• The process develops at the dermoepidermal junction in toxic epidermal necrolysis.
• TEN is believed to be an immunologic problem.
• Corticosteroid use is not a primary part of therapy
25. Impetigo
• A 3 year old child is seen by a pediatrician because he has developed multiple isolated lesions on his
face and neck. Physical examination reveals many lesions up to 4 cm in diameter with golden crusts,
while in other sites small blisters and weeping areas are seen.Impetigo is the most likely diagnosis.
• Impetigo contagiosa may be caused by Staphylococcus aureus (most common) or Group A beta
hemolytic streptococci or by both.
• Bullous impetigo caused by S. aureus mostly
• Impetigo may predispose to glomerulonephritis.
• Impetigo does not produce scar on healing.
• Commonest skin infection in children is Impetigo Contagiosa.
• 'Honey colored' crusts are characteristic of Impetigo.
• Impetigo is a contagious bacterial infection.
• Impetigo is a pyoderma.
• Treatment for impetigo is Dicloxacillin.
• Pigment production by staphylococcus aureus occurs in Bullous Impetigo.
• Nikolsky's sign is seen in Bullous Impetigo.
26. Pityriasis Rosea

• Pityriasis rosea is a self limiting disease.
• Hanging curtain sign seen in Pityriasis Rosea.
• Lesions of pityriasis rosea are distributed mostly on the trunk.
• A 25 year old male presents with multiple erythematous annular plaques with peripheral collarette
of scales arranged predominantly over trunk.Pityriasis Rosea is the most probable diagnosis.
• Herald patch ,moderate itching,low grade fever may be seen in Pityriasis Rosea.
• 'Fir-tree' type of distribution is seen in Pityriasis Rosea.
• HHV-7 viral association is found in pityriasis rosea .
• Etiology of Pityriasis rosea is Herpes Virus.
• Christmas tree appearance in skin is seen in Pityriasis Rosea.
27. Dermatitis
• Parthenium causes allergic contact dermatitis through air.

• Most common cause of plant induced dermatitis in India is Parthenium.
• A 3 year old child has eczematous dermatitis on extensor surfaces. His mother has a history of
Bronchial asthma. Diagnosis should be Atopic Dermatitis.
• Commonest site of Atopic dermatitis is Elbow( Antecubital fossa).
• Dennie -Morgan fold, Hertoghe’s sign, Hyperlinearity of palms are features of Atopic Dermatitis.
• Facial pallor, Pityriasis alba, Keratosis pilaris are skin findings in Atopic Dermatitis.
• Langerhan cell histiocytosis produce a seborrheic dermatitis like lesions in an infant.
• Air-borne contact dermatitis can be diagnosed using Patch test.
• 36 year old farmer presented to dermatology department with pruritic erythematous lesions on
arms, forearms, face and retroauricular area after removal of weeds in his farm. A diagnosis of
phytodermatitis was made. Parthenium Hyterophus is the most likely plant responsible for this
condition.
• A child presents with seborrheic dermatitis, lytic skull lesions, ear discharge and
hepatosplenomegaly; likely diagnosis is Histiocytosis X.
• Contact dermatitis is a type IV hypersensitivity.
• In contact dermatitis T cells play major role.
• Doxycycline has maximum propensity for photodermatitis.
• Baby with recurrent infection of ear & discharge & seborrheic dermatitis with hepatosplenomegaly
with cystic skull lesions. Diagnosis is Langerhan's Cell Histiocytosis.
• Minor clinical feature in diagnosis of atopic dermatitis are - Dry skin, Morgagnian fold, Pitriasis alba.
• Most common precipitant of contact dermatitis is Nickle.
• Exfoliative dermatitis is seen in : Pityriasis rubra pilaris, Psoriasis, Drug hypersensitivity.
• Gold poisioning leading to exfoliative dermatitis is treated by Steroid.
• Most common cause of allergic contact dermatitis in Indian female is Detergents.
• Berloque dermatitis is due to contact with cosmetics.
• Photosensitive dermatitis are Psoriasis,Pellagra, Pemphigus.
• Atopic dermatitis may be associated with Conjunctivitis, Keratoconus, Cataract.
• Dennies Morgan fold is indicative of Atopic Dermatitis.

• The day after playing in the high grasses of a neighbour's fields, this boy develops an erythematous,
and itchy rash on his arms, legs, and neck.Spongiotic Dermatitis best describes this inflammatory
condition.
• RAST test is used in diagnosis of Allergic Dermatitis.
• Hanifin & Rajke is the diagnostic criteria for Atopic Dermatitis.
28. Lichen Planus
• A combination therapy with steroids and Dapsone is used in generalised Lichen Planus.
• LP is characterized by shiny, violaceous, flat-topped polygonal papules which retain the skin lines.
• Wickham’s striae are white lines which traverse the surface of the papules.
• A focal increase in thickness of the granular layer and infiltrate corresponds to the presence of
Wickham’s striae.
• Mouth lesions are seen in Lichen Planus.
• Skin, hair and oral mucosa commonly involved in Lichen Planus.
• Features of Lichen planus are Pruritus, Purple, Papule
• Max. Joseph's space is a histopatho-logical feature of Lichen Planus.
• Civatte bodies are found in Lichen Planus.
• Following is seen in a case of Leprosy:Basal cell degeneration; Colloid bodies seen; Epidermal
hyperplasia in chronic cases.
• A young lady presents with lacy lesions in oral cavity and genitals, and her proximal nail fold has
extended onto the nail bed. Lichen Planus is the likely diagnosis.
• A 30 year old male present with pruritic flat-topped polygonal, shiny violaceous papules with
flexural distribution. the most likely diagnosis is Lichen Planus.
• Lymphatic infiltration in supradermal layer is seen in Lichen Planus.
• Lichen Planus may be associated with Hepatitis C.
• Topical Steroids are the mainstay of therapy in Lichen Planus.
• Spontaneous remissions may be seen in 6month to 2years.
• Characterstic nail finding in lichen planus is Pterygium.
• Most characteristic Feature of lichen planus is Wickham Striae.
• The most characteristic finding In lichen planus is Basal Cell Degeneration.
• Nail deformity commonly seen in lichen planus are Pterygium,Longitudnal grooves,Oncholysis.
• Wood's lamp is not used for diagnosing Lichen Planus.
• Lichen planopilaris,Lichen hypertrophica, Lichen pigmentosa are the types of Lichen Planus.
• Lichen scrofulosorum is a type of cutaneous TB, not the lichen planus.
• Koebner phenomenon may be seen in Lichen Planus.
• The role of Lichen Planus in predisposing Squamous cell carcinoma of Oral cavity is uncertain.
29. Acrodermatitis Enterohepatica
• Lifelong treatment required in Acrodermatitis enteropathica.

• Dose of zinc used in acrodermatitis enteropathica is 2 mg/kg.
• Acrodermatitis enteropathica is a rare autosomal recessive disorder caused by an inability to
absorb sufficient Zinc from the diet.Symptoms improve with zinc supplementation
• Acrodermatitis enteropathica causes diarrhoea and dermatitis but no dementia.
• Denuded skin around mucocutaneous junction is seen in Acrodermatitis enteropathica .
• A child with alopecia, hyperpigmentation psoriatic dermatitis in genitals & mouth and
hypogonadism is likely to be suffering from Zn deficiency.
30. Pityriasis Rubra Pilaris
• Isolated patches of normal skin are found in Pityriasis Rubra Pilaris.

• Cephalocaudal distribution is seen in Pityriasis Rubra Pilaris.
• Exfoliative dermatitis is seen in Pityriasis Rubra Pilaris.
• Keratodermic sandles is a feature of Pityriasis Rubra Pilaris.
31. Psoriasis
• Most common site affected by psoriasis is extensor surface.

• A 24 year old lady with a past history of psoriasis presents with fever and multiple pus filled lesions
in a generalized distribution.Methotrexate is the drug of choice.
• The only definite indication for giving systemic corticosteroids in pustular psoriasis is extensive
lesions.
• The Drug of choice for a pregnant woman in 2nd trimester with pustular psoriasis is Prednisolone.
• Methotrexate is the drug of choice in the treatment of erythrodermic psoriasis.
• Lithium, Beta blocker ,Hydroxychloroquine are known to exacerbate psoriasis.
• Methotrexate used in the treatment of pustular psoriasis acts by inhibiting dihydrofolate reductase.
• Limpet-like cone-shaped lesions in psoriasis refers to Ruipoid Psoriasis.
• Nail changes in Psoriasis includes: Pitting: It is the most frequent change ,Subungual hyperkeratosis
,Onycholysis ,Thickening and yellowish discoloration of nail plate, Oil spots.
• HLA associated with psoriasis is HLA-CW6.
• A topical retinoid recently introduced for the treatment of psoriasis is Tazarotene.
• Histopathological features of psoriasis include - compact hyperkeratosis, orthokeratotic stratum
corneum supra papillary thinning, Munromicro abscess in stratum corneum , Kogoj's spongiform
pustule, exaggeration of rette pattern and parakeratotic stratum corneum (i.e. nuclei are
retained) with marked epidermal thickening (but absent or thinned stratum granulosa).
• Bleeding spots seen on removal of scales in psoriasis is called as Auspitz sign.
• The important feature of psoriasis is Scaling.
• 10% of cases of psoriasis are associated with arthritis.
• Worsening of psoriasis is seen during winter.
• In psoriasis,no scaly, red lesions are seen in inframammary and natal area.
• Abscess may be seen in Psoriasis.
• Least common site involvemnet in psoriasis is CNS involvement.
• Psoriasis is exacerbated by- Lithium , B- blockers , Antimalarials,Metformin,Interferon-Alpha.
• Treatment of Psoriasis includes PUVA and Methotrexate.
• Treatment of pustular psoriasis is Retinoids.
• A patient with psoriasis was started on systemic steroids. After stoping the treatment, patient
developed universally red scaly skin with plaques losing their margins all over his body. The most
likely cause is Erythrodermic Psoriasis.
• A patient with psoriasis was started on systemic steroids. After stopping treatment, the patient
developed generalized pustules all over the body. The cause is most likely to be Pustular Psoriasis.
• The only indication of giving corticosteroids in pustular psoriasis is Psoriatic Erythroderma with
pregnancy.
• DOC for a pregnant woman in 2" trimester with pustular psoriasis is Prednisolone.
• Only definitive indication of systemic steroids in psoriasis is Impetigo Herpetiformis.
• Photosensitive Dermatitis are Psoriasis, Pellagra, Pemphigus, SLE, Congenital erythropoietic
porphyria.
• Diathronol ointment is used for Psoriasis.
• Silver plaques are a feature of Psoriasis.
• Koebner's phenomenon seen in Psoriasis.
• Thimble pitting of nails is seen in Psoriasis.
• Vitamin D analogue calcitriol is useful in the treatment of Psoriasis.
• Grattage test is used for Psoriasis.
32. Systemic Sclerosis
• Diffuse cutaneous systemic sclerosis is characterised by early pulmonary fibrosis.

• Late stages of limited systemic sclerosis patients may develop Pulmonary arterial hypertension
(PAH), Interstitial lung disease, Hypothyroidism, Primary biliary cirrhosis.
• Limited cutaneous systemic sclerosis have Anticentromere autoantibody positivity
• Increased serum antibodies to human cytomegalovirus are seen in Systemic Sclerosis.
• The incidence of SSc is increased among miners exposed to silica
• Bleomycin, pentazocine and cocaine may produce systemic sclerosis like illness
• Secondary Raynaud's phenomenon is associated with SLE, systemic sclerosis, Atherosclerosis,
Buerger's disease, RA.
• Features of Systemic Sclerosis are Calcinosis;Sclerodactyly & Raynaud's phenomena.
• A 35 year old lady complains dysphagia, Raynaud's phenomenon, sclerodactyly. Investigations show
antinuclear antibody. The likely diagnosis is Systemic Sclerosis.
• ANA (antinuclear antibody) may be seen in Systemic Sclerosis.
• Antitopoisomerase antibodies (Scl 70) are characteristic of diffuse systemic sclerosis .
• Trunk involvement is present in generalized (diffuse) systemic sclerosis.
• Raynaud's phenomenon seen years before skin changes in generalized (diffuse) systemic sclerosis..
• Calcinosis , Sclerodactyly , Hyperpigmentation (Melanin deposition) may be seen in Systemic
Sclerosis.
• The term mixed connective tissue disease is used to describe a disease with clinical features that
are a mixture of the features of SLE, systemic sclerosis, and Polymyositis.
33. Pigmentation Disorders

• Acquired symmetric hyper pigmentation of the sun exposed skin of the face and neck, which is
strongly associated with pregnancy & use of oral contraceptives is called Melasma.
• A melanocytic naevus surrounded by a depigmented halo is called Sutton's Nevus.
• A giant congenital melanocytic nevus is usually of the size:>20 cm.
• Salmon patch ,Port wine stain, Naevus aneamicus are examples of vascular malformation.
• 28 year old pregnant female came to you with complaints of brownish pigmentation on the bridge
of nose and cheek. She noticed it after returning from her vacation at beach. There is no pain or
itching at the affected site. Chloasma is the most likely diagnosis.
• There is no need of treatment for Mongolian Spots.
• The most common presentation of a blue rubber bleb nevus syndrome is assymetric iron deficiency
anemia.
• The most likely diagnosis is a case of intractable convulsions mental defect and facial nevus is
Sturge Weber Syndrome.
• Maximum malignant potential is in Junctional Nevus.
• Malignant change in nevus is characterised by- Darkening, Hemorrhag, Itching.
• Common sites for mongolian spot are Lumbosacral Area.
• Hyperpigmentation (hyper melanosis) of skin is seen in endocrine disorders like Addison's
disease, acromegaly, Nelson's syndrome, Cushing's (ectopic ACTH) syndrome, carcinoid syndrome,
pheochromocytoma, and hyperthyroidism (Grave's disease) but not in hypothyroidism or
myxedeme.
• Melanoma, dyskeratosis congenita & lentigines lichen planus cause hyperpigmentation.
• Freckles (or ephelides), Melasma (chloasma or mask of pregnancy), Mongolian spots, Cafe au lait,
Becker's nevus or melanosis (pigmented hairy epidermal nevus), nevus of Ota and nevus of Ito
cause hyperpigmented patches
• Pityriasis alba, pityriasis versicolor, pinta, yaws, syphilis (secondary syphilis - leukoderma
syphiliticum), tuberculoid and indeterminate leprosy,Nevus depigmentosus (or achromicus), nevus
anaemicus, Sutton's (Halo) nevus (leukoderma acquisitum centrifugum), hypomelanosis of Ito and
Piebaldism - all can cause hypopigmentation (hypomelanosis).
• The best results in treatment of capillary nevus have been achieved by Argon Laser treatment.
• Salmon patch usually disappears by 1 year age.
• Melasma, during pregnancy is seen on face.
• A 15cm hyperpigmented macule on an adolosent male undergoes changes such as coarceness,
growth of hair & acne. Diagnosis is Becker Nevus.
34. Rosacea
• An 76 year lady had a history of a red facial rash suffered venous eczema of legs. She was treated
for acne rosacea by her GP. On examination, she had bluish pigmentation on both the legs.
Minocycline is likely to have caused this.
• A 40-year-old woman presents with a 2-year history of erythematous papulopustular lesions on the
convexities of the face. There is a background of erythema and telangiectasia. The most likely
diagnosis in the patient is Rosacea.

• Rosacea is a chronic disease affecting fair skinned middle aged adults characterised by flushing and
telangiectasia in early stage, papules and pustules in inflammatory stage, papules and induction
and rhinophyma in chronic stage.
• ion the skin is erythematous, with dilated blood vessels, nodules and pustules without any
comedones. Rosacea is the MOST likely diagnosis in this patient.
• Rhinophyma is a complication of glandular form of acne rosacea.
• A 25-year old girl presented with erythematous papules on the face as seen in the figure. The
lesions were exacerbated on excessive sweating, sun exposure and emotional disturbance.Acne
Rosacea is the diagnosis.
• Potato nose is seen in acne rosacea.
35. Acne
• Acid that is increased in acne comedones is Palmitic Acid.

• A teenager girl with moderate acne is also complaining of irregular menses. Drug of choice willl be
Cyproterone Acetate.
• Oral retinoid is indicated in the treatment of Acne Vulgaris.
• A 17 year old girl with acne has been taking a drug for the last two years. She now presents with
blue black pigmentation of nails. The likely medication causing the above pigmentation is:
Minocycline.
• Isotretinoin is the treatment for nodulocystic acne vulgaris.
• Acne agminata also known as lupus miliaris disseminatus faciei or facial idiopathic granulomatous
with regressive evolution is a disorder of uncertain etiology.It is not a variant of Acne.
• Varients of Acne,includes Acne conglobata, Acne fulminans, Pomade acne.
• Cheilitis is the most common side effect of Isotretinoin used for acne vulgaris.
• Acne Vulgaris is due to involvement of Pilosebacceous Gland.
• Adapalene is used in treatment of Acne Vulgaris.
• Causative factor for acne include Androgen, Bacterial contamination, Hypercornification of
duct,Keratin,Cell nucleus.
• Only food is not a causative factor for Acne.
• Comedones are characteristics of Acne Vulgaris.
• 19 years old girl has multiple papulo pustular erythematous lesions on face and neck, the likely
diagnosis is Acne Vulgaris.
• Treatment of Acne includes 13 cis retionol; Minocycline; Erytromycin; Cryotherapy; Estrogens; UV
light.
• Recalcitrant Pustular Acne is treated by Retinoid.
• Minocycline is useful for inflammatory acne.
• Retinoids is useful for comedonal acne.
• A 24-year-old girl presented with complains of acne. On examination, multiple nodules, cysts and
intercommunicating sinuses were seen.Oral Isotretinoin will be the treatment of choice.
• SAPHO syndrome is manifested by synovitis, acne, pustulosis, hyperostosis and osteitis.
• Difference in acne rosacea & acne vulgaris is absence of comedone.
• Testosterone hormone is responsible for acne.
36. Nail Abnormalities
• Digital clubbing is seen in Endocarditis ,Pulmonary arteriovenous fistula ,Tricuspid atresia.

• Onycholysis is seen in Allergic dermatitis ,Psoriasis ,Antineoplastic therapy.
• A 60-year-old woman complains to a physician because several of her toe nails are discolored.
Physical examination demonstrates crumbling, friable nails with distal-lateral separation from the
nail bed. Hyperkeratotic debris is present under the affected part of the nail. Trichophyton is the
most likely pathogen.
• Nails is formed in 10-12 week of IUL.
• Mees line is seen in Arsenic poisoning.
• Pterygium of nails is seen in Lichen Planus.
• Thimble Pitting of nails is seen in Psoriasis.
• Tinea ungum effects Nail plate.
• A patient presented with scarring alopecia, thinned nails, hypopigmented macular lesions over the
trunk and oral mucosa. The diagnosis is Lichen Planus.
• 10 year old chid has violaceous papule and pterygium of nails. The diagnosis is Lichen Planus.
• Koenen's periungual fibromas are seen in > 50% of cases with Tuberous Sclerosis.
• Nail and half nail sign, seen in uremia is increased capillary density at the distal half of the nails.
• Causes of Unilateral Clubbing
• Aneurysm of Aorta, innonimate artery, suhclavian artery or axillary artery
• Brachial AV fistulas / malformations
• Infected arterial grafts
• Pancoast tumors
• Arsenic poisoning presents with abdominal pain, diarrhea, Mees line on nails and
myelosuppression.
• A middle aged man presented with paraesthesia of hands and feet. Examination revealed presence
of 'Mees' lines in the nails and raindrop pigmentation in the hands.
• The most likely diagnosis is Arsenic poisoning.
• Muehrcke lines in nails are seen in Nephrotic Syndrome.
• A 60-year old male presented with discoloration, thickening and tunneling of 2 fingernails and one
toenail. KOH mount will clinch the diagnosis at the earliest.
• Lovibond profile sign is seen in Clubbing.
• 40 yr old with koilonychias, iron deficiency & dysphagia, diagnosis is Plummer Vinson Syndrome.
37. Alopecia
• Rapid, diffuse, excessive hair loss after 3 months of pregnancy is due to Telogen Effluvium.
• An 8-yrs-old male presents with multiple patches of alopecia and severe pruritus. A bright blue-
green fluorescence is seen on examination of the scalp with a wood lamp. Pathogen most likely
responsible is Microsporum Canis.
• Pitting of nails can be seen in Alopecia Areata.

• Causes of scarring alopecia: Tinea capitis infection and kerion, Staphylococcal folliculitis, Syphilis,
Herpes simplex and zoster, Lupus vulgaris ,Lichen planus ,Lupus erythematosus, Sarcoid,
Scleroderma, Basal cell carcinoma.
• Non scarring alopecia occur in: Androgenic type ,Telogen effluvium, Alopecia areata
,Trichotillomania,Psoriasis.
• Cicatrising alopecia with perifollicular blue-gray patches is likely to be associated with whitish
lesions in buccal mucosa which is characteristic of Lichen planus.
• Favus is a form of Tinea capitis . It is caused by Tinea schoenlein .It causes cicatricial alopecia.
• The Hamilton Norwood scale is used for Male Androgenetic Alopecia.
• A woman presents to a dermatologist because she has lost almost all the hair on her body,
including scalp hair, eyebrows, eyelashes, armpit and groin hair, and the fine hairs on her body and
extremities. She most likely has a variant of Alopecia Areata.
• A 40 year old, formerly obese woman presents to her physician. She was very proud of having lost
36Kg. during the previous 2 years, but now noticed that her "hair is falling out." On questioning, she
reports having followed a strict fat-free diet. Her alopecia is probably related to a deficiency of
Vitamin A.
• Severe painful sensorimotor and autonomic neuropathy along with alopecia may suggest poisoning
with Thallium.
• A female patient presents with diffuse alopecia to you. She had suffered from typhoid fever 4
months back. Most probable diagnosis is Telogen Effluvium.
• A 30 year old female developed diffuse hair loss 3 months after delivery of her first child. The
probable diagnosis is Telogen Effluvium.
• Pseudo pelade is synonym of Cicatrical Alopecia.
• In DLE (a form of SLE) there is cicatrial alopecia & in SLE there is non cicatrial alopecia; thus SLE has
both forms of alopecia.
• Alopecia aerate is presumed to be Autoimmune in etiology.
• Exclamation mark hairs is seen in Alopecia Areata.
• Male with patchy loss of scalp hair and grey hair in the eyebrows and beard diagnosis is Alopecia
Areata.
• Alopecia areata is treated by Minoxidil.
• An 8 yr old boy presents with boggy swelling and easily pluckable hair, Diagnosis is Tinea Capitis.
• A 8 year old child has localized non cicatrial alopecia over scalp with itching and scales. The
diagnosis is Tinea Capitis.
• Moth eaten alopecia is seen with Syphilis.
• Hypogonadism, reduced immunity and alopecia may be a deficiency manifestation of Zinc.
• Most common type of non scarring alopecia is Androgenic.
• Alopecia thin brittle nail, sparse hair with thin enamel diagnosis is Ectodermal Dysplasia.
• Patchy hair loss with velvety skin points to the diagnosis of Hyperthyroidism.
• A child presenting with localized patches of complete hair loss with normal appearance of scalp.
Diagnosis is Tinea Capitis.
38. Immune mediated Bullous Disorders

• In pemphigus vulgaris,antibodies are present against Intercellular membrane.
• A person presents with hemorrhagic fluid in tense blister at dermoepidermal junction. Most
probable diagnosis is Pemphigoid.
• Epidermal bullae are seen in Pemphigus Vulgaris.
• Dermatitis Herpetiformis shows deposition of IgA in dennal papilla.
• The “dilapidated brick wall” appearance is classically seen in the histopathology of Hailey Hailey
disease.
• A 30 year old pregnant woman presents to a physician with painful oral ulcers. Physical
examination demonstrates widespread erosions of her mucous membranes. Close examination
reveals a friable mucosa, but no well-defined aphthous ulcers. Biopsy of perilesional mucosa
demonstrates acantholysis; direct immunofluorescence demonstrates an intraepidermal band of
IgG and C3. Pemphigus Vulgaris is the most likely diagnosis.
• A 30 year old male presents with itchy papulo-vesicular lesions on the extremities, knees, elbows
and buttocks since one year. Direct immunofluorescence staining of the lesions showed IgA
deposition at dermoepidermal junction. Dermatitis Herpetiformis represents the most probable
diagnosis.
• A 40 year old male developed persistant oral ulcers followed by multiple flaccid bullae on trunk and
extremities. Direct immunofluorescence examination of a skin biopsy showed intercellular IgG
deposits in the epidermis. The most probable diagnosis is Pemphigus Vulgaris.
• Pemphigus Vulgaris is associated with acantholysis.
• A 45 yr old female developed recurrent oral erosions followed by multiple flaccid bullae on trunk
and extremities. A tzanck smear showed acantholytic cells and direct immunofluoroscence showed
intercellular IgG deposits in the epidermis. The most probable diagnosis is Pemphigus Vulgaris.
• Itching associated with linear IgA deposition in dermal papillae is a feature of Dermatitis
Herpetiformis.
• Penicillin, cephalosporins, penicillamine, rifampicin, captopril, piroxicam, phenylbutazone are drugs
commonly associated with drug induced pemphigus.
• Pemphigus vulgaris is characterized by Positive Nikolsky’s sign ,Oral erosions,Intraepidermal bulla,
Tzanck smear showing acantholytic cells.
• Pemphigus vulgaris is an intraepidermal blistering disease due to antibodies against desmogleins
(epidermal attachment complexes).It presents with flaccid blisters and oral erosions in a middle
aged person.
• Fogo selvagem is a type of Pemphigus Foliaceous.
• U-serrated pattern in direct immunofluorescence is seen in Epidermolysis Bullosa aquisita.
• Linear IgA disease presents with a "string of pearl appearance".
• Direct immunofluorescence (DIF) is of great value in the early diagnosis of pemphigus vulgaris.
• Oral mucosal lesions are seen in Pemphigus Vulgaris.
• 'Bulla spread sign' is seen in Pemphigus Vulgaris.
• Acantholytic cells in Pemphigus are derived from Stratum Spinosum.
• 'Row of tombstones ' appearance is seen in Pemphigus.
• Subepidermal lesion are seen in Bullous Pemphigoid,Dermatitis herpatiformis,Burns.
• Acantolytic cells in pemphigus is- Cell with hyperchromatic nuclei and perinuclear halo.
• Nikolsky sign is positive in Staphylococcal scalded skin syndrome , Toxic epidermonecrolysis ,
Pemphigus,Herpes Zoster,Herpes Simplex.

• Genetic predisposition is seen in Epidermolysis Bullosa.
• Hailey - hailey disease is Benign familial chronic pemphigus.
• Commonest/rarest veriety of Pemphigus is Pemphigus Vulgaris/Vegetans.
• Antibody are formed against desmogleins in Pemphigus Vulgaris.
• A 50 year old male known case of myasthe-nia with erythemated shallow erosions with few blisters
and scales. Oral mucosa is not involved. Immunopathology demonstrates IgG deposition on
keratinocytes and auto antibodies against Dsg -1. The diagnosis is Pemphigus Foliaceous.
• Paraneoplastic pemphigus may be associated with non Hodgkin's lymphoma (NHL), Chronic
lymphocytic leukemia (CLL), Castleman's disease, thymoma and spindle cell tumors. And pemphigus
folliaceus is associated with thymoma & /or mysthenia gravis.
• A 56 year old male lallu presents with painful bullous lesion in lower extrimity, the most likely
diagnosis is Bullous Pemphigoid.
• A 85 year old woman with Nikolsky sign-ve, blisters on thigh & trunk, lesions come on & off.
Pemphigoid is the cause .
• Inter cellular IgG deposition in epidermis is seen in Pemphigus.
• Direct immunofluorescence is positive in Pemphigus.
• Linear IgA disease presents with severely pruritic, subepidermal blisters. On DIM, linear (not
granular) deposits of IgAQ is seen along EBM. It is a separate & distinct entity different from
dermatitis herpetiformis and so gluten free diet is not required
• A 65-year old male presented with tense blisters associated with itching on normal looking skin
with urticarial plaques as seen in the figure. Bullous Pemphigoid is the most likely diagnosis.
• Tense itching bulla is seen in Bulllous Pemphigoid.
Psychiatry
1. Obsessive Compulsive Disorder
• It is a disorder of thought content.

• Features of OCD are Ego-Alien(Ego Dystonic),Insight ,Failure to resist,Irrationale
Thought,Persistence of idea.
• Defence mechanism in OCD includes Repression,undoing and displacement.
• Area of brain involved in OCD is Basal Ganglia.
• Combination of behaviour & drug therapy is the treatment of choice.
• Behavioural Therapy includes particular forms of Cognitive behavior therapy (exposure and
response prevention) .
• First-line medicines for OCD are selective serotonin reuptake inhibitors (SSRIs; (fluoxetine,
fluvoxamine, sertraline, paroxetine, citalopram, escitalopram) and clomipramine , a tricyclic
antidepressant.

• In OCD treatment is based on Serotonergic receptor.
• Other secondary medicines used are Carbamazepine,Lithim,etc .
• Drug of choice for OCD is SSRIs.
• Selective serotonin reuptake inhibitors (SSRIs) are US-FDA approved drugs of first choice (line) for
Major Depression, Obscessive - compulsive disorder (OCD), Premenstrual dysphoric disorder, Post
traumatic stress disorder (PTSD), Panic disorder, Eating disorder (bulimia nervosa), and Social
phobia (social anxiety disorder).
• Psychoanalytic psychotherapy is also used as a treatment modality in OCD.
2. OBSESSIVE-COMPULSIVE DISORDER
• Obsession to Dirt and contamination is a common finding of OCD

• ½ of the people with OCD later develop sever depressive episode.
• Obsessive Compulsive Disorder is associated with intrusive thoughts (obsessions) and unusual
rituals and activities (compulsions).
• Ego's defence mechanism "Undoing" is typically seen in OCD
• Perfectionism interfering with performance, Compulsive checking behaviour ,Preoccupation with
rule are find in OCD
• Irritational thought,Resisting the idea, Persistence of idea are find in OCD
• Abnormal thought possession is found in OCD
• Repression,Undoing,Denial & Displacement are Defence mechanism in OCD
• Patient is conscious about the disorder in OCD
• Irresistible desire to do a thing repeatedly is seen in OCD
• Area of brain involved in OCD is Basal ganglia
• Compulsive hair pulling that produces bald spots is called Trichotillomania
3. Phobia
• The woman who cannot urinate in a restroom because of embarrassment is probably suffering
from social phobia.
• Agoraphobia is a disorder characterized by Avoidance of situations in which it occurs ,Presence of
panic symptoms, Avoidance of being outside alone
• Phobia is neurosis
• Commonest type of phobia seen in clinical practice is Agoraphobia
• Displacement is the defense mechanism in phobia
• Patient of contamination phobia was asked by therapist to follow behind and touch everything he
touches in patients house Therapist kept talking quietly & calmly all the time .This procedure is
called modelling
• Systemic de-sensitization therapy is used for phobia
• In Agoraphobia behavioural therapy is helpful
• Thanatophobia – fear of death
• Claustro phobia- Fear of closed spaces
• Acrophobia – fear of high places.
• Definitive treatment of all types of phobias is behavioural therapy
• Systemic desensitization,Psychodynamic therapy,Exposure therapy are the method of
treating Agoraphobia
• SSRI is first line treatment for Panic disorder, Social phobia, Post traumatic stress disorder
4. MANAGEMENT OF OBSESSIVE-COMPULSIVE DISORDER
• Drug of choice for OCD is Fluoxetine

• Clomipramine is used for treatment of OCD
• In psychoanalytic terms, obsessive compulsive disorder is fixed at Anal stage
• Treatment of choice for OCD is Combination of behavior and drug therapy
• In OCD treatment is based on Serotonergic receptor
• Exposure & response prevention ,Psychoanalytic psychotherapy, Clomipramine are the treatment
modalities of OCD
5. Post traumatic Stress Disorder
• Recall of events and avoidance of similar experiences in PTSD

• The principal features of Post traumatic stress disorder (PTSD) are painful re-experiencing of the
event (reliving experience, frightening dream with unrecognisable content in children),
avoidance (avoiding the things or places involved in the trauma), emotional numbing and constant
hyper arousal (anger, irritability, difficultly falling asleep etc).
• SSRIs are drug of choice for Post traumatic stress disorder
6. PANIC DISORDER
• Sudden onset breathlessness, anxiety, palpitation & feeling of impending doom suggest panic
attacks
• Patient showing Chest pain, sweating, restlessness, dyspnoea, and palpitation which
is asymptomatic with supportive measures is diagnosed to have panic disorder
• Patient afraid of dying, experiencing chest pain, a sensation of choking, nausea, and tingling
sensations, face is flushed and sweating, high pulse and respirations rate but 15 minutes later
symptoms are dissipating & normal ECG suggest Panic disorder
• Behaviour therapy is useful in panic disorder
• Panic attack is Acute anxiety
• Panic attack is associated with a disturbance in Serotonin, GABA,Dopamine, CCK, pentagastrin
• SSRI is first line treatment for panic disorder
• Agoraphobia associated with panic disorder
7. Generalized Anxiety Disorder
• Muscle tension,Irritability,Restlessness but not Fear of impedending doom are seen in general
anxiety disorder
• Lithium is not used in treatment of general anxiety disorder
• SSRIs are not effective in treatment of general anxiety disorder
8. Psychosexual Phases
• Theory of "Psychosexual development" was given by Sigmund Freud

• Life span of Sigmund Freud was 1856-39 and he passed most of his life in Austria
• Oedepius complex has been described by Sigmund Freud
• Oedipus complex (given by sigmund freud) is seen in Boys of 3 - 5 years of age
9. Sexual Perversions
• Catamite is Young passive victim of sodomy

• Faecal smell,Tear of Frenulum,Relative Constriction of shaft of penis is seen in accuse of sodomy
• Unnatural sexual offences are Sodomy & Buccal coitus
• Bestiality is Having intercourse with an animal
• Sec. 377 IPC deals with sodomy
• Fetishism is a sexual perversion characterized by Sexual pleasure derived from inanimate objects
• Taking off ones clothes and running naked in a public race is called Exhibitionism
• Anal intercourse between two males or between a male and female is called sodomy
• Exhibitionism is punishable under Sec 294 IPC for imprisonment upto 3 months or fine or both.
• Heterosexual penile anal intercourse is called Buggery/Sodomy
10. Bulimia Nervosa
• Repeated episodes of excessive eating followed by purging by use of laxatives is seen in Bulimia
nervosa
• Anorexia nervosa can be differentiated from bulimia by Peculiars patterns of food handing
• The main differnce between anorexia nervosa and bulimia nervosa depends on weight
• Bilateral parotid enlargement with repeated episodes of uncontrolled eating is seen in Bulimia
nervosa
11. REM Sleep
• Brain is very active but muscles are virtually paralyzed in REM sleep
• Irregular breathing,depressed Muscle tone in the body ,active dreaming are seen in REM sleep
• Disturbances in sleep due to depression are associated with Decreased REM (rapid eye movement)
latency
• Bruxism is not seen in REM sleep
• Neurotransmitter For REM sleep is acetylcholine
• REM sleep Shows ? rhytm on EEG
• The condition known as REM sleep is Referred to as paradoxical sleep.
• Nightmare is seen in REM sleep
• Growth hormone secretion is decreased by REM sleep
12. Schizophrenia
• Lateral and third ventricle enlargement ,Deficits in smooth-pursuit eye movements,Increased

incidence of abnormally slow electroencephalogram tracings are seen in schizophrenia
• 3rd person auditory hallucination,Inappropriate emotions,Formal thought disorder
& incongruent affect are seen in schizophrenia
• Neurotransmitter which is implicated in both positive and negative symptoms in schizophrenia
is Dopamine
• 0.5% is the incidence rate of schizophrenia in general population
• Schizophrenia and depression both have Social withdrawal,Poor personal care,Decreased interest
in sex, suicidal tendencies
• Schizophrenia is a disorder of thoughts
• Split personality,Systemized delusion & Third person hallucination are the features that is
suggestive of Schizophrenia rather than organic psychosis
• Maximum heritability is seen in Schizophrenia I
• Incidenceof schizophrenia in India is 1 -5%
• Eugen Bleuer's fundamental symptoms include Ambivalence,Autism and Affect disturbance
• Schneider's first rank symptoms (SFRS ) is seen in schizophrenia
• The primary disturbance in schizophrenia is Formal Thought Disorder
• Waxy flexibility,Delusion of reference & Formal thought disorder are characterstics
of schizophrenia
• Auditory Hallucination & Catatonia is seen in schizophrenia
• Van Gogh Syndrome is seen in schizophrenia
• Schizophrenia mostly occurs in Adolescents
• Auditory Hallucination in schizophrenia respond earliest to treatment
• Gradual onset of suspiciousness, muttering and smiling without clear reason, decreased
socialization, violent outbursts, and lack of interest in studies ,blunt affect, thought broadcast, a

relatively preserved cognition, impaired judgment and insight are suggestive symptoms
of schizophrenia
• Neologism is characteristically seen in schizophrenia
• Perseveration is Persistent and inappropriate repetition of the same thoughts Characteristic of
schizophrenia
• Four A's of schizophrenia was described by Eugen Bleuler's
• Drugs abuse with symptoms similar like paranoid schizophrenia are seen in Amphetamine
13. TREATMENT & PROGNOSIS IN SCHIZOPHRENIA
• Good prognosis in schizophrenia is indicated by Late Onset ,Catatonic features ,Pyknic Built ,No
Family history, Acute onset ,Emotions are preserved ,Type I
• Subtle involuntary movements of hands, feet, lips, and tongue on decreasing the dose of
haloperidol is increase initially as the medication is decreased
• Resistant,negative symptoms & Refractory Schizophrenia is an indication for the use of Clozapine
• Drugs used in the treatment of schizophrenia have in common their ability to Block dopamine
receptors in the brain
• In Schizophrenia treated with CPZ (chlorpromazine) if develops auditory hallucination again should
be given Clozapine
• After the initiation of haloperidol if the patient shows be restlessness, fidgety, irritability and
cannot sit still at one place should be treated with betablocker
• Schizophrenia patient treated with Clozapine medication may develope purposeless involuntary
facial and limb movements, constant chewing and puffing of cheeks
• Bad prognostic indicator of Schizophrenia are Family history ,Poor Prognostic Factors,Younger age
of onset ,Disorganized type,Asthenic built,Chronic type,Blunting of affect or atypical Feature
Present,Type II
• Common Drugs used in schizophrenia include Chlorpromazine,Haloperidol,Olanzapine
14. Schizophrenia Types
• Type II Schizophrenia is characterised by prominent negative symptoms, intellectual deterioration,

enlarged cerebral ventricles and poor response to neuroleptics.
• Most common type of schizophrenia is paranoid
• Paranoid Schizophrenia is associated with best prognosis
• Catatonic features are seen in schizophrenia they are also seen in Severe depression & Conversion
disorder
• Schizotype is a personality disorder of DSM-IV which is not classified as PD & is placed with
schizophrenia in ICD
• Somatic passivityDelusions of control, persecution and self reference is a feature of Paranoid
schizophrenia

• Patient presents with psychomotor acitivity,Stuptor, waxy flexibility, negativism & rigidity Diagnosis
is Catatonic schizophrenia
• Grimacing and Mannerism is Catatonic Schizophrenia
• Schizophrenia with late onset and good prognosis is Catatonic SZP
• In Schizophrenia early onset with poor prognosis is seen in Hebephrenic
• Defect of conation is typically seen in Catatonic schizophrenia
• Paranoid schizophrenia is mimicked by intake of Amphetamine
15. Pica syndrome
• Pica is a pre-school problem seen in children most commonly below 3 year

• Pica is associated with lead poisoning
16. PSYCHOSOCIAL THEORY
• BY ERIK.H.ERICKSON (1963)
• Erik Erikson was a follower of Sigmund Freud who broke with his teacher over the fundamental
point of what motivates or drives human behavior.
• For Freud it was biology or more specifically the biological instincts of life and aggression.
• His developmental theory of the "Eight Stages of Man" was unique in that it covered the entire
lifespan rather than childhood and adolescent development.
17. Cognitive theory
• In Piaget's theory of cognitive development 'out of sight, out of mind' and 'here and now' is seen
in Sensory-motor stage
• Concrete thinking stage of cognitive development is 5-10 years
18. AUTISM
• Developed Isolated area of talent ,No attribution of Parental attitude and behavior
& delayed Emergence of speech and social smile is often suggestive of childhood autism
• A 5-year-old boy with normal motor skills has severe language delay, shows no interest in
interacting with other children or with adults, and spends a lot of time spinning around. The most
likely diagnosis for this child is Infantile autism
• A 3 year old child presents with developmental delayed in speech. He has difficulty in
communication and social interactions. His teachers and parents are worried that he is not making
any friends. He is observed to have unusual routines and repetitive activities is diagnosed to have
autism.
• The parents of a 4-year-old girl Mili is worried that she is isolating herself from people. She seems
to be deeply involved in her own games and keeping her toys in a particular order. She does not
speak full sentences yet. All other developmental milestones were normal. She does not leave
parents when she is taken out to a party or shopping. She finds it difficult to concentrate on reading
and has not managed to write alphabets is diagnosed to have autism.
• A 6-year-old boy is observed to be peculiar by his teacher. Children attempt to play with him but his
response is to either ignore them or get angry at their advances. This response in someone with
autism might best be described as Lack of social reciprocity.
• Autism Starts before 2-3 years of age
• Autism is Social and language communication problem
19. DEFENCE MECHANISM
• A student justifying his bad marks in an examination saying that the teacher did not give him the
marks that he deserve because he does not like him, is an example of Projection defence
mechanism.
• Anticipation & Altruism is a mature defence mechanism
• Ego's defence mechanism "Undoing" is typically seen in Obsessive compulsive neurosis
• One of the important defence mechanism is Repression
• Projection, Undoing,Conversion & Reaction formation are defence mechanisms of ego
• Defence mechanism in OCD Repression,Undoing & Displacement
20. Alzheimer's Disease
• In Alzheimer's disease Cortical atrophy of temporoparietal cortex is involved.

• Recent memory loss is feature of Alzheimer's disease
• Degenerated neurofilaments seen in patients with Alzheimer's disease are Neurofibrillary tangles
• Neurofibrillary tangles, Senile (neurotic) plaques & Amyloid angiopathy are feature of Alzheimer's
disease
• Trisomy 21 is associated with alzheimer's dementia
• The area of the brain resistant to Neurofibrillary tangles of Alzheimer's disease is Lateral geniculate
body
• Galantamine, Rivastigmine & Donepezil are used for treatment of Alzheimer’s disease
• Protein involved in Alzheimer's disease is Apo E gene
• Biochemical etiology of Alzheimer's disease relates it to Acetylcholine
• Dementia of Alzheimer's type is associated with Depressive symptoms, Delusions, Apraxia and
aphasia
• Alzheimer's disease is Common in 5th and 6th decade
• Alzheimer's disease is Atrophied gyri widened sulci
• In Alzheimer's disease number of senile neural plaques correlates (increases) with age
• In Alzheimer's disease there is presence of tau protein suggest neurodegeneration
• In Alzheimer's disease number of neurofibrillary tangles is associated with the severity of dementia
• Area of brain resistant to NFTs in Alzheimer's disease Lateral geniculate body
• Biochemical etiology of Alzheimer's disease relates to acetylcholine
• The fixative used in histopathology 10% buffered neutral formalin
• Donepezil is a cerebroactive drug. It is used in Alzheimer's disease (AD).
Radiology
1. Frontal Sinus
• Caldwell view is the best method to see frontal sinus in patients with recurrent frontal sinusitis
• Frontal sinus drain into Middle meatus
• Most superior sinus in the face is Frontal sinus
2. PET Scan
• PET scan uses FDG tracer material.

• The scan with highest sensitivity to detect adrenal metastasis due to bronchogenic carcinoma is:PET
Scan.
• A patient presented with a 4 cm tumour in the left pariental lobe for which he underwent surgery
and radiotherapy. After 2 months, he presented with headache and vomiting. FDG-PET Scan would
best characterize the lesion in this patient.
• Gold standard investigation for recurrent gastrointestinal stromal tumor is PET -CT.
• PET Scan is the best for differentiating recurrence of brain tumour from radiation therapy induced
necrosis.
• Radiation induced necrosis can be diagnosed by PET Scan.
• To detect distant metastasis in pancreatic cancer the imaging modality which is BEST used
is Positron-emission tomography.
3. MRI Scan
• Double line sign on MRI is seen in AVN of Hip.

• Absolute Contraindications for the MRI scan:
• Electronically, magnetically, and mechanically activated implants
• Ferromagnetic or electronically operated active devices like automatic cardioverter defibrillators
• Cardiac pacemakers

• Metallic splinters in the eye
• Ferromagnetic haemostatic clips in the central nervous system (CNS).
• The working of an MRI machine is based on the properties of Protons.
• HIV patients with low CD 4 counts if presents with multiple ring enhancing lesions on MRI is
suggestive of Tuberculoma, Primary CNS lymphoma and Toxoplasmosis.
• Spinal Cord infarctions appears as spinal cord edema in MRI scan.
• A 40-years-old female patient presented with recurrent headaches. MRI showed an extra-axial,
dural based and enhancing lesion. The most likely diagnosis is Meningioma.
• MRI Scan is the investigation of choice for assessment of depth of penetration and perirectal node
involvement in rectal cancer.
• Painful limp in a six year old boy with limitation of hip movements and tenderness in the groin
region confirms a diagnosis of Perthe’s disease. MRI is the investigation of choice to
include/exclude a diagnosis of Perthe’s disease.
• A 25 year old person presents with acute onset of fever and focal seizures. MRI scan shows
hyperintensity in the temporal lobe and frontal lobe with enhancement. The most likely diagnosis is
Hepres Simplex Encephalitis.
• The lack of a dural tail on MRI differentiates acoustic neuromas from cerebellopontine angle
meningiomas.
• In MRI the field used is 1.1 tesla.
• MRI is not better than CT for detection of Calcifies Lesions.
• MRI is useful for evaluating bone marrow.
• MRI is useful for localizing small lesion in the brain.
• MRI rooms are shielded completely by a continuous sheet or wire mesh of copper or aluminum to
shield the imager from external electromagnetic radiations, etc. It is called Faraday Cage.
• Atrophy of hippocampus, fornix and mamillary body are established MRI findings in Mesial
Temporal Sclerosis.
• Epidermoids can be differentiated from arachnoid cyst characteristically by hyper-intense diffusion
weighted images because of restricted diffusion of epidermoid cyst.
• MRI/CT appearance of lateral meningocele is widened Neural Foramen.
• T1 and T2 images are a feature of MRI Scan.
• A patient is suspected to have vestibular Shwanomma, the investigation of choice for its diagnosis is
Gadolinium Enhanced MRI.
• A middle aged female presents with prolonged history of back pain followed by slowly progressive
weakness of both lower limbs, spasticity and recent onset difficulty in micturation. On neurological
examination there is evidence of dorsal myelopathy. MRI scan of spine shows a well-defined mid-
dorsal intradural homogenous contrast enhancing mass lesion. The likely diagnosis is Spinal
Meningioma.
• A patient presented with unilateral proptosis, which was compressible and increases on ending
forward. No thrill or bruit was present. MRI shows a retro-orbital mass with enhancement. The
likely diagnosis is Orbital Varix.
• Best diagnostic modality to diagnose avascular necrosis is MRI Scan.
• Contrast used for MRI is Gadolinium.
• Investigation of choice in a patient brought with traumatic paraplegia is MRI Scan.
• MRI is a noninvasive imaging technique that does not involve exposure to ionizing radiation.

• Ideal investigation for fistula-in-ano is MRI.
• A bone bruise or contusion is best identified using MRI Scan.
• CSF on MRI appears Hypointense on T1 weighed image and hyperintense on T2 weighed image.
• Best imaging modality in patients with breast implants is MRI Scan.
• Investigation of choice for a pregnant lady with upper abdominal mass is MRI.
• In aortic dissection most accurate investigation is MRI Scan.
• The most sensitive and specific investigation in renal artery hypertension is MRI.
• MRI of the adrenal glands may distinguish adrenal adenoma from carcinoma.
• MRI is the best choice to evaluate radiologically a posterior fossa tumor.
• Current gold standard to detect ductal carcinoma in situ breast is MRI.
• A 14 yr old boy with abnormal movements. MRI shows involvement of bilateral striatum, thalami,
puns, centrum semiovale and asymmetrical diffuse white matter involvement. Wilson's Disease
could be the possible diagnosis.
• Penetrating iron particle in eye ,MRI investigation will not be used is such a case.
• Investigation of choice for spinal TB is MRI.
4. CT Scan
• Most sensitive and specific investigation for screening of Renovascular hypertension is Spiral CT
Angiography.
• Investigation of choice for juvenile nasoangiofibroma is Contrast enhanced CT Scan.
• CECT is the investigation of choice in a patient with blunt abdominal trauma with hematuria.
• Presence of calcification on an intracranial lesion is best made out by CT Scan
• Initial Investigation of choice of subarachnoid hemorrhage is CT Scan.
• Trauma to spleen in a stable patient is best diagnosed by CT scan.
• Endoscopic sinus surgery prerequisite is CT scan of PNS.
• Investigation of choice for Acute pancreatitis is CT Scan.
• IOC for ureteric stone with acute colic is Non Contrast CT scan.
• IOC for interstitial lung disease is CT scan.
• Investigation of choice for bronchiectasis is CT scan.
• IOC for pleural effusion is CECT.
• Best diagnosis of pancreatic cancer (head) is by CT scan.
• About non contrast CT scan in head injury:
• Extra dural haematomas are usually lens shaped.
• Acute subdural hematoma appears as crescent shadow of increased density.
• Subarachnoid haemorrhage appears as areas of increased density in basilar cisterns.
• In a patient with renal cell carcinoma with a thrombus in the IVCrenal vein, CT scan is the best for
diagnosis.
• In a case of Cushing's Syndrome,Adrenal CT scan distinguishes adrenal tumour from cortical
hyperplasia.
• Most diagnostic of pulmonary embolism in a high-risk case is Multidetector CT angiography
• Investigation of choice for small intestine tumor: CT scan with contrast.
• Investigation of choice for vascular ring around airway is CT scan.
• Investigation of choice for a lesion of temporal bone is CT scan.
• Slip ring technology is useful for CT scan.
• Preferred imaging modality for choanal atresia is CT scan.
• Most reliable test for spinal tuberculosis is CT guided Biopsy.
• NCCT head is the investigation of choice for evaluation of acute head injury.
5. USG
• To detect a 4 mm nodule in the pancreas, the investigation of your choice would be Endoscopic
USG.
• USG examination of an 8 weeks pregnant female shows a gestational sac with absent fetal parts.
The diagnosis is Blighted Ovum.
• Basanti, a 28yrs aged female with a history of 6 weeks of amenorrhea presents with pain in
abdomen; USG shows fluid in pouch of douglas. Aspiration yields dark colour blood that fails to clot.
Most probable diagnosis is Ruptured Ectopic Pregnancy.
• Young lady presents with acute abdominal pain and history of 1 1/2 months amenorrhoea. On USG
examination there is collection of fluid in the pouch of douglas and empty gestational sac. Diagnosis
is Ectopic Pregnancy.
• USG sign of fetal death:Heart beat absent; and Spalding sign.
• Contrast used in USG is Sonavist.
• USG is sensitive in Gall Stone,Blunt abdominal trauma.
• Piezoelectric crystals are made use of that is safe from radiation also,in USG.
• Midline hypoechoic mass with dilated lateral ventricles (on USG), bruit on auscultation,
hydrocephalus and high output cardiac failure in neonates/ infants is diagnostic of vein of galen
malformation.
• Ultrasonography is the investigation of choice to confirm diagnose of hypertrophic pyloric stenosis
with accuracy > 95% (approching almost 100%). USG visualizes thickened and elongated pyloric
canal. USG criteria for diagnosis include >16 mm pyloric length and >4mm pyloric muscle wall
thickness.
• Thickened gall bladder wall in USG seen in? Acute cholecystitis ,Mucosal thickening, Cholesterosis.
• Features of cholecystitis on USG : Thick fibrosed gallbladder wall , Stone impacted at neck of gall
bladder , Perigallbladder halo.
• Focal and diffuse thickening of gall bladder wall with high amplitude reflections and 'comet tail'
artifacts on USG suggest the diagnosis of Adenomyomatosis.
• Ectopic pregnacny, characteristic finding in USG is absence of gestational sac in uterus.
• Most accurate assessment of gestational age by USG is done by Crown Rump Length.
• 20 yr old man with progressive proptosis which increases on bending forward. It is compressible
and has no bruit or thrill. USG showed "hyperintense" mass with shadowing of mass. The diagnosis
is Orbital Varix.
• Ultrasound is the first radiological investigation done to evaluate obstructive or any jaundice. It is
both sensitive and specific for diagnosing gallbladder stones and biliary tract dilatation..
• USG is very sensitive for ascites.USG can detect as little as 100 ml of peritoneal fluid.

• Peritoneal deposits could also be detected on USG, but with difficulty. CECT and MR are the
preferred investigation for peritoneal deposits in that order..
• Ultrasound findings of pyelonephritis include the following:
• Renal enlargement
• Compression of the renal collecting system
• Decreased echogenicity (secondary to edema) or increased echogenicity (potentially from
hemorrhage)
• Loss of corticomedullary differentiation
• Poorly marginated mass(es)
• Gas within the renal parenchyma
• Focal or diffuse absence of color Doppler perfusion corresponding to the swollen inflamed areas.
• Pseudo kidney is thickened bowel loop on USG,which is seen in Intussception.
• A 3 year old girl presents with recurrent UTI. On USG shows hydronephrosis with filling defect and
negative shadow of bladder with no ectopic orifice.Diagnosis is Ureterocele.
• Investigation of choice for blunt trauma abdomen in unstable patient is USG.
• Investigation of choice for screening of proximal internal carotid artery stenosis is Doppler Flow
USG.
• Gold standard investigation for diagnosing cystic echinococcus is USG.
• Initial investigation for an amoebic liver abscess is USG.
• Investigation of choice for acute cholecystitis is USG.
• Investigation of choice for gall bladder stone is is USG.
• Common anomalies that can be seen in USG are:
• Cranial anomalies-anencephaly, hydrocephalus.choroid plaexus cysts
• Spinal anomalies-Spina bifida occulta and Spina bifida aperta
• Fetal heart
• Fetal abdomen and abdominal wall-Esophageal atresia, omphalocoele, gastroschisis
• Hydrops fetalis.
• Best time for diagnosing fetal abnormalities by USG is 13-19 weeks of pregnancy.
• Embryonic structure, identified earliest on USG, for confirmation of pregnancy is Gestational Sac.
• Best time to do USG in pregnancy, if it is to be done once in entire pregnancy, would be 18-22
weeks.
• Non invasive method for locating an expelled Cu-T is USG.
• Snow storm appearance of USG is seen in H.Mole.
• Initial IOC for intussesception is USG.
• Transvaginal USG can detect fetal cardiac activity in 5 weeks.
• Best parameter by USG to assess fetal maturity is Biparietal Diameter at 12 weeks.
• Antenatal diagnosis of hydrocephalus is done by USG.
• Acoustic shadow on USG is due to Reflection.
• The earliest congenital malformation that can he detected on USG is Anencephaly.
• Lactating women with painful breast, 1st investigation to be done should be USG.
• USG feature: String of pearls/ Necklace appearance is seen in PCOD.
• Investigation of choice for acute appendicitis in children is USG.
• First trimester USG finding in Down syndrome is Nuchal Translucency.
• Investigation of choice for varicose veins:Duplex Ultrasound.

6. Radionuclide Scanning
• The best method of investigation is case of acute cholecystitis is Radionuclide Scanning.

• Neuroendocrine tumors (NET) can be best detected by Radionuclide Scanning.
• Radionuclide scan is done for parathyroid adenoma is Sesta MIBI scan.
• A patient presents with acute renal failure (ARF) and complete anuria. The USG is normal. DTPA
Scan(Radiorenogram) will give best information regarding renal function.
• Investigation of choice for locating Parathyroid gland is Tc-Thallium Substraction Scan.
• Functional Analysis of Kidney is best done by Radionuclide Scanning.
• The most sensitive test to detect GI bleeding is Radiolabelled, erythrocyte scanning .
• Best Diagnosis for Ectopic gastric mucosa of meckels diverticulum is Radionuclide Scan(Technetium-
99 scan).
• Thallium Scan is performed to detect reversible myocardial ischemia.
• In radionuclide imaging, the most useful radiopharmaceutical agent for skeletal imaging is Tc-99m
linked to methylene diphosphonate (99m Tc-MDP).
• Tc-99 pyrophosphate is used for defining hot spots in myocardial infarction/avid infarct imaging
• 99m Tc-Sc is used in imaging of reticuloendothelial system (liver/ spleen), gastric emptying, GI
bleeds
• Gallium 67 is used for tumours/abscess.
• Gamma camera is used for measuring the radioactivity and Radionuclide Scanning.
• Scans used for:
• Hot spot in MI: Technetium scan
• Pancreatic scanning: Selenium 75
• Parathyroids: Sestamibi scan
• Renal GFR estimation: Tc 99DTPA scan
• Vesicourethral reflex: MAG3 Tc 99 scan
• Thyroid scan: 1-131
• Radionuclide Scan is initial investigation of choice for a patient presenting with solitary nodule of
thyroid.
• Curie is a unit for quantity of radionuclide disintegrating per second.
• Investigation of choice in parathyroid pathology is Technetium-thallium subtraction scan.
• DTPA radionuclide is best suited for measurement of GFR.
• Biliary radionuclide scanning (HIDA scan) may be of help in the atypical case. Lack of filling of the
gallbladder after 4 hours indicates an obstructed cystic duct and, in the clinical setting of acute
cholecystitis, is highly sensitive and specific for acute cholecystitis. A normal HIDA scan excludes
acute cholecystitis.
7. ERCP,MRCP,HIDA Scan
• Biliary radionuclide scanning (HIDA scan) may be of help in the atypical case. Lack of filling of the
gallbladder after 4 hours indicates an obstructed cystic duct and, in the clinical setting of acute
cholecystitis, is highly sensitive and specific for acute cholecystitis. A normal HIDA scan excludes
acute cholecystitis.
• Best screening method for Mirizzi syndrome is: ERCP.
• Risk factors for post-ERCP pancreatitis are minor papilla sphincterotomy, sphincter of Oddi
dysfunction, prior history of post-ERCP pancreatitis, age 2 contrast injections into the pancreatic
duct..
• Elective ERCP with sphincterotomy is considered in patients with persistent / incipient biliary
obstruction, those who are poor candidates for cholecystectomy, and for those in whom there is
strong suspicion for bile duct stones after cholecystectomy. ERCP with stent placement is indicated
for pancreatic ductal disruptions..
• Urgent ERCP is indicated in patients who have severe acute biliary pancreatitis with cholangitis.
• ERCP in pancreatitis is done to know about Gall Stones.
• Magnetic resonance cholangio pancreatography (MRCP) is a non - invasive alternative to evaluate
biliary tree.It is used to obtain the image.
• Best investigation for acute cholecystitis is HIDA Scan.
• ERCP is the gold standard for diagnosing CBD stones..
• ERCP, sphincterotomy and balloon clearance is now the standard treatment for stone in the
common bile duct.
• ERCP may provide direct diagnosis of the distal CBD pathology and may be therapeutic as well for a
CBD stone or stricture..
• 5 days after CBD surgery there is a small leak. ERCP and Stenting will be the best T/t.
• ERCP is the most sensitive test for detecting pancreatic cancer but CT scan is the inv. of choice.
• Most common complication after ERCP is Acute pancreatitis.
• Best investigation for diagnosis of ampullary gall stone with obstructive jaundice is ERCP.
• Chain of lakes appearance on ERCP is seen in Chronic Relapsing Pancreatitis.
• On HIDA scan. gall bladder is not visualized.
• Magnetic resonance cholangiopancreatography (MRCP) is not a cause of Acute pancreatitis.
• Principle of MRCP:Use of heavily T2-weighted image without contrast to create the three
dimensional image of the biliary tree using MIP algorithm.
• A 3-month-old child with history of passage of clay colored stools and dark yellow urine since one
month was given steroids and ursodeoxycholic acid. On further investigation, he was found to have
direct bilirubin of 6 mg%. HIDA Scan is the most sensitive investigation for the diagnosis of above-
mentioned condition.
8. Renal Diagnostics(Pyelogram,Urogram,Nephrogram,Cystourethrogram,Cystometry,DTPA Scan)
• Radiological sign of Papillary Necrosis on Excretory Urogram:

• a.Tracks and horns of contrast medium arising ,from the calyceal fornices (representing necrosis
around the papillary margin.)
• b.Egg in a cup appearance (due to central necrosis producing central pool of contrast within the
papillae)
• c. Ring shadow (Papillary sloughing produces a central lucent filling defect with a surrounding ring
of contrast medium).
• Bead cystogram is used for the diagnosis of Stress incontinence.
• Cystogram is used to evaluate bladder filling defects (tumors, diverticula) and bladder perforation.
• Cystography and cystourethrography are important radiologic techniques for detecting
vesicoureteral reflux and may be used in the workup of patients with urinary stress incontinence.
• CT cystography (CT of the pelvis after the instillation of dilute contrast medium into the bladder)
has been shown useful in the evaluation of traumatic bladder rupture.
• Cystometry is the investigation of choice in a suspected case of detrusor instability or dyssynergia..
• A dense persistent nephrogram may be seen in : Acute ureteral obstruction , Severe
hydronephrosis , Dehydration.
• Non-visualisation of kidney in excretory urogram is seen in Renal Vein Thrombosis.
• Retrograde pyelography is useful to locate the site of PUJ obstruction
• Flower 'Vase' pattern of the pelvis in an intravenous urogram is seen in Horse Shoe Kidney.
• "Spider leg" deformity in excretory urogram occurs in Polycystic Kidney.
• Most reliable investigation in bladder rupture is Retrograde Cystogram.
• The posterior urethra is best visualized by Voiding Cystogram.
• A patient presented with ARF with complete anuria, but a normal ultrasound.Next investigation
would be Radio-renogram.
• Investigation of choice in Vesico-ureteric Reflux is Voiding Cystourethrography.
• Reflex nephropathy is diagnosed mainly by Micturationg Cystourethrogram.
• In intravenous pyelography, one contracted kidney indicates Chronic Pyelonephritis.
• Nephrogram phase of IVP is because of dye in Proximal Convoluted Tubule.
• Polycystic Kidney is diagnostic of the 'Rim sign' in a nephrogram.
9. Barium Studies
• Apple core sign in barium enema is seen with Colon Carcinoma.

• "Bird of Prey" sign is seen in the radiographic barium examination of Sigmoid Volvulus.
• On radiography widened duodenal 'C' loop with irregular mucosal pattern on upper gastrointestinal
barium series is most likely due to Duodenal Ulcer.
• Corkscrew esophagus on barium swallow is seen in Diffuse Esophageal Spasm.
• Barium swallow shows a beak like appearence in Achalasia Cardia.
• The lead pipe appearance of the colon on a barium enema is seen in Crohn's involvement of colon.
• Diffuse esophageal dilatation on barium swallow is seen in Achalasia and Trypanosomiasis.
• Ileocecal tuberculosis presents with stricture of terminal ileum, widening of ileocecal angle and
pulled up contracted cecum on barium study.
• Main indications for water soluble contrast barium enema are neonatal low
gastrointestinal obstruction, suspected post -necrotizing enterocolitis strictures, Hirschsprung's
disease and after colonic surgery.
• On barium swallow the grade IV esophageal varices appear as mucosal folds below the carina.
• Second swallowing in barium meal studies is found in Pharyngeal Pouch.
• Most useful investigation in sliding hernia in female is Barium Meal.
• Colonic diverticulosis is best diagnosed by Barium Enema.
• The area of the colon which is least visualized by barium studies is Sigmoid Colon.
• In intestinal obstruction, investigations needed is Intestinal Barium Meal.
• Intusssusception is usually relieved by Barium Enema.
• Complete Rx of intussception is indicated by free passage of barium in the terminal ileum.
• A lady presented with non progressive dysphagia only for solids. Barium study showed proximal
esophageal dilatation with distal constriction. The most likely diagnosis is Lower Esophageal Ring.
• A young patient presents with history of dysphagia more to liquid than solids. The first investigation
you will do is Barium Swallow.
• Substance utilized for barium meal follow through study is Barium Sulphate.
• 'Thumb print' appearance on Barium enema is found in Bowel Ischemia.
• 'Carman meniscus sign' in barium meal is pathognomic of Malignant Gastric Ulcer.
• Reversed "3" sign on barium studies is seen in Carcinoma of head of Pancreas.
• Saw tooth' appearance on barium enema may be seen in Diverticular Disease of Colon.
• Barium meal picture of carcinoma stomach shows: Filling defect , Loss of rugosity , Small capacity of
stomach.
• Coiled spring appearance on barium enema is seen in Intussception.
• 'Scalloping' of the edge of sigmoid colon on barium enema seen in Pneumatosis Intestinalis.
• Pipe stem appearance in barium enema is seen in Ulcerative Colitis.
• The X-ray finding of small intestinal malabsorption syndrome is Flocculation of Barium.
• Left atrial enlargement is best seen with Barium swallow right anterior oblique view.
• Posterior displacement of the oesophagus on barium meal in left atrial enlargement.
• Barium meal is a less useful diagnostic procedure in a case of acute haematemesis.
• Common features of malignant gastric ulcer on barium meal : Carman's meniscus sign , Radiating
folds which do not reach the edge of the ulcer ,Lesser curvature ulcer with a nodular rim.
• On barium swallow posterior indentation is seen due to Aberrant right subclavian.
10. Angiography ,Venograpgy,Lymphangiography
• Indications for penile angiography : Peyronie's disease , Erectile dysfunction , Arteriovenous

malformation.
• The major disadvantage of mesenteric angiography in the setting of GI bleeding is it does not
identify the specific cause of bleeding.
• A patient presents with sudden onset of blurring vision, micropsia and central scotoma. Fundus
examination shows an oval area of retinal elevation in the macula and fundus angiography shows a
smokestack configuration of fluorescein dye leaking from the choriocapillaris. He is most likely
suffering from Central Serous Chorioretinopathy.
• Fluorescein angiography done in a case of Cystoid Maculae Edema shows leakage of fluorescein dye
from the perifoveal retinal capillaries and peripapillary region, and accumulating in a flower-petal
pattern around the fovea.
• Best test to determine etiology of SAH is inter-arterial digital Substraction Angiography.
• In patient with high clinical suspicion of pulmonary thromboembolism, best investigation would be
CT Angiography.
• Lens and cornea are avascular structures of eye that's why fluorescein angiography can't be used to
identify lesions.
• Dye is injected in carotid artery in cerebral angiography.

• The initial investigation of choice for a post cholecystectomy biliary stricture is Magnetic Resonance
Cholangiography.
• The gold standard for the definitive diagnosis of the extrahepatic biliary atresia is Peroperative
Cholangiography.
• In cholangiography CBD stone appears as Meniscus Sign.
• Cholangiography via T-tube done after 10-14 days of cholecystectomy.
• Dye used in IV cholangiography is Biligraffin.
• Lymphangiograpgy of the leg is performed by Dissecting lymphatics through an incision on the
dorsum of the foot .
• Premature filling of veins is a manifestation in cerebral angiography of Arteriovenous
Malformation.
• The glomus tumor invasion of jugular bulb is diagnosed by Jugular Venograpgy.
• Magnetic Resonance Angiography is the most specific screening test for renovascular hypertension.
• Contrast Enhanced Arteriography (Angiography) is the most definitive diagnostic procedure for the
diagnosis of Renal Artery stenosis while Magnetic Resonance Angiography (MRA) is the most
sensitive and specific non invasive test (screening test) for its diagnosis.
• Cerebral angiography was performed by Egas Moniz.
• Angiography is the investigation of choice in Central Serous Retinopathy.
• A young adult presents with proptosis and pain in eye after 4 days of trauma to eye. Chemosis,
conjunctival congestion and extraocular muscle palsy with inability to move eye are seen.
Investigation of choice is Digital Substraction Angiography.
• Transfemoral route is the preferred route for cerebral angiography.
• Investigation of choice for diagnosing lung sequestration is Angiography.
• Vessels catheterized on carotid angiography are 2 internal carotids and 1 vertebral.
• CT scan shows a suharachnoid haemorrhage following symptoms of sudden headache and
paralysis. Next investigation of choice is: 4 vessel Angiography.
• Coronary CT angiography is best for Coronary Plaque lesions.
• Puff of smoke appearance on cerebral angiography is seen in Moyamoya disease.
• Fluorescein angiography is used in :?
• Diabetic retinopathy
• Neoplasm
• Papilloedema
• Central serous retinopathy
• Retinitis pigmentosa and other retinal degeneration
• Choroidal diseases : Choroidal neovascularization
• Vascular occlusions (CRVO, CRAO)
• Eale's disease
• Cystoid macular edema.
• Deep vein thrombosis post-operatively is diagnosed by Ascending venography.
11. Radiation

• Back ground radiation is a low level, wide spread (ubiquitous), constantly present radiation from
natural sources that is usually not detrimental to life.
• About Electromagnetic radiation: Infrared is a EM radiation , Compton scattering occur for
intemediate energy.
• Amount of radiation delivered to an organ is defined as absorbed dose.
• Equivalent dose is a measure of biological damage caused by the absorbed dose depending on the
relative effectiveness of type of radiation; and effective dose is a measure to assess the risk of
carcinogenesis & genetic defect by calculating an imaginary total body dose depending on
equivalent dose for each organ and relative sensitivity of each organ to radiation.
• Alpha is the most ionizing radiation.
• Functional basis of ionising radiation depends on removal of orbital electron.
• Radiation produces its effect on tissue by charring of nucleoprotein,Denaturation of DNA.
• Radium emits α rays; β-rays; γ -rays.
• Maximum permissible radiation dose in pregnancy is 0.5 rad.
• Most common hormone deficiency seen after intracranial radiation therapy is Growth hormone.
• MC cancer due to Radiation is Leukemia.
• Mucositis and Enteritis are late effects of radiation therapy.
• Most common early (acute) manifestation of local skin reaction is erythema which is followed by
desquamation.
• 'Stochastic effects' of radiation:Probability of effect is a function of dose.
• Low dose radiation cause Lung cancer; AML; Cervical cancer.
• Dose of radiation during whole body exposure that leads to haematological syndrome is 2 Gy.
• USG is based on piezoelectric effect of lead-zirconate titanate and MRI is based on gyromagnetic
property of proton (hydrogen nucleus). Both are associated with no risk of radiation exposure.
• The radiation exposure in decreasing order is CT scan > Barium enema > Dynamic cardiac scan > PET
> Bone scan > IVU > Xray.
• Radiation is an etiological agent for papillary carcinoma thyroid & external radiation is used in
treatment of anaplastic cancer thyroid.
• Total skin electron irradiation is used for Mycoses Fungoides.
• The source of endogenous radiation is Potassium.
• Terrestrial radiation is maximum in Kerela.
• Effect of radiation above threshold level is non-stochastic effect.
• 0.05 mm is the approximate penetrating ability of alpha particle radiation at tissue level.
• Unit of one of radiation absorbed is Gray.
• The maximum permissible level of occupational exposure to radiation is 5 rad per year.
• Testicular tumour most sensitive to radiation is Seminoma.
• Differentiated thyroid carcinoma particularly papillary variety frequently follows accidental
irradiation of thyroid in infancy and childhood.
• Most common type of cataract following radiation is Posterior Subcapsular.
• Bone Tumour which can occur following exposure to radiation is Osteosarcoma.
• Dactinomycin requires a dose adjustment in patient during radiotherapy in order to prevent
radiation toxicity.
• Radiation of 5 Gy will kill patients in 4-6 weeks.
• 6-10 Gy radiation dose is needed for permanent testicular sterilization in normal male.

• Treatment for post-radiation skin lesion like desquamation is observation alone.
• Malignant Melanoma is least sensitive to radiation.
• MRI and USG are not using ionising radiation.
• Least affected by radiation is Cartilage.
• Mantle irradiation is used in Hodgkin's Disease.
• One gray of radiation is equal to 100 rad.
• Cell most sensitive to radiation is Lymphocyte.
• Commonly used type of radiation in radiotherapy is Gamma Rays.
• Radiation protection shields are made up of: Lead.
• Anaplastic Carcinoma responds best to radiation.
• Thickness of lead apron to prevent radiation is 0.5 mm.
• Acute radiation sickness is characterised by:Hematological symptoms , CNS symptoms ,
Gastrointestinal symptoms.
• Least sensitive structure to radiation is Vagina.
• Intracavitary radiation is given in Carcinoma of Cervix.
• The most common presentation of radiation carditis is Pericardial Effusion.
• Features of radiation include Fluorescein , Biological ,Photographic.
• The radiation tolerance of whole liver is 40 Gy.
• 8 Gy in one fraction of radiation therapy is recommended for pain relief in bone metastases.
• Planned radiation volume is more than targetted radiation volume.
• 80-85 and 85-90 gy is the maximum radiation dose to point A for early and advanced Ca cervix.
• SI unit of dose of radiation absorption is BPD.
• Foam Cells in vessel wall is the characteristic histological finding of chronic radiation pneumonitis.
• Phase of the Cell cycle which is most sensitive to radiation is G2M.
• Ionizing radiation commonly used for disinfection is Gamma Rays.
• Unit of radiation exposure is Roentgen.
• Units of potency
• Roentgen and coulomb per kilograme → Units of exposure. It is the amount to which a person is
exposed.
• Red and Gray→ Units of absorbed dose. It is the amount which is absorbed per gram of Ɵssue.
• Rem and Sievert → Product of the absorbed dose and the modifying factor. Represent the degree
of potention danger to health
12. CHEST XRAY
Chest Xray in the image shows:
• Visible pleural edge (green arrow)

• Lung markings not visible beyond this edge.
• Left sided rib fracture (yellow arrow)
• The trachea and mediastinal structures are not displaced so there is no 'tension'.
Probable diagnosis is Left sided Pneumothorax due to rib fracture

13. PULMONARY EDEMA
Causes include:
• Pneumonia
• Inhalation of toxins - such as chlorine, mustard gas, smoke
• Circulating toxins - such as histamine, septicaemia
• Disseminated intravascular coagulation
• Intravenous drug use like heroin
• heart failure:
Atrial, e.g. mitral stenosis
Ventricular, e.g. myocardial infarction, hypertension
• Pulmonary embolism, reperfusion

• IV fluid overload, e.g. from multiple blood transfusion
• Chest injury
• Acute LVF may be trigerred by a major event such as MI in a previously healthy heart
• An increase in the left ventricular diastolic pressure causes the pressure in the LA, pulmonary veins
and pulmonary capillaries to rise.
• When the hydrostatic pressure of the pulmonary capillaries exceeds the oncotic pressure of the
plasma (about 25-30 mm Hg), fluid moves from the capillaries into the alveoli
14. PRODUCTION OF XRAYS
• X-ray tubes produce x-ray by accelerating electrons to high energies (PG1 04, MP 01). The x-ray
tube filament (cathode) is heated to incandescense so that it emits electrons (liPn'r 9°' TN 9°) by
thermoionic emmision. A high voltage is applied between filament (cathode) and target (anode) so
that the electrons are attracted towards anode and the electrons from the filament are accelerated
away from the negatively charged filament to positively charged target. When the electrons hit the
anode (the target), x-rays are produced. These x-rays are used to take all conventional radiography
(plane x-ray) and computed tomograph (CT).
• You should know that these x-rays are photon. When electron strikes it produces photon by either
of two mechanisms:?
15. METHODS OF xray examination
• Simple radiography : - When we use the term x-ray in radiology, it usually means simple
radiography. It is also called plane x-ray. In simple radiography an x-ray beam is passed through the
patient to a photographic plate (x-ray plate).
16. New imaging techniques in USG
Ultrasound:
• Initial imaging modality of choice in obstructive jaundiceQ

• It can identify intra- and extrahepatic biliary dilatationQ
• Ascites can be detected by ultrasound.
• USG is IOC for acute calculous cholecystitis, chronic cholecystitis and cholilithiasis
Ultrasonography
• Initial imaging modality of choice in obstructive jaundice°

• It is operator dependent and maybe suboptimal due to excessive body fat and intraluminal bowel
gasp
USG can demonstrate
Size of GB and CBDQ Biliary calculiQ

Thickness of GB wall Occasionally, presence of stones within the biliary treeQ
Presence of inflammationQaround GB
17. TECHNETIUM-99M BONE SCAN
Bone scan/ nuclear medicine technique:
• The patient is injected with a small amount of radioactive material such as 600 MBq of technetium-
99m-MDP and then scanned with a gamma camera, a device sensitive to the radiation emitted by
the injected material.
• Two-dimensional projections of scintigraphy may be enough, but in order to view small lesions (less
than 1 cm) especially in the spine, single photon emission computed tomography (SPECT) imaging
technique may be required. About half of the radioactive material is localized by the bones. The
more active the bone turnover, the more radioactive material will be seen.
• Not all tumors are easily seen on the bone scan.
• Some lesions, especially lytic (destructive) ones, require positron emission tomography (PET)
18. BARIUM STUDIES

• MCU is the most accurate method of demonstrating vesicoureteric reflux, and as this is important
in children with urinary tract infection and reflux nephropathy.
• The ascending urethrogram gives excellent anatomical information concerning the distal urethra as
far as the distal sphincter mechanism.
• Ultrasound and CT are the investigations of choice in the diagnosis and staging of renal tumours.
• Dynamic CT is more accurate than angiography in detecting a small neoplasm.
• Antegrade pyelography is an accurate method of demonstrating precisely the site of an obstruction
to the upper urinary tract.
19. Boron Neutron Capture Therapy (BNCT)
• he nucleide then undergoes a nuclear reaction with the localized release of substantial amount of
energy and kills the tagged cancer cells but does not damage the surrounding untagged normal
cells.
• At present moderated neutron beams from nuclear reactors are used but there is ongoing work in
developing high current particle accelerator to produce low energy thermal or epithermal beams
for BNCT.
20. RADIOTHERAPY
• The postoperative radiotherapy in Willm's tumor is started within 10 days of surgery. Delay in
starting RT beyond 10 days leads to tumor cell repopulation and increase in relapse rate.
• Indication of RT in Willim's tumor are:
1.Stage II, III, IV with unfavourable histology (UH)
2. Stage III & IV with favourable histology (FH)
3.Metastatic disease
4. Clear cell sarcoma of kidney in all stages.
• Cytotoxic drugs and radiation cause cellular damage which leads to release of 5-HT from intestine
and activation of emetogenic 5-HT3 receptors. Therefore, 5-HT3 receptor antagonists (e.g.
ondenstron) are the DOC for this condition.
• Cisplatin is the most common culprit causing chemotherapy induced nausea and vomiting.
• Drugs used to treat chemotherapy induced nausea and vomiting are:
i) 5-HT3 antagonists (drug of choice): Ondansetron, dolasetron, palonosetron, granisetron.

ii) Other drugs: Dexamethasone, methylprednisolone, metoclopramide, BZDs (lorazepam) and
aprepitant.
• Cisplatin can induce vomiting within 24 hours or after 2 days. DOC for the early vomiting is
ondensetron while for delayed vomiting is aprepitant (substant P antagonist).
21. isotopes used in medicine
• Which of the following radioactive isotopes is not used for brachytherapy?

• Iodine-131
• All of the following radioisotopes are used as systemic radionucleide, except:
• Iridium — 192
• Which of the following radioisotopes is commonly used as a source for external beam radiotherapy
in the treatment of cancer patients -
• Cobalt-60
• One of the following radioisotopes is used for interstitial therapy:
• Iridium 191
• Isotopes have same atomic
• Number
• Radioisotopes which is used in teletherapy:
• Co-60
All isotopes are used for thyroid except:
• 1-122
• Radioactive isotopes that are used in treatment of cancer are
• Cesium; b i.e. Cobalt
• Which of the following radioactive isotopes is not used for brachytherapy:
• Iodine -131
• Which of the following radioisotopes is commonly used as a source for external beam radiotherapy
in the treatment of cancer patients
• Cobalt - 60
• Which of the following chemicals or isotopes is used in cardiac ventriculography?
• 99m Technitium is used as an isotope in Cardiac Ventriculography. It is a medical imaging technique
used to detemine the cardiac functions. Ejection fraction, stroke volume and cardiac output can be
measured by the procedure. Gallium is used to find out places where inflammation is present.
Most common radio-isotopes used as a source for external beam radiotherapy in the treatment of
cancer:
• Cobalt 60 is commonly used as a source for external beam radiotherapy in the treatment of cancer
patients

22. CRANIOSPINAL IRRADIATION
• Craniospinal irradiation is employed in the treatment of medulloblastoma.

• Craniospinal irradiation is employed in the treatment of:Medulloblastoma
23. Total Body Irradiation (TBI
• Craniospinal irradiation is employed in the treatment of:Craniospinal irradiation is employed in the

treatment of medulloblastoma.
• Craniospinal irradiation is employed in the treatment of:Medulloblastoma
Anaesthesia
1. Brachial Plexus nerve block
• Interscalene approach to brachial plexus block does not provide optimal surgical anaesthesia in the
area of distribution of ulnar nerve
• Pneumothorax is a common complication of brachial plexus nerve block
• Persistent paresthesia of forearm is due to injury to the peripheral nerve seen as complication of
axillary nerve block
2. Epidural anaesthesia
• Lower Segment Caesarean section (LSCS) can be carried out under Combined Spinal Epidural
anaesthesia
• In pregnant patients with mitral stenosis, mitral regurgitation, aortic stenosis or aortic regurgitation
epidural anaesthesia is the preferred route during labour.
• 2% concentration of lignocaine is used in epidural anaesthesia
• Epidural anaesthesia in pregnancy is Given through Epidural space
• Epidural anaesthesia in pregnancy Decreased venous return,Bladder
distension,Hypotension,Nausea & Hypotension
• Hypopnoea, Total spinal analgesia, Urinary retention are the complications of Epidural anaesthesia
in pregnancy
• T10 – S5 level of block outside dura is desired for painless delivery by epidural anaesthesia
• Epidural anaesthesia is preferred over spinal anaesthesia because of Prolonged duration of effect

3. Spinal Anaesthesia
• In spinal anaesthesia drug is deposited between Piamater and arachnoid

• First fibres to be blocked in spinal anaesthesia is Sympathetic preganglionic
• Hypotension and Bradycardia is seen in patients given high spinal anaesthesia
• A Lower Segment Caesarean section (LSCS) can be carried out under Spinal anaesthesia
• The most effective method to prevent hypotension during spinal anaesthesia is Preloading with
crystalloids
• Headache after spinal anaesthesia is believed to be due to loss of CSF
• Post spinal headache can last for 2 weeks
• 5% lignocaine is used for spinal anaesthesia.
• Increased intracranial pressure is the contraindications Spinal anaesthesia
4. INTUBATION
• Submental intubation is the choice in a patient with Le-fort II, Le-fort III, & naso-ethmoid fracture
• Difficult oral intubation may be associated with Receding lower jaw, Poor mobility of mandible
& Protruding upper incisor tooth
• Mallampatti classification is used for Inspection of oral cavity before intubation
• Blind nasal intubation is indicated in TM joint ankylosis, Impossible laryngoscopy & CSF otorrhea
• In severe maxillofacial trauma with low Sp02 the immediate management is Orotracheal
intubation
• Merits of nasotracheal intubation is Good oral hygiene
• Miller's sign, TMJ ankylosis & Micrognathia are related to difficult intubation
• An anaesthetist is using Mallampati classification for Inspection of oral cavity before intubation
• TM joint ankylosis, Impossible laryngoscopy & CSF otorrhea are indication for blind nasal
intubation
• Indication for endotracheal intubation are Pulmonary toilet, Maintenance of a patent airway & To
provide positive pressure ventilation
• RTA leading to ribs fracture producing flial chest and respiratory distress is managed with IPPV with
oral intubation
• During intubation of a child, type of endotracheal tube and blade of laryngoscope is Uncuffed tube
with straight blade
• A child presented in the casuality with fever, unconcous & papilloedema should be Intubated
• Endotracheal intubation reduces normal anatomical dead space
• Laryngea Mast Airway Intubation can be done
• During laryngoscopy and endo-tracheal intubation Flexion of the neck, Extension of Head at the
atlanto-occipital joint & In a straight blade laryngoscope, the epiglottis is lifted by the tip are the
maneuver to be performed
• Nasal intubation is contra indicated in CSF Rhinorrhea
• Both Oral and Nasal intubation are Acute Tracheo - Laryngo - bronchitis
• Intubation dose of pancuronium is 0.08 mg/Kg

• Suxamethonium muscle relaxants if used for endotracheal intubation might lead to cardiac arrest
in patient who had extensive soft tissue and muscle injury
• During endotracheal intubation, unilateral breath sounds, no air heard entering the stomach and
no gastric distension is suggestive of entry of the endotracheal tube into Right main bronchus
• Proper technique of endotracheal intubation involves Flexion of the neck and extension of the
atlantooccipital joint
• Sore throat is the most common complication related to intubation
• Neck flexion at atlanto-occipital joint is contraindicated during endotracheal intubation
• Injury resembling endotracheal intubation injuries is Manual strangulation
• In infant with respiratory distress fastest and accurate method to confirm intubation
is Capnography
• The laryngoscope shall be held in Left hand by a right handed person for the purpose of intubation
• The first priority in management of a case of head injury with open fracture of shaft of femur
is Intubation
• Standard method to differentiate between endotracheal and esophageal intubation is End tidal CO2
• Alternative to succinylcholine which muscle relaxant can be used while endotracheal intubation
is Mivacurium
• Drug used for emergency intubation is Propofol
• Infra ocular pressure rises in Intubation & laryngoscopy
5. LARYNGOSCOPY
• Acute laryngeal spasm during indirect laryngoscopy is seen in Acute epiglottitis

• During laryngoscopy and endo-tracheal intubation The laryngoscope is lifted upwards levering over
the upper incisors maneuver is not performed
• Anaesthesia used in microlaryngoscopy is Pollarad tube with infiltration block
• In a direct laryngoscopy Cricothyroid, Lingual surface of epiglottis & Arytenoids can be visualized
• Hidden areas of larynx viz. infrahyoid epiglottis, anterior commissure, ventricles and subglottic
region and apex of pyriform fossa are difficult to visualize by indirect laryngoscopy.
• Microlaryngoscopy was started by Kleinsasser
• The procedure that should precede microlaryngoscopy is Rhinoscopy
• laryngoscopy showing diagnosis of multiple juvenile papillo-matosis of the larynx should be
followed by Microlaryngoscopic surgery
• lntra ocular pressure rises in Intubation & laryngoscopy
6. MALIGNANT HYPERTHERMIA
• Receptor responsible for malignant hyperthermia is Ryanodine receptor

• Agent causing malignant hyperthermia is Succinylcholine
• Hyperkalemia, Metabolic acidosis & Hypertension are seen in malignant hyperthermia
• Halothane,Lidocaine, Isoflurane & Suxamethonium trigger malignant hyperthermia
• Sevoflurane is contraindicated for induction of anaesthesia in patient with H/O malignant
hyperthermia
• Increased muscle metabolism by excess of calcium ions causes increased heat production in
malignant hyperthermia
• Malignant hyperthermia is best treated with Dantrolene sodium
• End-tidal CO2 is increased to maximum level in Malignant hyperthermia
• Difference between thyrotoxicosis and malignant hyperthermia is Elevated serum CPK level in MH
• Malignant hyperthermia is caused due to Increased intracellular Ca
7. ETOMIDATE
• Etomidate is an intravenous induction agent that suppress steroidogenesis

• Etomidate may cause adrenal cortex suppression
• Etomidate causes pain at site of injection
• In RTA following splenic rupture with hemodynamically unstablity the induction agent of choice in
this case would be etomidate
• Etomidate is not suitable for continuous intravenous use in a cardiac dysfunction case as it
suppress the release of steroids from adrenals
• Etomidate produce cardiac stability in coronary artery disease patients
• Etomidate causes Coronary insufficiency
• Drugs contraindicated in acute intermittent porphyria is Etomidate & Thiopentone
• A intravenous anesthetic agent that is associated with hemodynamic stability, maintenence of CPP
with post operative nausea, vomiting and myoclonus is Etomidate
• Burn case with splenic injury indicated for laproscopy should be given Etomidate as ideal
anaesthetic agent of choice
• Etomidate causes Decreased steroid, Decreases Intracranial tension & Nausea and vomiting
8. KETAMINE
• Ketamine is the anesthetic agent of choice in a case of status asthmaticus

• A child is taken to operation theatre for correction of right-to-left shunt in Tetralogy of Fallot will be
administered ketamine anesthesia
• Ketamine increases arterial blood pressure
• ketamine inhibits polysynaptic reflexes in the spinal cord
• Ketamine functionally "dissociates" the thalamus
• Highest analgesic effect is a feature of Ketamine
• Emergence Delirium is characteristic of Ketamine
• Hallucinations are seen after Ketamine
• Ketamine should be avoided in presence of increased arterial pressure
• Inducing agent of choice in shock is Ketamine
• Dose of Ketamine is 2 mg/kg I/v
• Increased Cardiac Oxygen demand is caused by Ketamine
• ICT is raised due to Ketamine
• Cerebral metabolism and 02 consumption are increased by Ketamine
• Ketamine is a direct myocardial depressant
• With use of ketamine Emergence phenomenon are more likely if anticholinergic premedication is
used
• Ketamine may induce cardiac dysarythmias in patients receiving tricyclic antidepressants
• Ketamine has Vasodialator and negative ionotropic effect
• ketamine shows Psychomimetic emergence
• Ketamine can be used in Status asthamaticus, For analgesia & sedation, Obstetric hemorrhage
• Ketamine is contraindicated in Ischemic heart disease
• The induction agent of the choice in surgery of cyanotic heart disease is ketamine
• General anaesthetic agent causing sympathetic stimulation is ketamine
• Ketamine is contraindicated in head injury, Hypertension, glaucoma
• Ketamine acts an NMDA receptors
• Intraocular pressure is increased by ketamine
9. NITROUS OXIDE
• Use of nitrous oxide is contraindicated in Tympanic membrane

grafting,Pneumoencephalography,Vitreoretinal surgery,Cochlear implant, Microlaryngeal surgery
& Vitreoretinal surgery
• Nitrous oxide should be avoided in middle ear surgery when tympanic grafts are used
• Gas stored in liquid form is Nitrous oxide
• Nitrous oxide causes bone marrow supression
• Blue cylinder with blue shoulder is the colour coding for Nitrous oxide gas cylinder for UK and ISO.
• Nitrous oxide is a low potency anaesthetic agent as Nitrous oxide has a low lipid solubility and and
its MAC value of 105%.
• PIN index for nitrous oxide is 3-5
• At the end of anaesthesia after discontinuation of nitrous oxide and removal of endotracheal tube,
1000/0 oxygen is administered to the patient to prevent Diffusion Hypoxia
• Nitrous oxide shows Blunts ventilatory response to hypoxia
• Laughing gas is Nitrous oxide
• Nitrous oxide Causes megaloblastic anemia
10. XENON
• In Patient with mitral stenosis, & liver compromise Xenon inhalational agent is preferred
• Rapid induction and recovery is seen in Xenon
• Xenon have Low potency
• Xenon is Non explosive
• Minimal cardiovascular side effects is seen with Xenon
• Xenon inhibits Ca. pump and low blood gas solubility
• Xenon acts through NMDA receptors
11. FENTANYL
• A patient after undergoing thoracotomy complains of severe pain. He can be managed by I.V
fentanyl
• Chest wall rigidly is the common side effects is seen with fentanyl
• A 25 year old overweight female was given fentanyl-pancuronium anesthesia for surgery. After
surgery and extubation she was observed to have limited movement of the upper body and chest
wall in the recovery room. She was conscious and alert but voluntary respiratory effort was limited.
Her blood pressure and heart rate were normal. The likely diagnosis is Incomplete reversal of
pancuronium
• Propofol, fentanyl, isoflurane are the most preferred for short day care surgeries
• Drug used for Epidural Analgesic is Fentanyl
• Management of chronic pain includes Epidural fentanyl
12. Ether
• Ether was first used by Morton

• Disadvantages of anaesthetic ether are slow Induction , Irritant nature & Cautery cannot be used
• In formal ether concentration technique, Sediment layer contain parasites
• Stages of anesthesia were established by ether
• Ether have no effect on heart
• The plane of surgical anesthesia during ether anesthesia is defined as From onset of regular
respiration to cessation of spontaneous breathing
13. LIGNOCAINE
• Dose of lignocaine for spinal anesthesia is 5%

• Maximum safe dose of lignocaine with adrenaline is 7 mg/kg wt
• Maximum safe dose of lignocaine for spinal anesthesia is 25-100 mg
• Concentration of lignocaine is used in epidural anaesthesia is 2%
• Maximum dose of lignocaine which can be given with adrenaline for ocular blocks is 7mg/kg
• Local anaesthetics acts by blocking nerve conduction.
• Small fibers and non myelinated fibers are blocked more easily than large myelinated fibers.
• Lignocaine is used as anesthetic and class IB antiarrhythmic in 2% jelly, 4% injection form
• 2-10% is the concentration of lignocaine used for topical anaesthesia
• High first pass metabolism is seen in Lignocaine
• Lignocaine is used in Ventricular tachycardia
• Best used in digoxin induced arrhythmia Lignocaine
• Drug of choice in lignocaine toxicity is Diazepam
• Lignocaine can be used in Ventricular fibrillation, Spinal anaesthesia & Epidural anaesthesia
• A patient selected for surgery was induced with Thiopentone iv through one of anti cubital vein
complains of severe pain of whole hand. The next line of management IV lignocaine through same
needle
• Lignocaine is a amide
• Lignocaine in high dose produces Convulsion, Respiratory depression & Hypotension
• Adrenaline is added to Lignocaine injection for Less bleeding at the site, Higher doses can be given
& Prolonged duration of action
• Lignocaine Can penetrate through mucous membrane
• Lignocaine can precipitate malignant hyperthermia
• Percentage of adrenaline with lignocaine for local infilteration is 1:50000
14. PUDENDAL NERVE BLOCK
• To provide anesthesia to a patient in the third stage of labor, an obstetrician palpates the ischial
spine transvaginally, then injects a local anesthetic. Injection of anesthetic at this approximate
location will most likely block Pudendal nerve
• A patient with external hemorrhoids develops pain while passing stools. The nerve mediating this
pain is Pudendal nerve
• Pudendal Nerve Block Involve S2S3S4
15. CARDIOPULMONARY RESUSCITATION
• Bag and mask ventilation in newborn resuscitation is contraindicated in diaphragmatic hernia

• Color, Heart rate & Muscle tone are used in a preterm infant to assess need for resuscitation
• 3 year old child with weight – 15 kg, SPO2 – 88, BP unrecordable, RR – 40/minute VF the energy
for DC shock so as to revert to it to normal rhythm will be 60 J
• A lady with placenta previa delivered a baby. She had excessive bleeding and shock. After
resuscitation most likely complication would be Loss of menstruation
• Indications for giving intravenous calcium gluconate during cardiopulmonary resuscitation
are Hypocalcemia, Calcium channel blockers toxicity & Cardiac arrest due to hyperkalemia
• Mechanism of action of epinephrine in cardiopulmonary resuscitation is Increase SA node activity
• Naloxone is not used during resuscitation of a child whose mother is on Methadone
• Components of neonatal resuscitation Maintenance of temprature, respiration & circulation
• Meconium aspiration is done for 3 times but no breathing occurs. Next step in resuscitation would
be Trikling of sole
• 1st mouth suctioning done in neonatal resuscitation
• Max. length of nasal suctioning is upto 3 cm and mouth suctioning is upto 5 cm in neonatal
resuscitation
• Dose of i.v. adrenaline in term infant is during neonatal resuscitation 0.1-0.3 ml/kg in 1:10,000
• Bag and mask ventilation in newborn resuscitation is contraindicated in Diapharagmatic herina
• The outcome following resuscitation of cardiac arrest is worsened if during resuscitation patient is
given5% Dextrose
• First step in CPR (cardio pulmonary resuciatation) should beAirway maintainance
• Adrenaline in CPR Can be given intratracheally
• I.V. route better than intracardiac for adrenaline in CPR
• According to 2005 AHA guidelines true about no of chest compression in CPR is 90/min including
neonate
• During cardiac resuscitation Rupture of Lungs, liver or stomach can occur
• The 2010 AHA Guidelines for CPR during Basic Life Support Recommend is Compression- Airway –
Breathing (C-A-B)
• The 2010 AHA Guidelines for CPR during Basic Life Support for neonates Recommends Airway –
Breathing – Compression (A-B-C)
• Adrenaline is given if cardioversion fails in CPR
• The best chances of recovery after successful cardiopulmonary resuscitation are seen in Ventricular
Tachycardia
• Resuscitation time of the human retina following ischaemia is 1 to 2 hours
• Ratio of chest compression to breathing during cardiopulmonary resuscitation in newborn patient
admitted in ICU is 3:1
• Endotracheal Concentration of adrenaline in CPR for pediatric is 1: 1,000
• Chest compression during CPR depth is 2 inches
• During cardiopulmonary resuscitation in adult, chest compressions are given at the rate of 100
compressions/min
• Fluid of choice for resuscitation of burn patient is Ringer lactate
• Oral fluids must contain salts in burn patients
• Half of the calculated volume of fluid should be given in first 8 hours in burn patients
• During CPR, artifacts due to rib fracture most commonly seen in 4th — 6th ribs
• Drug used in neonatal resuscitation are Adrenaline, Sodium bi carbonate & Naloxone
• The ideal parameters for cardiac massage in cardiopulmonary resuscitation are Force should
depress sternum by 11/2 inches, Compressions to be given over lower third of sternum & Force
should depress sternum approximately 1/3 of chest wall diameter
• Machine used noninvasively to monitor an external chest compression during cardiopulmonary
resuscitation is Zoll AED - plus automatic external defibrillator
16. Central Venous Catheterization
• Pneumothorax is a fairly common complication of placement of central venous catheter.

• Following central vein catheterization pneumothorax can occur as late as 48 – 72 hours.
• While inserting a central venous catheter, a patient develops respiratory distress because
of Pneumothorax
• Most common complication of central venous catheter Catheter related infection
• Enterococcus fecalis is most common infection following central venous catheter
• A pt. developed resp. distress and hypoxemia after central venous catheterization through int.
jugular vein, reason for this is Pneumothorax
• MC late complication of central venous line is Sepsis
Internal Medicine
1. Jugular Venous Pulse
JUGULAR VENOUS PULSE
• a wave – right atrial contraction.

• c wave – bulging of tricuspid valve into the right atrium during RV isovolumetric contraction
• v wave – increase in volume in venecava during systole, when tricuspid valve is closed
Abnormalities:
Giant 'a' wave
• Tricuspid stenosis
Cannon 'a' waves
• Complete heart block
Accentuated `a-x' descent
• Cardiac tamponade
Reduced v-y descent
• Tricuspid stenosis
2. Pseudohypoparathyroidism
PSEUDOHYPOPARATHYROIDISM

• Etiology:
• There is tissue resistance to the effects of PTH, so PTH concentrations are markedly elevated
• Type 1 a or Albright's hereditary osteodystrophy (AHO) - GNAS1 mutation is inherited on
the maternal chromosome
• Clinical features:
• Hypocalcemia
• Hyperphosphatemia
• Short fourth/fifth metacarpals and metatarsals with associated Cataract
3. Cluster Headache
Symptoms:
• Young adult men

• The pain is unilateral, deep, usually retro orbital, excruciating, non-fluctuating and explosive in
quality
• A core feature of cluster headache is periodicity. Pain recurs at the same hour each day for 8 to 10
weeks a year; followed by a pain-free interval
• Patients are generally perfectly well between episodes
• Often occurs at night 2 hrs after sleep, wakes up the patient from sleep
• Associated with vasomotor phenomenon – rhinorrhea, conjunctival injection, nasal
congestion, lacrimation, ptosis or Horner's syndrome
4. Ataxia telengiectasia
ATAXIA TELANGIECTASIA
• Gene involved – ATM gene on chromosome 11 which encodes Atm protein kinase, a member of
phosphatidyl inositol 3-kinase family.
• Only phacomatotic hereditary condition transmitted in the autosomal recessive mode, where
combined immunodeficiency is associated with cerebellar ataxia, telangiectasia, ovarian dysgenesis
& chromosomal abnormalities.
• Presents in the first decade of life with progressive telangiectatic lesions and ataxia & chorio-
athetoid movements associated with deficits in cerebellar function and nystagmus
5. Friedrich's Ataxia
FRIEDREICH'S ATAXIA

• Etiology:
• The classic form of Friedreich's ataxia has been mapped to 9q13-q21.1, and the mutant
gene, frataxin, contains expanded GAA triplet repeats in the first intron. There is homozygosity for
expanded GAA repeats in >95% of patients.
• Characteristic Diagnostic features:
• Chronic Slowly progressive cerebella,- ataxia
• Absent lower limb deep tendon reflexes with an extensor plantar response
• Associated features,
• Cardiomyopathy
• Diabetes
• Spine or foot deformity
6. Rhabdomyolysis
RHABDOMYOLYSIS
Causes:
• Crush or Anoxic injuries

• Drugs: Statins
Clinical & Laboratory findings
• Myalgias and weakness are usually present.
Complications:
• Myoglobinuria
• Acute Renal Failure
7. Diffuse Large B Cell Lymphoma
• The most common variant of Non-Hodgkin's Lymphoma in India is Diffuse Large B cell Lymphoma.
• Immunophenotype of Diffuse Large B Cell Lymphoma:
• They will demonstrate markers of mature B lymphocytes as well as germinal centre markers- CD 19-
CD 20 - CD 10- BCL-6- slg- BCL-2 (see in 10% to 20% associated with t(14:18)).
• Incidence of Diffuse Large B Cell lymphoma is more common in males.
• Most common extranodal site for non - hodkin's lymphoma is Stomach.
• 60-80% of intestinal lymphomas are B cell lymphomas, mostly diffuse large B cell type of Non
Hodgkin's lymphoma of the distal small intestine and especially in the ileo-cecal region
• Most common ocular lymphoma is B Cell Non Hodgkin's Lymphoma.
• B cell lymphoma, Burkit lymphoma, Non Hodgkin's lymphoma, mantle cell lymphoma are common
in orbit.
• The paraneoplastic hypercalcemia in lymphoma is due to ectopic production of 1,25
dihydroxyvitamin D.
• 5 year survival rate of Diffuse large B cell lymphoma is 46%.
• Cytogenic Abnormality associated with Diffuse Large B Cell Lymphoma is t(3;-)(q27;-)t(17;-)(p13;-).
• Oncogene associated with Large B Cell Lymphoma is BCL-6,p53.
• Working formulation in staging of non-hodgkins lymphoma is based on Morphology of Cells.
• Follicular cell lymphoma falls under the low grade non-Hodgbkins lymphoma .
• Lymphomas with a follicular histological pattern have a longer survival than those of diffuse
pattern.
• Diffuse small, mixed , as well as large cell Lymphoma falls in the Intermediate form of Non-
Hodgkin's Lymphoma.
• The classification proposed by the International Lymphoma Study Group for non-Hodgkin's
lymphoma is known as REAL Classification.
• The IPI (International Prognostic Index) score system is calculated by the sum of the presence or
absence of 5 variables :age ≥ 65 y, performance status ≥ 2, elevated lactate dehydrogenase (LDH),
Ann Arbor stage III or IV, and ≥2 extranodal sites of disease.
• Distinction between a poorly differentiated carcinoma and a lymphoma can be made by
immunoperoxidase staining of the tumour tissue with antibodies directed against Cytokeratin.
• Immunohistochemical stains is used for the diagnosis of lymphomas is CD45 (leucocyte common
antigen).
• Ritumixab is used in the treatment of B-cell lymphomas: Low grade lymphomas, mantle cell
lymphomas, relapsed aggressive B cell lymphomas, CLL;SLE and Rheumatoid Arthritis.
8. Lucid Interval
• Lucid Interval is seen in Extradural Hemorrhage/Hematoma,Intradural Hemorrhage/Hematoma and

Insanity.
9. Criggler Najjar Syndrome
• Deficiency of Diglucuronide is present in Criggler-Najjar syndrome Type-II.
10. Reactive Arthritis
• Keratoderma blennorrhagica is seen in reactive arthritis.

• Most common organism associated with reactive arthritis is chlamydia trachomatis.
• HLA B 27 associated reactive arthritis, urethritis and conjunctivitis is associated with Ureaplasma
urealyticum infection
• Reactive arthritis is a result of exposure to four Shigella species S. sonnei, S. boydii, S. flexneri, and
S. dysenteriae, S. flexneri,chlamydia trachomatis,Ureaplasma urealyticum, Campylobacter jejuni,
Salmonella enteritidis, and Yersinia.
• Asymmetric & painful oligoarthritis is a feature of reactive arthritis
• Reactive arthritis Most common among young men
• Asymmetrical Enthisistis, sacroilitis,Dactylitis & anterior uveitis are associated with reactive arthritis
• HLA B27 & HIV affects severity of reactive arthritis
11. Prophylaxis & Treatment Of Typhoid Fever
• Carrier are treated by β-lactamase inhibitors

• The number of doses recommended for oral Ty21a typhoid vaccine is 3
• Vi polysaccharide vaccine for typhoid is administered subcutaneously or intramuscularly
• Ty21a is an oral vaccine in typhoid
• Vi polysaccharide of bacterial cell used for vaccination
• Treatment of choice for salmonella typhi is Ciprofloxacin
• Typhoid Vi polysaccharide vaccine is usually administered in children above the age of 2 years
• Vi polysaccharide is a subunit vaccine
• Chemoprophylaxis is not required in Typhoid
• Ty21a is the live attenuated vaccine in typhoid
• Typhoid oral vaccine is given on 1, 3, 5 days
• Immunity lasts for 3 years Need a booster
• For a typhoid endemic country like India, the immunization of choice is Typhoral 21 A oral vaccine
12. Hepatitis B Acute & Chronic Infections
• Serum analysis yields elevated ALT, HBsAg, Anti-HBc, HBeAg, and bilirubin in active
chronic hepatitis B
• DNA polymerase,Ig M anti-HBc antibody, HBsAg (+) is a marker of acute hepatitis B infection
• Liver biopsy in acute hepatitis due to hepatitis B virus is likely to show ballooning degeneration,
Councilman body or acidophil body, dropout necrosis, and bridging necrosis
• The incidence of chronic carrier state in liver disease is due to hepatitis B infection.
• The patterns of glomerular injury in HBV related chronic liver disease shows Membranous
nephropathy, Minimal change nephropathy, Mesangial proliferative
glomerulonephritis, Membranoproliferative glomerulonephritisIgA nephropathy
• Most widely accepted mechanism associated with nephropathy in chronic HBV patients
is Deposition of immune complex particles attributed to viral antigens and host antibodies
• Adult infection is usually symptomatic in chronic hepatitis B
• 90 % chance for chronic infection if HBV infection occur at birth
• Mild chronic hepatitis B has 5 year survival 97 %
• Complications of acute HBV include Fulminant hepatitis, Cirrhosis,Hepatocellular
carcinoma, Chronic hepatitis, Gianotti - crosti syndrome, Glomerulonephritis, Essential mixed
cryoglobulinemia, Polyarteritis nodosa (PAN), Hepatocellular carcinoma
• Best means of giving hepatitis B vaccine is Intramuscular deltoid
• Ground glass hepatocytes are seen in HBV chronic infection
• Increased SGPT & SGOT with HBs Ag antigen positive HBe Ag antigen negative and anti-HBe
antibody positive shows chronic active hepatitis is diagnosed as HBV precore mutant
• Marker of level of liver injury in cases of hepatitis B is HBV DNA
• Hepatitis B associated with Polyarteritis nodosa
• Hepatitis B vaccine should be given as per which schedule 0,1,6 months
• Antiviral therapy with interferon is indicated in patients with active viral replication (is HBV DNA)
and elevated ALT levels
• Extrahepatic Manifestations of Hepatitis B include Aplastic Anemia ,Cryoglobulinaemia, Diabetes
mellitus, Dermatomyositis-like syndrome ,Gianotti- Crosti syndrome, Glomerulonephritis, Guillain-
Barre syndrome, Myasthenia gravis, Pericarditis and myocarditis, Pancreatitis, Peripheral
Neuropathy, Polyarteritis Nodosa ,Polyarthritis, Polymyalgia rheumatica, Polymyositis, Porphyria
cutanea tarda ,Psychosis, Raynaud's syndrome, Serum sickness like illness, Splenomegaly and lymph
node enlargement, Skin alterations, Thrombopenic. purpura ,Thyroiditis ,Urticaria
• Positive HBs Ag with Other serological tests for hepatitis negative & normal liver enzymes are
suggestive of inactive HBV carrier
13. Anorexia Nervosa
• Amenorrhea, anorexia, weight loss and with milk discharge from the nipples are seen in Anorexia
nervosa
• Leukopenia, Amenorrhea, Self induced vomiting are seen in Anorexia nervosa
• Increased commitment to work ,Distortion of body image,Body weight < 85% of the predicted are
seen in Anorexia nervosa
• Weight loss,Dehydration,Mood changes are commonly seen in Anorexia nervosa
• Physical findings in anorexia nervosa are Emaciation, Hypotension, Bradycardia ,Hypothermia, Skin
dryness and flakiness, Lanugo ,Peripheral edema, Petechiae on extremities ,Sallow complexion
,Salivary gland hypertrophy, Dental enamel erosion, Osteoporosis ,Russell's sign ,Scars and calluses
on the back of the hand, Amenorrhea ,Mood changes
• Increase in free fatty acids,ketone bodies & Decrease in glycogen is seen within 24 hrs of starvation
in a 19-year-old patient with Anorexia Nervosa
• Hypophosphatemia and cardiorespiratory failure are the dangerous adverse effect of this type of
re-feeding in Anorexia Nervosa
• Anorexia Nervosa with euthyroid sick syndrome shows Low T3, Low T4, increased rT3, Normal TSH
• Anorexia nervosa can be differentiated from bulimia by Peculiars patterns of food handing
• Main difference between anorexia nervosa and bulimia nervosa lies in Weight
• In anorexia nervosa Bulimia may be seeen in 50% cases
• In anorexia nervosa Decreased FSH levels is seen
• BMI index is higher than normal Population in anorexia nervosa
• Malabsorption Syndrome is most common cause of anorexia nervosa
14. Peutz Jegher's Syndrome

• Peutz Jeghers polyps present most commonly in Jejunum
• Hamartomatous Polyps in Peutz Jegher’s Syndrome have less only 39% chances of malignant
transformation
• Polypectomy on colonoscopy is treatment of choice in Peutz Jegher’s Syndrome
• Melanosis on oral mucosa are the oral sign of Peutz Jegher’s Syndrome
15. Hashimoto's Thyroiditis
• Follicular destruction ,Increase in lymphocytes ,Oncocytic metaplasia is seen in Hashimoto's

Thyroiditis.
• Orphan Annie eye nuclei is not seen in Hashimoto's Thyroiditis.
• Thyroid follicular infiltration by lymphocytes along with the presence of Hurthle cells is
characteristic of Hashimoto's disease.
• Hashimoto's thyroiditis is an autoimmune disorder.
• In case of an Autoimmune disease,following is present: T cells recognise self antigen , Hashimoto's
thyroiditis is an example, Polyclonal B cell activation.
• Higher incidence among females is present in an Autoimmune disease.
• In hashimoto's disease serum antibodies are mainly against Thyroid follicles and thyroglobulin.
• There is increased risk of developing B-cell lymphoma in Hashimoto's thyroiditis.
• 'Hurthle cells' are seen in Hashimoto's thyroiditis.
• Most common cause of Thyroiditis is Hashimoto's thyroiditis.
• Antithyroid nuclear antibodies are not seen in Hashimoto's thyroiditis.
• Antithyroid microsomal antibodies ,Anti TSH receptor antibodies and Increased level of thyroid
hormones may be seen in Hashimoto's thyroiditis.
• Enlargement of thyroid gland with tenderness is most commonly seen in Hashimoto's thyroiditis.
• Anti-TPO antibodies are present in Hashimoto's thyroiditis.
16. Marfan's Syndrome
• "Marfan - like syndrome" is associated with Homocystinuria.

• Mutation in Marfan's syndrome is Fibrillin I.
• Ectopia Lentis may be associated with Marfan's Syndrome.
• Marfan's syndrome most commonly involves Ascending Aorta.
• The major criteria to diagnose Marfan's syndrome includes presence of at least four skeletal
abnormalities, ectopia lentis, dilation of the ascending aorta with or without dissection, dural
ectasia, and a blood relative who meets the same criteria, with or without a DNA diagnosis.
• Marfan syndrome is an autosomal dominant disorder with features of subluxated lens of the eye
and mitral valve prolapsed.
• The chromosomal defect in a case of Marfan's syndrome lies in Gene on chromosome 15 encoding
fibrillin.
• Acute aortic reguritation can occur as a complication of Marfan's syndrome.
• The drug which can be used to delay the progression of aortic dilatation in marfan syndrome is
Propranolol.
• Pregnancy is better avoided in Marfans syndrome with a dilated aortic root.
• Features of Marfan's syndrome are Arachnodactyly/ spider fingers ,Flat foot ,High
palate,Dislocation of the lens and Mitral regurgitation.
• Retinitis pigmentosa is not associated with Marfan's syndrome.
• Cystic medial necrosis responsible for aortic dilatation and rupture is seen in Marfan's syndrome.
• Dissecting haematoma is a clinical complication occurring in Marfan's syndrome.
• In Marfan's syndrome, Aortic aneurysm occurs most commonly in Ascending Aorta.
• Supratemporal lental subluxation is seen in Marfan's syndrome.
• Superior rib notching may be caused by Marfan's syndrome.
• Bilateral ptosis is not seen in Marfan's syndrome.
• Mitral valva prolapse is the most common cardiovascular manifestations of Marfan's Syndrome.
• Aortic regurgitation may be seen in Marfan's Syndrome.
• Blue Sclera may be associated with Marfan's Syndrome..
• Renal artery stenosis is not associated with Marfan's Syndrome.
• Revised Ghent Criteria are used for the diagnosis of Marfan's Syndrome
17. Sturge Weber Syndrome
• Rail-road calcification in the brain are found characteristically in Sturge weber syndrome.
• The most probable diagnosis in a child who has got a vascular plaque like lesion over the lateral
aspect of forehead mainly involving ophthalmic and maxillary division of trigeminal nerve. which
has remained unchanged since birth and he is also on valproate for seizure disorder is Sturge weber
syndrome.
• A neonate has a large, purplish, slightly raised lesion on the skin of the forehead near the temporal
area. As the child grows, the lesion grows as well and becomes increasingly prominent. This lesion
may be a component of Sturge weber syndrome.
• Mental retardation(60% cases), Seizure (upto 85 % cases) and Rail road track appearance is seen in
Sturge Weber Syndrome.
• Diffuse choroidal hemangioma may be seen in upto 40% of the cases in Sturge Weber Syndrome.
• Sturge Weber Syndrome is characterised by nevus flammeus.
• Sturge Weber's syndrome is associated with ,Seizures,Hemiatrophy of cerebral cortex and Gyriform
calcification in brain.
• The most likely diagnosis is a case of intractable convulsions mental defect and facial nevus
is Sturge weber syndrome..
• Pheochromocytoma is associated with following familial syndromes :
• MEN syndrome type 2A & type 2B ,Von Recklinghausen (Neurofibromatosis type I) ,Von Hippel
lindau syndrome, Sturge weber Syndrome, Familial paraganliomas 1,2, & 3.
• Sturge Weber Syndrome is not associated with brain tumors.
• Large haemangioma of lid and cheek along with glaucoma is seen in Sturge Weber Syndrome.
18. Henoch Schonlein Purpura

• Henoch Schonlein purpura presents with deposition of Ig A
• Cresentic Glomerulonephritis may be seen in Henoch Schonlein purpura
• Henoch Schonlein purpura shows abdominal pain, rashes, palpable purpura and, arthritis
• Hypersensitivity angitis is seen in Henoch schonlein purpura
• The most common leukocytoclastic vasculitis affecting children is Henoch Schonlein purpura
• Non blanching macules, papules and petecheal hemorrhage on lower extremities, mild abdominal
pain, and skin biopsy showed IgA deposition along blood vessels and perivascular neutrophilic
infiltrate is seen in Henoch Schonlein purpura
19. Atrial Blood Gas
• In Respiratory and metabolic acidosis ABG analysis show: pH 7.2,↑ PaC02, ↓HC03
• Reading of ABG analysis as ↓ PaCO2, Normal PaO2 and pH 7.5 shows Respiratory alkalosis
• Use of Intraarterial cannula in major surgery for Sample for ABG
• ABG revealing pH- 7.5, PCO2 24 mmHg, PO2 88 mm of Hg with excessive hyperventilation treated
for Respiratory alkalosis
20. Wernicke Korsakoff Psycosis
• Alcoholic presents with psychosis and memory loss is suggestive of Wernicke’s Korsakoff psychosis
• Opthalmoplegia, ataxia, Psychosis are features of Wernicke's Korsakoff Syndrome
• Mammilary body,Thalamus & Hippocampus are affected in Wernicke's Korsakoff Syndrome
• Thalamus is responsible for the amnestic defect in Wernicke's Korsakoff syndrome
• Wernicke-Korsakoff's syndrome is due to the deficiency of thiamine
21. Nephrotic Syndrome
• In nephrotic syndrome Transferrin, Albumin & Ceruloplasmin are reduced

• Oral cyclosporine for Steroid resistant nephrotic syndrome secondary to FSGS not responsive to
methylprednisolone
• Edema in nephrotic syndrome is due to Hypoalbuminemia & Sodium and water retention
• Finnish of nephrotic syndrome is caused by defect in Nephrin protein
• The most common gene defect in idiopathic steroid resistant nephrotic syndrome NPHS 2
• Action of Tolbutamide, Diazepam & Valproate is reduced with nephrotic syndrome and
hypoalbuminemia.
• Nephrotic syndrome increases the susceptibility to coronary artery disease
• Hypercoagulation in nephrotic syndrome is a result of Loss of Antithrombin III
• Muehrcke lines in nails are seen in nephrotic syndrome

• Nephrotic syndrome is the hall mark of Membranous Glomerulopathy,Minimal change disease
& Focal segmental Glomerulosclerosis
• Basic abnormality in a case of nephrotic syndrome is proteinuria
• Membranoproliferative glomerulonephritis is common in both nephritic syndrome and nephrotic
syndrome
• Patient with nephrotic syndrome on longstanding corticosteroid therapy may develop
Hyperglycemia,Neuropsychiatric symptoms & Suppression of the pituitary adrenal axis
• Patient with congenital nephrotic syndrome requires renal biopsy
• Serum albumin level below 2.5g/dl l is seen in nephrotic syndrome in child
• Hyperglycemia ,Neuropsychiatric symptoms & Suppression of the pituitary adrenal axis are the side
effects of long term steroid therapy in nephrotic syndrome
• Malaria causing nephrotic syndrome is P. malariae
• Most common cause of nephrotic syndrome in adult in Membranous glomerulonephritis
• Most common cause of nephrotic syndrome in children is Minimal change disease
• A child had hematuria and nephrotic syndrome (minimal change disease) shows Glomerular
function is lost due to loss of poly charge on both sites of glomerular foot process
• Lipid cast are seen in Nephrotic syndrome
22. AML
• DIC is seen most commonly seen in M3

• Bad prognosis in AML is indicated by Monosomy
• AML with gum infiltration, hepatosplenomegaly M4
• Aplastic anemia can progress to AML
• Non specific esterase is present in AML
• T (15,17) is the chromosomal translocation in AML M3
• Chloroma is due to AML
• AML is characterized by Auer rods
• Acute promyelocytic leukaemia (AML—M3) includes Hyper granular and micro granular type
• Hereditary - Down syndrome, Klinefelter syndrome, Patau syndrome, Fanconi anemia, Bloom
syndrome, Ataxia telangiectasia, Kotsman syndrome.
• Polycythemia vera may cause AML
23. Acute Lymphoblastic Leukemia
• Age of onset between 2-8 years,female, Early pre-B cell,Initial WBC count less than 50000
& Hyperdiploidy are good prognostic factor
• t(9:22), t(8:14), t(4:11),t (12 : 21) translocation shows bad prognosis
• Presence of mediastinal mass shows bad prognosis

24. CML
• Imatinib is the drug of choice for CML

• BCR ABL gene mutation is seen in CML
• Chromosomal translocation seen in CML is 9:22
• Imatinib used in CML acts by Competitive inhibition of ATP binding site of Abl kinase
• Phildalphia chromosome is mostly seen in CML
• Decrease in "Alkaline phosphatase" is seen in CML
• Thrombocytopenia, Lymphadenopathy & High HbF are the features of juvenile CML
• Size of splenomegaly indicates prognosis in CML
• Basophillic leucocytosis occurs in CML
• CML in children is associated with Down's syndrome
• Best Rx for CML is Allogenic stem cell Transpintation
25. Transfusion complication
• Hyperkalemia,Hypomagnesaemia, Hypocalcaemia,Citrate toxicity , Hypothermia are

the Complication of blood transfusion
• Metabolic alkalosis is most likely to occur after recieving several units of blood transfusion
• Most common blood transfusion reaction is Febrile non hemolytic reaction
• Blood transfusion reaction is Type II hypersensitivity
• In a 3 year old child, most common cause of hepatitis B is Blood transfusion
• Mismatched blood transfusion manifests intraoperatively as Hypotension & Excessive bleeding
from site of wound
• Massive transfusion in previous healthy adult male can cause hemorrhage due to Dilutional
thrombocytopenia
• Complement mediated Hemolysis is seen in Acute Hemolytic blood transfusion reactions
• Triad following massive blood transfusion includes Alkalosis, hypothermia, hyperkalemia
• Most common cause for complication of blood transfusion is Human error
• Hypothermia ,Hypocalcemia, Hypokalemia, Hypernatremia are seen in Massive blood transfusion
26. Hepatocellular Carcinoma
• Tumor marker for primary hepatocellular carcinoma are Alpha feto protein, PIVKA-
2, Neurotensin,Vit B12 binding globulin
• Yttrium 90 microspheres are used in treatment of hepatocellular carcinoma
• Liver transplantation offers the only chance of cure in those with unresectable case of
hepatocellular carcinoma
• High incidence in East Africa and South east Asia with worldwide incidence parallels the prevalence
of hepatitis B of hepatocellular carcinoma

• Hepatomegaly ,Raised a- fetoprotein levels, Raised alkaline phosphatase are seen in hepatocellular
carcinoma
• Sorafenib a tyrosine kinase inhibitor is used to treat hepatocellular carcinoma
• Transarterial chemoembolization (TACE) is used in the treatment of unresectable hepatocellular
carcinoma without portal vein thrombosis. The drug commonly used for TACE is Doxorubicin
• Hepatocellular carcinoma has propensity to invade the portal or hepatic vein
• Radiofrequency ablation ,Percutaneous Ethanol Injection and Resection are curative treatment
modalities for hepatocellular carcinoma
• Most common cause of malignant portal vein thrombosis is Hepatocellular carcinoma
• Mallory hyaline is seen in Hepatocellular carcinoma
• Liver biopsy is diagnostic for Hepatocellular carcinoma
• Raised titre of HBV and HCV antibodies is seen in Hepatocellular carcinoma
• Fibrolameller type is having good prognosis in hepatocellular carcinoma
• The most unlikely clinical feature of Hepatocellular carcinoma is jaundice
• In hepatocellular carcinoma, risk factor most important is Cirrhosis
27. Status epilepticus
• The initial drug of choice for status epilepticus is Lorazepam

• Causes of status epilepticus in a child Hyponatremia
• Status epilepticus is the complication (s) of meningitis in a child
• A child in status epilepticus should be given Clonazepam, Phosphenytoin & Diazepam
• In status epilepticus, drug of choice is IV diazepam
28. Diabetes Ketoacidosis
• High Anion Gap Acidosis is seen in Diabetic Ketoacidosis

• A patient with diabetic ketoacidosis in coma should be given immediate insulin therapy
with Potassium supplementation
• Increase in glucagon/insulin ratio, increased CAMP and increased blood glucose is seen in diabetic
ketoacidosis
• Decreased Bicarbonate is seen in diabetic ketoacidosis
• Oxygen dissociation curve shifts to right in diabetic ketoacidosis
• Orbital mucormycosis is a complication of diabetic ketoacidosis
• Somatostatin is used in Diabetic ketoacidosis
• The drug of choice for managing hyperglycemia in diabetic ketoacidosis is Regular insulin
• Cause of death in diabetic ketoacidosis in children is Cerebral edema
29. Hyperparathyroidism
• Secondary hyperparathyroidism is seen in Chronic renal failure, Vitamin D deficiency, Medullary
carcinoid syndrome & Malabsorption syndrome
• Adenoma is the most common surgically repairable cause of hyperparathyroidism
• Characteristic subperiosteal bone resorption in Hyperparathyroidism is best seen at Radial border
of middle phalanx
• MEN 1 is characterized by symptoms of hyperparathyroidism, tumor in pancreas, adrenal cortical
hyperplasia, pituitary adenomas, islet cell tumor with cutaneous angiofibromas
• Subperiosteal resorption and thickness of skull is increased in hyperparathyroidism
• Salt and pepper appearance of the skull on Xray is seen in hyperparathyroidism
• Chronic thiazide therapy causes persistent hypercalcemia due to hyperparathyroidism
• Brown’s tumour is seen in hyperparathyroidism
• Primary hyperparathyroidism, phaeochromocytoma may be associated with Medullary carcinoma
of the thyroid
• Treatment of choice for primary hyperparathyroidism secondary to parathyroid hyperplasia
is Removal of all glands leaving 50 mg of tissue as remnant
• Ca++↑ P04 ↓ is seen in hyperparathyroidism
• Secondary hyperparathyroidism due to Vitamin D deficiency shows Hypophosphatemia
• Hyperparathyroidism can cause nephrocalcinosis
• Tertiary hyperparathyroidism is Secondary hyperparathyroidism with chief cell adenoma
• Superior rib notching is/are caused by Hyperparathyroidism
• The symptoms of Hyperparathyroidism include Constipation , muscle weakness ,Anorexia ,weight
loss, Polydipsia & polyuri
• Subcutaneous Calcifications are seen in Hyperparathyroidism
• Peptic ulcer is associated with Primary hyperparathyroidism
• The initial treatment of choice for secondary hyperparathyroidism in renal osteodystrophy
is Phosphate binder
• The commonest cause of primary hyperparathyroidism is Solitary adenoma of parathyroid
• Secondary hyperparathyroidism causes rugger jersy spine in known case of chronic renal failure
• Tufting of the terminal phalanges is seen in hyperparathyroidism
• Floating teeth is seen in hyperparathyroidism
• Absence of lamina dura seen in hyperparathyroidism
• CPPD crystals are seen in hyperparathyroidism
• Osteitis fibrosa cystica is seen with hyperparathyroidism
30. Cystinosis
• Fanconi syndrome with nephrocalcinosis has a variant of dent disease

shows Hypercalciuria,Proteinuria & Rickets
• Photophobia and blond hair, Presence of cystine within leukocytes & Fanconi syndrome are seen
in cystinosis
• Fanconi's syndrome is caused by Old and degraded tetracycline
• Fanconi's syndrome is associated with malignancy
• Fanconi's syndrome have defect in DNA repair mechanism
31. Parkinsonism
• Patient presenting with pellagra, parkinsonism, convulsions, anemia and kidney stones has
deficiency of Pyridoxal phosphate
• Tyrosine Hydroxylase enzymes is believed to be deficient in Parkinsonism
• Mangnese (Mn) is associated with secondary Parkinsonisms
• Hypokinesia, Rigidity & Static tremors are seen in Parkinsonism
• Dinesh, a 56 yr aged man presents with complaints of slowness of movements, postural instability,
tremors, rigidity and memory loss. Most likely diagnosis is Parkinsonism
• Subthalamic Nucleus is the most commonly used site for Transcranial Magnetic Stimulation to
reduce frequency of Parkinsonism symptoms
• Parkinsonism like features are evident in surviving patients of CO poisoning
• Deep brain stimulation used in treatment of Parkinsonism
32. CHURG-STRAUSS SYNDROME
• Asthma ,Granuloma, Perpheral eosinophilia, Glomerulonephritis, Multisystem involvement of

vessels are seen in churg- strauss syndrome
• Mononeuritis multiplex ,regular attacks of bronchial asthma preceded by allergic
rhinitis, cutaneous purpura with eosinophilia is suggesitve of churg- strauss syndrome
• Lung is characteristically involved in churg- strauss syndrome
• Churg Strauss Syndrome is associated with pulmonary eosinophillic pneumonia
• Churg Strauss Syndrome is small vessels vasculitis
• Mononeuritis multiplex is common in Churg Strauss Syndrome
• Churg Strauss Syndrome is Often associated with Allergic Rhinitis
• Lower Respiratory Tract involvement is more frequently seen in Churg Strauss Syndrome in
comparison to Wegener's Granulomatosis
33. KAWASAKI DISEASE
• Kawasaki disease is a Mucocutaneous lesions

• Kawasaki disease is Associated with coronary artery aneurysm in up to 25% of untreated case
• Kawasaki disease is Seen in children
• child with bilateral non purulent conjunctivitis and 4 enlarged cervical lymph nodes , Conjusted
pharynx pharynx ,trunk covered with polymorphous rash and palmar erythema and desquamation
of finger tips with Bilateral pedal oedema is suggested to have Kawasaki disease
• Pedal edema, Truncal rash & Pharyngeal congestion are the component of Kawasaki disease
• Kawasaki disease is associated with Erythema,Red eye,Rash, Posterior cervical lymphadenopathy
& Conjuctivitis
• child with fever, non-purulent conjunctivitis, rashes, cervical lymphadenopthy, hepatomegaly
eruptions on trunk & proximal extremities, bilateral bulbar conjunctivitis without discharge and
fissuring -crusting- red lipsand desquamation of fingers and toes showing coronary artery aneurysm
on ECG is the most likely diagnosed to have Kawasaki disease
• Strawberry tongue, Pedal Edema & Cervical Lymphadenopathy are clinical manifestation of
Kawasaki disease
• The type of arteritis which may lead to myocardial infarction in children is Kawasaki disease
• Immunoglobulin are the treatment of choice for Kawasaki disease
34. BECHET'S SYNDROME
• Bechet's disease is characterized by Hypopyon

• Posterior uveitis,Iritis & Optic Neuritis are seen in Bechet's disease
• HLA marker of bechet's syndrome is HLA-B51
• Recurrent oral ulcers that are small with a yellow floor surrounded by an erythematous halo on lips
& also has multiple, tender nodules on skin are diagnosed to have bechet's syndrome
• Recurrent orogenital ulceration with arthritis is seen in bechet's syndrome
• Thalidomide is used in bechet's syndrome
• Pathergy test is used for bechet's syndrome
35. POLYARTERITIS NODOSA
• Drug abuser presents with fever , weight loss, hypertension, nodular skin rash, and peripheral
neuropathy showing ESR is 100 mm/L, and RBC casts are seen on urinalysis is suffering
from Polyarteritis nodosa
• Palpable purpura are seen in Polyarteritis nodosa
• Fibrinoid necrosis may be observed in Polyarteritis nodosa
• Loss of appetite, nausea and vomiting, and fatigue with confirm diagnosis of hepatitis B & icteric 2
shows vulnerable to the development of Polyarteritis nodosa
• Polyarteritis nodosa is a necrotizing vasculitis of small and medium-sized muscular arteries
• Involvement of the renal and visceral arteries is characteristic of Polyarteritis nodosa
• Granulomas, significant eosinophilia, and are not observed in Polyarteritis nodosa
• Patient with Severe abdominal pain with Guaiac test on stool demonstrates occult blood is taken to
exploratory laparotomy, at which a small area of infarcted small bowel is found and surgically
removedHistologic studies on the removed section of bowel demonstrate a recent thrombus
occluding a small muscular artery. The adjacent vessel wall shows fibrinoid necrosis with a mixed
inflammatory infiltrate containing neutrophils, eosinophils, and mononuclear cells is diagnosed to
have Polyarteritis nodosa
• Polyarteritis nodosa poses the greatest risk for development of pre-eclampsia
• Digital gangrene , palpable peripheral pulses is suggestive of Polyarteritis nodosa
• In polyarteritis nodosa, aneurysms are seen in Kidney, Liver & Pancreas
• Neuropathy is seen in polyarteritis nodosa
• Hepatitis B associated with polyarteritis nodosa
• Fibrinoid necorsis with neutrophilic infiltration is seen in PAN
36. Takayasu arteritis
• Most common causeof renal artery stenosis in children in India is Takayasu Aortoarteritis
• Takayasu arteritis commonly effects Renal arteries
• Takayasu arteritis are associated with granulomatous pathology
• Most common cause of renovascular hypertension in children in India is Takayasu Aortoarteritis
• Aortic arch syndrome is also known as Takayasu Aortoarteritis
• Takayasu Aortoarteritis is Large vessel vasculitis
• Takayasu Aortoarteritis is Pulseless disease
• Takayasu's arteritis predispoase to Aortic dissection
• A young female presents with diminished pulses in the upper limb and hypertension. The most
likely diagnosis is Takayasu's arteritis
• Reversed Coarctation is seen in Takayasu Arteritis
• Takayasu arteritis mainly affects Subclavian artery
• Renal artery stenosis may occur in Takayasu arteritis
• Blood pressure difference between left and right limbs in Takayasu arteritis
• Takayasu arteritis Shows Strongly positive mantoux
37. HYPOVOLEMIC SHOCK
• After trauma, hypovolemic shock can be due to Pelvic fracture, Blunt trauma to abdominal viscera
or Hemothorax
• 6 months old child is brought with vomiting & diarrhea. RR-45/min, HR-130/min, SBP-85 mm of Hg.
Capillary refilling time is 4 secs. Diagnosis is Early compensated hypovolemic shock
• Heart is spared from vasoconstriction during hypovolemic shock
• Features of hypovolemic shock are Oliguria, Low B.P & Acidosis
• Most common cause of death due to burns in early period is hypovolemic shock
• Hypovolemic shock after blunt trauma of the abdomen with splenic tear should undergo immediate
surgery
• The most serious complication of a pelvic fracture is hypovolemic shock
• Most common form of shock is hypovolemic shock
• In hypovolemic shock Constriction of capacitance vessels & arterioles in the skin with Decrease in
cardiac output is seen
• Hemorrhage leads to hypovolemic shock
38. GRANULOMATOSIS WITH POLYANGIITIS (WEGENER'S)

• In Wegeners glomerulonephritis characteristic feature seen in Focal necrotizing glomerulonephritis
• 90% of Wegener’s will have antibodies to Proteinase-3
• Renal biopsy with focal necrotizing glomerulitis with crescent formation & intermittent hemoptysis
and intermittent chest pain & chest x-ray demonstrate caviated multiple opacities , palpable
purpura on the legsare suggestive of Wegener's granulomatosis
• In Wegener's glomerulonephritis, the characteristic features seen is Granulomas in the vessels wall
• Wegener's glomerulonephritis, is more common in patients with alfa 1 antitrypsin deficiency
• Lung Wegener's granulomatosis involve Lung with Kidney
• Respiratory symptoms i.e. cough, hemoptysis and glomerulonephritis with raised c-ANCA in serum
is indicative of Wegener's granulomatosis
• In Wegeners glomerulonephritis characteristic feature seen in Granuloma in the vessel wall & Focal
necrotizing glomerulonephritis
• In Wegener's granulomatosis cytoplasmic anti neutrophilic antibodies are directed
against Proteinase 3
• RPGN caused by Wegener's granulomatosis
• Cresentic glomerular deposits are seen in Wegener's granulomatosis
• A person with involvement of upper respiratory tract, lungs and kidney shows evidence of
granulomas on histo pathology. The most likely diaglosis is Wegener's Granulomatosis
• Bilateral conductive deafness, palpable purpura on the legs and hemoptysis with Radiograph of the
chest showing a thin-walled cavity in left lower zone. Investigations reveal total leukocyte count
12000/mm3, red cell casts in the urine and serum creatinine 3mg/dL This may lead to diagnosis
of Wegener's granulomatosis
• Wegener's granulomatosis does not affect liver
• Lower Respiratory Tract involvement is more frequently seen in Churg Strauss Syndrome in
comparison to Wegener's Granulomatosis
• Ocular manifestations of Wegener's granulomatosis include Proptosis, Nasolacrimal duct
obstruction & Necrotizing scleritis
• Steroids is treatment of choice for Wegener's granulomatosis
• Anti-neutrophil cytoplasmic antibodies (ANCA) is seen in Wegener's Granulomatosis
39. TEMPORAL ARTERITIS
• Temporal arteritis More common in females

• Temporal arteritis Can leads to sudden bilateral blindness
• Temporal arteritis Mostly affects elderly
• Large vessel vasculitis is Temporal arteritis
• Polymyalgia rheumatica, Anemia & Sudden blindness are seen in Temporal arteritis
• Granulomatous inflammation is seen in Temporal arteritis
• Temporal arteritis Involves large to small sized areteries
• Segmental nature of the involvement is seen in Temporal arteritis
• An elderly female presents to the emergency department with history of fever, headache and
double vision. Biopsy of temporal artery revealed panarteritis. The most likely diagnosis is Temporal
arteritis
• The investigation of choice for diagnosis of Giant cell Arteritis is Temporal Artery biopsy
• A 64 year old lady Kamla complains of severe unilateral headache on the right side and blindness
for 2 days. On examination there is a thick cord like structure on the lateral side of the head. The
ESR is 80 mm/hr in the first hour. The most likely diagnosis is Temporal Artery biopsy
• Arterial biopsy of elderly male shows fragmentation of elastic lamina, lymphocyte infiltration and
giant cells indicates temporal arteritis
• Giant cell arteritis is a feature of temporal arteritis
40. CARDIOGENIC SHOCK
• In cardiacshock BP < 90 mm of Hg
• Drug of choice for cardiogenic shock is Dopamine
41. SEPTIC SHOCK
• The Reynold's pentad of fever, jaundice, right upper quadrant pain, septic shock and mental status
change in typical of Cholangitis
• Endotoxin causes Septic shock
• Peripheral resistance is decreased in Septic shock
• Veno constriction, Direct toxic endothelial injury & Activation of complement are pathogenetic
mechanisms operate in septic shock
• Septic shock in children 1st response is TC.O. due to vasodilatation
• Hypotension is a late sign in Septic shock in children
• The most important cause of the death in septic shock is Cardiac
• Renal failure in patients with septic shock occurs primarily from Acute tubular mecrosis
• Warm periphery is noticed in Septic shock
• Septic shock is due to Lipopolysaccharide
42. NEUROGENIC SHOCK
• Peripheral resistance is decreased in Neurogenic shock

• Neurogenic shock is characterized by Decreased peripheral vascular resistance
• Feature of neurogenic shock is Bradycardia and hypotension
43. COR PULMONALE

• Sudden death, right sided heart failure cor pulmonale or cardiovascular collapse occur when 60% or
more of pulmonary artery is obstructed with emboli
• Kerley B line, Pleural effusion & Cardiomegaly are radiological features of Chronic Cor pulmonale
• Secondary Polycythemia may be seen in Cor pulmonale
• Chronic Cor pulmonale is seen in COPD,Kyphoscoliosis,Intermittent pulmonary embolism, Cystic
fibrosis & Primary pulmonary hypertension
• The most common cause for chronic cor pulmonale is COPD
• The most common cause of acute cor pulmonale is Pulmonary thromboembolism.
44. INFECTIVE ENDOCARDITIS
• Diagnostic criterion for infective endocarditis includes Rheumatoid factor, Positive blood culture
& Positive ECG
• Infective endocarditis due to pseudomonas is most commonly seen with Intravenous drug abuse of
pentazocin
• Patient with Rapidly progressive malaise, fever, and chills,subungual splinter hemorrhages and a
systolic murmur Leading to death due to MI may be suffering from Acute infective endocarditis
• IE have most friable vegetation
• Staphylococcus aureus is the most common cause of acute infective endocarditis
• In a hospital cardiac care unit, there are three patients with different cardiac conditions: a 52 year
old man with dilated cardiomyopathy, an 18 year old girl with mitral valve prolapse, and a 30 year
old man with infective endocarditis of the mitral valve. Risk of systemic thromboembolism is the
common feature seen
• Tricuspid valve is most likely to be involved by infective endocarditis following a septic abortion
• Salmonella typhi is least likely to cause infective endocarditis
• ASD is the least common cause of infective endocarditis
• Blood culturefor staph. aureus is positive in Infective endocarditis
• A patient of RHD developed infective endocarditis after dental extraction. Most likely organism
causing this is Streptococcus viridans
• The group of organism HACEK , causing infective endocarditis include Haemophilus, Actionobacillus
& Eikenella
• Infective endocarditis is common in MR & AR
• Non-sterile vegetations are seen in Infective endocarditis
• In Infective endocarditis cause due to I.V. drug abuse is Candida is a common cause
• Staphylococeus aureus is commonest organism for IE in I.V. drug abuse
• Myocardial ring abscess, MI & Focal and diffuse glomerulonephritis are complication of infective
endocarditis
• In Infective endocarditis vegetation are friable and easily detachable from the cardiac valves
• In infective endocarditis Roth spots, Osiers nodes & Glomerulonephritis are immune mediated
• Diagnostic criterion for Infective Endocarditis include Positive Echocardiogram, Positive Blood
culture & Positive Rheumatoid Factor
• Infective endocarditis is commonly seen in Small VSD, Tetralogy of fallot & TDA
• Roth's spots are seen in Infective endocarditis
• Myocardial abscess, Vegetations along cusps & Perforation of cusp are the feature of Infective
endocarditis
• Acute Infective Endocarditis with abscess formation is most commonly associated
with Staphylococcus
• 3 culture sets separated by at-least 1 hour over 24 hours is recommended for culture sampling in
Infective Endocarditis
• Antiboiotic Prophylaxis for infective endocarditis is indicated in Coarctation of aorta
• Infective endocarditis after tooth extraction is probably due to Streptococcus viridans
45. AORTIC STENOSIS
• Dicrotic nature of aortic notch is lost in Aortic Stenosis

• Aortic Stenosis is common manifestation of congenital Rubella
• Aortic stenosis is an absolute contraindication for exercise testing
• The pressure-volume curve is shifted to the left in Aortic stenosis
• In heart patient the worst prognosis during pregnancy is seen in Aortic stenosis
• Aortic stenosis in young age is due to Bicuspid valve
• Calcification of the aortic valve is seen in Aortic stenosis
• Severity of Aortic stenosis is determined by Late ejection systolic murmur & ST -T changes
• Pure left sided failure may be seen with Aortic stenosis
• William's syndrome is associated with Congenital Supravalvular Aortic stenosis
• Angina pectoris and Syncope are most likely to be associated with Aortic stenosis
• Triad of angina, syncope and congestive heart failure can be suspected to have Aortic stenosis
• Aortic stenosis is a valvular heart diseases is most commonly associated with sudden death
• In severe aortic stenosis ST segment changes in ECG
• Delayed peak of systolic murmur is seen in a patient with severe aortic stenosis
• In Patient of Aortic stenosis with Exercise Stress testing terminated at 11 minutes due to
development of fatigue and dyspnea. Regional pressure gradient was observed to be 60 mm Hg
between the two sides of the aortic valve.Best Management is Aortic valve replacement
• Sub-valvular Aortic Stenosis is known to be associated with AR, VSD & Coarctation of Aorta
• The most common complication of Sub-valvular Aortic Stenosis is Aortic Regurgitation
• Aggravation of symptoms of angina in a patient when given nitrates is seen in Idiopathic
hypertrophic subaortic stenosis
• Pressure difference of 5mm Hg between the two upper limbs occurs in Supra –valvular aortic
stenosis
• Most common cause of death in aortic stenosis patients is IHD with ventricular fibrillation
• Vasopressor of choice in anesthesia for a patient of aortic stenosis, who develops hypotension
during surgery is Phenylephrine
46. MITRAL STENOSIS
• Pregnant patient will be benefited by having a forceps-assisted vaginal delivery at the time of
delivery in case of MS
• Features of Mitral stenosis on X-ray are Double contour of right border,Pulmonary
hemosiderosis,Straightening of left heart border, Lifting of left main bronchus ,Posterior
displacement of esophagus on barium swallow& Splaying of carinal angle
• In Patient with mitral stenosis with some liver compromise Xenon inhalational agent is preferred
for surgery
• In Pregnant patient with H/o MS & MR for normal delivery best analgesia is Epidural anaesthesia
• In Pregnant patient with mitral stenosis class II and Rheumatic heart disease Give Prophylactic
antibiotics, Apply Outlet forceps in 2nd stage of labor & Give iv furosemide at delivery of placenta
• In Pregnant patient with mitral stenosis class II and Rheumatic heart disease Methergin at delivery
is contraindicated
• Surgical correction of mitral stenosis during pregnancy is ideally done at14 weeks
• A case of severe mitral stenosis is associated with Pulsatile liver, Atrial fibrillation & Increase in the
length of murmur
• A patient known to have mitral stenosis and atrial fibrillation, presents with acute onset of
weakness in the left upper limb which recovered completely in two weeks. The most likely
diagnosis is Ischemic stroke
• Most common heart disease associated with pregnancy is Mitral stenosis
• Surgery for mitral stenosis during pregnancy is ideally done at 14 weeks
• During pregnancy corrective cardiac surgery is commonly indicated in Mitral stenosis
• In a diastolic murmur in mitral area with ECG showing mitral valve orifice to be 0.8 cm2. The cause
of her murmur is Severe mitral stenosis
• Loud S1 in Mitral stenosis is seen in Prolonged flow through mitral valve
• Kerley B lines seen in Mitral stenosis
• A 25 year old primigravide with mitral stenosis and mitral regurgitation is under labor. She wants
normal delivery which would be the best way to provide analgesia in this lady Neuraxialblockde
analgesia
• Mid-diastolic Murmur with presystolic accentuation is typically seen in Mitral stenosis
• A wide and notched P wave is typically seen in MS
• Mitral stenosis is associated with Right ventricular hypertrophy
• Pulsatile liver, Atrial fibrillation & prolonged murmur is seen as severity of mitral stenosis increases
• Severity of mitral stenosis is assessed by Length of murmur & S2-OS gap
• MC cause of morbidity and mortality late in the course of mitral stenosis Recurrent pulmonary
emboli
• Austin Flint Murmur is commonly mistaken for the murmur of Mitral stenosis
• An old lady with mitral stenosis underwent hysterectomy for uterine fibroid and died after
developing pulmonary edema. The order of cause of death in international certificate is Pulmonary
edema, hysterectomy, mitral stenosis
• A wide and notched P wave is typically seen in MS
• Heart sounds heard in chronic mitral stenosis is Mid diastolic murmur, Opening snap & Loud S I
47. LACTIC ACIDOSIS

• In the management of diabetes mellitus, lactic acidosis is commonly caused by Metformin
• Lactic acidosis is seen in Methanol poisoning, Respiratory failure & Circulatory failure
• Deaths from lactic acidosis in diabetes mellitus is associated with therapy with Phenformin
• Lactic acidosis is a side effect ofPhenformin & Metformin
• A child presents with metabolic lactic acidosis along with hyperammonemia and convulsion is due
to Reye's syndrome
• Thiamine deficiency lead to lactic acidosis
• Congenital lactic acidosis may occur d/t defect in PDH complex
• True about cause of Lactic Acidosis is that it is mainly caused by intake of Biguanides
• Lactic acidosis causes high anion gap metabolic acidosis
• Increased anion gap is seen in Lactic acidosis
• Linezolid may cause Lactic acidosis
• Extensive Ileal resection can cause Lactic acidosis
48. METABOLIC ALKALOSIS
• Metabolic alkalosis is seen in Thaizide diuretic therapy,Bartter's syndrome, Prolonged vomiting

& Cushing's disease
• An adolescent male presents with Hypokalemia, Metabolic Alkalosis, Hypercalciuria and
Nephrocalcinosis. His Blood Pressure is normal. The likely diagnosis is Bartter Syndrome
• The commonest cause of metabolic alkalosis is Pyloric stenosis
• A child had repeated vomiting and developed metabolic alkalosis. The treatment given is I.V.
normal saline and potassium
• In Metabolic alkalosis Less ammonia is excreted in urine
• Metabolic alkalosis and hypokalemia is seen in Cushing Syndrome
• Metabolic alkalosis is seen in Primary mineralocorticoid excess
• In severe metabolic alkalosis Hypocalcaemia, Hypoxia & Tetany is seen
• In a case of hypertrophic pyloric stenosis, the metabolic disturbance is Metabolic alkalosis with
paradoxical aciduria
• In Accelerated HTN metabolic defect seen is Metabolic alkalosis
• 20 mEq (mmol) of potassium chloride in 500 ml of 5% dextrose solution is given intravenously to
treat Metabolic alkalosis
• Persistent vomiting in G.O.O. causes Hypokalemic metabolic alkalosis
• Thiazide cause Metabolic alkalosis
• MOST common biochemical abnormality seen in congenital pyloric stenosis is Metabolic alkalosis
• Metabolic alkalosis is seen with long term use of loop diuretics
49. BECHET'S SYNDROME

• Bechet’s syndrome is a multisystem disorder with recurrent oral and genital ulcerations and ocular
involvement.
• HLA- B51 associated
• Recurrent aphthous ulcerations
• Genital ulcers
• Skin- folliculitis, eythema nodosum, sweet syndrome, pyoderma gangrenosum, acne.
• Eye involvement- scarring and bilateral panuveitis, Iritis/Posterior uveitis/Optic neuritis.
• Nondeforming arthritis
• Pseudo aneurysms
50. Myaesthenia Gravis
• Myasthenia gravis is a neuromuscular disorder characterized by weakness and fatigability of

skeletal muscles.
• An autoimmune disorder mediated by anti acetylcholine receptors at post synaptic membrane and
inhibits nicotinic receptors.
• Failure of transmission at many neuromuscular junctions results in weakness of muscle contraction.
• Myaesthenia gravis is antibody mediated (type II) hypersensitivity.
• Weakness and fatigability of skeletal muscles.
• Fluctuating weakness of voluntary muscle.
• Lids and extracocular muscle of eyelid- diplopia and ptosis.
• Facial weakness produces snarling expression.
• Tongue weakness leads to dysarthric mushy quality.
• Anti- AchR radioimmunoassay
• Electrophysiological testing
• Single- fibre electromyography
• Edrophonium chloride (Enlon) 2 mg + 8 mg IV, highly probable diagnosis.
• Drugs against MG-
• Antibiotics- aminoglycosides (streptomycin), Quinolones(ciprofloxacin), Macrolides(erythromycin)
• Beta- blocking agents- propranolol
• LA – procaine
• Magnesium
• Quinines
• Nondepolarizing muscle relaxants- tubocurarine, gallamine
• Botulinum toxin
51. PAROXYSMAL NOCTURNAL HEMOGLOBINURIA (PNH)
• PNH caused due to mutations in "PIG-A" (Phosphatidyl Inositol Glycan) gene.

• PIGA gene is responsible for biosynthesis of Glycosyl Phosphatidyl Inositol (GPI).

• Mutation in PIGA gene causes defective production of GPI resulting in undue to sensitivity of RBC's
to CRP.
• A stem cell disorder affecting all the three cell lines (RBCs, leucocytes & platelets) is PNH.
• Flow cytometry is the confirmatory test for PNH.
• Hams test is the best screening test for PNH.
• Eculizumab, an anti-C5 monoclonal antibody is used for treating PNH.
• PNH presents with chronic hemolytic anemia, pancytopenia with hypocellular marrow &
venous thrombosis.
• Venous thrombosis of hepatic veins is main cause of death in PNH - Budd Chiari syndrome.
• Reduces serum ferritin levels noted, due to hemoglobinuria & hemosiderinuria.
• Main CRP mutated is Membrane Inhibitor of Reactive Lysis (MIRL, CD59).
• PNH is associated with a decreased leukocyte alkaline phosphate scape.
52. Addison's Disease
ETIOLOGY-
• Autoimmune adrenalitis (autoimmune polyglandular syndromes)

• Tuberculosis in India
CLINICAL FEATURES-
• Characterised by loss of both glucocorticoids and mineralocorticoids.

• By Glucocorticoid insufficiency- Hypoglycaemia, Hyponatremia
• By Mineralocorticoids insufficiency- postural hypotension, Hyponatremia, Hyperkalemia,
Hypercalcemia
• Hyperpigmentation in palmar, dorsal foot, nipples and axillary region and oral mucosa.
DIAGNOSIS-
• Short cosyntropin test

• Cortisol level < 18-20 μg/dl sampled.
• ACTH stimulation test
TREATMENT
• Glucocorticoids replacement- hydrocortisone

• Mineralocorticoid replacement- fludrocortisone

53. Cushing Syndrome
• Cushing syndrome is caused to ACTH- producing adenoma.
ETIOLOGY
• Pituitary corticotrope adenomas

• Iatrogenic hypercortisolism (most common)
• Ectopic tumour ACTH production
• Cortisol- producing adrenal adenomas
• Adrenal carcinoma
• Adrenal hyperplasia
Clinical features-
• Body fat-weight gain, rounded face (moon face), buffalo hump.

• Eye- loss of diurnal variation
• CVS- hypertension, hyperkalemia, edema, artherosclerosis.
TREATMENT-
• Treatment of choice- removal of pituritary corticotrope tumour (transphenoidal approach)

• Pituitary irradiation
• Metyrapone and ketoconazole
54. Thyrotoxicosis
• Thyrotoxicosis is defined as the state of thyroid hormone excess.

• Primary Hyperthyroidism
• Grave’s disease
• Toxic multinodular goiter
• Thyrotoxicosis without hyperthyroidism
• Subacute thyroiditis
• Hyperactivity, dysphoria, systolic hypertension
• CVS- Tachycardia, midsystolic murmur, means lerman scratch (2nd left intercoastal space), systolic
ejection click.
• Fatigue, weight loss, diarrhea, polyuria, glycosuria, proximal muscle weakness.
• Eye- Lid retraction or lag, proptosis, myxedema, unilateral exopthalmos
• Thyroid dermopathy
• Joffroy’s sign- absence of wrinkling on forehead when patient looks up.
• Scintigraphy is a preferred test
TREATMENT-
• Antithyroid drugs- thionamides (Carbimazole for child, pregnancy), methimazole, Propylthiouracil
(pregnancy- preferred)
• Thyroidectomy
• Radioiodine
• Propranolol (? blockers)used for adrenergic symptoms
55. Thyroid Storm
• Thyroid storm or thyrotoxic crisis is rare and is a life threatening exacerbation of hyperthyroidism.
ETIOLOGY
• Acute illness (stroke, infection, trauma, diabetic ketoacidosis)

• Surgery
• Inadequate control of hyperthyroidism
• Radioactive treatment of hyperthyroidism
TREATMENT-
• Propylthiouracil (drug of choice)

• Stable iodide blocks thyroid hormone synthesis via Wolff- Chaikoff effect.
• Potassium iodide
• Porpranolol
• Glucocorticoids
• Calcium channel blocker
56. Reactive arthritis
Definition
• Reactive arthritis is a systemic disorder ,defined by the development of conjunctivitis, urethritis,

arthritis, and mucocutaneous lesions following an episode of infection elsewhere in the body.
Pathophysiology:
• Human leukocyte antigen B27 (HLA-B27) haplotype is frequently associated.
Organism Responsible
• Reactive arthritis (ReA) is most commonly triggered by Shigella (usually flexneri > sonnei, boydii,
dysenteriae) > Chlamydia trachomatis, Salmonell, Yersinia (enterocolitica, pseudotuberculosis),
Campylobacter jejuni > Clostridium difficile, Campylobacter coli, toxic E.coli > Ureoplasma
ureallyticum, Mycoplasma genitalium > Chlamydia pneumoniae URTI
• Adolescents and young men are most likely to acquire reactive arthritis after they have urethritis.
Clinical features:
• The arthritis is most commonly asymmetric and frequently involves the large weight-bearing joints
(chiefly the knee and ankle)
• The mucocutaneous lesions may include balanitis, stomatitis, and keratoderma blennorrhagicum,
indistinguishable from pustular psoriasis.
• The Characteristic skin lesions- Keratoderma Blenorrhagica, consist ofvesicles that become
hyperkeratotic, ultimately forming a crust before disappearing. These are seen in palms and soles
57. HYPOKALEMIA
• Hypokalemia
Associated with:
• Diuretics
• Thiazide,
• Bumetanide,
• Furosemide,
• Ethacrynic acid
• Theophylline intoxication,
• Cortisol,
• Villous adenoma of colon etc.
• ECG changes of hypokalemia:
• ST segment depression,
• Increased U wave amplitude etc.
• Hypokalemic Metabolic Alkalosis with Hypercalciuria in a patient with normal blood pressure
suggests a diagnosis of Bartter Syndrome.
• Hypokalemic metabolic alkalosis with normal blood pressure may be seen in both Banter Syndrome
and Gitelman's Syndrome. Presence of Nephrocalcinosis from Increased Urinary excretion of
Calcium is typically seen in Bartter's
• Syndrome and distinguishes Bartter's Syndrome from Gitelman's Syndrome (Decreased Urinary
Calcium Excretion). Liddle's Syndrome also causes Hypokalemic metabolic alkalosis but this disorder
is typically associated with Hypertension (Blood Pressure is elevated)
Presentation Diagnosis
Hypokalemic Metabolic alkalosis with Liddle's Syndrome
Hypertension
Hypokalemic Metabolic Alkalosis without Banner Syndrome (Increased Urinary Ca
Hypertension Excretion)
Gitelman Is Syndrome (Decreased Urinary Ca

Excretion)
• Hypokalemia is associated with ST depression, prolonged PR interval, Flattened or Inverted T

waves, Prominent U waves and rarely S - A block
• Hypokalemia is associated with a prolonged QU interval and not a prolonged QT interval (Refer
previous question) Increased PR interval with ST depression therefore remains the single best
answer of choice.
• Note:
• QT interval is prolonged in Hypocalcemia
• QT interval is decreased in Hypercalcemia 2
• Hypokalemia can be due to increased loss. Non renal causes are
1. Gastrointestinal loss (Diarrhea)
2. Integumentary loss (Sweat)
MUST KNOW:
• The loss of K+ in sweat is very low except in extremes of physical exertion

• Direct gastric losses of K+ is also minimal (Vomiting, NG aspiration)
• It can lead to hypochloremic alkalosis
• It lead to persistent kaliuresis due to secondary hyperaldosteronism
• Celiac disease, ileostomy, villous adenoma, VIPomas, and chronic laxative cause significant
hypokalemia
• Colonic pseudo-obstruction (Ogilvie's syndrome) can lead to hypokalemia from secretory diarrhea
• Hypokalemia is a feature of Gitelman's syndrome
• Mechanism: Mineralocorticoid excess
• Similar mechanism seen with
Primary and secondary hyperaldosteronism
Malignant hypertension
Renin secreting tumors
Renal artery stenosis
Hypovolemia
Bartter’s syndrome
• Apparent mineralocorticoid excess leads to hypokalemia in
Liddle's syndrome
11 beta dehydrogenase-2 deficiency
58. sickle cell anemia

Laboratory findings of sickle cell anemia :?
• Moderate to severe anaemia.

• Peripheral smear will show
• Sickle cells
• Target cells
• Howell-Jolly bodies because of autosplenctomy.
• A postive sickling test with a reducing substance like sodium metabisulfite.
• Sickle cell anemia is caused by replacement of normal Hemoglobin by sickled hemoglobin (HbS).
• HbS is formed by replacement of Glutamine by Valine at position 6
• This substitution replaces the polar Glutamine residue with a nonpolar Valine.
• The replacement of Glutamine by Valine generates a sticky patch on the surface of HBS.
• The sticky patch is present on both oxygenated and deoxygenated HbS
• The deoxygenated HbS also contains a complementary site for the sticky patch.
• In oxygenated hemoglobin this complementary site is masked.
• When HbS is deoxygenated the sticky patch present on its surface binds to the complementary
patch on another deoxygenated HbS molecules.
• This binding leads to polymerization of deoxyhemoglobin S forming long fibrous precipitates.
• These extend throughout the erythrocyte and mechanically distort it, causing lysis and multiple
secondary clinical effect.
• So, if HbS can be maintained in an oxygenated state or if the concentration of deoxygenated HbS
can be minimized, formation of these polymers will not occur and sickling can be prevented
(Remember the complementary site for the sticky patch remains masked in case of Oxygenated
HbS).
Role of HbA in polymerization
• Unlike HbS, HbA does not contain any sticky patch, but it does have a binding site for the sticky
patch of HbS.
• Thus it can bind to HbS through its receptor site but this binding cannot extend the polymer
because HbA does not contain any sticky patch to promote binding to still another hemoglobin
molecule.
• So HbA interferes with the polymerisation and aggreation of HbS and reduces the intensity of sickle
cell anemia.
59. sarcoidosis
Diffuse Effusion is an uncommon atypical manifestation in Sarcoidosis reported in up to 5% of patients.
• Parotid enlargement is a classic feature of sarcoidosis and bilateral involvement is the rule
• Neurological disease is reported in 5-10% of patients with sarcoidosis
• Facial nerve palsy is the single most common neurological manifestation of sarcoidosis seen in up
to 50% of patients with Neurosarcoidosis.
• Angiotensin converting enzyme (ACE) levels are raised in sarcoidosis
Lung involvement in sarcoidosis
• Most common involved organ (90%).

• Characterized by B/L hilar adenopathy.
• Cavitations are rare
• Pleural effusion are rare (1-2%)
60. KWASHIORKOR
• Kwashiorkor is a major type of protein energy malnutrition characterised by inadequate intake of

proteins.
CLINICAL FEATURES-
• Easy hair pluckability

• Edema
• Skin breakdown
• Poor wound healing
• Infection
• Muscle wasting
• Fatty liver
• Moon face
• Retarded growth
• Psychomotor changes
LAB DIAGNOSIS-
• Decrease serum proteins (albumin)
61. Marasmus
• Marasmus is a state in which all body fat stored has been exhausted due to starvation without
systemic inflammation.
CLINICAL FEATURES
• Growth retardation
• Loss of subcutaneous fat
• Wasting of muscles
• Infections
• Chronic diarrhea
• Vocarious appetite
• Monkey facies
• Baggy pant appearance
• Weight loss
LAB DIAGNOSIS
• Blood urea is low

• Blood glucose is low
62. Hypothyroidism
• Hypothyroidism is caused due to iodine deficiency.

• Primary
• Autoimmune hypothyroidism- hashimoto’s thyroiditis
• Iatrogenic
• Drugs- lithium, ethionamide, p-aminosalicyclic acid(antitubercular drug)
• Congenital hypothyroidism
• Iodine deficiency (in India most common cause)
• Infiltrative disorder- scleroderma, hemochromatosis
• Yellowing of skin occurs due to accumulation of increase carotene.
• Primary hypothyroidism- T4 is low and TSH elevated
63. Congenital hypothyroidism
• Neonatal hypothyroidism is due to thyroid gland dysgenesis, inborn errors of thyroid hormone
synthesis.
CLINICAL FEATURES
• Common symptoms- tiredeness, weakness, dry skin, cold extremities, weight gain, hoarse voice,
growth retardation.
• CVS- Bradycardia, peripheral oedema
• Nervous system- carpel tunnel syndrome, paresthesia,mental retardation, large anterior
fontanelle
• Menorrhagia, delayed puberty
• Puffy face, hands and legs, protruded tongue
• TREATMENT-Levothyroxine

64. Subacute Thyroiditis
• Subacute causes- viral infection, silent thyroiditis, mycobacteria infection, drug induced
(amiodarone)
• Chronic- autoimmunity (Hashimoto’s thyroiditis, Riedel’s thyroiditis, parasitic infection, traumatic.
• Subacute thyroiditis also termed as de Quervain’s thyroiditis, granulomatous thyroiditis or viral
thyroiditis.
• High ESR
• During initial phase of follicular destruction, radioactive uptake is low
• Decreased T3 & T4 and TSH increased.
• Histology- MULTINUCLEATED GIANT CELLS.
65. Silent thyroiditis
• Painless thyroiditis or silent thyroiditis occurs with underlying autoimmune thyroid disease
(subacute thyroiditis).
• Postpartum thyroiditis occurs with subacute thyroiditis in women 3-6 months after pregnancy.
• The risk of of recurrence in subsequent pregnancy is 70%.
• Thyrotoxicosis lasting 2-4 weeks followed by hypothyroidism for 4-12 weeks.
• Thyroid function may be normal after 1 year.
66. Blind Loop Syndrome
• Blind loop syndrome or stagnant bowel syndrome is bacterial proliferation due to functional stasis
or anatomic stasis.
CLINICAL FEATURES
• Watery diahrroea/ stearrhoea- deficiency of vitamin B12

• Macrocytic anaemia due to bacterial growth.
• INVESTIGATIONS- Hydrogen breath test
67. Scleroderma
• Systemic sclerosis (scleroderma) is a generalised multisystem connective tissue disorder.

• Onset in the fourth and fifth decade.
• Limited cutaneous systemic sclerosis- patients have “CREST” syndrome (calcinosis, Raynaud’s,
oesophageal involvement, sclerodactyly, telangiectasia)

CLINICAL FEATURES-
• Skin- sclerodactyly, Ranaud’s phenomenon, calcinosis, telangiectasia, skin thickening.

• Musculoskeletal features- Arthralgia, flexor tenosynovitis
• GIT- oesophagitis, dysphagia, malabsorption
• Cardiorespiratory features- pulmonary fibrosis, pulmonary hypertension
• Renal features- hypertensive renal crisis
68. Blood Products
• Red cell concentrate- ABO compatibility is essential

• Fresh Frozen Plasma (FFP)-
• Replace coagulation factors (fibrinogen, albumin, Factors II, V, VII, IX, X, XI) and used for thrombotic
thrombocytopenic purpura.
• Stored at -400C – 500 C
• Cryoprecipitate-
• Replace fibrinogen, factor VIII and von Willebrand factor.
• Contain Factor VIII
• IV Immunoglobulin- Used in hypogammaglobulinaemia
69. Hyperphosphatemia
• Hyperphosphatemia is defined as serum phosphate concentration >1.8 nmol/L (5.5mg/dL) results

impaired glomerular infiltration, hypoparathyroidism, excess of phosphate into the ECF.
ETIOLOGY-
• Impaired renal phosphate excretion
a) Renal insufficiency
b) Hypoparathyroidism
c) Parathyroid suspension
d) Pseudohypoparathyroidism
e) Acromegaly
CLINICAL FEATURES

• Hypocalcaemia
• Metastatic calcification
Surgery
1. Hypospadias
• Hypospadias is most common congenital malformation of urethra.

• M/c Type - Glandular
• Cryptorchidism is not a feature of hypospadias. But it may be seen associated with hypospadias in
8-9% of cases
• Ventral chordee is seen in hypospadias while Dorsal chordee is a feature of epispadias
• Meatal stenosis may be associated with hypospadias and needs meatotomy for correction
• The best time for surgery for hypospadias is between 6-12 months of age"
2. Facial Nerve Reanimation
• Immediate onset paralysis due to fracture of mastoid (temporal bone) requires surgery
(decompression, re-anastomosis or cable nerve graft).
• In Facial nerve is injury during parotid surgery Best management would be immediate repair
• Treatment of choice for CSOM with vertigo and facial nerve palsy is immediate mastoid exploration
• Crocodile tears Occurs due to improper regeneration of facial nerve
3. Thyroglossal Cyst
• Most common site of thyroglossal cyst is Subhyoid.

• Thyroglossal cyst moves upwards on protrusion of tongue.
• Thyroglossal cyst is located within 2 cm of the midline.
• Thyroglossal cyst is the frequent cause of anterior midline neck masses in the first decade of life.
• Excision of the thyroglossal cyst along with the track and the body of the hyoid bone is the
treatment of choice (Sistrunk’s operation)

• The most common site of a swelling in a 16 year old girl presenting with a painless swelling in the
midline of the neck and moves up and down with swallowing and with protrusion of the tongue is
Subhyoid.
• The cause of swelling in a child presenting with a midline swelling beneath the arch of the hyoid
bone might be Thyroglossal cyst.
• In thyroglossal cyst, Papillary carcinoma may arise.
• Thyroglossal cyst is an example of painless midline swelling.
• Hyoid bone is closely associated with Thyroglossal cyst/fistula.
• In the management of thyroglossal cyst,Central portion of hyoid excised.
• Sistrunk's operation is used in Thyroglossal fistula and Thyroglossal cyst.
• Thyroglossal cyst move on deglutition(other causes are pre-tracheal lymph nose and thyroid
nodule).
• Thyroglossal fistula develops due to Incomplete removal or infection of thyroglossal cyst
4. BLOW OUT FRACTURE
• CT can fairly accurately determine the size of the fracture and its relationship to the orbital soft
tissues
• Blow out fracture of the orbit, most commonly leads to fracture of Posteromedial floor of orbit
• Restriction of lateral and upward gaze of eyeball and diplopia with enophthalmos following history
of trauma is suggestive of blow out fracture
• Diplopia, 'Tear drop" sign , Positive forced duction test & enopthalmous are signs of blow out
fracture
5. Glasgow Coma Scale(GCS)
• Eye opening , Motor response, Verbal response are used for gradation of coma in Glasgow coma
scale
• Glasgow coma scale score for head injury, eye opening seen with painful stimulus, localize pain
and inappropriate verbal response is 10
• Glasgow coma scale is the best prognostic factor in a case of head injury
• According to the Glasgow Coma Scale (GCS), a verbal score of 1 indicates No response
• Glasgow Coma Scale score in a conscious person is 15
• Glasgow coma scale Ranges from 3 – 15
• Glasgow coma scale are Less than 7 is classified as coma
• Glasgow coma scale More than 9 excludes coma
• Mild head injury is having Glasgow coma scale of 10-15
• Low score in Glasgow coma scale indicates deteriorating brain function
• According to the Glasgow Coma Scale (GCS), a verbal score of 1 indicates No response
• A person with 'Inappropriate speech' evaluated by the 'Glasgow Coma Scale' will have a verbal
score of 3
• Glasgow coma scale in death is 3
6. Cleft Lip
• Cleft of the upper lip that extends upward toward the left nostril and left anterior cleft of the
primary palate just deep to the cleft lip. These defects are most likely due to a failure of Maxillary
process to fuse the medial nasal process
• Isolated cleft lip and palate is Multifactorial
• Cleft lip, cleft palate, polydactyly, microcephaly with holoprosencephaly, ectodermal scalp defect is
seen in Trisomy 13
• Repair of cleft lip should be undertaken at 10 weeks
• Millard repair is used for treatment of Cleft lip
• A midline cleft lip is present when there is failure of fusion between Medial nasal processes
• Drug likely to be consumed by the mother causing cleft lip is Isotretinoin
• Commonest type of cleft lip is Combined with cleft palate
• In cleft lip operation all the stitches are removed on 4th day
• Unilateral clefts are most common on Left side
• Le Mesurier's method,Tennison's method, Millard's method are used in cleft lip surgery
• Unilateral cleft lip is associated with Posterior displacement of alar cartilage
7. Cellulitis
• Cellulitis is commonly caused by S aureus , streptococcus pyogenes & Clostridium perfringens.

• Vancomycin, Teicoplanin and Linezolid are all active against most Methicillin-resistant
Staphylococcus aureus (MRSA) infection causing cellulitis
• Cellulitis of floor of mouth can lead to Ludwigs angia
• Pasteurella multocida is the most common causative micro organism of cellulitis in case of cat bite
• Treatment of spreading streptococcal cellulitis is penicillin
• cellulitis of lower limb Are Infection of skin & subcutaneous tissue showing distinct margins
with Fever & malaise
• Orbital cellulitis is caused by
• Pneumococcus(on culture show greenish colonies and optochin sensitivity)
• Apophysomyces species(severe panophthalmitis with cellulitis shows irregular branching aseptate
and broad hyphae)
• Aspergillus(hyaline, narrow, septate and branching hyphae)
8. Zenkers diverticulum

• Zenkers diverticulum is also called as Pharyngoesophageal diverticulum, pharyngeal pouch &
hypopharyngeal diverticulum
• An aged patient with symptoms of foul breath & regurgitation of food which is eaten 3 days ago, it
is a typical presentation of Zenker's diverticulum.
• Zenkers diverticulum is an acquired, false, pulsion diverticulum that affects patients older than 50
years
• Lateral X-rays on barium swallow are often diagnostic of Zenkers diverticulum
• Zenkers diverticulum is an outpouching in the posterior pharyngeal wall immediately above upper
esophageal sphincter
• Zenkers diverticulum when enlarges, it tends to deviate from the midline, mostly to the left
• Zenker’s diverticulum originates from the posterior wall of the esophagus through triangular area
of weakness
• Treatment of Zenker’s diverticulum is simple excision
• Commonest complication of Zenker's diverticulum is Aspiration pneumonia & Lung abscess
9. Sigmoid Volvulus
• Coffee bean sign is seen in Sigmoid volvulus

• A plain abdominal X-ray in a patient with a sigmoid volvulus will show a distended bowel
loop with its apex in Rt. Hypochondrium
• Bird of Prey sign is seen in the radiographic barium examination of Sigmoid volvulus
• Sigmoid volvulus is more common than caecal volvulus
• Sigmoid volvulus is More common in psychiatric patients
• Definitive treatment of sigmoid volvulus is sigmoid colectomy
• Rotation in sigmoid volvulus nearly always occur in anticlockwise direction
• Age of 60-70, neurological impairment, psychiatric condition ,Band of adhesion & Long pelvic meso
colon with Narrow attachment are some Predisposing factors for sigmoid volvulus
10. Heller Cardiomyotomy
• Heller's operation is done for Achalasia cardia

• Dysphagia to both solids and liquids along with episodes of intermittent chest pain & Barium
swallow showing dilated lower esophagus are best treated by Heller's myotomy
11. Dermoid Cyst
• Ovarian mass in x-ray pelvis showing a radio-opaque shadow suggest Dermoid cyst
• Dermoid cyst of ovary is teratoma Frequently undergo torsion
• Most common ovarian tumour in pregnancy is Dermoid cyst
• Dermoid cyst of ovary contains derivatives from all 3 germ layers Endoderm,Mesoderm & Ectoderm
• Dermoid cyst is Commonly more than 10 cm
• Dermoid cyst Has sebaceous material
• Dermoid cyst diagnosed during pregnancy should be removed surgically at 14-16 week
• Dermoid cyst are commonly seen in skull
• Most common orbital cyst in children is dermoid cyst
12. Penetrating injury
• Penetrating injury to neck is defined as Violation of platysma

• Sympathetic ophthalmitis results due to Penetrating injury of ciliary body
• Esophageal injury is Most common after penetrating injury
• Esophageal injury Can lead to mediastinal collection
• Barium swallow is diagnostic of esophageal injury
• Organ most commonly damaged in penetrating injury of abdomen is Liver & Small intestine
• Commonest cause of death in penetrating injury of chest is Tracheobronchial injury
13. Cholelithiasis
• Solitary gall stone 1.5 cm in size without symptoms can be treated with Cholecystectomy if it
develops biliary colic
• Mercedes Benz sign is seen in Gall stone
• Gall stones in children is caused by Chronic hemolytic disease (sickle cell anemia,
spherocytosis),Obesity & Prematurity with complicated medical or surgical course
• Open cholecystectomy for cholelithiasis is considered a clean contaminated wound
• History of epigastric pain radiating to back along with an enlarged (edematous) pancreas revealing
cholelithiasis on ultrasonography suggests a diagnosis of Acute Pancreatitis.
• Illeo cecal junction is the most common site of intestinal obstruction caused by a gall stone
• Radio-opaque stones is a contraindication for medical management of Gall stones
• Cholelithiasis is particularly seen in association with Somatostatinoma malignancy
• Gall stones in hemolytic anaemia are Pigmented
• Childhood cholelithiasis is seen in Neimann Pick's disease
• Investigation of choice for gall stone is USG
• The commonest site of obstruction in Gall stone ileus is Distal ileum
• The treatment of gall stone ileus is Removal of obstruction
• Gall stones is More common in female
• Coronary artery disease with asymptomatic gall bladder stones should not be treated with
surgery
• Indication for medical treatment in gall stone is stone size less than15mm
• Ursodeoxycholic acid is Gall stone dissolving drug

• Multiple Gall stones & 8 mm dilation with 4 stones in CBD, best treatment modalities are
Cholecystectomy with choledocholithotomy at same setting
• Recurrent attacks of cholelithiasis, U/S examination shows a dilated CBD of 1 cm is best treated
with ERCP
• The Gall stone pain is referred to the shoulder through C3-05
• Commonest type of gall stone is mixed
• 10% Percent of gall stones are radio opaque
• A gall stone gets impacted most commonly in Ampulla of vater of common bile duct
• Gall stones contains Cholestrol, Phosphate, Carbonate
• Cholesterol gall stones are due to Increased cholesterol,Decreased bile salts,Decreased entero
hepatic circulation
• Elective open cholecystectomy for cholelithiasis is the surgical procedures is considered to have a
clean-contaminated wound
• Best investigation for diagnosis of ampullary gall stone with obstructive jaundice is ERCP
14. Inguinal Hernia
• Enlarged right hemi-scrotum with a mass that appears to be originating at the level of the external
inguinal ring. With the patient completely relaxed, the physician is able to reduce the mass by
pushing it back through the external inguinal ring. With the mass reduced, the physician instructs
the patient to perform a Valsalva maneuver, upon which a protrusion is felt at the external inguinal
ring. Once the mass is reduced, the testicle appears normal in size and consistency, this is
suggestive of inguinal hernia
• Direct inguinal hernia swelling is doughy in consistency , dull on percussion & reducible but
reduction is difficult towards the end is suggestive of Epiplocele
• Pain could indicate obstruction in inguinal hernia
• Family history of inguinal hernia,Weight lifter,COPD are the risk factors for inguinal hernia
• Sup. Inguinal ring is an opening in external oblique aponeurosis
• Indirect inguinal hernia lies Lateral to inferior epigastric vessels
• For differentiating Inguinal hernia and femoral hernia the landmark will be Pubic tubercle
• Bubonocele: in this case the hernia is limited in the inguinal canal.
• In children, if inguinal (indirect) hernia is present in one side, then processus vaginalis is intact on
other side
• Direct hernia is less likely to undergo strangulation
• Hernia on Rt side is more common than Lt side
• In case of female commonest hernia is Indirect inguinal hernia
• Aspiration of the sac for diagnosis,X-ray abdomen,USG abdomen are not done in case of obstructed
inguinal hernia
• Truss cannot prevent progression of Sliding type of inguinal hernia
• Transillumination distinguishes indirect inguinal hernia from hydrocele
• Most common type of hernia is indirect inguinal hernia
• Incompletely descended testis Early repositioning can preserve function,It may lead to sterility, if
bilateral & May be associated with indirect inguinal hernia
15. TREATMENT OF INGUINAL HERNIA
• During surgical repair of hernia, the sac of a strangulated inguinal hernia should be opened
at Fundus
• Congenital hydrocele is treated by herniotomy
• Hernia in children is treated with herniotomy
• Absorbable mesh should not be used for surgery
• Surgery can be done using laparoscopy
• A pt. operated for direct inguinal hernia developed anethesia at the root of the penis and adjacent
part of the scrotum the nerve likely to be injured is Ilioinguinal nerve
• During repair of indirect inguinal hernia, while releasing the constriction at the deep inguinal ring,
the surgeon takes care not to damage Inferior epigastric arterySpermatic cord
• Most important step in the repair of an indirect inguinal hernia is Narrowing of the internal ring
16. Duodenal Atresia
• Treatment of duodenal atresia is Duodenoduodenostomy

• Double bubble sign is seen in Duodenal atresia
• Anomaly associated with duodenal atresia is Down syndrome
• A newborn presenting with intestinal obstruction and constipation showed, on abdominal X ray,
multiple air fluid levels is suggestive of Duodenal atresia
• Most common cause of Acute Intestinal Obstruction in neonates is Duodenal atresia
• Commonest cause of intestinal obstruction in down's syndrome is Duodenal atresia
• Antenatal double bubble appearance on ultrasound is due to Duodenal atresia
17. rectal prolapse
• Well’s operation,Lahaul’s operation,Ripstein’s sling operation are abdominal procedure for rectal
prolapse
• A young male patient presents with complete rectal prolapse. The surgery of choice is Abdominal
Rectopexy
• Chronic dysentery, abdominal pain, and rectal prolapse in children is caused by Trichuris trichura
• Treatment of rectal prolapse in childhood is Thiersch wiring
• Delorme's Procedure is used for Rectal prolapse
18. Pyloric Stenosis

• Congenital hypertrophic pyloric stenosis of infancy most commonly occurs in first born male child
• Congenital hypertrophic pyloric stenosis of infancy usually presents at 3 to 4 weeks of life
• In Congenital hypertrophic pyloric stenosis of infancy Baby is hungry soon after vomiting
• Hypokalemic,Hypochloremic metabolic alkalosis are the Metabolic abnormalities associated with
Congenital Pyloric Stenosis
• A 3 week old patient presenting with vomiting and failure to thrive is found to have pyloric stenosis
should be treated with correction of electrolyte disturbances
• Drug which can cause Hypertrophic Pyloric stenosis is Erythromycin
• The pyloric tumour is best felt during feeding is the most characteristic feature of congenital
hypertrophic pyloric stenosis
• Ultrasonography is the diagnostic test in hypertrophic pyloric stenosis
• Clinical features of pyloric stenosis in infants are Abdominal lump,Constipation,Weight Loss &
Metabolic alkalosis
• The vomiting in pyloric stenosis may or may not be projectile, however non bilious vomiting after
feed is the characteristic feature.
• Remsted's operation is done for pyloric stenosis
• Patient with low serum calcium posted for pyrolic stenosis surgery should undergo Serum protein
level investigation before administration calcium supplement
• USG findings of congenital pyloric stenosis shows > 95% accuracy,Segment length >16mm
& Thickness >4mm
• Single bubble appearance string sign or double neck sign and shoulder sign is seen in X-ray finding
of pyloric stenosis
• In congenital pyloric stenosis the defect usually lies in Circular muscle fibres antrum
19. Blunt Injury to abdomen
• Blunt injury abdomen, patient was hemodynamically stable, next investigation is X-ray abdomen
• Blunt injury of abdomen by RTA with established Airway & stable respiration , Blood collection for
cross matching & IV fluid adminisration is the next line of management
• In Renal injury following blunt injury to abdomen management will include Diagnostic peritoneal
lavage,IVP,Exploratory laparotomy
• Preferred incision for abdominal exploration in Blunt injury abdomen is Always Midline incision
• Blunt injury abdomen, patient was hemodynamically stable, next investigation is FAST
20. Liver Transplantation
• Hepatitis C is the Most common indication for Liver transplantation

• Patient of hepatitis C treated with orthotopic liver transplantation which shows rising transaminase
and bilirubin levels after an year should be given immunosuppresent to prevent T-lymphocyte
mediated rejection injury to hepatic endothelial cells

• Liver transplantation offers the only chance of cure in those with unresectable hepatocellular
carcinoma
• Donor bile duct with recipient bile duct or Roux en Y choledochojejunostomy is the best way to get
bile drainage in donor liver In orthotropic liver transplantation
• The best available treatment for portal hypertensive gastropathy is Liver transplantation
• Indications of Liver transplantation are Biliary atresia,Sclerosing cholangitis & Cirrhosis
• According to Pugh's classification moderate to severe hepatic insufficiency is managed by liver
transplantation
• Liver transplantation was first done by Starzl
• In late stage of PSC treatment is liver transplantation
21. Sub Phrenic Abcess
• Non-specific gas pattern in bowel and an air-fluid level in LUQ seen in Abdominal radiograph after
Splenectomy is suggestive of Subphrenic abscess
• Subphrenic abscess is toxemia
• Complain of right hypochondrial pain with plain chest x ray showing elevated right hemidiaphragm
is seen in Subphrenic abscess
22. Varicocele
• varicocele Can present as a late sign of renal cell carcinoma

• varicocele Has bag of worm like feeling
• varicocele Can lead to infertility
• Hypernephroma May present with rapidly developing varicocele
• Varicocele is common on left testis because Left tesicular vein drains into left renal vein which has
high pressure
• Indications of surgery in Varicocele are Small testis, Pain, Oligospermia
• Varicocele of pampiniform plexus of veins has Negative transillumination test, is Reducible,
shows Cough impluse
• Incompetent valves of testicular vein are responsible for varicocele
• Femoral catheterization with spermatic vein ablation is done in recurrence
• Drainage of venous blood from testes following division of testicular vein for treatment of
varicocele is by Cremasteric vein
23. Ureterocele
• In IVP, Adder head appearance is seen in Ureterocele

• Recurrent E.coli infection in urine with Ultrasound of abdomen showing Hydroureter and
Hydronephrosis & Micturating cysto - urethrogam showing filling defect in urinary bladder is
suggestive of Ureterocele
• Cobra head deformity is characterstic of Ureterocele
24. Hydrocele
• Funicular hydrocele is a communicating hydrocele

• Congenital hydrocele is treated by Herniotomy
• Hydrocele are Brilliantly transilluminant swellings
• Edema of foot and Hydrocele is caused by W.Bancrofti
• Lord's Plication is done for Hydrocele
• Congenital hydrocele in infant showing inguinal swelling which is smooth, transparent, fluctuating
&receives an impulse when the child coughs or struggles
• Vaginal hydrocele remains in the scrotum
• Hernia with hydrocele is Gibbon's hernia
• No-scalpel vasectomy is for contraception is contraindicated in Hydrocele
• Lord's and Jaboulay's operation is done for Hydrocele
• Hydrocele is a type of Exudation cyst
25. Hepatic Resection
• Adenocarcinoma with invasion of muscular layer is treated with Wedge hepatic resection with
lymph node dissection
• Patients with solitary hepatic metastases without clinical or radiographic evidence of additional
tumor involvement is treated with partial liver resection.
• Hepatic resection is done in hydatid disease of liver
• The minimum amount of normal perfused liver parenchyma to be left intact when a hepatic
resection is planned is 20%
26. Cholecystectomy
• Contraindication for laparoscopic Cholecystectomy is Coagulopathy,Obstructive pulmonary

disease, End-stage liver disease
• Asymptomatic gall stone of 1.5cm can be treated with Cholecystectomy only, if she develops biliary
colic
• The technique of laproscopic cholecystectomy was first described by Erich Muhe
• Anaesthetic of choice in laparoscopic cholecystectomy is Propofol
• Open cholecystectomy for cholelithiasis is considered a clean contaminated wound
• Acute Cholecystitis with medically controled symptoms is further treated with Laparoscopy
cholecystectomy immediately
• The treatment of choice for mucocele of gallbladder is Cholecystectomy
• Howel-Jolly bodies may be seen after Cholecystectomy
• Treatment of chronic cholecystitis is Cholecystectomy
27. Splenectomy
• Autospleenectomy" is a feature seen in:sickle cell anemia
28. Barrett's Esophagus
• Metaplasia of esophageal squamous epithelium into columnar in distal esophagus

• It is consequence of severe reflux esophagitis
• MC type of columnar epithelium is intestinal epithelium (Intestinal metaplasia)
• Barrett's Esophagus is a pre-malignant condition.
• Barrett's esophagus leads to Adenocarcinoma.
• Chronic reflux is a casue of Barrett's Esophagus.
• Established metaplasia doesn’t reverse in a case of Barrett's Esophagus.
• Barrett's Esophagus is more common in men.
• Long esophageal segment is involved in Barrett's Esophagus.
• Barrett's esophagus does not lead to Odynophagia.
• Methylene Blue dye is used in a patient of Barrett's esophagus undergoing chromoendoscopy for
detection of cancer.
• A screening endoscopy for Barrett's esophagus may be considered in patients with a chronic
history (>10 year) of GERD symptoms.
• Endoscopic biopsy is the gold standard for confirmation of Barrett's esophagus.
• The classification system used for barrett's esophagus is Prague.
• In Barrett's esophagus, esophageal lining is changed to Columnar epithelium.
• Barrett's esophagus is lower oesophagus lined by columnar epithelium.
• Barrett's esophagus can lead to Stricture and Peptic ulcer.
• Barrett's esophagus is more common in males.
• Barrett's esophagus does not responds to conservative management.
• Patient is usually asymptomatic in a case of Barrett's Esophagus.
• Histology of the lesion in a case of Barrett's esophagus shows mucus secreting goblet cells.
• Diagnosis of Barrett's esophagus is made by demonstration of columnar mucosa, which on
histopathology shows Intestinal type of metaplasia.
29. MALLORY-WEISS SYNDROME

• Mallory - Weiss syndrome is seen in alcoholics
• A male executive, 50 year of age is seen in casualty with hematemesis & forceful retching with
history of alcohol intake is diagnosed with Mallory - Weiss syndrome
• Esophagogastroduodenoscopy is the BEST method to diagnose a case of Mallory weiss tear
• Superficial mallory weiss tear heals completely within 48 hours
• 26 year old women in the first trimester of pregnancy with retching and repeated vomiting with
large hematemesis. Her pulse rate is 126/minute and blood pressure is 80 mm Hg systolic. The most
likely diagnosis is Mallory - Weiss syndrome
• Mallory weiss Syndrome is caused due to tear in Gastro esophageal junction.
• Mallory weiss syndrome is partial thickness rupture occurs at Gastric cardia
• Mallory weiss syndrome often occurs in Patient who abuse analgesics & pregnant females
30. Thyroid Carcinoma
• Thyroid carcinoma associated with hypocalcemia is Medullary carcinoma

• FNAC cannot distinguish between a Follicular Adenoma and a Follicular Carcinoma
• In Medullary carcinoma thyroid Patients should be screened for RET point mutation on
chromosome 10
• Medullary carcinoma thyroid Secretes calcitonin
• Medullary carcinoma thyroid Contains amyloid
• Papillary carcinoma of thyroid have Excellent prognosis
• Amyloid deposition is seen in Medullary carcinoma thyroid
• Total thyroidectomy is done in Medullary carcinoma thyroid
• Parafollicular cells involved in Medullary carcinoma thyroid
• Medullary carcinoma thyroid is TSH dependent
• Radionuclide scan is is initial investigation of choice for a patient presenting with solitary nodule of
thyroid
• Percentage of cold thyroid nodules likely to be malignant are 20%
• Psammoma bodies are seen in Seminaoma
• Medullary thyroid carcinoma is associated with MEN II
• Multiple,round figures in histopathological picture of a patient suffering from carcinoma is due to a
mineral deposition can be diagnosed to have Adenocarcinoma of Lung, Meningioma or
papillary thyroid carcinoma.
• Medullary thyroid carcinoma is classically associated with calcitonin induced amyloid deposition
31. CARCINOMA OF THYROID MANAGEMENT
• Ligation of inferior thyroid artery during thyroidectomy is done maximally away from the gland
• Thyroxine can be given in Papillary thyroid carcinoma
• After thyroidectomy for medullary carcinoma of thyroid recurrence of tumour can be determined
by Carcinoembryonic antigen
• Marker for follow-up of patient undergone total thyroidectomy for papillary carcinoma of thyroid
is Thyroglobulin
• In treatment of papillary carcinoma thyroid, radioiodine destroys the neoplastic cells predominantly
by ri rays
• A female presented with severe secretory diarrhea and the thyroid carcinoma can be treated
by Surgery only.
• Complications of total thyroidectomy is Hypercalcaemia
• The drug used in the management of medullary carcinoma thyroid is Cabozantinib
• A 27-year-old female presented with long-standing nodule in right lobe of size 2 cm x 2 cm and
underwent right hemithyroidectomy. Histopathological findings are suggestive of Papillary
carcinoma
32. Varicose Vein
• Direct Pressure and Elevation is the first treatment of choice in a case of rupture of varicose veins
at the ankle
• Varicose veins is associated with migratory thrombophlebitis
• Sclerotherapy for varicose vein is contraindicated in Deep vein Thrombosis
• Pulsatile varicose veins in lower limbs is seen in Klippel trenaunay syndrome
• After the division of testicular vein for treatment of varicose vein, venous drainage of testes is
by Cremasteric veins
• Varicose veins are seen in DVT & AV fistula
• Most commonly varicose veins are seen with Long saphenous vein
• 5% oily phenol is an appropriate sclerosant for venous sclerotherapy.
• Surgery in varicose veins is NOT attempted in presence ofDeep vein thrombosis
• A pt presented with pulsating varicose veins of the lower limb. Most probable diagnosis is Klippel
Trenaunay syndrome
• Injection sclerotherapy for varicose veins is by using phenol
• Commonest complication of varicose vein stripping is Ecchymosis
• Pulsating varicose vein in a young adult is due to Arteriovenous fistula
• An operated case of varicose veins has a recurrence rate of About 10%
• Operations for varicose veins are best accomplished by Stripping
• Gold standard diagnostic test in varicose veins is Duplex imaging
• Trendelenburg's operation is done for Varicose veins
• Investigation of choice for varicose veins Duplex ultrasound imaging
• Arteriovenous fistula, Deep venous thrombosis & Pregnancy may cause varicose veins
• Drug used for sclerotherapy of varicose veins are Polidocanol, Sodium tetradecyl
sulfate, Ethanolamine Oleate,
• Perthe's test, Tourniquet test & Trendelenberg test are done for varicose veins
• Patient presents with varicose vein with sapheno-femoral incompetence and normal perforator can
be managed with Endovascular stripping, Sapheno-femoral flush ligation & Saphenofemoral flush
ligation with striping

33. Intususseption
• Claw Sign" is seen in Intussusception.

• A 10 month old infants present with acute intestinal obstruction. Contrast enema X-ray shows the
intussusceptions. Peyer's Patch Hypertrophy is the most likely cause.
• A 15 year old child presents in the OPD with acute abdominal pain. He also gives history of blood
and mucous in the stool. On P/A examination a mass is palpable. The MOST probable diagnosis in
this patient is Intussusception..
• Recurrent obstruction, mass per abdomen and diarrhoea in a child is suggestive of which
of Intussusception..
• Recurrent intussusception occurs in about: 5-10%.
• Vaccination causing intussusception is Rota Virus.
• Commonest cause of intestinal obstruction in children is Intussusception..
• A 10 month old infants presents with acute intestinal obstruction. Contrast enema X-ray shows the
intussusceptions, likely cause is Peyer's Patch Hypertrophy.
• Meckel's Diverticulum can be a leading point of intussusception.
• Most common type of Intussusception is -Deo Colic.
• Intussuscepiens is the outer layer.
• Features of intussusception are- Target sign.
• A child was operated for intussusceptions. He underwent resection of the affected ileal
segment which revealed a tumor. The most likely tumor would be Villous Adenoma.
• Recurrent pain abdomen with intestinal obstruction and mass passes per rectum goes in favour of
Intussusception.
• Commonest cause of intussusception is Hypertrophy of submucosa peyer's patches.
• A 12 month old male child suddenly draws up his legs and screams with pain. This is repeated
periodically throughout the night interspersed with periods of quiet sleep. When seen after 12
hours the child looks pale, has just vomited andpassed thin blood-stained stool; there is a mass
around umbilicus. Intussusception is the most likely diagnosis.
• Signe-de-Dance is -Empty right iliac fossa in intussusception.
• Coiled spring appearance on barium enema is seen in intussusception.
• A 6 months old child woke up in night, crying with abdominal pain, which got relieved on passing
red stool. Intussusception is the most likely diagnosis.
34. Choledochal Cyst
• Choledochal Cyst is associated with anomalous junction of the pancreatic and biliary duct.
• Surgical removal is the treatment of choice in a case of Choledochal Cyst.
• Choledochal cyst if ruptures ,can cause biliary peritonitis.
• Type I is the most common.
• In case of choledochal cyst, side-to-side choledochoduodenostomy is NOT recommended because
of the risk of recurrent cholangitis.
• Conjugated hyperbilirubinemia in infancy may be seen in Choledochal Cyst.
• Choledochal Cyst presents with Pain, lump and progressive jaundice.
• Saccular diverticulum of extrahepatic bile duct in choledochal cyst is classified as Type-II.
• Choledochal Cyst may predispose to Cholangiocarcinoma.
35. Suture and Suture Materials
• Kelly's suture is done in Stress incontinence.

• If suture marks are to be avoided, sutures of face should be removed by 3-5 days.
• In abdominal surgery Lembert sutures refers to Seromuscular Sutures.
• Surgically used suture material polydioxanone (PDS) undergoes hydrolysis and complete
absorption.
• Vicryl is a delayed absorbable synthetic suture material and is a Co-Polymer of glycolide and lectide.
• Isopropyl Alcohol is used as preservative for packing catgut suture.
• Best suture for common bile duct is non synthetic absorbable.
• Absorbable sutures are:Plain and Chromic Catgut,Polyglactin,Polyglyconate,Polyglycolic
Acid,Polydiaxone,Polyglycaprone.
• Non-absorbable sutures are:Silk,Linen,Surgical Steel,Linen,Polyester,Polybutester,Polypropylene.
36. Laproscopy
• Best gas used for creating pneumoperitonium at laparoscopy is CO2.

• Laparoscopy is best avoided in patients with COPD.
• Best tubal function test is Laproscopy.
• The intra - abdominal pressure laparoscopy should be set between 10-15 mm of Hg.
• A female presents with primary amenorrhea and absent vagina, the next investigation to be done
is Laproscopy.
• Salpingitis / Endosalpingitis is best confirmed by Hysteroscopy with Laproscopy.
• During laparoscopy the preferred site for obtaining cultures in a patient with acute pelvic
inflammatory disease is cul-de-sac or fallopian tube.
• Gold standard for diagnosis for PID is diagnostic Laproscopy.
• Shoulder pain post laparoscopy is due to CO2 retention.
• Best investigation to diagnose ectopic pregnancy is Laproscopy.
• A lady presented in the emergency department with a stab injury to the left side of the abdomen.
She was hemodynamically stable and a contrast enhanced CT scan revealed a laceration in spleen.
Laparoscopy was planned however the patient's p02 suddenly dropped as soon as the
pneumoperitoneum was created. Gaseous Embolism through Splenic Vessels is the most likely
cause.
• A 45 year old female presents with symptoms of acute Cholecystitis. On USG there is a solitary
gallstone of size 1.5cm. Symptoms are controlled with medical management. Immediate
Laproscopic Cholcystectomy is the next most appropriate step in the management of this patient.
• Laparoscopic and dye test are done doing secretory phase of the cycle for finding out the tubal
factors of infertility.
• Laparoscopy is the primary method used for diagnosing endometriosis..
• Advantage of carbon dioxide in laproscopy are : Non-irritant , Non-inflammable , No tissue reaction
37. Achalasia Cardia
• Mode of treatment for achalasia is associated with high rate of recurrence : Botulinum toxin.
• Progressive Dysphagia,Regurgitant vomitting is a presenting problem.
• Dilated and Tortuous Esophagus is seen in Achalasia Cardia.
• The cause is degeneration of ganglion cells of auerbach's myenteric plexus.
• Treatment includes heller’s cardiomyotomy, forceful dilation by pneumatic balloon, repeated
injection botulinum toxins and drugs improving motility of esophagus.
• Esophagectomy is not a treatment modality for achalasia cardia.
• Barium swallow shows a dilated esophagus with tapering narrowing in the terminal end of
esophagus, described as ‘BIRD BEAK’ appearance.
• Fluoroscopy shows loss of normal peristalsis in the lower third of the esophagus..
• Dysphagia equal for both solid and liquid from the very onset suggests motor disorder i.e achalasia
and diffuse esophageal spasm.
• The characteristic esophageal manometry finding in achalasia cardia is Impaired lower esophageal
sphincter relaxation and absent peristalsis.
• It is believed that cause of ganglion cell degeneration in achalasia is an autoimmune process
attributable to a latent infection with human herpes simplex virus 1 combined with genetic
susceptibility.
• The malignancy which is a close mimicker of achalasia is Carcinoma of gastric fundus.
• The most sensitive diagnostic evaluation for achalasia cardia is Esophageal Manometry.
• The pharmacologic agents used in Achalasia are:
1. Nitrates
2. Calcium channel blockers
3. Botulinum toxin
4. Sildenafil- phosphodiesterase inhibitors, effectively decrease LES pressure.
• In pneumatic dilatation for the treatment of achalasia, the cylindrical balloon dilator is dilated upto
3-4 cm.
• Achalasia is associated with increased risk of Squamous Cell carcinoma of Esophagus.
• Uniform dilation of esophagus is seen in Achalasia Cardia.
• Elevated resting LES tone is seen in Achalasia.
• A 40-year-old female patient presented with dysphagia to both liquids and solids and regurgitation
for 3 months. The dysphagia was non-progressive.Achalasia cardia is the most likely diagnosis.
• 'Pencil tip' deformity is seen in Achalasia Cardia.
• Heller's operation treatment of choice in Achalasia Cardia.
• Radiologic feature suggestive of Achalasia cardia is? Absence of gastric air bubble , Air fluid level
in mediastinum ,Sigmoid esophagus.
• Maximum dilatation of esophagus occurs in Achalasia Cardia.
• Amyl nitrite inhalation is used to distinguish patients of achalasia from those with pseudoachalasia.

• Non visualization of gastric fundic bubble with air-fluid level in retrocardiac region suggests
Achalasia Cardia.
38. Gastritis
• Increased production of macrocytic red blood cells would mostly likely be associated with chronic
gastritis (Type A) resulting from autoimmune destruction of parietal cells.
• A patient of peptic ulcer disease, when investigated endoscopically showed chronic antral gastritis.
Warthin Starry Stain will be able to stain the specimen.
• Type B gastritis:It is called as antral predominant gastritis as antrum is involved predominantly.
However, it is misnomer as the inflammatory process may progress to body and fundus and causing
pangastritis.
• Autoimmune gastritis is less common of the two forms and is characterized by :- Presence of
antibodies against parietal cells and intrinsic factor and Involvement of body and fundus with
sparing of antrum.
• Endoscopic biopsy from a case of H.pylori related duodenal ulcer is most likely to reveal Antral
predominant Gastritis.
• Atrophic Gastritis is a predisposing factors for gastric carcinoma.
• Erosive gastritis commonly occurs at Body and Fundus.
• H. pylori causes Type B gastritis.
• Most important side effect of aspirin is Gastritis.
39. Pyloric Stenosis
• Regarding congenital hypertrophic pyloric stenosis of infancy : It most commonly occurs in first
born male child,It usually presents at 2 to 4 weeks of life,Baby is hungry soon after vomiting,Non
bilious Vomitting.
• The classical electrolyte abnormality associated withpyloric stenosis is hypokalemic, hypochloremic
metabolic alkalosis, presumably due to ongoing gastric acid loss from vomiting. Paradoxical
acidurea is sometimes noted (with progressive Hypokalemia and hypovolemia) because the kidney
excretes protons in exchange of sodium in an attempt to conserve fluid".
• A 3 week old patient presenting with vomiting and failure to thrive is found to have pyloric
stenosis. Correction of electrolyte disturbances should be the next step of management.
• Drug which can cause Hypertrophic Pyloric stenosis is Erythromycin.
• Most characteristic feature of congenital hypertrophic pyloric stenosis:The pyloric tumour is best
felt during feeding.
• Treatment of choice is Finney’s pyloroplasty in Hypertrophic Pyloric Stenosis.
• Clinical features of pyloric stenosis in infants are Abdominal lump , Constipation , Weight Loss.
• The vomiting in pyloric stenosis may or may not be projectile, however non bilious vomiting after
feed is the characteristic feature.
• Peristalsis is seen from left to right across the upper abdomen in Hypertrophic Pyloric Stenosis.
• A 6 year old boy presenting with palpable abdominal mass in the epigastrium. (There is no bile in
vomitus).The clinical diagnosis is Pyloric Stenosis.
• The traditional Ramstedt procedure is performed through a short transverse skin incision in a case
of Hypertrophic Pyloric Stenosis.
• A 10 days old neonate is posted for pyloric stenosis in surgery. The investigation report shows a
serum calcium level of 6 mg/dL. The information which you would like to know before you
supplement calcium to this neonate is Serum Protein.
• Ultrasonography is the investigation of choice to confirm diagnose of hypertrophic pyloric stenosis
with accuracy > 95% (approching almost 100%). USG visualizes thickened and elongated pyloric
canal. USG criteria for diagnosis include >16 mm pyloric length and >4mm pyloric muscle wall
thickness. Gastric residues are low b/o recurrent emesis.
• Xray feature of Pyloric Stenosis is Single bubble appearance.
• A robust male baby with vigorous feeding and immediate vomiting at 2 months of age. Most
probable diagnosis is Congenital Hypertrophic Pyloric Stenosis.
• Dilated Stomach with minimal gas is seen in Pyloric Stenosis.
• In congenital pyloric stenosis the defect usually lies in -Circular muscle fibres in antrum.
• String sign is seen in: Crohn's disease ,TB of the ileocaecal region , Idiopathic hypertrophic pyloric
stenosis.
40. Hemorrhoid
• Pain of External hemorrhoids is carried by Pudendal Nerve.

• Internal Hemorrhoids is ideal for the treatment with injection of sclerosing agents.
• Hemorrhoids is the most common cause of fresh lower gastointestinal bleed in India.
• A jaundiced, 43 year old alcoholic male presents to the emergency room complaining of bright red
blood in his last two stools. He denies pain on defecation or changes in his bowel habits.
Hemorrhoids would be the most likely finding on sigmoidoscopic examination.
• External hemorrhoids below the dentate line are painful.
• Five-day self subsiding pain is diagnostic of thrombosed external hemorrhoids.
• Hemorrhoids are probably the most common cause of Lower GI Bleed .
• MC complication following hemorrhoidectomy is Urinary retention.
• Treatment of choice for 3rd degree hemorrhoids is Hemorrhoidectomy.
41. Anal Fissure and Fistula
• Intersphincteric fistula is the most common type of ‘fistula in ano’.

• Anal fissure is best diagnosed by characteristic history of bleeding PR and pain during defecation
and clinical examination.
• Treatment of acute fissure in ano : Conservative , Dilatation under GA , Lateral sphincterotomy.
• Fistula in ano is not a cause of acute anal pain.
• Sentinel pile indicates Anal Fissure.
• Rectal examination should not be done in Anal Fissure.
• The treatment of choice in fistula in ano is Fistulotomy.
• Internal sphincterotomy is the treatment of choice for Fissure in Ano.
• High or low fistula in ano is termed according to its internal opening present with reference to
Anorectal ring.
• Multiple fistula in ano commonly occurs in Tuberculosis and LGV.
• Lateral internal sphincterotomy is useful for Anal Fissure.
42. Ulcerative Colitis
• The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of
crypts (cryptitis), frank crypt abscess, and hemorrhage or inflammatory cells in the lamina propria.
• Crohn's disease is frequently associated with "skip lesions," discontinuous areas of active disease in
the colon and small intestine with intervening segments that appear normal.
• Pseudopolyps are more commonly found in ulcerative colitis than Crohn's disease.
• For patients of ulcerative colitis associated with primary sclerosing cholangitis :They may develop
biliary cirrhosis , may have raised alkaline phosphatase ,increased risk of hilar Cholangiocarcinoma.
• Ulcerative Colitis is associated with:
• Dermatologic: Erythema nodosum ,Pyoderma gangrenosum
• Rheumatologic: Peripheral arthritis, Ankylosing spondylitis, Sacroiliitis
• Ocular:Conjunctivitis ,Anterior uveitis/iritis ,Episcleritis
• Hepatobiliary: Hepatic steatosis ,Fatty liver ,Cholelithiasi ,Primary sclerosing cholangitis
• Urologic: Calculi ,Ileal bladder fistulas
• Metabolic bone disorders
Thromboembolic disorders.
• Ulcerative colitis (UC) is a chronic inflammatory condition causing continuous mucosal
inflammation of the colon without granulomas on biopsy, affecting the rectum and a variable
extent of the colon in continuity, characterised by relapsing and remitting course.
• Distal colitis with respect to ulcerative colitis refers to Left sided colon distal to splenic flexure is
only involved.
• Parameters of truelove witts criteria : Bloody stools/day ,Pulse, Temperature, Haemoglobin, ESR,
CRP.
• In clinical practice, ‘remission’ mean a stool frequency ≤3/day with no bleeding and no urgency.
Sigmoidoscopy to confirm mucosal healing is generally unnecessary.
• Steroid refractory ulcerative colitis is said to be present in a patients who have active disease
despite Prednisolone up to 0.75 mg/kg/day over a period of 4 weeks.
• Baron Endoscopic scores for ulcerative colitis
• Score 0: Normal: matt mucosa, ramifying vascular pattern clearly visible, no spontaneous bleeding,
no bleeding to light touch
• Score 1: Abnormal, but non-haemorrhagic: appearances between 0 and 2
• Score 2: Moderately hemorrhagic: bleeding to light touch, but no spontaneous bleeding seen ahead
of the instrument on initial inspection
• Score 3: Severely haemorrhagic: spontaneous bleeding seen ahead of instrument at initial
inspection and bleeds to light touch.
• Occasional severe constipation is seen in ulcerative colitis patients with Proctitis.
• Pancolitis and Pseudopolyps may be seen in Ulcerative Colitis.
• Ulcerative colitis involves the rectum and extends proximally in a retrograde fashion to involve the
entire colon (pancolitis) in more severe cases.
• Malabsorption may be seen in ulcerative colitis.
• Sulfasalazine is used in ulcerative colitis.
• Pyoderma gangrenosum is seen in Ulcerative Colitis.
• Rx of choice in case of chronic ulcerative colitis is Proctocolectomy with Ileo-Anal Anastomosis.
• Surgical treatment of Ulcerative Colitis :Done in cases where medical treatment fails & Pouch
surgery done.
• Complications of ulcerative colitis : Perforation ,Toxic megacolon, Carcinoma.
• As the inflammation is purely mucosal in ulcerative colitis, strictures are highly uncommon. Any
stricture diagnosed in a patient with ulcerative colitis is presumed to be malignant until proven
otherwise.
• Ulcerative colitis involves mucosa and superficial submucosa with deeper layers unaffected except
in fulminant disease.
• Pt with recurrent diarrhoea, pseudopolyp, lead pipe appearance on Ba enema has Ulcerative Colitis.
• Risk of Malignancy in Ulcerative Colitis is more in :Onset in childhood ; Extensive involvement of
colon,Takes atleast 10 years to develop,Associated with dysplasia of the rest of the colon.
• Primary sclerosing cholangitis is the most serious extraintestinal manifestation of ulcerative colitis
and it does not resolve with colectomy.
• Most common post operative complication of ileo anal pouch anastomosis in ulcerative colitis is
Pouchitis.
• Sulphonamide is used for the treatment of ulcerative colitis is Salazopyrin,Sulfasalazine.
• Procedure of choice in ulcerative colitis with acute perforation is Total Colectomy with Ileostomy.
• Best treatment for Remission of Acute ulcerative colitis is Prednisolone.
• A 20 year old male presents with mucus and repeated gastrointestinal bleeding. Patient is positive
for ANCA. The most likely diagnosis is Ulcerative Colitis.
• A 25 year old male presents with a history of chronic diarrhea. Pathological examination
reveals cryp. titis and crypt abscesses. The likely diagnosis is Ulcerative Colitis.
• 5-amino salicylic acid is drug of choice for ulcerative colitis.
• Methotrexate has not been shown to be effective for treating active ulcerative colitis or for
maintaining remission.
• Malignant potential is seen in both ulcerative colitis and Crohn's disease, but ulcerative colitis is a
more important risk factor than Crohn's.
• First radiological sign of ulcerative colitis is loss of Haustrations.
• Pipe stem colon is seen in Ulcerative Colitis.
• Agents that may be used for treatment of ulcerative colitis
• 5-ASA
• Glucocorticoids
• Azathioprine and 6 mercaptopurine
• Cyclosporine or TNF alpha therapy (Infliximab).
• Tacrolimus

43. Crohn's Disease
• Most common cause of death in Crohn's disease is due to Malignancy.

• A 26 year old man has had Crohn’s disease of the ileum for 10 months and has been treated with
several drugs. He now suffers from muscle weakness, centripetal obesity, and a round, plethoric
face. These side effects are most likely associated with the long-term use of Prednisone.
• Crohn's disease is frequently associated with "skip lesions," discontinuous areas of active disease in
the colon and small intestine with intervening segments that appear normal..
• Pseudopolyps are more commonly found in ulcerative colitis than Crohn's disease..
• Crohn's disease may be caused by Clostridium Difficile.
• String sign of Kantor is seen in Crohn's Disease.
• The endoscopic finding which suggests crohns in a patient with chronic diarrhea among the
following is Anorectal lesions.
• Comb sign in CT abdomen is seen in Crohn's Disease.
• Creeping fat is a feature of Crohn's Disease.
• Skip granulomatous lesions ,Transmural involvement,Cobblestone appearance,Crypt Abscess
,Fissuring ulcer ,hrough and through involvement of thickness of bowel wall are seen in Crohn's
Disease.
• Extra intestinal manifestations of Crohn's disease: Migratory polyarthritis,Sacroiliaitis , Hepatic
pericholangitis , Clubbing , Ankylosing spondylitis,Erythema Nodosum,Uveitis ,Primary sclerosing
cholangitis.
• Anti-Saccharomyces cerevisiae antibodies are seen in Crohn's Disease.
• Skip lesions of colon with epitheloid granuloma are usually seen with Crohn's Disease.
• Fistula is most common in - Crohn's Disease.
• Yellowish exudates at multiple sites seen in colonoscopy indicates Crohn's Disease.
• Megaloblastic anemia is seen in Crohn's Disease.
• The established biological therapy for Crohn's disease is Anti TNF alpha-antibody.
• Immumodulators used in Crohn's disease :-i) Anti-TIVF-a : Infliximab, adalimumab,
certolizumbab ii)Anti-Integrin therapy : Natalizumab.
• An eight year old boy had abdominal pain, fever with bloody diarrhea for 18 months. His height is
100 ems and weight is 14.5kg. Stool culture was negative for known enteropathogens. The
sigmoidoscopy was normal. During the same period, child had an episode of renal colic and passed
urinary gravel. The mantoux test was 5 x 5 mm. The most probable diagnosis is Crohn's Disease.
• 14 year old girl with history of abdominal pain (periumbilical), postprandial, passing blood in stools,
fever, weight loss since ten months. She also has episodes of passing blood in stools. Crohn's
Disease may be the likely diagnosis.
• A patient gives chronic history of diarrhoea and blood in stool presents with multiple fistulae in the
perineum and multiple stricture in small intestine. The diagnosis is Crohn's Disease.
• Inflammatory bowel disease found in children is Ulcerative Colitis and Crohn' Disease.
• In a 27 yr old male most common cause of a colovesical fistula would be Crohn' Disease.
• A patient of Crohn's Disease, underwent resection anastomosis. Now presents on 7th post-op day
with anastomotic site leak from a fistula. Everyday leakage volume adds up to 150-200m1. There is
no intraabdominal collection and the patient is stable without any complaints. The next line of
management would be:Do conservative treatment and leave him and hope for the spontaneous
resolution.
• Crohn's disease can be seen in Mouth to anus.
• A patient with Crohn's disease was opened for and an inflammed appendix found. The treatment of
choice is Appendicectomy.
• Reccurence is common after surgery in Crohn's Disease.
• Transmural inflammation is seen in Crohn's Disease.
• Crohn's Disease is not a commoner cause of intestinal perforation.
• Enteo-enteric fistula is seen in Crohn's Disease.
• First radiological sign of Crohn's disease in terminal ileum is Aphthoid Ulceration.
• Terminal ileum is MOST commonly affected by Crohn's Disease.
44. Hirschsprung disease
• Gold standard: full thickness rectal biopsy (absence of ganglion cells)

• In the newborn period, this is performed at the bedside using a special suction rectal
biopsy instrument
• Barium enema – abnormal segment is contracted, normal segment is dilated
• Anorectal manometry – absence of anorectal reflex which is diagnostic
45. Diverticulosis
• Colonic diverticulosis is best diagnosed by Barium enema.

• The commonest site of diverticulosis is Sigmoid Colon.
• A patient complains to his physician of chronic constipation. On the instruction of his physician, the
patient increases his dietary fiber, but his constipation persists. The physician refers the patient to a
gastroenterologist. Colonoscopy reveals over fifty 2-3 mm openings into the bowel mucosa. No
bleeding is seen, and the intervening mucosa appears normal. Diverticulosis is the most likely
diagnosis.
• Protrusion of mucosa through muscular layers at point of blood vessel is seen in Diverticulosis..
• Massive bleeding per rectum in a 70 yr old patient is due to Diverticulosis.
46. Appendicitis
• During an operation for presumed appendicitis, the patient appendix is found to be markedly
thickened and feels rubbery to firm. The serosa is edematous and inflamed and the mesentery is
thickened with fat growing about the bowel circumference. Most likely diagnosis is Ileal Crohn’s
disesase.
• In a case of retrocecal appendicitis ,extension movement aggravates pain.
• A female who underwent laproscopic appendicectomy for acute appendicitis, on post op. day 2
bumped her nose on to a table. She developed difficulty in breathing and examination showed a
swelling in the anterior part of the nasal septum. Next line of management is Incision and Drainage.

• Three hours after an uneventful appendectomy, a previously healthy (except for appendicitis) 78
year old man becomes disoriented and confused. He repeatedly asks the nurses where he is, and
his speech pattern is disorganized and rambling. His temperature is 37 C (98.6 F), blood pressure is
120/80 mm Hg, pulse is 70/min, and respirations are 18/min. The patient is uncooperative, but
shows no physical abnormalities. Mental status examination is not possible because of an altered
level of consciousness. Laboratory studies show no abnormalities.Delirium is the most likely
diagnosis.
• A 23-year-old man is admitted to the hospital through the emergency department with probable
appendicitis. He has been having right lower quadrant abdominal pain for several days, which has
been becoming increasingly worse. His temperature 39.2 C (102.6 F), blood pressure is 80/40 mm
Hg, Pulse is 120/min, and Respiratory rate is 35/min. The abdomen is rigid with guarding. Multiple
petechiae and purpura are present, and the patient is oozing blood from his oral mucosa. According
to the patient's wife, he has not had bleeding problems in the past. The fact the abdomen is rigid
with guarding suggests Peritonitis.
• ALVARADO SCORE in Appendicitis:
Migratory right iliac fossa pain 1

Anorexia 1
Nausea/ vomiting 1
RLQ tenderness 2
Rebound tenderness 1
Elevated temperature 1
Leukocytosis 2
Left shift 1
Total 10
• Ochsner-Sherren regimen is used in the management of Appendicular mass.

• Rovsing’s sign, Obturator sign and Psoas sign are seen in appendicitis..
• Appendicitis like syndrome is caused by : Yersinia enterocolitica ,Yersinia pseudotuberculosis ,
Pasteurella septica.
• Appendicitis is diagnosed by TLC & DLC and USG.
• When acute appendicitis is suspected, it can be confirmed by Clinical examination,USG and CT scan.
• Diffuse peritonitis in acute appendicitis is caused due to early rupture of Appendix.
• Earliest symptoms in acute appendicitis is pain.
• Acute Appendicitis is due to Faecoliths & Worms of ileo-caecal region.
• Early complications arising after appendicectomy for acute appendicitis are Ileus , Intestinal
obstruction, Pulmonary complications.
• All are useful in acute appendicitis : Antibiotics ,Analgesics , IV Fluids.
• About McBurney's incsion:Most suitable if the diagnosis of appendicitis is definite,If it is converted
into a muscle cutting incision it is called Rutherford Morison's incision,Inguinal hernia is a sequlae of
the incision.
• Diffuse peritonitis following appendicitis is usually seen -when appendicular perforation occurs
early (within 24 hours).
• Aaron's Sign is seen in Acute Appendicitis.
• The term "Left sided appendicitis" as popularly called is nothing but Diverticulitis.
• Clinical features of appendicitis:
• Central abdominal pain moving to right iliac fossa
• Nausea, vomiting, anorexia
• Low-grade pyrexia (37.2-37.7 degree celsius)
• Localised tenderness in right iliac fossa
• Right iliac fossa peritonism
• Percussion tenderness is a kinder sign of peritonism than rebound.
• Investigation of choice for acute appendicitis in children is USG.
47. BUDD-CHIARI SYNDROME
• Diagnosis suspected when CT shows a large congested liver

• Hepatic venography via transjugular approach confirms the diagnosis
• Patients presenting with acute fulminant liver failure, established cirrhosis, complications of portal
hypertension: liver transplantation is the treatment
• If cirrhosis is not established: TIPSS, portocaval shunt or mesoatrial shunt
• Patients usually need lifelong warfarin therapy
48. Meckel's Diverticulum
• Meckel's diverticulum is best diagnosed by Tc99 pertechnetium scan.

• Meckel's diverticulum arises from Ileum.
• Meckel Diverticulum is a failure of the intraabdominal portion of the umbilical vesicle to atrophy.
• Meckel's Diverticulum:It occurs in 2% population ,It is a is a 'true' diverticulum and consists of all
the 3 layers of the gut - the mucosa, the muscularis & outer scrosa. It arises from antimesenteric
border,Located 60 cm from the cecal valve,
• The most common location for a Meckel's diverticulum is the Terminal Ileum.
• Vitellointestinal Duct represents the embryological origin of Meckel’s diverticulum.
• Meckel's Diverticulum may present with bleeding per rectum and Intussusception.
• Peroforation may occur in Meckel's Diverticuum.
• Heterotopic gastric muscosa can ulcerate and cause a brisk gastrointestinal bleed.
• A fibrous band between the apex and umbilicus can cause intestinal obstruction.
• Best Diagnosis for Ectopic gastric mucosa of meckels diverticulum is Radionuclide Scan.
• A wide mouth meckels diverticulum is found. accidently on laparotomy. The treatment of choice
would be to leave as such.
• Heterotopic epithelium is present in 50-60% cases.
• Has three layers with artery.
• Complications of Meckel's Diverticulum:Hemorrhage,Intussception and Strangulation.
• Uncommon complication of meckels diverticulum is Malignancy.
• Meckels diverticulum is located at 2 feet proximal to ileococcal valve on antimesentric border.
• The commonest presentation of meckel's diverticulum is Lower GI Bleeding.
• Lined by heterotopic epithelium.
• 3-5 % of Population,
• More common in females.
49. Peritonitis
• Primary peritonitis is more common in females because ostia of Fallopian tubes communicate with
abdominal cavity.
• A posteriorly perforating ulcer in the pyloric antrum of stomach is most likely to produce initial
localized peritonitis or abscess formation in Omental Bursa(lesser sac).
• A patient with abdominal injury presents to the emergency department with signs of peritonitis and
shock. His airway and breathing were secured and IV fluids were started with 2 large bore cannulas.
The next line of management should be Exploratory Laparotomy under general Anesthesia.
• Apart from Escherichia coli,Bacteroides is the other most common organism implicated in acute
suppurative bacterial peritonitis.
• A 23-year-old man is admitted to the hospital through the emergency department with probable
appendicitis. He has been having right lower quadrant abdominal pain for several days, which has
been becoming increasingly worse. His temperature 39.2 C (102.6 F), blood pressure is 80/40 mm
Hg, Pulse is 120/min, and Respiratory rate is 35/min. The abdomen is rigid with guarding. Multiple
petechiae and purpura are present, and the patient is oozing blood from his oral mucosa. According
to the patient's wife, he has not had bleeding problems in the past. The fact the abdomen is rigid
with guarding suggests Peritonitis.
• Meconium peritonitis is an aseptic peritonitis which can occur in late intrauterine life, during birth
or just after delivery.It occurs due to intestinal perforation usually as a result of some form of
neonatal intestinal obstruction.
• Total parenteral nutrition is the management of choice in a patient presenting with peritonitis and
massive contamination because of duodenal leak.
• Prophylaxis against spontaneous bacterial peritonitis ( SBP) in case of cirrhosis with ascites is
indicated in prior history of SBP.
• The characteristic ascitic fluid findings in the setting of secondary bacterial peritonitis are Ascitic
fluid PMN > 250 cells/mm 3 with at least two of the following criteria
1. Ascitic fluid total protein > 1 g/dl
2. LDH greater than the upper limit of the normal of the serum
3. Glucose < 50 mg/dl
• In patients with SBP, along with cefotaxime albumin infusion is indicated in the setting , when
1.Serum creatine is > 1 mg/dl

2. BUN > 30 mg/dl
3. Total bilirubin is > 4 mg/dl
• Primary bacterial peritonitis (PBP) occurs most commonly in conjunction with cirrhosis . Other
conditions which may cause PBP are Metastatic malignant disease, Postnecrotic cirrhosis, Chronic
active hepatitis, Acute viral hepatitis, Congestive heart failure, Systemic lupus erythematosus
Lymphedema.
• PBP is commonly present with fever, but it can present without any symptoms too.
• Most common infection in a child nephrotic syndrome is spontaneous bacterial peritonitis.
• Most common cause of peritonitis in adult male is perforated Appendix.
• Primary peritonitis with pneumococcus is associated with Nephrotic Syndrome.
• Early surgery is indicated in Biliary and Typhoid Peritonitis.
• Most common cause of generalised peritonitis in a 40 year old adult male is Duodenal ulcer
perforation.
• Intra-abdominal calcificaition in a plane X-ray abdomen is most often seen in Meconium
Peritonitis.Plain X-ray abdomen of this condition reveals calcification on liver and spleen.
• Meconium peritonitis should always be considered when a baby is born with tense abdomen.
• Systemic complications of peritonitis Bacteraemic/endotoxic shock Bronchopneumonia/respiratory
failure,Renal failure,Bone marrow suppression ,Multisystem failure.
• A 25 years old female presents with pyrexia for ten days, develops acute pain in periumblical region
spreading all over the abdomen. Typhoid enteric perforation and peritonitis would be the most
likely cause.
• Spontaneous peritonitis in cirrhosis patients; the polymorphonuclear cells are more than 200
cells/cumm.
• About preoperative optimization for perforation peritonitis:Patients may require large volume of
crystalloid infusion,Hypovolemia and sepsis contribute to tissue underperfusion,Base deficit >6 is
marker of significant metabolic acidosis.
• The most common intraperitoneal abscess following peritonitis is Pelvic.
• Paralytic ileus is caused by Peritonitis.
• Diffuse peritonitis in acute appendicitis is caused due t early rupture of Appendix.(within 24 hours).
• A patient was on long term antibiotic therapy for peritonitis. During the course of treatment, he
develops mucus diarrhea. Most likely cause of diarrhea is antibiotic associated diarrhea.
• In a case of Acute peritonitis,CT scan may aid in the diagnosis and Upright films shows free air
under the diaphragm.
50. LUNG SEQUESTRATION
• Sequestration of lung is seen in Posterior part of left lung

• Abdominal aorta supply to the segment involved in intralobar sequestration of the lung
• Bronchogenic sequestration is seen in Left lower lobe

• Chronic left lower lobe pneumonitis On contrast bronchography, the area involved with the
pneumonitis does not fill whereas the area around it does fill. The most likely diagnosis Pulmonary
sequestration
• Intralobar sequestration of lung takes its blood supply from Descending abdominal aorta
• Diagnosis of lung sequestration by CT scan
• Investigation of choice for diagnosing lung sequestration is Angiography
51. AMPUTATION
• Myodesis is employed in amputations is indicated for Tumor, Ischemia & children

• Myodesis is contraindicated in cases of severe dysvascularity in which blood supply to the muscle
appears compromised.
• Tarso Metatarsal amputation is also known as Lisfranc amputation
• Amputation is required in Gas gangrene, Buerger's disease & Diabetic gangrene
• In flap method of amputation, bone is kept shorter than the level of amputation
• Ring sequestrum is seen in Amputation stump
• MES score evaluates chances of amputation in a traumatized limb
• Age, B.P & Velocity of trauma evaluate the chances of amputation in a limb
• In below elbow amputation the length of stump should be 15-20 cm
• Distance from Olecranon in amputation should be 15-20 cm
• Phantom limb Follows amputation
• Pain due to post-amputation neuroma is best treated by Surgical Excision
• Most Imp. technical consideration at the time of doing below knee amputation is Post. flap should
be longer than the anterior flap
• Extensive surgical debridement, decompression or amputation may be indicated in Progressive
synergistic gangrene, Acute haemolytic streptococcal cellulitis & Acute rhabdomyolysis
• Liability for wrong limb amputation can be considered under Both civil and criminal
• Most common cause of amputation in India is RTA
52. AMELOBLASTOMA
• Ameloblastoma is the Most common odontogenic tumour

• Ameloblastoma is Generally benign
• Ameloblastoma is Common in 3rd to 5th decade
• Most common jaw tumor is Ameloblastoma
53. RANULA
• Structure damaged most commonly during Surgery on Ranula is Submandibular duct

• Ranula is Translucent, Retention cyst of minor salivary gland
• Ranula is cystic swelling in the floor of mouth
• Ranula is Retention cyst of sublingual gland
• Plunging may be a feature in ranula
54. HYDRONEPHROSIS
• Presence of hydronephrosis in staging of carcinoma cervix denotes FIGO disease Stage III-B
• In follow up of BPH, most important indication of surgery is Bilateral hydronephrosis
• Whitaker test is done for diagnosing hydronephrosis
• IOC in Posterior urethral valves of newborn with hydronephrosis is Micturating Cystourethrogram
• Hydronephrosis with dilated renal pelvis and cortical thinning with a normal ureter treated
with Pyeloplasty
• Micturating cysto urethrogram shows bilateral Grade IV vesicoureteral reflux with Ultrasound
abdomen showing bilateral hydronephrosis is suggested for Ureteric re-implantation
• Recurrent E.coli infection with Hydroureter and Hydronephrosis as U/S finding & Micturating cysto
- urethrogam shows filling defect in urinary bladder are suggestive of Ureterocele
• Rim sign in IVP is seen in Hydronephrosis
• Bilateral impacted ureteric stones with hydronephrosis & RBCs with pus cells in urine should be
imediately treated with stent drainage
• Inadvertent surgical occlusion of the ureter leads to Complete renal atrophy & Hydronephrosis
• Unilateral hydronephrosis is due to Carcinoma of prostate
• During investigation of hydronephrosis, isotope renogram is useful mainly in Distinguishing
between non-obstructed system
• In follow up of BPH, most important indication of surgery is Bilateral hydronephrosis
• Catheterization with Foley catheter is mandatory for acute urinary retention with bilateral
hydronephrosis .Spontaneous voiding may return, but a catheter should be left indwelling for 3
days while detruson tone returns
• History of recurrent ureteric calculi presented with fever treated with Right-sided nephrectomy
suggest diagnosis of Chronic pyelonephritis with hydronephrosis
• Intra uterine hydronephrosis of 32-34 weeks-management Require serial USG and other associated
anomalies
55. sebaceous cyst
• Usually sebecous cyts are found in the soul.
56. hypertrophic scar and keloid

• Local recurrence is common after excision
• It appears a few days after surgery
• Made up of Dense collagen
• riamcinolone acetonide is the drug used for intralesional injection of steroid.
• Intralesional injection of steroid (Triamcinolone acetate) is now recommended as the first line of t/t
for keloids [Ref Schwartz 9/e p226 (8/e p241)]
• Intralesional injection of Triamcinolone is also the t/t of choice for intractable hypertrophic scars.
Success is enhanced when it is combined with surgical excision [Ref CSDTI 3/e p1105 (11/e, p1243)]
• Other modalities of tit used for keloids are:
Surgery
• surgical excision alone leads to a high recurrance rate.

• there are fewer recurrances when surgical excision is combined with other modalities such as
intralesional corticosteroid injection, topical application of silicone sheets or the use of radiation or
pressure.
• surgery is recommended for debulking large lesions.
Radiation therapy
• it may produce unpredictable results and has obvious potential side effects including neoplastic
degeneration; and has high recurrance rate when used alone.
Silicone sheet application
Pressure application
Topical retinoids
• Precancerous leading to cancer

• There is no evidence of malignancy in keloids.
• Keloids have equal incidence in both males & females
Keloids It is a scar which shows extreme overgrowth so that scar tissues grows beyond
the limits of original wounds and shows no tendency to resolve.
Keloids grow on particular sites, these are ?
a) Central chests (probably most common, not sure)
b) Back
c) Shoulder
d) Earlobes
• Other points about Keloids & hvpertrophic scars

Hypertrophic scars (FITS) and keloids represent an overabundance of fibroplasia in the
dermal healing process. They are both characterized by excessive collagen deposition versus
collagen degradation.
HTS rise above the skin level but stay within the confines of the original wound and often
regress over time.
Keloids are defined as scars that grow beyond the border of the original wound and rarely
regress spontaneously.
Both HTS and keloids occur after trauma to the skin, and may be tender, pruritic, and cause
a burning sensation.
Keloids are more prevalent among dark pigmented ethnicitics (i.e. Africans, Asians &
Hispanics)
HTS usually develop within 4 weeks after trauma Keloids tend to occur 3 months to years
after the trauma.
The long acting steroid Triamcinalone is used for treating keloid.
• Other treatment modalities include laser, silicone sheets, cryotherapy, interferon, fluorouracil,
radiation.
Keloids can result from surgery, burns, skin inflammation, acne, chickenpox, zoster,
folliculitis, lacerations, abrasions, tattoos, vaccinations, injections, insect bites, ear piercing,
or may arise spontaneously.
• Keloids tend to occur 3 months to years after the initial insult, and even minor injuries can result in
large lesions.
• They vary in size from a few millimeters to large, pedunculated lesions with a soft to rubbery or
hard consistency.
• Although they project above surrounding skin, they rarely extend into underlying subcutaneous
tissues.
• Certain body sites have a higher incidence of keloid formation, including the skin of the earlobe as
well as the deltoid, presternal, and upper back regions.
• They rarely occur on eyelids, genitalia, palms, soles, or across joints.
• Keloids rarely involute spontaneously, whereas surgical intervention can lead to recurrence, often
with a worse result.
Also know
• Treatment of hypertropic scars/Ref: CSDT13/e pI105 (11/e p1243)]

• Since nearly all hypertrophic scars undergo some degree of spontaneous regression, they are not
t/t in early phases. If the scar is still hypertrophic after 6 months surgical excision and primary
closure of the wound is indicated.
Other modalities used for t/t of HTS.
• Pressure application - particularly useful for burn scars.

• Silicone sheet application
• Intralesional injection of triamcinolone is the t/t of choice for intractable HTS riamcinolone
acetonide is the drug used for intralesional injection of steroid.

57. Paronychia
• It is a fungal infection.
58. FELON
• Terminal pulp space infection

• A felon is a closed-space, purulent infection of the fingertip pulp.
• Felons are closed-space infections of the fingertip pulp.
• Staphylococcus aureus is the most common cause.
• Thumb and index finger are the most commonly affected digits.
• Felons are characterized by marked throbbing pain, tension, and edema of the fingertip pulp.
• A felon is an infection of the distal pulp space of a digit, usually secondary to a puncture wound.
This is a closed space at the level of the distal interphalangeal joint. Since the infection cannot
spread proximal to this point, pain is throbbing and intense. Late osteomyelitis may develop in the
distal phalanx if the felon is not opened appropriately.
59. oesophageal carcinoma
• Predisposing factors include 8:

• alcohol and smoking: for squamous cell carcinoma and adenocarcinoma
• achalasia
• asbestosis
• Barrett oesophagus: for adenocarcinoma
• coeliac disease
• ionising radiation
• caustic stricture/lye stricture
• Plummer-Vinson syndrome
60. Boerhaave syndrome
• Boerhaave syndrome is a barogenic injury resulting from a sharp increase in the intraluminal
pressure against a closed cricopharyngeus.
• Perforation typically occurs at the weakest point in the esophagus, usually in the left lower
esophagus below the diaphragm in adults, whereas in very young patients, the perforation is
usually into the right pleural cavity.

• Alcoholism and overindulgence in food and drink are primary risk factors. Both can lead to emesis,
which is a major component of the classic presentation.
• No genetic predilection is apparent
61. CHOLANGIOCARCINOMA
• Mucin producing adenocarcinomas that arise from bile ducts

• Types: intrahepatic, hilar or central (65%) and peripheral (30%)
• Nodular tumors arising at the bifurcation of the common bile duct are called Klatskin tumors and
are often associated with a collapsed gallbladder
62. BARIATRIC SURGERY
Gastric bypass surgery
• Main article: Gastric bypass surgery

• A common form of gastric bypass surgery is the Roux-en-Y gastric bypass, designed to reduce the
amount of food a person is able to eat by cutting away a part of the stomach. Gastric bypass is a
permanent procedure that helps patients by changing how the stomach and small intestine handle
the food that is eaten to achieve and maintain weight loss goals.[21] After the surgery, the stomach
will be smaller. A patient will feel full with less food.
• The gastric bypass had been the most commonly performed operation for weight loss in the United
States, and approximately 140,000 gastric bypass procedures were performed in 2005. Its market
share has decreased since then and by 2011, the frequency of gastric bypass was thought to be less
than 50% of the weight loss surgery market. [10]
• A factor in the success of any bariatric surgery is strict post-surgical adherence to a healthy pattern
of eating.
63. Whipple's triad
• Whipple's triad includes symptoms of hypoglycaemia, low blood glucose measured at the time of
symptoms and symptoms resolved on correction of hypoglycemia
• Insulinomas are a 13 cell endocrinal tumour of the pancreas.
• The symptoms are produced due to excessive secretion of insulin causing hypoglycemia
• Most of the insulinomas are solitary and benign.
• Only about 10-15 % of insulinomas are malignant. (Keep in mind that all other endocrine tumours
of pancreas are usually malignant).

Classic diagnostic criteria is Whipple's triad
• Signs and symptoms of hypoglycemia during fasting.

• Blood glucose below 2.8 mmol/L (50 mg/dl) during symptomatic episodes.
• Relief of symptoms by intravenous administration of Glucose.
• Classical presentation of insulinoma (Whipple's triad)
• Fasting hypoglycemia
• Plasma glucose levels < 2.8 mmo1/1
• Relief of symptoms on intravenous administration of glucose
64. SHORT BOWEL SYNDROME
• Cyanocobalamine (Vitamin B12) deficiency is the most common deficiency in patients with short
bowel syndrome associated with loss of ileum (Heal resection) since vitamin B12 is absorbed only in
the ileum
• Short Bowel Syndrome may be associated with deficiency offal-soluble vitamins (Vitamin A, D, E
and K) and water soluble Vitamin B12 (when ileum is resected / non functional).
• The most common deficiency is determined essentially by the specific segment of the small
intestine (jejunum or ileum) that is resected / non functional
• Short bowel syndrome is characterized by increased gastrin levels (hypergastrinemia) due to
reduced small intestinal catabolism of gastrin
• Short bowel syndrome is a condition in which extensive resection of the small bowel results in
malabsorption, fluid and electrolyte loss and malnutrition. Short bowel syndrome can occur at any
age from neonates through the elderly. Patients present with diarrhea, steatorrhea, increase in
renal calcium oxalate calculi and cholesterol gallstones.
• Etiology: In neonates can result from jejunoileal atresia, gastrochisis, omphalocele and necrotizing
enterocolitis (bowel is resected). In adults it occur after bowel resection secondary to trauma,
chrons disease and mesenteric vascular disease. Following resection of the small intestine, the
residual intestine undergoes adaptation of both structure and function that may last for up to 6–12
months.
65. ACUTE APPENDICITIS
Appendicitis is more common in men The risk of perforation is:
• Less than 10 years old = 50%

• 10-50 years old = 10%
• Over 50 years old = 30%
Clinical features of appendicitis:

• Central abdominal pain moving to right iliac fossa
• Nausea, vomiting, anorexia
• Low-grade pyrexia (37.2-37.7 degree celsius)
• Localised tenderness in right iliac fossa
• Right iliac fossa peritonism
• Percussion tenderness is a kinder sign of peritonism than rebound
• Rovsing's sign = pain in right iliac fossa on palpation of the left iliac fossa
• Perforation of appendix in acute appendicitis commonly leads to an abscess cavity walled off by the
small bowel loops and the omentum, forming a phlegmon. Rarely the appendix may perforate
freely into the peritoneal cavity and cause generalized peritonitis. This usually occurs in cases of
early rupture of the appendix as inflammatory process did not get time to be localized by the
omentum and bowel loops.
• Usually the rupture of appendix is a late sequelae of appendicitis, usually occurring 48 to 72 hours
from the onset of symptoms.
• Management of appendicitis: [Ref Sabiston 18/e p1339; Schwartz 9/e p1084]
• The treatment of appendicitis is appendectomy. (It can be done open or laparoscopically)
• Prophylactic antibiotics are indicated preoperatively. Postoperative antibiotic coverage is of no use
in simple (uncomplicated) acute appendicitis. If perforated or gangrenous appendicitis is found,
antibiotics are continued until the patient is afebrile and has a normal white blood cell count.
• Perforated Appendicitis (Maingot's 11/e p603)
• Rupture is suspected in the presence of fever with a temperature of >39°C (102°F) and a white
blood cell count of >18,000 cells/mm3.
• The management of perforation depends on the nature of the perforation.
• If the perforation is free causing intraperitoneal dissemination of pus and fecal material, urgent
laparotomy is done for appendectomy and irrigation and drainage of the peritoneal cavity.
• If the perforation is contained it would result in an appediceal mass or abscess. This is managed as
described under.
• Appendiceal Abscess/ Mass
• Patients who present late in the course of appendicitis with a palpable or radiographically
documented mass (abscess or phlegmon) are treated with?
• conservative therapy and interval appendectomy 6 to 10 weeks later.
• (conservative management includes intravenous antibiotics and fluids as well as bowel rest.)
• Patients with large abscesses, greater than 4 to 6 cm in size, and especially those patients with
abscess and high fever, benefit from abscess drainage.
• Patients who continue to have fever, persistent pain and leukocytosis or develop complications like
bowel obstruction after several days of nonoperative treatment are likely to require immediate
appendectomy during the same hospitalization, whereas those who improve promptly may be
considered for interval appendectomy. Bailey lists Criteria for stopping conservative treatment and
going for appendectomy
• A rising pulse rate
• increasing or spreading abdominal pain
• increasing size of the mass

66. HIRSCHSSPRUNGS DISEASE
• Swenson procedure– aganglionic bowel is removed & coloanal anastomosis is done

• Duhamel – normal ganglionated colon pulled behind the abnormal segment & stapled
• Soave – endorectal mucosal dissection within the aganglionic distal rectum followed by pull
through of normal segment & coloanal anastomosis.
67. ANAL FISTULA
• An abnormal communication between anal canal and recto with exterior

• Even though multiple openings are seen in perianal skin – the internal opening is always single
• Causes: persistent anal gland infection, TB, Crohn's disease, lymphogranuloma venereum,
actinomycosis, rectal duplication, foreign body and malignancy
• More common in men
• Usual presentation – intermittent purulent discharge (may be bloody) and pain (which increases
until temporary relief occurs when the pus discharges)
• A previous episode of acute anorectal sepsis that settled (incompletely) spontaneously or with
antibiotics, or which was surgically drained
68. EXTERNAL HEMARRHOIDS
• External haemorrhoids relate to venous channels of the inferior haemorrhoidal plexus

• They are not true haemorrhoids; Commonly termed as perianal hematoma
69. INTERNAL HEMARRHOIDS
• Internal hemorrhoids are characteristically seen in 3, 7 and 11 o'clock positions

• Nature of bleeding is characteristically separate from the motion and is seen either on the paper on
wiping or as a fresh splash on the pan
• Pain is not commonly associated with bleeding
• Secondary internal haemorrhoids arise as a result of a specific condition (most important –
anorectal cancer)
70. VOLVULUS
• “Definitive treatment of sigmoid volvulus is sigmoid colectomy”

• Management of sigmoid volvulus
• Unless there are obvious signs of gangrene or peritonitis, the initial management of sigmoid
volvulus is resuscitation followed by endoscopic decompression (by using rigid
proctosigmoidoscopy or flexible sigmoidoscopy or colonoscopy) ; a rectal tube is inserted and kept
to maintain decompression. Endoscopic decompression is contraindicated if there is evidence of
strangulation or perforation.
• Although endoscopic decompression is successful in majority of patients, recurrence rate is quite
high. Therefore elective sigmoid colectomy is performed as the definitive procedure after the
patient is stabilized and adequate bowel preparation done.
• Emergency laparotomy is performed if strangulation or perforation is suspected or if attempts of
endoscopic decompression fail.
Volvulus refers to torsion of a segment of the alimentary tract, which often leads to bowel
obstruction. The most common sites of volvulus am the sigmoid colon and cecum.
In sigmoid volvulus, rotation nearly occurs in the anticlockwise direction.
Volvulus of other portions of the alimentary tract, such as the stomach, gallbladder, small bowel,
splenic flexure, and transverse colon, are rare
Predisposing factors includes a high residue diet and constipation.
• The definitive treatment of sigmoid volvulus is sigmoid colectomy.

• Unless there are obvious signs of gangrene or peritonitis, the initial management of sigmoid
volvulus is resucitation followed by endoscopic decompression (by using rigid
proctosigmoidoscope or flexible sigmoidoscope or colonoscope); a rectal tube is inserted and kept
to maintain decompression) Endoscopic decompression is contraindicated if there is evidence of
strangulation or perforation.
• Although endoscopic decompression is susccessful in majority of patients, recurrence rate is quite
• Emergency Laparotomy is performed if strangulation or perforation is suspected or if attempts of
endoscopic decompression fail.
• Volvulus describes a condition in which there is rotation of a segment of the intestine on an axis
formed by its mesentery resulting in partial or complete obstruction of the lumen and may be
followed by circulatory impairment of the bowel.
• Most common site is colon, among which following are involved in descending order - Sigmoid
volvulus (- 75%)
• Cecal volvulus (< 25%)
• Transverse colon
• Splenic flexure
• Sigmoid volvulus
• Most common site of volvulus
• Volvulus can occur in any segment of large bowel that is attached to a long and floppy
mesentery that is fixed to the
• retroperitoneum by a narrow base of origin. The mesenteric anatomy is such that volvulus is most
commonly seen in sigmoid colon.
• Associated predisposing factors are :
• age : average age of presentation is 60-70 yrs. - chronic constipation
• institutionalized or neurologically impaired or psychiatric patients (their medication may decrease
intestinal
• motility, or they may fail to pass stool regularly, leading to fecal loaded large bowel predisposing to
volvulus) - diet high in fibre and vegetables (as in third world countries)
• Signs and symptoms are those of acute or subacute intestinal obstruction.
• X-ray picture is dramatic
• there is a markedly dilated sigmoid colon with the appearance of a bent inner tube or coffee bean
appearance. Inferior convergence of the dilated loop points towards left side of pelvis.
• contrast enema demonstrates the point of obstruction with the pathognomic 'birds beak' or 'bird of
prey' or 'ace of spades' sign.
• Unless there are obvious signs of gangrene or peritonitis, the initial management
is resuscitation followed by endoscopic decompression and detorsion.
• Decompression/detorsion can be achieved by placement of rectal tube through a proctoscope or
the use of a colonoscope.
• If detorsion / decompression cannot be achieved with either the rectal tube or colonoscope,
laprotomy with resections of the sigmoid colon is done.
• Even if detorsion of the sigmoid volvulus is successful, risk of recurrence is high (approx. 50%).
Hence an effective sigmoid colectomy is indicated after the pt. has stabilized.
• Any evidence of bowel gangrene or perforation contraindicates non-operative decompression and
an immediate surgical exploration is done.
• Cecal volvulus
• The condition commonly referred to as cecal volvulus is actually a cecocolic volvulus and consists of
an axial rotation of the terminal ileum, cecum and ascending colon.
Cecal bascule - is a condition in which the cecum folds in a cephalad direction anteriorly over
a fixed ascending colon. This causes intermittent bouts of abdominal pain because the
mobile cecum causes intermittent episodes of Isolated cecal obstruction. It is relieved
spontaneously as the cecum falls back into its normal position.
Cecocolic volvulus is possible because of lack of fixation of the cecum to the
retroperitoneum.
Associate predisposing factors are:
• previous surgery
• pregnancy
• malrotation
• obstructing lesion of the left colon
• Cecocolic volvulus affects a younger age group (late 50s) than sigmoid volvulus (60s & 70s).
• X-ray picture
• dilated cecum usually occupying the left upper quadrant.

• haustral markings can be seen in the distended cecocolic segment and is a distinguishing feature
from sigmoid colon in which generally there are no haustra.
• Management
• According to Schwartz Surgery - Cecal volvulus, unlike sigmoid volvulus can almost never be
detorsed / decompressed endoscopically. As vascular compromise occurs early in the course of
cecal volvulus, surgical exploration is necessary when the diagnosis is made. Right hemicolectomy is
the procedure of choice.
• Sabiston surgery writes that - 'Although there have been reports of detorsion of cecocolic volvulus
with a colonoscope most cases require operation to correct the volvulus and prevent ischemia."
Volvulus neonatorum
• o The fetal alimentary canal returns from the extraembryonic coelom into the abdomen at 8-10
weeks, and the bowel undergoes rotation and fixation at certain points by the attachment of its
mesentery to the posterior abdominal wall.
• o When the process is incomplete or deviates from the normal plan, the result is malfixation or
malrotation.
• o Commonly, the normal oblique attachment of the mesentery from duodenojejunal flexure of the
caecum is absent, and the small bowel is attached to the posterior abdominal wall by a narrow stalk
based around superior mesenteric vessels. The caecum is undescended, i.e., situated in the right
hypochondrium and abnormally fixed by peritoneal bands running laterally across the second part
of duodenum.
• o The poorly attached small bowel undergoes volvulus around the axis of the 'universal mesentery',
which is twisted so that the flow of blood is cut off, producing a strangulating obstruction of the
small bowel. This typically occurs in the newborn, hence the term Volvulus neonatorum'. The
terminal ileum and caecum are drawn into the volvulus and are wrapped around the stalk of the
mesentery in two or three tight coils.
Clinical feature
• o A young infant, previously healthy, starts bile-stained vomiting during the first few days of the
live. Abdomen is
• soft and non-distended; however, abdominal distension may occur which is limited to upper
abdomen (epigastrium). o No obstruction may occur in the first day or two after birth and
meconium may be passed normally. Then, with
• variable suddenness, bowel actions cease with onset of obstruction.
• o The signs vary, depending on the degree of intestinal obstruction versus ischemia. When
strangulation occurs there are signs of schock, especially pallor and a vague mass of congested
bowel may be palpable in the centre of abdomen. Blood or blood-tinged mucus may be passed
rectally.
• o Ischemia may result in gangrene and perforation.
Investigations

• o Barium contrast studies with fluoroscopy (Barium meal follow through) is the investigation of
choice as X-ray is not reliable in early stages of volvulus.
• o However, if the perforation is suspected, barium contrast should not be used because of risk of
perotinitis. Water soluble contrast studies (iodine based) should be used. Plain X-ray of
abdomen/chest is the initial investigation to demonstrate free air under the diaphragm in
suspected cases of perforation.
• Types II, III, and IV hiatal hernias are all subtypes in which the herniation includes a visceral
structure other than the gastric cardia. Type II and III paraesophageal hernias, the gastric fundus
also herniates
• Type II and III paraesophageal hernias -the stomach inverts and lead to anupside down stomach,
gastric volvulus, and even strangulation of the stomach.
• In a case of suspected perforation plain x-ray should be performed. It shows free air under the
diaphragm and confirms the diagnosis of perforation.
• Definitive treatment of sigmoid volvulus is sigmoid colectomy”
Management of sigmoid volvulus
1. Unless there are obvious signs of gangrene or peritonitis, the initial management of sigmoid volvulus
is resuscitation followed by endoscopic decompression (by using rigid proctosigmoidoscopy or
flexible sigmoidoscopy or colonoscopy) ; a rectal tube is inserted and kept to maintain
decompression. Endoscopic decompression is contraindicated if there is evidence of strangulation or
perforation.
2. Although endoscopic decompression is successful in majority of patients, recurrence rate is quite
3. Emergency laparotomy is performed if strangulation or perforation is suspected or if attempts of
endoscopic decompression fail
4. A volvulus is the twisting strangulation of an intestinal segment around an axis which is formed by
an axis or an adhesion.
5. Ascaris infection is acquired by ingestion of the eggs, usually from contaminated soil.
• The ingested eggs hatch in the duodenum to produce larvae, which cross the small intestinal wall to
enter the bloodstream.
• They then pass through the heart to lodge in the lungs.
• They leave the lung capillary bed to enter the airspaces.
• They then ascend the bronchial tree into the oropharynx, where they are again swallowed.
• This time, they return to the small intestine where they develop into mature worms that can live in
the host for up to two years.
• A gravid female worm may produce up to 250,000 eggs daily, which are shed in stool.
• The passage of the larvae through the lungs often produces cough and/or wheezing, and may, in
severe cases, produce fever, dyspnea, fleeting patchy pulmonary infiltrates (Loeffler pneumonitis
with prominent eosinophilia), and rarely hemoptysis.
• Passage through the heart is usually asymptomatic, as the larvae are small.
• A single adult worm, but not usually larval forms, can migrate into the biliary tree, leading to biliary
colic, cholangitis, or gallstone formation; obstructive jaundice uncommonly occurs.
• The pancreas and stomach are not common sites for complications of ascariasis.
1. Plain Xray abdomen finding in Sigmoid Volvulus
1. Characteristic bent inner tube or coffee bean appearance with convexity of loop lying in the right
upper quadrant (opposite to the site of obstruction)
2. Contrast study (gastrografin enema) - bird beak appearance i.e. narrowing at the site of voivulus.
71. paralytic ileus
Pharmacologic Management of Post op paralytic ileus (P01):
• Minimizing the sympathetic inhibition of gastrointestinal motility, decreasing inflammation and

stimulation of gastrointestinal 11-opioid receptors are the ultimate goals of pharmacologic
management.
A) Minimizing sympathetic inhibition
• Both propranolol, a nonspecific 13-receptor antagonist, and dihydroergotamine, an a-receptor

antagonist, have been investigated for treatment of POI.
• Neostigmine is an acetylcholinsterase inhibitor that causes an increase in cholinergic
(parasympathetic) activity in the gut wall, which is believed to thereby stimulate colonic motility.
• Use of edrophonium chloride and bethanechol chloride, which competitively inhibit acetylcholine
on the binding site of acetylcholinesterase, has been reported to show improvement of POI.
• Cisapride is a serotonin (5-HT)4 receptor antagonist that promotes acetylcholine release from
postganglionic nerve endings in the myenteric plexus and is thought to indirectly improve
gastrointestinal motility.
• Metocloprimide is suspected to enhance gastrointestinal motility without stimulating gastric
secretion, but its use has not been substantiated for POI.
B) Decreasing inflammation
• Decreasing inflammation may be indicated in patients who are about to undergo major intestinal
surgery, as this is thought to be an important contributing factor to POI.
• Nonsteroidal anti-inflammatory (NSAIDs) agents can be used in conjunction with opioid analgesics
for their dual effects on pain control and inflammatory inhibition.
C) Stimulation of gastrointestinal iii-opioid receptors
• Stimulation of gastrointestinal .1-opioid receptors can theoretically influence gastrointestinal

motility directly; therefore, blocking the peripheral gastrointestinal effects of centrally acting
opioids used for analgesia may help prevent POI.
• Two novel drugs are being investigated for this reason: alvimopan and methylnaltrexone.
• Both drugs are If-opioid receptor antagonists, and both appear to offer promising results for
preventing prolonged POI.
• Opioid therapy for postoperative or chronic pain is frequently associated with adverse effects, the
most common being dose-limiting and debilitating bowel dysfunction, so alvimopan and
methylnaltrexone may also be useful in the treatment of chronic opioid bowel dysfunction.
• The currently available opioid antagonists such as naloxone are of limited use because they also act
at central opioid receptors to reverse analgesia and elicit opioid withdrawal.
• Alvimopan and methylnaltrexone are peripherally acting if-opioid receptor antagonists that have
been studied in patients undergoing abdominal and pelvic surgery and have been shown in several
studies to significantly accelerate gastrointestinal recovery. Alvimopan received FDA approval for
the treatment of POI on May 20, 2008.
D) Alternative medications
• Bisacodyl administration versus placebo twice daily starting on postoperative day 1, patients who
received bisacodyl had significantly earlier bowel movements than those who received placebo (25
h v. 56 h), but further studies are needed to assess the effect of laxatives on POI.
• Paralytic ileus, also called pseudo-obstruction, is one of the major causes of intestinal obstruction in
infants and children. Causes of paralytic ileus may include:
• Chemical, electrolyte, or mineral disturbances (such as decreased potassium levels)
• Complications of intra-abdominal surgery
• Decreased blood supply to the abdominal area (mesenteric artery ischemia)
• Injury to the abdominal blood supply
• Intra-abdominal infection
• Kidney or lung disease
• Use of certain medications, especially narcotics
Management:
• Nil per os (NPO or "Nothing by Mouth") is mandatory in all cases.

• Nasogastric suction and parenteral feeds may be required until passage is restored.
• There is no place for the routine use of peristaltic stimulants. Bowel movements may be stimulated
by prescribing lactulose, erythromycin or, in severe cases (Ogilvie's syndrome), neostigmine.
• If possible the underlying cause is corrected (e.g. replace electrolytes).
• In older children, paralytic ileus may be due to bacterial, viral, or food poisoning (gastroenteritis),
which is sometimes associated with secondary peritonitis and appendicitis.
Causes of Paralytic ileus
• Postoperative - a degree of ileus usually occurs after any abdominal procedure and is self-limiting,
with a variable duration of 24-72 hrs. Post op ileus may be prolonged in the presence of
hypoproteinemia or metabolic abnromality.
Paralytic ileus is a state in which there is failure of transmission of peristaltic waves
secondary to neuromuscular failure.
The resultant stasis leads to accumulation of fluid and gas within the bowel with
associated distention, vomiting, absent or diminished bowel sounds and absolute
constipation.
Radiological picture shows dilated gas filled bowel loops with multiple air-fluid level.
The picture is similar to mechanical small bowel obstruction; the only differentiating point
is presence of gas in colon and rectum in paralytic ileus.
• Other clinical differentiating features of paralytic ileus from mechanical small bowel obstruction
are.
1) Pain - Pain is colicky in mechanical obstruction. Pain is not a feature of paralytic ileus and if present
is a steady, diffuse pain.
2) Bowel sounds - Bowel sounds are hypoactive or absent in paralytic ileus in contrast to hyperactive
bowel sounds in mechanical obstruction.
72. WILKIES SYNDROME
• Barium meal is diagnostic

• Duodeno-jejunostomy is the treatment
73. ACUTE PERITONITIS
• Moderately raised amylase levels are diagnostic of peritonitis.

• A DPL with more than 500 leukocytes/mL is considered positive and suggests peritonitis.
• The fluid in bacterial peritonitis generally demonstrates low pH and glucose as well as elevated
protein and LDH levels. The drop in peritoneal fluid pH (and P02) is more pronounced in mixed
infections and severe bacterial contamination, with increased numbers of anaerobic bacteria in
these circumstances.
• USG and CT scan are increasingly used to identify the cause of peritonitis (acute pancreatitis).
74. TUBERCULAR PERITONITIS
• Post-primary, due to activation of long standing latent focus

• Through Blood spread, diseased mesenteric LN, perforated intestine, fallopian tube
75. PELVIC ABSCESS
• Vaginal drainage of a pelvic abscess (posterior colpotomy) is indicated when a pelvic abscess
extends into the pouch of Douglas.
76. PEPTIC ULCER (GASTRIC AND DUODENAL ULCER)

• Most important factors causing peptic ulcer
• H pylori infection
• NSAID use
• Sequelae of peptic ulcer surgery
• Recurrent ulceration
• Small stomach syndrome
Follows most ulcer operations, does not occur following Highly selective vagotomy
Due to loss of receptive relaxation
Gets better with time
Revisional surgery is not necessary
• Bile vomiting (Afferent loop syndrome)
Following gastrectomy, best treatment is Roux-en-Y diversion
In patients with gastroenterostomy, small Pyloroplasty may be performed
• Dumping syndrome (Post cibal syndrome)
More common after partial gastrectomy with the Billroth II reconstruction.
Much less common following the Billroth I gastrectomy or after vagotomy and drainage
procedures
• Efferent loop obstruction
More than 50% of cases occur within the first postoperative month
• Alkaline reflux gastritis
Although the diagnosis can be made by taking a careful history HIDA scans usually
demonstrate biliary secretion into the stomach and even into the esophagus.
Most patients had gastric resection and Billroth II anastomosis
• Post vagotomy diarrhea
Patient managed as for early dumping
Octreotide not effective
77. Portal hypertensive gastropathy
• Portal hypertensive gastropathy (PHG) is the ectatic blood vessels in the proximal gastric body and
cardia causing oozing of the blood.
• Less severe grades of PHG appear as a mosaic or snakeskin pattern and are not associated with
bleeding.
• Severe PHG with diffuse bleeding is treated by β-adrenergic receptor blockers or possibly with
placement of a TIPS or surgical portacaval shunt.
• The best treatment is liver transplantation
• Classification of Portal Hypertensive Gastropathy
McCormack Tanoue NIEC = New Italian Endoscopic

Club.
Mild Grade I Mosaic pattern

Fine pink speckling (scarlatina- Mild reddening Mild: diffuse pink areola
type rash)
Superficial reddening Congestive mucosa Moderate: flat red spot in the
pink areola
Mosaic pattern Severe: diffuse red areola
Severe Grade II Red mark lesion
Discrete red spots Severe redness and a fine reticular Discrete
pattern separating the areas of
raised edematous mucosa
Diffuse hemorrhagic lesion Confluent (diffuse)
Grade III Black brown spot
Point bleeding + grade II
• NIEC = New Italian Endoscopic Club.
78. GASTROINTESTINAL STROMAL TUMORS (GIST)
• Tyrosine kinase inhibitors imatinib and sunitinib are approved for the treatment of Gastrointestinal
Stromal Tumors (GIST)
79. LYMPHOMA
• Burkitt's lymphoma is a tumor of mature B cells that express surface IgM, CD19, CD20, CD10, and
BCL6, a phenotype consistent with a germinal center B-cell origin.
• Unlike other tumors of germinal center origin, Burkitt lymphoma almost always fails to express the
antiapoptotic protein BCL2
• Burkitt's lymphoma is a B-cell lymphoma
• As this a tumor of mature B-cells it expresses IgM, CD 19, CD20, CD 10 and BCL 6 a phenotype
consistent with a B-cell origin.
• However, unlike other tumors of germinal center origin, Burkitt lymphoma almost always fails to
express the antiapoptotic protein BCL-2.
• All forms of Burkitt lymphoma are associated with translocations of c-Myc gene on chromosome 8.
• The usual translocation is t (8 : 14).
• Other less common translocations are t (2 : 8) and t (8 : 22).
• Most of the patients in United States with Burkitt's lymphoma present with peripheral
lymphadenopathy or an intro abdominal mass.
• The disease is typically rapidly progressive and has a propensity to metastasize to CNS.
• Chemotherapy is the treatment of choice in Burkitt's Lymphoma.
• Burkitt's Lymphoma was one of the first cancers shown to be curable by chemotherapy.

• Molecular pathogenesis of Burkitt's lymphoma
• All forms of Burkitt's lymphoma are associated with translocation of the c-MYC gene an
chromosome 8.
• The translocation partener is usually IgH locus on chromosome 14, i.e., t (8; 14); But may also be Igk
on chromosome 2, i.e., t (2; 8) or IgX on chromosome 22, i.e., t (8; 22).
Mantle cell lymphoma
• Mantle cell lymphoma is a type of non-hodgkin lymphoma characterized by presence of tumor cells
which closely resemble the normal mantle zone of B-cells that surround germinal centers.
• Immunophenotype of mantle cell lymphoma
• Mantle cell lymphoma is neoplasm of B cells.
• Therefore it expresses B cell marker :
• CD19,CD20
• Surface immunoglobulin heavy chain (IgM and IgD).
• Either /c or X light chain.
• As the tumor cells are derived from Mantle zone, they are positive for B cell marker of mantle zone
i.e., CD-5.
• Mantle cell lymphoma is CD23 negative, this feature distinguish it from chronic lymphocytic
leukemia (CLL) which is positive for both CD5 and CD23.
• The other characteristic marker of mantle cell lymphoma is cycline DI.
Cytogenetic abnormalities.
• Mantle cell lymphoma is associated with an 11 : 14 translocation involving the IgH locus on
chromosome 14 and the cyclin DI locus on chromosome 11.
• This leads to increased expression of cyclin D 1, which promotes GI to S phase progression during
the cell cycle.
• 65 years old man with splenomegaly, lymphodenopathy CD-23 negative and CD-5 positive B-cell
suggest the diagnosis of mantle cell lymphoma.
Clinical features of mantle cell lymphoma
• It is usually present in fifth to sixth decade with male preponderance.

• The most common presentation is painless lymphodenopathy.
• Splenomegaly may occur.
• Occasionally, multifocal mucosal involvement of the small bowel and colon produces lymphomatoid
polyposis→ of all forms of NHL, mantle cell lymphoms is most likely to spread in this fashion.
• Prognosis of hodgkin lymphoma mainly depends on the histological type and staging.
Histological type
Best prognosis Lymphocytic predominent

Worst prognosis Lymphocytic depletion type

Best Prognosis Lymphocytic predominance type
Worst prognosis Lymphocytic depletion type
Most common HL Nodular sclerosis type
Most common type HL in India Mixed cellularity type
Least common type HL Lymphocytic depletion type
• Post transplant lymphoma is most commonly associated with Epstein-Barr virus
Oncogenic DNA virus Oncogenic RNA virus

Human papilloma virusQ Hepatitis C virusQ
Epstein-Barr virusQ Human T-cell leukemia virus type-1Q
Hepatitis B virusQ Helicobacter pyloriQ
Epstein-Barr Virus
• Epstein-Barr virus infection may lead to the following clinical conditions:

• Infectious mononucleosis
• EBV-associated malignancies:
• Burkitt's lymphomaQ
• Lymphomas in immunodeficient persons such as AIDS patients and transplant recipientsQ
• Nasopharyngeal carcinoma in persons of Chinese origin
• Post-Transplant Lymphoproliferative Disorder (PTLD)
• PTLD is associated with replication of EBV in B cells induced by enhanced immunosuppression,
primarily observed
• in patients who have received more than one course of polyclonal antilymphocyte globulin (ALG)
or monoclonal
Clinical Features:
• Clinical presentation of PTLD includes fever, malaise and lymphadenopathyQ
Diagnosis:
• The diagnosis is made by tissue biopsyQ
Treatment:
• Polyclonal PTLD: Discontinuation of immunosuppression and antiviral therapyQ

• Monoclonal PTLD: Radiation, chemotherapy and occasionally surgical resection. Antibody against
CD20Q
• represents a novel approach in treating monoclonal PTLD with favorable outcome.Q
(LCA or CD45):
"LCA or CD45 is expressed brightly in normal lymphocytes as well as in most of the
lymphoproliferative disorder. It is also variably expressed in other leukocytes. It is absent in
erythroid cells." -Iochims Lymph Node Pathology 4/43
S-100: S-100 is a marker that comes positive in chondrocytes, schwann cells, fat cells,
oligodendrocytes and other neural crest origin cells and tumors.
HMB-45: HMB-45 is a activated melanocytic marker expressed in melanoma cells.
Cytokeratin: Cytokeratin is expressed in normal and malignant epithelial cells.
Choice Cancers associated

Sjogren NHL mainly MALT-oma involving salivary glands>stomach
syndrome
Ataxia Elevated incidence of cancers, approximately 100-fold in comparison to the general
telengectasia population. In children, more than 85% of neoplasm cases are acute lymphocytic
leukemia or lymphoma. In adults with ataxia-telangiectaisa, solid tumors are more
frequent
Lynch-II Gastrointestinal cancer associated with endometrial/ovarian carcinoma. Early onset
syndrome brain tumor and lymphoma also seen in children
Lymphoa is a well-known complication of Sjogren's syndrome Most lymphomas are

extra-nodal, low grade marginal B cell lymphomas.
Development of Lymphoma in Sjogren's syndrome is suggested by low C4

complement levels.
Lymphoma in Sjogren's syndrome
The development ofLymphomas in patients with Sjogren syndrome is suggested by

:-
Persistent parotid gland enlargement
Purpura
Leukopenia
Cryoglobulinemia
Low C4 complement levels
• he stomach is the most frequent extranodal site for lymphomas. Microscopically, the vast majority
of gastric lymphoid tumors are non-Hodgkins lymphomas of B cell origin, Hodgkins ds involving the
stomach is extremely uncommon."
• Most patients notice the reddish discoloration of the surface of the eyeball (conjunctiva).
• As the tumor enlarges, patients seek medical attention.
• Conjunctival lymphomas can become large enough to displace the eyeball, and restrict eye
movement. Eye movement restriction can cause diplopia (double-vision).
• If the tumor extends behind the eyeball, it can be pushed forward (proptosis). Rarely, and if large
enough, orbital lymphoma can press on the optic nerve and cause loss of vision.
• If discovered early, prompt treatment offers the best chance for recovery of vision.
• n 1964, researchers at the National Cancer Institute developed the first combination chemotherapy
that cured a number of patients who had relapsed following a standard radiation therapy regimen.
This drug combination was called MOPP and was, for a long time, the standard treatment for
Hodgkin's disease:
• Mustargen (mechlorethamine, nitrogen mustard)
• Oncovin (Vincristine, VCR)
• Procarbazine (Matulane)
• Prednisone (Deltasone, Orasone)
• MOPP has been mostly replaced by another combination chemotherapy called ABVD (Adriamycin,
Bleomycin, Vinblastine, Dacarbazine), which is now the standard chemotherapy regimen for
Hodgkin's disease.
• However, MOPP may be used if there are lung or heart conditions present or allergies to any of the
medications in the ABVD combination. Additionally, 30% to 40% of people will relapse after
treatment with ABVD, which will require 'salvage' treatment with MOPP.
• VAD combination chemotherapy is used for multiple myeloma and CHOP combination
chemotherapy is used for B cell chronic lymphoid leukemia
• Reed-Sternberg cells (also known as lacunar histiocytes for certain types) are different giant cells
found on light microscopy in biopsies from individuals with Hodgkin's lymphoma (aka Hodgkin's
disease; a type of lymphoma), and certain other disorders. They are usually derived from B
lymphocytes.
• nvolvement of another organ (kidney) by Gi lymhonlma of duodenojejunal flexure classifies it as a
stage IV lymphoma.
Gastrointestinal lymphomas are staged using a modified Ann Arbor Classification:
• IE: Tumor confined to small intestine

• IIE: Spread to regional lymphnodes
• IIIE: Spread to non resectable nodes beyond regional nodes
• IVE: Spread to other organs
• Development of Lymphoma in Sjogren's Syndrome is suggested by Low C4 Complement levels
• Lymphoma in Sjogren's syndrome (Extra-nodal, low grade marginal B cell Lymphomas)
• The development of Lymphomas in patients with Sjogren Syndrome is suggested BY :
Persistent Parotid gland enlargement
Purpura
Leukopenia
Cryoglobulinemia
Low C4 complement levels
• Lymphoma is a well-known complication of Sjogren's syndrome; Most lymphomas are extra-nodal,
low grade marginal B cell Lymphomas

• Stromal polips are infrequent primary gastric malignancies classified as Gastrointestinal Stromal Cell
Tumors (GSIT). These are not associated with MALT Lymphomas
MALT Lymphomas presents at extranodal sites (Harrisons)
MALT Lymphomas are also called 'Extranodal Margmal zone B cell Lymphomas of MALT
type' and typically occur at extranodal sites as suggested by the terminology
MALT Lymphomas are predisposed by H.Pylori (Harrison) Gastric presemation
of 11141.1" Lymphoma is associated with H. Pylori injection – Harrisons
MALT Lymphomas are sensitive to chemotherapy Extensive MALT Lymphomas (Ire most
Oen treated with single agent chemotherapy such as chloramhticil- Harrison
Acute Lymphoblactic leukemia (ALL) may he associated with t(4;11), t(9;22) or 1(8; 14) but
association with 1(9; 20) is not seen.
Type of Leukemia Translocation Deletion (-) / Trisomy (+)

Chronic myelocytic t(9; 22)'Philadelphia ?
leukemia (CML) chromosome
Acute Myoblastic t(8; 21), t(9;22) +8, 7-, 5-, 7q, 5q?
Leukemia (AML)
Acute Monocytic Leukemia t(9; 11), t(11; ?
23)
Acute Promyelocytic t(15; 17)
leukemia (M3)
Acute lymphoblastic t(4; 11), t(9; t(8; 14) 20q?
leukemia (ALL) 22),
Chronic lymphocytic +12
leukemia (CLL)
Erythroleukemia - 7q-, 5q?
Polycythemia Rubravera - 20q?
• The treatment of choice for Burkitt's Lymphoma is chemotherapy and not Radiotherapy.
• 'Burkitt's lymphoma responds well to short term high dose chemotherapy. Treatment of Burkitt's
lymphoma in both children and adults should begin within 48 hours of diagnosis and involves the
use of intensive combination chemotherapy regimens' – Harrisons
• Burkitt's Lymphoma is a B cell lymphoma
• Burkitt's Lymphoma are tumors of mature B cells – Robbins 7th/677
• t (8;14) translocation is the most common translocation in Burkitt's Lymphoma Burkitt's
lymphomas are associated with translocation of the c-MYC gene on chromosome 8. Translocation
• t (8; 14)
• t (8; 22)
• t (2; 8)
• Burkitt's Lymphoma may present with an abdominal mass

• Most Burkitt's Lymphoma presents at extranodal sites but may present with lymphadenopathy
• Extranodal sites of involvement include the mandible and abdominal viscera
`Burkitt's Lymphomas may present with peripheral lymphadenopathy or an intraabdominal mass' –
Harrison
CNS involvement is frequent
• The disease is rapidly progressive and has a propensity to metastasize to CNS, prophylactic therapy
to CNS is therefore mandatory.
• Burkitt's Lymphoma is the most rapidly progressive human tumor
• Burkitt's Lymphoma is typically associated with Epstein Barr virus (EBV).
• EBV is associated with upto 95% of cases of Endemic Burkitt's Lymphoma.
• EBV is associated with approximately 30% of cases of Sporadic Burkitt's Lymphoma and Immune
Deficiency associated Burkitt's Lymphoma.
• Infectious Agents Associated with the Development of Lymphoid Malignancies
Lymphoid Malignancy
• Thu-kites lymphoma
• Post–organ transplant lymphoma
• Primary CNS diffuse large B cell lymphoma
• Hodgkin's disease
• Extranodal NK/T cell lymphoma, nasal type
• Adult T cell leukemia/lymphoma
• Diffuse large B cell lymphoma
• 8111-kW's lymphoma
• Lymphoplasmacytic lymphoma
• Gastric MALT lymphoma
• Primary effusion lymphoma
• Multicentric Castleman's disease
• CNS, central nervous system; HIV, human immunodeficiency virus; HTLV. human T cell
lymphotropic virus; MALT, mucosaassociated lymphoid tissue; NK, natural killer
• Primary Effusion Lymphoma (PEL) is a rare variant of Immunoblastic Lymphomas seen primarily in
HIV infected patients.
• Primary Effusion Lymphoma (PEL) is a rare variant of Immunoblastic Lymphomas seen primarily in
HIV infected patients
• 'Two variants of Immunoblastic Lymphomas seen primarily in HIV infected patients are Primary
Effusion Lymphoma(PEL) and its solid variant Plasmacvtic lymphoma of the oral cavity'
• Centroblastic Lymphoma and Anaplastic Lymphomas are variants of Diffuse Large B call Lymphomas
and are distinct entities from I mmunoblastic Lymphomas
• Morphologic Variants of Diffuse Large B Cell Lymphomas ( DLBCL)
• Centroblastic
• Immunoblastic
• Anaplastic
• The most common variant of Non-Hodgkin's Lymphoma in India is Diffuse Large B cell Lymphoma
• Diffuse Large B cell Lymphoma is also the most common variant of Non-Hodgkin's Lymphoma in the
United States (Western Data)
• 'The majority of Non-Hodgkin's Lymphoma (NHL) in India are B-cell Lymphomas (around 80
percent). The distribution of Non-Hodgkin's Lymphoma (NHL) subtypes in India shows important
differences with those from the rest of the world. Diffuse large B-cell lymphoma remains the most
common form of NHL as in Western Data. However, Follicular lymphoma and mantle-cell
lymphoma are less common in India compared to Europe and the USA. T cell Lymphomas account
for approximately 16 percent of all NHL. T-cell lvmphohlastic lymphoma and anaplastic large T/null
cell lymphoma are more prevalent in India. Peripheral T-cell lymphomas and T/NK-cell lymphomas
of nasal and nasal types, which are common in many other Asian countries, are less prevalent.'
• Working formulation of NHL for clinical usage is as follows:
• Low grade
Small lymphocytic Q
Follicular, predominantly small cleaved cell Q
Follicular, mixed, small cleaved and large cell. Q
• Intermediate grade
Follicular predominantly large cell Q
Diffuse small cleaved cell
Diffuse mixed small and large cell.
Diffuse large cell.
• High grade
Large cell immunoblastic Q
Lymphoblastic Q
Small non cleaved cell.
• Note that all varieties of diffuse fall in the intermediate grade category only.
• International prognostic index' does not include Hemoglobin and Albumin as prognostic factors.
• Prognostic Factors according to International Prognostic Index for NHL
1 AgeQ : (Age 60 years carries adverse prognosis)

.
2. Stages : (Ann Arbor stage III or IV carries adverse prognosis)
3. LDH levelse : (Elevated LDH levels above normal carry adverse prognosis)
4. Performance status : (P.S 2 (ECOG) or
5. Number of Extranodal sites : (>1 extranodal site involvement carries adverse prognosis)
involvedQ
• International Prognostic Index for NHL

• Five clinical risk factors:
Age 60 years
Serum lactate dehydrogenase levels elevated
PerfOrmance status 2 (ECOG) or 70 (Karnofsky)
Ann Arbor stage III or IV
> / site of extratiodal involvement

n 1994, a group of hematopathologists, oncologists and molecular biologists came together
(International Lymphoma Study Group) and introduced a new classification, called the
'Revised European-American Classification of Lymphoid Neoplasms (REAL).
• WHO has now reviewed and updated the real classification resulting in inclusion of additional rare
entities.
• WHO Classification / Modified 'REAL' Classification
I. Precursor B-cell Neoplasm
• Precursor-B lymphoblastic leukemia/lymphoma
II. Peripheral B-Cell Neoplasms
• Chronic lymphocytic leukemia/small lymphocytic lymphoma

• B-cell prolymphocytic leukemia Lymphoplasmacytic lymphoma
• Splenic and nodal marginal zone lymphomas Extranodal marginal zone lymphomas
• Mantle cell lymphoma
• Follicular lymphoma
• Marginal zone lymphoma
• Hairy cell leukemia
• Plasmacytoma/plasma cell myeloma
• Diffuse large B-cell lymphoma
• Burkitt lymphoma
III. Precursor T-Cell Neoplasms
• Precursor-T lymphoblastic leukemia/lymphoma
iv Peripheral T-Cell and NK-Cell Neoplasms
• T-cell prolymphocytic leukemia

• Large granular lymphocytic leukemia Mycosis fungoides/Sezary syndrome Peripheral large cell
lymphoma, unspecified Anaplastic large cell lymphoma Enteropathy-associated T-cell lymphoma
Hepatosplenic y8 T-cell lymphoma
• Adult T-cell leukemia/lymphoma
• NK/T-cell lymphoma, nasal type
• NK cell leukemia
V. Hodgkins LF mphoma
• Classical subtypes
• Nodular sclerosis - Mixed cellularity
• Lymphocyte-rich
• Lymphocyte depletion Lymphocyte predominance

80. BARIATRIC SURGERY
• Types of Commonly Performed Bariatric Operations by Mechanism of Action:
Restrictive
• Laparoscopic adjustable gastric banding (LAGB)
• Sleeve gastrectomy (SG)
• Vertical banded gastroplasty (VBG)
Malabsorptive
• Biliopancreatic diversion (BPD)
• Jejunoileal bypass (JIB)
Combined restrictive and malabsorptive

• Roux-en-Y gastric bypass (RYGB)
• BPD with duodenal switch (DS)
81. RECURRENT PYOGENIC CHOLANGITIS
• Fever, right upper quadrant abdominal pain, and jaundice

• Biliary obstruction is usually incomplete and therefore marked jaundice and pruritus are not
common.
• Abnormal LFT
• Treatment of acute cases: percutaneous transhepatic cholangioscopic lithotomy (PTCSL)
• Definite treatment: surgery
82. LIVER TRANSPLANTATION
• In orthotropic liver transplantaion, the bile duct between recipent and donor liver are repaired in
end to end fasion or else Roux en Y choledochojejunostomy.
• Biliary atresia is an indication for Liver transplantation in children while primary Biliary Cirrhosis,
Sclerosing cholangitis and Hematochromatosis an established indications for Liver transplantation
in adults
Indication for Liver Transplantation:
Children
• Biliary atresia
• Neonatal hepatitis
• Congenital hepatic fibrosis
• Alagille's disease"
• Byler's disease
• a 1 -Antitrypsin deficiency
• Inherited disorders of metabolism
• Wilson's disease
• Tyrosinemia
• Glycogen storage diseases
• Lysosomal storage diseases
• Protoporphyria
• Crigler-Najjar disease type I
• Familial hypercholesterolemia
• Primary hyperoxaluria type I
• Hemophilia
Aduts
• Primary biliary cirrhosis

• Secondary biliary cirrhosis
• Primary sclerosing cholangitis
• Autoimmune hepatitis
• Carob's disease'
• Cryptogenic cirrhosis
• Chronic hepatitis with cirrhosis
• Hepatic vein thrombosis
• Fulminant hepatitis
• Alcoholic cirrhosis
• Chronic viral hepatitis
• Primary hepatocellular malignancies
• Hepatic adenomas
• Nonalcoholic steatohepatitis
• Familial amyloid polyneuropathy
• "Arteriohepatic dysplasia, with paucity of bile ducts, and congenital malformations, including
pulmonary stenosis.
• "Intrahepatic cholestasis, progressive liver failure, mental and growth retardation
• `Multiple cystic dilatations of the intrahepatic biliary tree.
• Hematochromatosis is also an indication for Liver Transplantation
• 'Among genetic and metabolic conditions, Hematachroatosis is the most common reason for Liver
Transplantation'
• The first human liver transplant was performed in 1963 by Dr. Thomas Starzl.
• Caval, portal vein, hepatic artery, and bile duct anastomoses are performed in succession, the last
by end-to-end suturing of the donor and recipient common bile ducts or by choledochojejunostomy
to a Roux-en- Y loop if the recipient common bile duct cannot be used for reconstruction (e.g., in
sclerosing cholangitis)."- Harrison 17/e p
• Bile duct anastomosis in orthotopic liver transplant is done by
• Choledochocholedochostomy or
• Roux-en-Y choledochojejunostomy
• Choledochocholedochostomy
• end to end anastomosis between donor CBD and the recipient CBD
• used when the recipient bile duct is not diseased
• preferred method of bile duct anastomoses
• Roux-en-Y choledochojejunostomy
• alternative bile duct anastomosis when choledochocholedocostomy is not possible, that is when
recipient extrahepatic bile duct is diseased (eg. sclerosing cholangitis), or small or when there is
significant recipient donor duct size mismatch.
• Liver transplantation is indicated for those children and adults, who in the absence of
contraindications suffer from severe, irreversible liver disease for which alternative medical or
surgical treatments have been exhausted or are unavailable.
• Most common indication
• in children ________ Biliary atresia
• in adults Cirrhosis
• Harrison 17/e writes- "Currently, chronic hepatitis C and alcoholic liver disease are the most
common indications for liver transplantation, accounting for over 40% of all adult candidates who
undergo the procedure."
Indications for ver Transplantation Adults
Children
Biliary atresia Primary biliary cirrhosis
Neonatal hepatitis Secondary biliary cirrhosis
Congenital hepatic fibrosis Primary sclerosing cholangitis
Alagille's disease Autoimmune hepatitis
Byler's disease Caroli's disease
al- antitrypsin deficiency Cryptogenic cirrhosis
Inherited disorders of metabolism Chronic hepatitis with cirrhosis
Wilson's disease Hepatic vein thrombosis
Tyrosinemia Fulminant hepatitis
Glycogen storage diseases Alcoholic cirrhosis
Lysosomal storage diseases Chronic viral hepatitis
Protoporphyria Primary hepatocellular malignancies
Crigler-Najjar disease type I Hepatic adenomas
Familial hypercholesterolemia Nonalcoholic steatohepatitis
Primary hyperoxaluria type I Familial amyloid polyneuropathy
Hemophilia
Contraindications to Liver Transplantation

Absolute Relative
Uncontrolled extrahepatobiliary infection Age >70
Active, untreated sepsis Prior extensive hepatobiliary surgery
Uncorrectable, life-limiting congenital anomalies Portal vein thrombosis
Active substance or alcohol abuse Renal failure
Advanced cardiopulmonary disease Previous extrahepatic malignancy (not
including nonmelanoma skin cancer)
Extrahepatobiliary malignancy (not including Severe obesity

nonmelanoma skin cancer)
Metastatic malignancy to the liver Severe malnutrition/wasting
Cholangiocarcinoma Medical noncompliance

AIDS HIV seropositivity
Life-threatening systemic diseases Intrahepatic sepsis
Severe hypoxemia secondary to right-to-left

intrapulmonary shunts (P02 < 50 mmHg)
Severe pulmonary hypertension (mean PA

pressure >35 mmHg)
Uncontrolled psychiatric disorder
83. CHOLEDOCHOLITHIASIS or COMMON BILE DUCT STONES
• Common bile duct stones will manifest: Jaundice,Itching,Clay coloured stools
84. Mirrizi syndrome
• Gallstone impacts in the wall causing pressure necrosis which further gets adherent to the CBD wall
• Occasionally leads to a cholecystocholedochal fistula
85. GALL BLADDER CARCINOMA
• Gallstones may be a predisposing factor

• Primary carcinoma of the gallbladder is an uncommon, aggressive malignancy that affects women
more frequently than men.
• Older age groups are most often affected, and coexisting gallstones are present in the vast majority
of cases.
• The symptoms at presentation are vague and are most often related to adjacent organ invasion.
Imaging studies may reveal a mass replacing the normal gallbladder, diffuse or focal thickening of
the gallbladder wall, or a polypoid mass within the gallbladder lumen.
• Adjacent organ invasion, most commonly involving the liver, is typically present at diagnosis, as is
biliary obstruction. Periportal and peripancreatic lymphadenopathy, hematogenous metastases,
and peritoneal metastases may also be seen. The vast majority of gallbladder carcinomas are
adenocarcinomas.
• Because most patients present with advanced disease, the prognosis is poor.
• The radiologic differential diagnosis includes the more frequently encountered inflammatory
conditions of the gallbladder, xanthogranulomatous cholecystitis, adenomyomatosis, other
hepatobiliary malignancies, and metastatic disease.
• The prevalence of lymphatic spread is high in gallbladder carcinoma. Lymphatic metastases
progress from the gallbladder fossa through the hepatoduodenal ligament to nodal stations near
the head of the pancreas.
• Three pathways of lymphatic drainage have been suggested: the cholecystoretropancreatic
pathway, the cholecystoceliac pathway, and the cholecystomesenteric pathway.
• The cystic and pericholedochal lymph nodes are the most commonly involved at surgery and are a
critical pathway to involvement of the celiac, superior mesenteric, and para-aortic lymph nodes.
86. BILE DUCT INJURIES
Management:
• Early repair not attempted. only drainage procedures carried out

• Ideal time of repair is 8 to 12 weeks to allow inflammation to subside
• Roux-en-Y -hepatico-jejunostomy
87. White bile
• On table diagnosis is done for white bile.
88. Pseudocyst
• Most common cause of pancreatic pseudocyst is Pancreatitis (90%). The second most common
cause is trauma (10%).
• The complication least likely to occur in a pseudocyst of the pancreas is Carcinomatous change
• Commonest complication of pancreatic pseudocyst ?
• Infection
• "Other than pain, infection is the most common complication" - Maingot's 10/e, p 1929
• Other complications are:
• Obstruction of GIT
• Hemorrhage
• Rupture
• Pseudoanetoysm - splenic artery is most frequently involved.
• Percutaneous aspiration is preferred only in cases of infected cyst and abcesses, other wise internal
drainage is the t/t of choice.
• Epigastric mass is the main symptom of pseudocyst.
• Increased level of amylase is usually elevated with pancreatic pseudocysts.
89. CHRONIC PANCREATITIS
A feeding tube jejunostomy is strongly advised during major foregut, or hepatic operation, during a
major trauma laparotomy, after pancreatic surgery; or in nutritionally bankrupt patients." - Essentials
of General Surgery by Lawrence 4/e p80.
Enteral route if possible should always be preferred over TPN.
GI tract surrounding pancreas (stomach, duodenum) undergoes paralytic ileus after a major
pancreatic surgery, thus oral feeding and feeding gastrostomy are not used.
A feeding jejunostomy would be ideal route after a major pancreatic surgery and is strongly
recommended.
• "Pseudocysts occur in up to 10% of patients with acute pancreatitis, and in 20 to 38% of patients
with chronic pancreatitis, and thus, they comprise the most common complication of chronic
pancreatitis."
• Areas of ductal dilatation alternating with areas of ductal stenosis are common finding in alcoholic
patients who have severe chronic pancreatitis.
• This type of duct obstruction cannot be relieved by a sphincteroplasty because of multiple areas of
stenosis along the duct.
• Although total pancreatectomy would be a beneficial approach, mortality and morbidity rate with
this procedure are extremely high.
• Thus the procedure of choice in this pt. is side to side pancreaticojejunostomy in which the duct is
opened longitudinally through the chain of lakes. A Roux-en-Y limb of jejunum should then be
brought up for anastomosis with the opened pancreas in side-to-side fashion
• he patient most likely has a pancreatic pseudocyst, which is a complication of pancreatitis.
Pancreatic pseudocyst is not a true cyst; it is lined by granulation tissue and collagen.

• It contains pancreatic juices and lysed blood, so rupture would spill the active digestive enzymes
onto the adjacent viscera, particularly the stomach, small intestine, and transverse colon.
• Digestive action produces potentially severe gastrointestinal hemorrhage.
Anaphylactic shock results from massive activation of the IgE-mediated branch of the immune
system.
• Pancreatic secretions do not elicit an IgE response.
• The classic abdominal cyst that ruptures, producing anaphylactic shock, is a hydatid cyst.
• Carcinomatosis is widespread serosal spread of a carcinoma, typically due to tumor spillage into a
body cavity.
• Although this may occur with pancreatic mucinous cystadenocarcinoma, this disease is far less
likely to occur than is pancreatic pseudocyst in a patient with chronic pancreatitis.
• Pancreatic pseudocyst is not an infective disease. Although septic abscesses do occur in the
abdomen, and may even complicate a pancreatic pseudocyst, the danger of rupture is more
associated with tissue destruction by pancreatic enzymes than with infection.
• When a patient has undergone a prolonged and complicated pancreatic surgery, the recovery of
the patient will require a form of nutrition that gives rest to the pancreas and protect the
pancreatic anastomosis.
• A feeding jejunostomy in such a case can provide supplementary nutrition and also gives protection
to the pancreatic anastomosis and cause minimal stimulation of pancreatic secretion thereby giving
rest to the pancreas.
90. INSULINOMA
• Xylose test is used in the diagnosis of malabsorption due to intestinal mucosal disease. This test is
not used for the diagnosis of Insulinomas
• Fasting blood glucose, C- peptide levels and Insulin Glucose Ratio are all used in the diagnosis of
Insulinomas.
Diagnosis of Insulinomas
• 6,uU/m1 when blood glucose in < 40 mg/dl " align="left" height="40" width="237">Serum insulin
levels (fasting)
• Serum glucose levels (fasting)
• Serum C- peptide levels (Elevated)
• Serum proinsulin levels (Elevated)
• Insulin / Glucose Ratio (> 0.3)
• Plasma fl-Hydroxybulyrate (Decreased)
• The most reliable test is a fast upto 72 hours with serum glucose, C-peptide and insulin levels
measurements every 4-8 hours
• The Gold standard test for diagnosis of Insulinoma is a supervised '72 hour fast' test
• Diagnosis of lnsulinoma requires demonstration of inappropriately high levels of plasma Insulin (
and C- peptide) in the presence of documented hypoglycemia (Achieved by 72 hour fast test).

• Absolute values of Insulin or C- peptide are not reliable in establishing a diagnosis unless
hypoglycemia is documented The '72 hour fast test' allows demonstration of hypoglycemia,
together will elevated levels of Insulin and C-peptide and thus becomes the most reliable – gold
standard test for establishing a diagnosis of Insulinoma
Diagnosis of Insulinoma: '72 hour fast' test
• The diagnosis of Insulinoma requires the demonstration of an inappropriately elevated plasma

insulin (and C-peptide) at the time of hypoglycemia
• The '72 hour fast' test involves supervised fasting for upto 72 hours or until hypoglycemia can be
documented (
• The test is considered positive if at any time when blood glucose levels drop to < 2.2mmo1/1 (40
mg/dl), the serum insulin levels are recorded to be greater than 6µU/ml. (and C- peptide levels >
100 pmo1/1)
• Studies indicate that 100% of patient with insulinoma will he detected after a supervised 72 hour
fast and hence this test is considered the gold standard test
• First 24 hours : 70-80% of patients with insulinoma can be detected
• Upto 48 hours : 98% of patients with insulinoma can be detected
• By 72 hours: 100% of patients with insulinoma can he detec
• nsulinomas and Sulfonylureas, both produce endogenous hyperinsulinemia leadink to the same
biochemical pattern. These can only be distinguished by directly measuring the drug
concentration of sullOnylureas in the plasma
• 'It is necessary to screen the plasma for sulphonylureas and other insulin secretagogues
(repaglinide, nateglinide) at the time of hypoglycemia since these produce an insulin, C- peptide„
proinsulin and glucose pattern, indistinguishable from that produced by an insulinoma' - Harrison
• Biochemical Patterns In Patients With Various Causes Of Hyperinsulinemic Hypoglycmia
• The most common site of Insulinomas is the Pancreas.
• sulinomas are usually single and not multiple (>90%) – Harrison's
• Insulinomas are endocrine tumors of pancreas derived from Beta cells.
• They are generally small (>90% < 2 cm), usually not multiple (90%) and only 5-15% are malignant
(usually benign).
Symptoms due to Hypoglycemia
• Most common symptoms are due to the effect of hypoglycemia on the central nervous system
(Neuroglycemic Symptoms)
• Confusion
• Headache
• Disorientation
• Visual difficulties
• Irrational behavior (even coma)
Symptoms due to Excessive Catecholamine Release secondary to Hypoglycemia
• Tremor
• Palpitation
• The most important examination is intraoperative ultrasound, which can identify a pancreatic
tumor in nearly all cases. It is more sensitive than any preoperative test." - CSDT
• nsulinomas invariably occur only in the pancreas, distributed equally in the pancreatic head, body
and tail".
• Harrison 17/e
• Insulinomas are a cell endocrinal tumur of the pancreas.
• Insulinomas are the most common pancreatic endocrine neoplasms.
• The symptoms are produced due to excessive secretion of insulin causing hypoglycemia
• Most of the insulinomas are solitary and benign,
• Only about 10-15% of insulinomas are malignant. (keep in mind that all other endocrine tumours of
pancreas are usually malignant).
• Symptoms of insulinoma ?
• The most common symptom is due to the effect of hypoglycemia on the central nervous system. -
These symptoms are - confusion, disorientation, visual difficulties, irrational behaviour, coma
• Other symptoms are due to increased secretion of catecholamines which includes sweating, tremor
and palpitations.
• Classic diagnostic criteria is - Whipple's triad
• Signs and symptoms of hypoglycemia during fasting.
• Blood glucose below 2.8 mmol/L (50mg/d1) during symptomatic episodes.
• Relief of symptoms by intravenous administration of Glucose.
• The most useful diagnostic test and the only one indicated in almost all patients is demonstration of
fasting hypoglycemia in the presence of inappropriately high level of insulin.
• The patient is fasted for 72 hrs or till the symptoms of hypoglycemia develop.
• When hypoglycemia develops, serum level of insulin is measured. A ratio of plasma insulin to
glucose > 0.3 is diagnostic.
• Localization of the tumour
• Once the diagnosis has been made, localization of the tumour is must for surgery.
• The most important examination for localization of tumour is intraoperative ultrasound, which can
indentify pancreatic tumour in all cases.
• It is more sensitive than any other method
• Other important methods of localization ?
• High resolution CT and MRI.
• Endoscopic ultrasound examination of pancreas.
• Selective arteriography
• T/T - Surgical excision is the t/t of choice ?
• Since most insulinomas are benign simple enucleation is done.
• "The most reliable test to diagnose insulinoma is a fast up to 72 h with serum glucose, C-peptide,
and insulin measurements every 4-8 h."—Harrison
• An insulinoma is an endocrine tumor of the pancreas derived from beta cells that ectopically
secretes insulin, which results in hypoglycemia.
• The clinical symptoms are because of.the effects of hypoglycaemia (sweating, tremor, palpitations,
confusion, headache, disorientation, visual difficulties, irrational behavior, or even coma)

• The diagnosis of insulinoma requires the demonstration of an elevated plasma insulin level at the
time of hypoglycemia. This is because insulinomas do not reduce the secretion of insulin in the
presence of hypoglycaemia. Whereas in a normal person, insulin levels would decrease with
decrease in blood glucose levels.
• The most reliable test to diagnose insulinoma is a fast up to 72 h with serum glucose, and insulin
measurements every 4-8 h.
• The test is terminated if the the patient becomes symptomatic or glucose levels are
• Diagnosis of insulinoma is made if:
• A serum insulin level of 6 microunit/mL or more in the presence of blood glucose values below 40
mg/dL ratio of plasma insulin to glucose is > 0.3
• In addition to the above criteria, some other measurements are also required before making the
diagnosis of insulinoma
• C-peptide level
• serum proinsulin level,
• serum sulfonylurea levels
• These additional tests are used because any hidden use of insulin or oral hypoglycemics taken by
the patient would resemble insulinoma causing high levels of insulin in presence of hypoglycaemia.
• The combination of elevated proinsulin levels (normal in exogenous insulin/hypoglycemic agent
users), elevated C-peptide levels (low in exogenous insulin users), antibodies to insulin (positive in
exogenous insulin users), and measurement of sulfonylurea levels in serum or plasma will allow the
correct diagnosis to be made.
91. urolithiasis
• Which one of the following gastrointestinal disorders predisposes to urolithiasis -short bowel
syndrome.
92. URETERIC CALCULI
• A 45-year-old male with history of recurrent ureteric calculi presented with fever. Right-sided
nephrectomy was performed. Gross view and histology have been provided.the diagnosis will be
uteric calculi.
93. UNDESCENDED TESTES
• Orchidopexy is usually done before 6 months of age

• Orchidectomy: if the incompletely descended testis is atrophic, if patient is past puberty & other
testis is normal
• In bilateral cases, testis is passed into the opposite scrotum through an opening in the scrotal
septum - Ombredanne's operation
• HCG or GnRH can be given when cryptorchidism is associated with hypogenitalism and obesity
94. ACUTE EPIDIDYMO-ORCHITIS
Epidemiology of Acute Epididymo-Orchitis
• Most Common Organism – Chlamydia (Gonococcal epididymitis still prevalent)

• Develops in 18% of men suffering from Mumps , usually when parotid swelling is waning
• Mumps epididymitis in absence of parotiditis occurs in infants
• Other Causes – Enteroviruses , Brucellosis, LGV
• Escherichia coli is an important cause of nonspecific epididymitis and orchitis in children with
congenital genitourinary abnormalities and in older men.
• Mycobacterium tuberculosis can cause tuberculosis of the epididymis and testes, characterized by
granuloma formation.
• Pseudomonas sp. has been implicated as an important cause of nonspecific epididymitis and
orchitis in older men.
Pathogenesis of Acute Epididymo-Orchitis
• May Follow Uretheral Instrumentation , prostatectomy
Signs & Symptoms (Clinical Features) of Acute Epididymo-Orchitis
• Scrotal Wall becomes red, edematous , shiny and become adherent to epididymis
• Orchitis without epididymitis is seen in SYPHILIS
• In differential diagnosis of epididymo-orchitis & torsion it is important that Elevation of testis in
epididymo orchitis relieves pain
• Acute tuberculous epididymitis – thickened vas
Complication of Acute Epididymo-Orchitis
• The Main Complication is testicular atrophy which may cause infertility (if B/L)
Diagnosis & Management of Acute Epididymo-Orchitis
• Doxycycline for Chlamydial infection, Plenty of fluids, scrotal support and analgesics

Pediatrics
1. Meconium Aspiration Syndrome
• Meconium stooling is seen in 90 percent of newborns within the first 24 hours, and most of the rest
within 36 hours.
• Patient with leakage of fluid and meconium stained liquor at 34 weeks of gestation is suffering from
preterm premature rupture of membrane (PROM)
• Meconium is excreted by a new born till 3 day
• Saffron coloured meconium is seen in post maturity
• Meconium aspiration syndrome occurs when infants take meconium into their lungs during or
before delivery.
• Meconium stained liquor (amniotic fluid) with respiratory distress soon after birth suggests the
diagnosis of meconium aspiration syndrome
• Complications: Persistent pulmonary hypertension
• Obstructive emphysema can occur as a result of passage of meconium in utero
• Chest X-ray: bilateral heterogeneous opacities (patchy infiltrates), coarse streaking of both lung
fields, areas of hyper expansion, atelectasis and air leak, increased AP diameter, flattening of
diaphragm
• Management: IV fluids, ventilator support,oxygen,Antibiotics
2. Congenital Diaphrgmatic Hernia
• The least important prognostic factor is delay in emergent surgery.

• The first clinical intervention is to Insert a nasogastric tube.
• Peristalsis in the thoracic cavity.
• Lung head ratio .
• Heart beat shifted to right.
• Apgar scores were 3, and 6 at 1 and 5 minutes. At 10 minutes child shows features of breathlessness on CXR.
• Gasless abdomen.
• Most common on left side and posterolateral part of diaphragm.
• X-ray shows left hemithorax with multiple air-filled structures and mediastinal shift to the right.
• Cause of death in congenital diaphragmatic hernia is pulmonary hypoplasia.
3. Kwashiorkor
• Flag sign is seen in kwashiorkor

• Kwashiorkor is characterised by Markedly retarded growth, psychomotor
changes,Dermatitis,Edema,Flag sign
• Apathy, Flaky paint dermatosis, Poor appetite & low albumin level is seen in Kwashiorkor
• In malnourished subjects, secretory IgA is generally reduced.

• In Kwashiorkor, the letter 'K' is post-fixed to denote Edema
4. Phenylketonuria
• In Phenylketonuria the main aim of first line therapy is Limiting the substrate for deficient enzyme
• Microcephaly, blue eyes, fair skin, and mental retardation in a 4 year old girl with a positive ferric
chloride test is indicative of Phenylketonuria
• A child brought with seizures and impairment of development is diagnosed having phenylketonuria.
Restriction of substrate of the deficient enzyme in the diet is the initial line of treatment in this
child
• The primary deficiency in the disease phenylketonuria occurs in the synthesis of Tyrosine
• Phenylketonuria is detected by Guthrie test
• Incomplete oxidation of phenylpyruvic acid results in Phenylketonuria
• Mousy odour urine is seen in Phenylketonuria
• Enzyme deficient in phenylketonuria is Phenylalanine hydroxylase
• In phenylketonuria FeCl3 test with urine gives green color
• Severe mental retardation,Enamel hypoplasia & Vomiting in early infancy is seen
in Phenylketonuria
• Brain damage in phenylketonuria is due to accumulation of Phenylalanine
• Phenylketonuria is Autosomal recessive disorder
5. Transient Tachypnea of New born (TTN)
• Newborn with an early onset of dyspnea with chest retractions, expiratory grunting and cyanosis
following an uneventful normal preterm labor. On examination no cardiac murmurs are heard and
the lungs appear clear. On a plain X-ray there is evidence of prominent pulmonary vascular
markings and fluid lines in the fissures. The cyanosis improves with minimal oxygen. The most
probable diagnosis is Transient tachypnea of the newborn
• Transient Tachypnea of New born (TTN) is due to delayed clearance of lung fluids
• X – ray may show prominent vascular markings with prominent interlobar fissure
• A diabetic female at 39 weeks of gestation delivered a baby by elective cesarean section. Soon after
birth the baby developed respiratory distress. Chest X-ray shows opacity in right middle lobe
fissure. The diagnosis is Transient Tachypnea of New born (TTN)
• Transient tachypnea of new born (TTN) is commonly seen in Elective caesarean section
• Onset of respiratory distress is immediately after birth and it rarely lasts beyond 48 hrs
• Respiratory rate in a 2 month old, to label it tachypnea is 60
6. Acute paralytic polio

• IM injections and increased muscular activity increases the risk of paralytic polio
• Vaccine associated paralytic poliomyelitis is suspected if AFP develops within45 days of receipt of
OPV
• In Paralytic poliomyelitis Anterior horn cell & Autonomous nervous system are affected
• Paralytic polio is under surveillance by WHO for notification by National health Authorities
• Anterior horn cells is affected in spinal paralytic polio
7. SHORT STATURE
• Characteristic of XO chromosomal defect are Short stature, Webbed necked & Infertility
• Characteristic of Noonan syndrome are anti-mongoloid slant, pulmonary stenosis, short stature and
undescended testis.
• 45 X karyotype is seen in female with short stature, wide spread nipples and primary amenorrhoea
• The most common cause of short stature is Constitutional
• Height more than 3.5 SD below the mean for chronologic age is seen in pathologic short stature in
a child
• Growth rate more than 2 SD below the mean for chronologic age is seen in pathologic short stature
in a child
• Height more than 2 SD below the target height when corrected for midparental height is seen
in pathologic short stature in a child
• Thyroid Dyshormonogenesis shows short stature, lethargy, & constipation with goiter & low T4 and
elevated TSH
• Mentally retarded, has short stature, gait disturbance, squint and proximal spasticity in the lower
limbs with a swelling in front of the neck which moves with deglutition arising due to a low intake
of iodine less than 25microg/d is diagnosed to have neurologic cretinism
• Short stature is seen in Maternal deprivation syndrome & Hypothyroidism
• Short stature, secondary to growth hormone deficiency is associated with Normal body proportion.
• Recurrent attacks of polyurea, short stature, Serum Creatinine - 6 mg%, HCO3 - 16 meq, Na - 134,
K+ 4.2 & USG showing bilateral small kidneys is diagnosed as Nephronophthisis
• Short limbs compared to trunk & short stature is seen in critinism
• Growth retardation and propensity to hypoglycemia,short stature, micropenis, increased fat and
high-pitched voice is most appropriately diagnosed with Growth hormone deficiency
• Short stature, secondary to growth hormone deficeincy is associated with Normal body proportion
• A child presents with antimongoloid slant, pulmonary stenosis, short stature and undescended
testis is showing symptoms of Noonan syndrome
• High risk pregnancy Short stature primi
• Bone age corresponds to chronological age in Familial short stature
• Webbing of neck, short stature, increased carrying angle, low posterior hair line, primary
amenorrhea and short fourth metacarpal are characteristics of Turner syndrome
8. DEVELOPMENTAL MILESTONES
• Milestones during the first year of life is Social smile, Head control, Sits up The correct sequence in
the developmental & Crawls
• The sequence and time of attainment of milestones may vary among individual children
• Development always proceeds in a cephalocaudal sequence
• Presence of primitive reflexes is essential for attaining voluntary actions
• Mirror play developmental milestones is first to happen
• Moro's Reflex is not present from 3 months
• Motor function develops and differentiates early in a term newborn
• The milestones achieved at 13 months in children are Index finger approach, Walking & Single
words
• Mental retardation can be proved if delayed milestones and slow or retarded growth seen upto 18
yr
• Object permanence milestone develop at 9 months
9. PRIMITIVE REFLEXES
• Persistent Moro’s reflex at 12 weeks indicates Brain damage

• Presence of primitive reflexes is essential for attaining voluntary actions
• Persistence of Moro's reflex is abnormal beyond the age of 3rd month
• Moro's reflex is abnormal after 12 weeks
• Persistant Moro's reflex at 6-7 months indicates Brain damage
• Persistence of Moro's reflex is abnormal beyond the age of 6th month
• Atypical moro's reflex is seen in # clavicle, Shoulder dislocation & Brachial plexus injury
• Asymmetric Moro's reflex at birth is indicative of Erb's palsy
10. NEONATAL SEPSIS
• Neonatal sepsis is associated with an increased risk of neurologic damage in a jaundiced newborn
• Most common cause of Neonatal sepsis in hospital in India is Klebsiella
• Preterni babies are predisposed to Neonatal sepsis
• Late initiation of breast feeding is a predisposition for Neonatal sepsis
• Premature rupture of membranes predisposes to Neonatal sepsis
• Early Neonatal sepsis is due to organism in maternal genital tract
• Environmental factors cause late Neonatal sepsis
• Least observed laboratory finding in Neonatal Sepsis is Neutrophilia
• Neonatal sepsis and meningitis most common cause Streptococcus agalactacea
• Early neonatal sepsis occurs within (hours) 72
11. NECROTIZING ENTEROCOLITIS
• Necrotizing enterocolitis is complication of formula fed baby over human milk fed baby
• Peritoneal drainage by putting drains in the flanks is the treatment of choice for low birth weight
preterm baby showing clinical features of necrotizing enterocolitis with perforation
• Probiotics have been found beneficial for use in Necrotizing enterocolitis
• Prematurity is considered the MOST important risk factor for necrotizing enterocolitis
• A preterm baby with Patent ductus arteriosus may show Necrotizing enterocolitis
• Pneumatosis intestinalis is diagnostic of Necrotizing enterocolitis
• Neonatal Necrotizing enterocolitis is characterized by Abdominal distension,Metabolic
acidosis, Pneumoperitoneum & Decreased bowel sounds
• A premature neonate on top feeding develop abdominal destension and bleeding per rectum with
acute Upper RTI is diagnosed to have Necrotizing enterocolitis
• A neonate is suspected to be suffering from necrotizing enterocolitis (NEC). On further examination
and investigation, he is diagnosed to be Bell's stage I NEC. The management of choice would
be Conservative management with IV fluids and antibiotics
12. HEMORRHAGIC DISEASE OF NEW BORN
• A newborn infant showing multiple hemorrhagic, cutaneous lesions and does not respond to sound
stimuli with periventricular calcifications in CT is most likely caused by Cytomegalovirus
• Late onset hemorrhagic disease of newborn is characterized by Onset at 4-12 week of
age, Intracranial hemorrhage
• Intramuscular vitamin K prophylaxis at birth has a protective role in hemorrhagic disease of
newborn
• Thrombin time is abnormal in classic hemorrhagic disease of newborn
• Biliary atresia can predispose late onset Hemorrhagic disease of newborn (HDN)
• Warfarin therapy is associated with late onset Hemorrhagic disease of newborn (HDN)
• Case of hemorrhagic disease of newborn bleed on 2nd day is associated with factor 2, 7, 9, 10
13. KERNICTERUS (BILIRUBIN ENCEPHALOPATHY)
• Kernicterus is due to Unconjugated Hyperbilirubinemia

• Yellowish staining of Basal Ganglia is seen in Kernicterus
• Prematurity is a risk factor for Kernicterus
• Sulfonamide may cause Kernicterus in newborn
• The late features of kernicterus include Sensorineural hearing loss, Choreoathetosis & Upward gaze
palsy
• Risk of kernicterus is increased in Low level of serum albumin, Prematurity & Acidosis
• Drugs that can be used in kernicterus Barbiturates
14. PHOTOTHERAPY
• Structural isomerization in phototherapy is chiefly responsible for reduction in serum billirubin

• Bronze baby syndrome is due to Phototherapy
• For A full term, 80 hrs old new born baby develops jaundice 20mg% should be the minimum level of
serum bilirubin to start phototherapy
• Infants receiving phototherapy Should have their eyes patched during therapy
• Infants receiving phototherapy May develop diaorrhea
• Ideal treatment of B/L retinoblastoma is phototherapy
• Ideal management for premature, healthy infant weighing less than 1 kg is having jaundice with
serum bilirubin level of 5 mg% is phototherapy
15. EXCHANGE TRANSFUSION
• Partial Exchange Transfusion is best management option in neonatal polycythemia

showing intolerance to feed /abdominal distension & 72%PCV
• A 32 weeks premature infants, 900gm weight on the third days. The serum bilirubin is 13 mg%. The
treatment of choice is Exchange transfusion
• In Rh Iso Imunisation, exchange transfusion is indicated if Cord blood hemoglobin is less than 10 g
%, Cord bilirubin is more than 5 mg & History of previous sibling affected
• Indications for exchange transfusion are Unconjugated bilirubin > 18 mg/100 ml, Cord hemoglobin
< 10 mg/100 ml & Bilirubin protein ratio > 3.5
16. Neonatal jaundice
• About 50% of affected infants have moderately severe neonatal jaundice is hereditary
spherocytosis
• Neonatal Jaundice first time appears in the 3rd week by Galactossemia, Hypothyroidism & Breast
milk Jaundice
• Defective hepatic conjugation is seen in Neonatal jaundice
• Hypothyroidism, Jaundice due to breast milk & Galactosemia are cause for neonatal jaundice
manifesting for the first time in the second week
• G6PD deficiency is Associated with neonatal jaundice
17. RESPIRATORY DISTRESS SYNDROME
• Neutrophils play a crucial role in the pathogenesis of alveolar-capillary damage in adult respiratory
distress syndrome (ARDS)
• Air bronchogram in chest x-ray favour the diagnosis of respiratory distress syndrome (RDS) in new
born
• Respiratory distress syndrome can be diagnosed prenatally by determining Lecithin / Sphingomyelin
ratio as RDS is caused by deficiency of surfactant
• Respiratory distress syndrome in premature infants is due to inadequate secretion
of Dipalmitoylphosphatidylcholine
• To prevent Respiratory Distress Syndrome dexamethasone injection is given to a lady of 32 weeks
pregnancy
• Hyaline membranes and collapsed alveoli is most likely be observed in the lung during an autopsy
of a 2 week old infant who died of neonatal respiratory distress syndrome
• Respiratory distress syndrome in the newborn is commonly associated with Diabetic
pregnancy, Prematurity & Following an elective cesarean section
• Hyaline membrane disease shows FRC below the closing volume
• In hyaline membrane disease the pathology in the lung consists of Fibrin
• Respiratory distress syndrome in infants is seen in Babies of diabetics & Premature rupture of
membrane
• The clinical sign of hyaline membrane disease generally first appears In the first 6 hours of life
• Intercostal retraction & RR > 60/ min are signs of neonatal respiratory distress syndrome
• A 31 week pregnant lady delivers a child. In 4 hrs baby develops dyspnoea and cyanosis. X-ray chest
shows ground glass appearance. The diagnosis Hyaline membrane disease
• X-ray appearance in hyaline membrane disease can be Homogenous ground glass
appearance, Reticulonodular shadow or normal x-ray
• Granulomatous appearance of lung with air bronchogram in neonates represents Hyaline
membrane disease
• Phosphatidyl glycerol estimation is a reliable method of diagnosis Phosphatidyl glycerol estimation
is a reliable method of diagnosis
• The dose of betamethasone in prenatal to prevent respiratory distress syndrome is 12 mg every 24
hours
• Failure to initiate and maintain spontaneous respiration following birth is clinically k/a respiratory
distress syndrome
• Diffuse Alveolar Damage is the most characteristic feature of Adult Respiratory Distress Syndrome
(ARDS)
• Diagnostic criteria for acute respiratory distress syndrome is Pao2/Fio2 ratio is
• Mortality rates ranges between 40 to 65% in ARDS
• Pneumonia is commonly associated with ARDS
• ARDS is seen after 6 hours of birth
18. BRONCHIOLITIS
• Fever and mild respiratory distress, wheeze and exaggerated breathlessness with hyperluscency in
Chest x-ray & obstructive pattern of PFT suggest Bronchiolitis Obliterans
• RSVH(respiratory syncitial virus or adenovirus) is the commonest etiological agent of Bronchiolitis
• Antiviral agent of choice in a child with bronchiolitis is Ribavirin
• Hyperinflation of the chest is seen in Bronchiolitis
• Intercostal and subcostal retractions and extensive rhonchi on auscultation & chest X-rayshowing
hyperinflated chest suggest Bronchiolitis
• Bronchiolitis in a self-limiting viral illness secondary to respiratory syncitial virus
• Bronchiolitis predisposes children for later development of asthma
• Egg shell calcification is seen in bronchiolitis
19. Kangaroo Mother Care (KMC)
• Kangaroo Mother Care (KMC) is best for transport of the newborn with maintainance of warm
temperature
• Kangaroo Mother Care (KMC) Can also be given by father
• Kangaroo Mother Care (KMC) is for Effective thermal control
• Kangaroo Mother Care (KMC) is especially for low birth weight body
• Skin to skin contact, Exclusive breast feeding & Early discharge and follow-up are the components
of Kangaroo Mother Care (KMC)
20. COARCTATION OF AORTA
• Infants of diabetic mother are likely to have Coarctation of aorta

• Coarctation of aorta is the most likely cardiac lesion in a young adult who complains of headache,
dizziness and intermittent claudication with exercise
• In postductal coarctation of aorta, vessels involved in the formation of collateral are Intercostal
artery, Internal thoracic artery & Superior epigastric artery
• In post-ductal coarctation of aorta, collaterals may be formed by Vertebral artery, Suprascapular
artery & Subscapular artery
• Coarctation of aorta is an absolute indication for caesarean section in pregnancy associated with
heart disease
• Infective endocarditis, CCF & Intra cranial hemorrhage are causes death in coarctation of Aorta
• A 1-month-old boy is referred for failure to thrive. On examination, he shows feature of congestive
failure. The femoral pulses are feeble as compared to branchial pulses. The most likely clinical
diagnosis is Coarctation of aorta
• The clinical features associated with coarctation of aorta in older children are Upper body
hypertension, Prominent pulsation in neck & Fatiguableness, tiredness in leg
• A 30 year old woman with coarctation of aorta is admitted to the labour room for elective
caesarean section. Which of the following is the anaesthesia technique of choice General
anaesthesia
• High incidence of associated Bicuspid aortic valve, Left ventricular Hypertrophy & Diminution of
femoral pulsations are seen in Coarctation of Aorta
• Coarctation of Aorta is most commonly associated with Bicuspid Aortic valve
• Coarctation of aorta is associated with Turner's syndrome, Bicuspid aortic valve & Pulmonary
stenosis
• Antiboiotic Prophylaxis for infective endocarditis is indicated in Coarctation of aorta
• In coarctation of aorta the rib changes are seen from 4-9th
• Coarctation of aorta causes rib-notching on the chest radiography
21. ENURESIS
• Nocturnal enuresis, Night terror & Nightmare is seen in parasomnia

• Enuresis persists, and the patient is placed on desmopressin acetate (DDAVP). This medication
works via Increase water permeability and reabsorption in collecting tubules
• Most useful drug in Enuresis is Trimipramine
• Lowest recurrence in nocturnal enuresis is seen with Bed alarms
• Desmopressin nasal spray is very effective in control of enuresis
• The behaviour therapeutic falls in management of enuresis, The pharmacological drug of choice for
this case is Imipramine
• The commonest cause of Enuresis in children is Genetic factors
• Best treatment for enuresis is Bed alarm
• Nocturnal enuresis may be considered normal upto 6 years
22. PATENT DUCTUS ARTERIOSUS
• Patent Ductus Arteriosus is a common heart lesion in rubella

• Patent Ductus Arteriosus Treatment is closure of defect by ligation and division of ductus
• Hypoxia and immaturity are important in maintaining the patency of Patent Ductus Arteriosus
• A neonate born with congenital rubella is diagnosed of having patent ductus arteriosus (PDA) may
lead to death due to Cardiac failure
• A preterm baby with Patent ductus arteriosus shows Necrotizing enterocolitis, Continuous murmur
& Congestive heart failure
• A premature infant is born with a patent ductus arteriosus. In closure can be stimulated by
administration of Prostaglandin inhibitors
• Direction of blood flow through the patent ductus arteriosus is from aorta to left pulmonary artery
• In patent ductus arteriosus connection is between Aorta and pulmonary artery
• Spontaneous closure in patent ductus arteriosus occurs in some term infants
• Bacterial endocarditis is more frequent with small PDA
• Recurrent chest infection and congestive failure may develop patent ductus arteriosus
• A premature infant is born with a patent ductus arteriosus. Its closure can be stimulated by
administration of Prostaglandin inhibitors
• Large PDA (Patent ductus arteriosus) leads to Endocardial valvulitis , Eisenmenger syndrome & CHF
23. Reye's syndrome
• Reye's syndrome – histological finding is Glycogen depletion

• A child with a history of viral infection presented with metabolic lactic acidosis along with
hyperammonemia and convulsion. The most probable diagnosis is Reye's syndrome
• Reye's syndrome following influenza is most commonly associated with Type B
• Reye's syndrome is diagnosed by using with stain Oil-red-0 stain
• Reye's Syndrome is cause by Adeno virus, Herpes & Influenza
• Reye's Syndrome fequently complicates viral infections
• Reye's Syndrome may be precipitated by salictylates
• Prothrombin time is prolonged in Reye's Syndrome
• Cerebral edema is seen in Reye's Syndrome
• Aspirin is associated with Reye's Syndrome
• Metabolic acidosis, Increased serum transaminases & Respiratory alkalosis are seen in Reye's
syndrome
• Reye's syndrome is characterized by encephalitis, fatty liver and following biochemical changes
like Moderate elevation of SGOT and SGPT, Hypoglycemia & Hypoglycorrhoea
• Cause of Reye's syndrome in children is Influenza virus
24. CEREBRAL PALSY IN CHILDREN
• Low birth weight is a risk factor for Cerebral palsy in children

• In Cerebral palsy in children Seizures are common
• Mental retardation is commonly associated with Cerebral palsy in children
• 8 days old neonate with extensor posture Cerebral palsy & Hypoxic ischemic encephalopathy
• Spastic quadriplegia type of cerebral palsy is commonly associated with scoliosis and other
orthopedic problems
• Features of cerebral palsy are Athetosis, Ataxia,Flaccid paralysis & Spasticity/Hypotonicity
• The common type of cerebral palsy seen in hospitals is Spastic
• Cerebral palsy in which upper limb is less affected than lower limb is Spastic diplegia
25. EBSTEIN'S ANOMALY
• X-ray chest showing globular cardiomegaly with oligemic lung fields in a child is suggestive
of Ebstein's anomaly
• Wolff-Parkinson-White disease may be associated with Ebstein's anomaly
• Ebstein's anomaly is characterized by Downward displacement of an abnormal tricuspid valve into
right ventricle
• Congenital heart disease associated with decreased pulmonary blood flow is Ebstein's anomaly
• Intracavitary electrocardiography is a diagnostic aid in Ebstein's anomaly
• Ebsteins anomaly is associated with Tricuspid atresia
• Ebstein's anomaly is seen with intake of Lithium

Obstetrics
1. Placenta accreta
• Abnormal attachment of the placenta through the uterine myometrium as a result of defective
decidual formation (absent Nitabuch's layer).
• Placental villi are attached to the myometrium in placenta accreta
• Invade the myometrium in placenta increta
• Penetrate through the myometrium & extend to the uterine serosa in placenta percreta
• The abnormal adherence may involve all of the cotyledons (total placenta accreta), a few to several
cotyledons (partial placenta accreta), or a single cotyledon (focal placenta accreta).
• Two-thirds of patients with this complication require hysterectomy.
• In fact, those with a prior cesarean section carry a 25% risk
• Doppler USG- helpful in diagnosis.
2. Prelabour rupture of membranes
• Premature rupture of membrane may result after Fothergill's repair

• Cervical incompetence is characterised by PROM
• Pregnant women with trichomoniasis if untreated are at increased risk of premature rupture of
membranes and preterm delivery.
• Threatened abortion at 32 weeks of pregnancy should be treated with Antibiotics to avoid PROM.
• Rupture of membrane is said to be premature when it occurs at Prior to 1st stage of labour
• In a 24-28 weeks pregnancy with premature rupture of membrane Steroids,Antibiotics
and Tocolytics can be given
• Risk factors for poor progress of labour include Premature rupture of membrane
• Premature rupture of membranes predisposes to neonatal sepsis
• Respiratory distress syndrome in infants is seen in PROM
3. Vesicovaginal Fistula
• The most appropriate method for collecting urine for culture in case of vesicovaginal fistula
is Foley's catheter
• Vesicovaginal fistula repair surgery, the drainage should be done for 14 days
• Vesicovaginal fistula by obstructed labour manifests After 1st week of delivery
• A 52 year old lady presents with constant leakage of urine and dysuria two weeks after a
complicated total abdominal hysterectomy diagnosed of Vesicovaginal fistula is suspected. The
most important test for the diagnosis is Triple Swab Test

• A 52 year old lady with a vesicovaginal fistula after abdominal hysterectomy is not responding to
conservative management. Most useful and important next investigation is Cystoscopy
• Obstructed labour is the MOST common cause of vesicovaginal fistula in India
• Vesicovaginal Fistula is the Most common genital fistula in India
4. Threatened Abortion
• Mifepristone is not used in Threatened abortion

• Ectopic pregnancy differs from threatened abortion by Manifests at an early age
• A lady presented with features of threatened abortion at 32 weeks of pregnancy should be
given Antibiotics along with other measures are used to prevent and treat preterm labour,
especially in the setting of chorioamnionitis which occur in case of ruptured membrane.
• A negative pregnancy test excludes the diagnosis of Threatened abortion
• In threatened abortion, the size of uterus Corresponds to duration of amenorrhea
• The clinical diagnosis of threatened abortion is presumed when a bloody vaginal discharge appears
through a closed cervical os during First half of pregnancy
5. Intrauterine Death
• Alpha fetoprotein levels are increased in Intrauterine Death

• Artificial rupture of membrane (ARM) is contraindicated in Intrauterine death
• Robert’s sign is associated with intra uterine death of the fetus
• Intra-aortic gas is the earliest conclusive evidence of intrauterine death
• Intrauterine death at 36 weeks is left untreated waiting for spontaneous expulsion
• DIC can be seen in Intrauterine death
• Spalding sign is seen in Intrauterine death
6. Fetal circulation
• The primitive uteroplacental circulation is functionally established during end of first month.
• Fetal blood is returned to the umbilical arteries and the placenta through the Hypogastric arteries
• The immunoglobulin which passes the placental barrier in humans is IgG
• Trophoblast, Fetal capillary endothelium & Mesoderm are components of placental barrier
• The liver and heart of the fetus receive blood with very high oxygen saturation
• Maximum level of alpha feto protein is seen in Fetal serum
• Heart receives blood with high oxygen saturation
• Fetal Hb shows high pO2 saturation compared to adult Hb because Affinity to binding to DPG is
different in fetal Hb

7. PLACENTA
• Human chorionic gonadotropin is produced by the human placenta having LH-like activity
• The placental hormone that participates in stimulation of ductal growth in the mammary gland
during pregnancy is Human chorionic somatotropin (HCS)
• HBV viruses is least likely to cross placenta
• Placenta develops from Placenta frondosum & Decidua basalis
• Trophoblast, Fetal capillary endothelium & Mesoderm are constituent of placental barrier
• At term, ratio of weight of fetus to weight of placenta is 6 : 1
• Syncytiotrophoblast is the inner most part of placenta
• In the placenta, maternal blood comes in direct contact with syncytiotrophoblast
• Chorionic gonadotropin, Chorionic thyrotropin & chorionic corticotropin are placental hormones
• Progesterone production require fetal steroidogenic tissue
• Weight of placenta at term is 500 grams
8. Amniotic Fluid
• Best method for the diagnosis of lung maturity is Phosphtidyl glycerol estimation in amniotic fluid
• The presence of increased levels of Acetyl cholinesterase in amniotic fluid is an indicator of open
neural tube defect in the fetus
• Nile blue sulphatase test in amniotic fluid is for Skin maturity
• Amniotic fluid contains acetyl cholinesterase enzyme can be a diagnosis of Open spina bifida
• Amniotic fluid is maximum at 38 weeks of pregnancy
• Amniotic fluid index (AFI) is calculated by adding the vertical depths of the largest pocket in each of
four equal uterine quadrants
• Fluid restriction may lower the AFI
• Significant hydramnios is defined by an index greater than 24 cm
• Prenatal diagnosis at 16 weeks of pregnancy can be performed using Amniotic fluid
• The amount of amniotic fluid at 12 weeks of pregnancy is 50 ml
• Amniotic fluid at 38 weeks in normal pregnancy is 800 cc
• pH range of amniotic fluid is 7.0 - 7.5
• pH of amniotic fluid at later weeks of gestation is 7.2
• Golden colour amniotic fluid is seen in Rh incompatibility
• The amniotic fluid is completely replaced in every 3 hours
• The major contribution of the amniotic fluid after 20 weeks of gestation is Fetal urine
• At 15 weeks of gestation, increased alpha fetoprotein in amniotic fluid is seen in Intrauterine death
• Risk of amniotic fluid embolism is greatest During labour
• Amniotic fluid is mainly produced by Fetus
• Surfactant appears in amniotic fluid at the gestational age of 32 weeks
• The amniotic fluid is in balance by Excretion by fetal kidneys, Maternal hemostasis & Fetal intestinal
absorption
• Antenatal screening is done using Cord blood, Amniotic fluid & Chorionic villi
• Lendrum's stain is done for Amniotic fluid embolism
9. Umbilical Cord
• Length of umbilical cord is 30-100 cms

• The folds of Hoboken are found in Umbilical cord
• Two arteries and the left vein are found in Umbilical cord
• Distal parts of the umbilical arteries form the medial umbilical ligaments, and the proximal portions
remain open as the superior vesical arteries
• Umbilical vein becomes Ligamentum teres
• The umbilical cord stump of a newborn most frequently sloughs off about the 10th day after
delivery
• Right vein disappear in umbilical cord
• Umbilical vein carries oxygenated blood
• Umbilical vesicle attains full development in 4 week
• Wharton's jelly, 2 arteries and 1 vein ,Allantois are the constituents of umbilical cord.
• Median umbilical ligament is derived from Urachus
10. Physiological Changes During Pregnancy
• Respiratory alkalosis is seen during pregnancy

• Decreased peripheral vascular resistance in pregnancy
• ↑ed cardiac output, & tidal volume is seen during pregnancy
• Shift of apical impulse laterally and upwards in left 4th intercostal space is physiological in last
trimester of pregnancy seen during pregnancy
• Fall in serum iron concentration,Increase in serum iron binding capacity & Increase in blood oxygen
carrying capacity are seen during pregnancy
• Globulin, Fibrinogen & Leukocytes are increased in pregnancy
• Sodium retention occurs in pregnancy
• Sr. potassium is decreased in pregnancy
• Increased BMR is seen in pregnancy
• Insulin resistance in pregnancy is because of Human placental lactogen & Progesterone
• During pregnancy the maternal blood volume increases by 50%
• Vital capacity remains unaltered in pregnancy
• Fibrinogen level increases in pregnancy
• Maximum increase in cardiac output occurs by 30th week
• Net weight gain in pregnancy is 24 lb or 12 kg
• In pregnancy Increased MCV & glomerular flow
• Fall in free T4/T3 in 3rd trimester
• TSH falls in the first and second trimester but increases in the third trimester
• There is an increase in Thyroid binding globulin
• Decrease in Urea , Creatinine & Reabsorption of glucose
• Tidal volume and resting minute ventilation increase during late trimester
• Functional residual capacity and the residual volume are decreased
• Total pulmonary resistance reduced
• Systemic vascular resistance is decreased during third trimester of a normal pregnancy
• Chorionic gonadotropin, Chorionic thyrotropin & Chorionic corticotropin are placental hormones
• Factor XIII reduction is consistent with normal pregnancy
• Decline of 5-10 mm of Hg is seen in in diastolic blood pressure in pregnancy
• Prolactin is Highest during pregnancy and fall during lactation
11. Diagnosis In Pregnancy
• Supine hypotension is characteristic of 3rd trimester of pregnancy

• Signs positive in early pregnancy are Hegar's sign, Palmer's sign & Goodell's sign and Osiander's
sign
• Braxton-Hicks contraction, Amenorrhea both are seen in 2nd trimester of pregnancy
• An expectant mother feels quickening at 16-20 weeks
• Hegar's sign is feeling the cervix and the body of bulky uterus separated because of softened
isthmus at 6 - 10 weeks of gestation
• Osiander's sign means Pulsation in the lateral vaginal fornix
• Chadwick's sign is Bluish discoloration of vagina
• Fetal movements, Fetal heart sounds & Fetal skeleton seen an X-ray are the definitive signs of
pregnancy
• Braxton — Hicks contractions Occur during most of the months of pregnancy
• In normal pregnancy ↑ed number of lactobacilli is seen in vagina
• Fat droplets occur in the cytoplasm of the epithelium in breast at pregnancy
• Cuboidal luminal epithelial cells of breast show vacuolization
• The terminal lobular units of breast are most affected during pregnancy
• In Pregnancy uterus shows both hypertrophy and hyperplasia at the same time
• Palmer’s sign indicate Rhythmic contraction of uterus
• Hegar's sign be elicited at 8 weeks
• pH of vagina in pregnancy is is 4-6
• Uterus reaches up to umbilical level at 24 weeks
• During pregnancyMelasma over face is seen
12. Methods of Obstetrical Examination
• Hasse's formula used in pregnancy to Estimate fetal age

• Best parameter for estimation of fetal age by ultrasound in 3rd trimester is Femur length

• Radio - immunoassay is the most sensitive method of quantitative measurement of human
chorionic gonadotrophin
• The earliest diagnostic test of pregnancy is Beta HCG
• Ideal number of antenatal visits 12-14
• Minimum number of antenatal visits should be 3
• Manual appreciation of fetal parts and fetal movement by examination is earliest possible
at 20 weeks of gestation
• Expected date of delivery is calculated by Nine calendar months plus 7 days, 280 days or 40
weeks,10 lunar months
• Head size, Fundal height & Abdominal circumference are used to assess intrauterine growth
retardation
• During early pregnancy, the trophoblastic cells secrete Human chorionic gonadotropin (hCG) in
order to maintain the corpus luteum
• HCG can be detected in the urine prior to the first missed period
• Leopold maneuver is used for Examination of abdomen
• Minimum hCG level that a urine pregnancy test can detect is 5 m IU/ ml
• Fetal blood, Maternal blood & Amniotic fluid can be used for establishing antenatal diagnosis
• Biparietal diameter, Abdominal circumference of fetus & Femur length are commonly used for
estimation of gestational age in mid trimester
• Plasma levels of hCG during pregnancy doubles every 2 days
• hCG is secreted by Syncytiotrophoblast
• HCG can be detected as early as 8-9 days after conception
• In pregnancy, calculation of EDD (expected date of delivery) considers First day of last menstruation
• Exact number of weeks between last menstrual period [LMP] and expected date of delivery
[EDD] 40 weeks
13. ROLE OF USG IN OBSTETRICS
• Transvaginal USG can detect fetal cardiac activity in 6 weeks

• Earliest detection of pregnancy by ultrasound is by Gestation sac
• Study of fetal parts in first trimester with least radiation hazard is USG
• Investigation of choice in diabetic mother with a doubtful abnormal fetus USG
• Earliest fetal anomaly to be detected by USG is Anencephaly
• Accurate diagnosis of anencephaly on ultrasound can be done at 10 weeks of gestation
• Ultrasound is done in 1st trimester for Multiple pregnancy, Fetal anomalies & To estimate
gestational age
• Congenital anomalies that can be identified by USG Hydrops fetalis, Esophageal atresia
& Anencephaly
• Best time for diagnosing fetal abnormalities by USG 13-19 weeks of pregnancy
• Embryonic structure, identified earliest on USG, for confirmation of pregnancy is Gestation sac
• First trimester USG finding in Down syndrome is Nuchal translucency
• Best parameter by USG to assess fetal maturity Biparietel diameter at 12 weeks
• Best time to do USG in pregnancy, if it is to be done once in entire pregnancy, would be18-22 weeks
• Most accurate assessment of gestational age by USG is done by Crown rump length
• Ectopic pregnacny, characteristic finding in USG is Absence of gestational sac in uterus
• Adenexal mass,Hyprechoic ring & Pseudo sac are signs /features of ectopic pregnancy on USG
• USG can detect gestation sac earliest at 5-6 weeks of gestation
14. Maternal Pelvis
• Most important diameter of pelvis during labour is Interspinous diameter of outlet

• Female pelvis as compared to the male pelvis has Shallow and wide symphysis pubis
• Maximum diameter of pelvic inlet is Transverse diameter
• Diagonal conjugate measurement at pelvic inlet can be assessed directly
• To obtain true conjugate 1.5 cm should be subtracted from the diagonal conjugate
• True pelvis refers to Lower part of pelvis
• Shortest diameter of the pelvic outlet is Posterior sagittal diameter
• Diagonal conjugate is defined as the distance between Lower border of symphysis pubis and the
sacral Promontory
• Interspinous diameter is the smallest diameter of the pelvis in the midplane
• A pelvis characterized by an anteroposterior diameter of the inlet greater than the transverse
diameter is classified as Anthropoid
• The smallest anteroposterior diameter of the pelvic inlet is called the Obstetric conjugate
• Deep transverse arrest is most commonly seen in Android pelvis
• Gynecoid is the most common type of female pelvis
• Subpubic angle is 85°
• The distance from the upper end of sacrum to lower border of pubis corresponds to Diagonal
conjugate
• Transverse diameter of the female mid-pelvic plane is 10.5
15. Fetal Skull
• Occipito frontal is the longest diameter of fetal skull after mentovertcal

• Sub occipitofrontal diameter of fetal skull is 10 cm
• The characteristics of caput succedaneum include Crosses midsuture line & It is a diffuse
edematous swelling of the soft tissues of the scalp
• Anterior fontanelle and supraobital ridge is felt in the second stage of labour in Brow
presentation On per vaginal examination
• Posterior fontanelies are osified at At term
• 6 number of fontanelles present in a new born child
• Closure of coronal sutures starts at age of 30-35 years
• Anterior fontanelle ossifies by 18 months
• Caput succedaneum in a newborn is due to Collection of sero-sanguineous fluid in the scalp
• The metopic suture closes by the age of 6 years
16. Normal labour-Causes and Physiology
• Prostaglandins are the first to cause uterine contraction and lowering of blood pressure
• Braxton — Hicks contractions Occur during most of the months of pregnancy
• True labour pain is Painful uterine contraction
• Formation of the bag of waters is seen in true labour
• Progressive descent of presenting part is seen in true labour pain
• Average pressure of uterine contractions during the first stage of labour is 30 mm Hg
• Engagement in primigravida occurs at Beginning of labour
• During uterine contraction of labour, the uterine blood flow Decreases
• True labour differs from false labour by Painful uterine contractions,Progressive effacement and
dilatation of the cervix & Pain often felt in front of the abdomen or radiating towards the thighs
• Pressure of normal uterine contractions is between 190-300 Montevideo units
• Bag of waters is a sure sign of labour
• Cervical ripening is mainly due to the action of PGE2
• Maximum cervical dilatation during labor is 10 cm
• True labour pains is represented by show
17. MECHANISM OF NORMAL LABOUR
• Flexion, Extension & Internal rotation and Descent are the cardinal movements of the head in
normal labour.
• Suboccipitofrontal is the commonest diameter of engagement
• Engagement in primigravida occurs at Beginning of labour
• Engagement of fetal head is When the widest diameter of the presenting part has passed through
the pelvic inlet
• Engagement of foetal head is with reference to Biparietal diameter
• The cardinal movements during normal labour occur inorder as Engagement, internal rotation,
delivery of head, restitution, external rotation
• One fifth of the head may be palpable per abdomen during engagement of the head
• The vertex will be at the level of ischial spine during engagement of the head
• The biparietal diameter has passed through the pelvic inlet in engagement
• The internal rotation in mentoposterior position is 3/8th of circle
• Maximum cervical dilatation during labor is 10 cm
• During active labor, cervical dilatation per hour in primigravida is 1 cm/hour
18. Stages of Normal Labour
• Latent phase of labour is followed by Accelerated phase

• CCF is most likely in pregnancy at 3rd stage of labour
• Second stage of labor starts from Full dilatation of cervix
• Expulsion of the fetus, Increase in contraction & Cervical dilatation are seen in 2nd stage of labor
• From full dilatation of cervix to complete birth of baby is 2nd stage
• Birth of infant to delivery of placenta is 3rd stage of labour.
• Pressure inside uterus in 3rd stage is 100-120 mm Hg.
19. INVERSION OF UTERUS
• After a full term normal delivery patient went into shock. Most probable cause is Inversion of
uterus
• Common cause of death in inversion of uterus Hemorrhage
• Complication of manual removal of placenta is Inversion of uterus
• Inversion of the uterus, a complication is noticed in Third satge of labour
20. VERSION
• Indication of internal podalic version is Transverse lie of second twin

• Contraindication to External Cephalic Version are Contracted pelvis, Antepartum hemorrhage
& Multiple pregnancy
• The danger of internal podalic version in obstructed labour is Rupture of lower uterine segment
• Internal podalic version is done under General anaesthesia
• Incorrect about external cephalic version is Done at 34 week, Abruption of placenta is a
complication & Done under general anesthesia
• External cephalic version is contraindicated in Twins, Placenta previa
• External cephalic version (ECV) is CONTRAINDICATED in PIH
• A full-term multigravida is having breech presentation. Ideal management in this case would
be External cephalic version followed by vaginal delivery
• Ideal management of 37 weeks uncomplicated breech pregnancy is External cephalic version and
trial of vaginal delivery
21. CORD PROLAPSE
• Least chances of cord prolapse are seen in Frank breech

• Cord prolapse is most commonly associated with Transverse lie
• Best treatment of Cord prolapse is Cesarean section
• Contracted pelvis, Hydramnios & Placenta previa are etiology of cord prolapse
22. Cesarean Section
• Indications for caesarean section in pregnancy are Aortic stenosis, M.R. & Aortic regurgitaion
• Lower Segment Caesarean section (LSCS) can be carried out under
• General anaesthesia
• Spinal anaesthesia
• Combined Spinal Epidural anaesthesia
• Absolute indication for caesarean section in pregnancy are
• Advanced Carcinoma Cervix
• Central Placenta Praevia
• Contracted Pelvis
• History of previous classical CS is the contraindication for trial of normal labour after caesarean
section
• Cephalopelvic disproportion is an absolute indication for Caesarean section.
• In classical caesarean section more chances of rupture of uterus is in Upper uterine segment
• Best management in Mento-posterior presentation Caesarean section
• Absolute indication for caesarean section is Type IV placenta previa
• Ideal management of a 37 weeks pregnant elderly primigravida with placenta praevia and active
bleeding is Caesarean section
• Placenat accrete complicates third stage of labour and is associated with a past history of caesarean
section
• Incidence of scar rupture in previous lower segment caesarean section 1%
• Risk of rupture of uterus with previous classical caesarean section is 4-8%
23. Ventouse Delivery
• There is Less maternal trauma by vacuum as compared with forceps

• Cephalohematoma is more common with vacuum extraction
• Retinal hemorrhage, intracranial hemorrhage and subgaleal hemorrhage are more common in
ventouse delivery than forceps
• Foetal macrosomia, Face presentation & Transverse lie are contraindications of ventouse
extraction
• Ventouse can be used to treat deep transverse arrest
• In deep transverse arrest with adequate pelvis, best mode of delivery will be Ventouse
• Ventouse extraction is done in Delay in first stage due to uterine inertia
• Ventouse extraction is done in Delay in descent of high head in case of second baby of twins
• Ventouse application, the prerequisite is Head engaged
• During application of the cup in Ventouse, 'knob' of the cup points towards Occiput
• Pressure in ventouse assisted delivery is 0.8 kg/sq.cm

24. Abnormal uterine action
• Bandl's ring is also called as Retraction ring

• Constriction ring Also called Schroeder's ring
• Constriction ring Can be caused by injudicious oxytocin use
• Inhalation of amyl nitrate relaxes the Constriction ring
• Cervical dystocia is usually present at Level of external os
• Hypertonic dysfunctional labour is characterised by early Fetal distress
• Bandl's ring is associated with Cephalopelvic disproportion
• Bandl's ring is seen in Obstructed labour & Injudicious use of oxytocins
25. Cervical Ripening
• Mifepristone is an antiprogestin agent used in Cervical ripening

• RU 486 is used in Cervical ripening
• Prostaglandin E2, Progesteron,Oxytocine & Misoprostol are used for cervical ripening during
pregnancy
• Induction of abortion is best by PGE2 gel
• Laminaria tent & Mifepristone & misoprostol are used in Ist trimester MTP
• Laminaria tent is made from seaweed
• Laminaria tent is used for the dilatation of the cervix
• Laminaria tent has got a thread to facilitate removal
• Bishops score includes Dilatation ,Effacement,Softening of cervix & Station of head
• Bishop scoring of more than 6 indicates labour has begun
• Prostaglandin tablet methods for induction of labour should not be used in patient with previous
lower segment caesarean section
• Bishop's classification is used for Requirement of induction for labour
26. Uterine rupture
• Indicators of impending uterine rupture during labour include Fetal distress, Hematuria & Fresh
bleeding per vaginum
• Uterine rupture is least common with LSCS
• In classical Cesarean section more chances of rupture of uterus is in Upper uterine segment
• The usual site of spontaneous rupture of the intact uterus during pregnancy is the Body of the
uterus
• Bleeding in rupture of the uterus associated with a large broad ligament hematoma is controlled
most simply by Ligation of hypogastric artery
• In Uterine rupture following illegal abortion air under both sides of diaphragm is visualized
• Risk of rupture of uterus with previous classical cesarean section is 4-8%

27. POST PARTUM HEMORRHAGE
• Uterine atony is the commonest cause of postpartum haemorrhage in multipara

• The amount of blood loss in postpartum haemorrhage is more than 500 mL
• Macrosomia, Twin pregnancy & Hydramnios are the complications during pregnancy that increase
the risk of postpartum hemorrhage (PPH)
• Anemia, Grandmultipara & APH are the risk factor for Post Partum Haemorrhage (PPH)
• The drugs are used in the treatment of postpartum haemorrhage are Misoprostol, Carboprost
& Methyl ergometrine
• Epidural analgesia,Cervical laceration, Prolonged labour & Over distension of uterus can lead
to postpartum hemorrhage
• The causes of post partum hemorrhage in a contracted uterus are Vaginal tear & Cervical laceration
• Maximum chances of post partum Hemorrhage are seen in Multiparity
• Post partum hemorrhage is blood loss of 500 cc or more within 24 hours of the beginning of
3Rd stage of labour
• During pregnancy, fibroid may have Post partum hemorrhage
• Post-partum hemorrhage is a common causes of maternal mortality
28. Rh NEGATIVE PREGNANCY
• To determine the correct amount of RhoGAM (anti-D immune globulin) that should be
given Kleihauer-Betke laboratory test should be done.
• The test used to differentiate between maternal and fetal blood in a given sample is Apt test
• Most severely affected child in Rh-isoimmunisation patient is Rh negative mother with Rh positive
in 2nd child
• In an Rh negative mother who has delivered an Rh positive baby, prophylactic anti D is indicated If
the Indirect Coomb's test (ICT) negative
• The dose of anti D gamma globulin given after term delivery for a Rh negative mother and Rh
positive baby is 300 micro gram
• The antigen lacking in Rh negative person is D
• Anti-D Rh is given for Rh positive father,Rh negative mother
29. Forceps Delivery
• Mitral valve stenosis patient benefit by having a forceps-assisted vaginal delivery at the time of
delivery
• Infant showing asymmetric Moro reflex involving the right arm, cynosis & labored respiration
with decreased breath sounds in the right chest post low forceps delivery may be due
to Ipsilateral paralysis of the diaphragm
• Retinal hemorrhage, intracranial hemorrhage and subgaleal hemorrhage are more common in
ventouse delivery than forceps
• Less maternal trauma by vacuum as compared with forceps
• Cephalohematoma is more common with vacuum extraction
• Forceps delivery is indicated in
• Face presentation
• Occipitoposterior
• After warming head in breech
• Prolonged second stage of labor
• In a case of prolonged labour, fetal occiput fails to spontaneously rotate anteriorly and caused
persistent occiput posterior presentation. The recommended management is Manual or forceps
rotation followed by forceps delivery
• The after coming head of breech chin to pubes is delivered by Manual rotation and extraction by
Piper's forceps
• For delivery of the aftercoming head in breech presentation Kielland's foceps, Das's variety
forceps & Mauriceau smellie, veit technique are used
• In face presentation, outlet forceps delivery can be accomplished successfully in Right mento-
anterior & Direct anterior positions
• Keilland's forceps facilitates correction of asynclitism of head
• The most important point of reference in the use of forceps is Station of biparietal diameter
• Head engaged and reached the pelvic floor can be treated using Outlet forceps
• Outlet forceps delivery is safest in maternal heart disease
• Prerequisite for applying forceps are
• Aftercoming head of breech
• there should be no CPD
• Foetal head should be engaged
30. PARTOGRAM
• Assessment of progress of labour is best done by Partogram

• Normal partogram include
• Descent of head in Y – axis
• Sigmoid shaped curve
• Alert line followed 4 hours later by action line
• Partogram helps in detecting Obstructed labour
• Partogram is a graphic record of Labour
• Partogram is the graphical record of cervical dilatation in centimeters against duration of labour in
hours
31. Preeclampsia
• Anti-phospholipid antibody, Gestational diabetes & Molar pregnancy are predisposing factor for
Preeclampsia
• Specific treatment of severe pre eclampsia is Magnesium sulfate
• Duration of latent phase of labour is affected by Pre-eclampsia
• Complete hydatidiform mole is associated with preeclampsia
• Pre-eclampsia is associated with placental abruption
• Low maternal serum 25-hydroxyvitamin D is associated with Pre-eclampsia
• There is decrease in in GFR is expected in a 30-year-old lady with pre-eclampsia
• Polyarteritis nodosa poses the greatest risk for development of pre-eclampsia
• Pregnant multigravida having pre-eclampsia & seizures should be treated with Pritchard's (MgSO4)
regimen
• Serum uric acid is known as ‘biochemical marker of pre-eclampsia’
• Doppler ultrasonography in IUGR & Preeclampsia shows notch in Uterine artery
32. Eclampsia
• Eclampsia, with given IV magnesium sulphate. The baby was resuscitated and transferred to the
NICU. 12 hours later, the baby showed hypotonia, lethargy, constricted pupils and two episodes of
seizures. The staging of HIE is 2
• The single most effective drug in eclampsia is Magnesium sulphate
• Hepatic infarcts are seen in Eclampsia
• Magpie’ regime for a patient with eclampsia is initiated following which respiratory rate is 6/minute
and the tendon reflexes are not elicitable should be managed with Inject calcium gluconate 10 ml
over 10 minutes
• Loss of deep tendon reflexesis the earliest sign of magnesium toxicity in a patient with eclampsia on
treatment with magnesium sulphate
• History of eclampsia classes as a high risk pregnancy
33. ECTOPIC PREGNANCY
• The commonest complication of pregnancy after complete treatment of genital tuberculosis

is Ectopic pregnancy
• Ectopic pregnancy is a reported complication of calendar method
• IUCD with highest incidence of ectopic pregnancy is Progestasert
• Condoms has the least risk of ectopic pregnancy
• In comparing laparoscopic salpingostomy vs. laparotomy with salpingectomy for the treatment of
ectopic pregnancy, laparoscopic therapy results in Decreased hospital stays
• Most sensitive diagnosis test for ectopic pregnancy Transvaginal USG
• The cause of fetal death in ectopic pregnancy is postulated as Vascular accident
• Hormone responsible for decidual reaction and Arias stella reaction in ectopic pregnancy
is Progesterone
• Medical treatment of ectopic pregnancy should be offered to those patients whose hCG level is less
than 10,000 IU/L and the size of the mass is less than 4 cms
• 6 weeks of amenorrhoea p,pain in abdomen; USG shows fluid In pouch of douglas. Aspiration yields
dark color blood that fails to clot. Most probable diagnosis is Ruptured ectopic pregnancy
• Acute abdominal pain , prolong amenorrhoea with collection of fluid in the pouch of douglas and
empty gestational sac are suggestive of ectopic pregnancy
• Ectopic pregnancy is most commonly associated with Tubal inflammatory diseases
• Most common manifestation of ectopic pregnancy is Pain abdomen
• In Interstitum part of fallopian tube ectopic pregnancy will have longest survival
• Ectopic pregnancy Associated with decidual reaction
• In ectopic interstitial ring sign is seen
• Potassium Chloride, Methotrexate & Actinomycin D are used in medical management of ectopic
pregnancy
• In Presence of fetal heart activity the medical treatment of Ectopic pregnancy is contraindicated
• Salpingo-oophorectomy is not done in ectopic pregnancy
• In a nulliparous woman, the treatment of choice in ruptured ectopic pregnancy is Linear
salpingostomy
• Ectopic pregnancy differs from threatened abortion by that it Manifests at an early age
• Commonest cause of ectopic pregnancy is Previous salpingitis
• Causes of ectopic pregnancy includes IUCD, & Tubal ciliary damage
• Commonest site of ectopic pregnancy is tube
• Commonest type of ectopic pregnancy with rupture is Isthmic
• In a young patient with abdominal pain and feature most suggestive of ectopic pregnancy
is Increase beta HCG in urine
• The most consistent sign in disturbed ectopic pregnancy is Vaginal bleeding
• The expelled products in ectopic pregnancy originate from Decidua vera
• Pathognomonic of ectopic pregnancy is Decidual casts
• Best endometrial reaction In ectopic pregnancy is Decidual reaction without chorionic villi
• Medical treatment of ectopic pregnancy is methotrexate
• Absolute contraindication to intra-uterine device is History of ectopic pregnancy
• Ectopic pregnancy is commonest in ampulla of fallopian tube
• Ectopic pregnancy can be ruled out on ultrasound by Finding foetus in uterus
34. MULTIPLE PREGNANCY- FEATURES AND DIAGNOSIS
• The placenta of twins may be Dichorionic and diamniotic in MZ twins

• Separate chorion and amnion is a feature of dizygotic twins
• Cephalic-cephalic is the commonest twin presentation
• Twin peak sign seen in Diamniotic dichorionic
• After embryonic disc fusion, conjoint twin is formed.
• According to Hellin's law chances of twins in pregnancy are 1 in 80
• Monochorionic monoamniotic twin occurs if division occurs > 8 days
• If division of fertilized egg occurs at 4-8th day what kind of mono zygotic twin pregnancy will it give
rise to Diamnionic monochorionic
• Commonest twin presentation is Vertex-vertex
• Identical twins may not have Same finger print pattern
• Most common type of twin pregnancy is Diamniotic monochorionic twins
• Twin pregnancy, but due to two different men is called Superfecundation
• Fraternal twins are Dizygotic twins
35. ABRUPTIO PLACENTA
• Consumptive coagulopathy is most commonly found in Abruption placenta

• Polyhydramnios Complications include placental abruption, uterine dysfunction, and postpartum
hemorrhage
• ARM + syntodrip + arrange blood is choice of management in IUFD with abruption placenta
• A pregnant patient presents with abdominal pain with twin gestation of 34 weeks and bleeding PV.
The most probable diagnosis is Abruptio placenta
• Abruptio placentae is the most frequent cause of spontaneous abortion in the first trimester of
pregnancy
• Cocaine abuse,Folic acid deficiency, Cigarette smoking & Pre-eclampsia are associated with
placental abruption
• Features of abruption placenta mixed variety includes acute intense abdominal pain followed by
slight vaginal bleeding, severe pallor, tense tender and rigid uterus, difficult to make out fetal parts,
absent fetal heart sounds, diminished urine output and markedly low hemoglobin.
• Page classification is the clinical classification system for abruptio placenta
• Couvelaire uterus is seen in Abruptio placentae
• Causes of DIC include Abruptio placentae
• Hypertension in the pregnancy is important predisposing factor for Abruptio placentae
• Abruptio placentae showsTender and hard uterus & Continuous bleeding per vaginum
36. POLYHYDRAMNIOS/ HYDRAMNIOS
• Complications include placental abruption, uterine dysfunction, and postpartum hemorrhage are
seen in polyhydramnios
• Polyhydramnios is associated with Diabetes,Anencephaly, Open spina bifida & Tracheo esophageal
fistula
• Amniocentesis is the treatment of choice in pregnant women with polyhydramnios and marked
respiratory distress at 35 weeks of gestation
• Cleft palate is associated with polyhydramnios
• Clinical signs of Hydramnios can be demonstrated when fluid collection is more than 2 ltr.
• Causes of Hydramnios are Twins,Oesophageal atresia or Anencephaly
• ARM is contraindicated in Hydramnios
• Feature of diabetes mellitus in pregnancy is Hydramnios
• Hydramnios is complicated by Placenta abruptio, Pre-eclampsia & Atonic Hemorrhage

37. Involution of the Uterus
• Retention of urine and constipation shows normal physiology of puerperium

• In normal puerperium in Involution of uterus At the end to the 6 weeks, becomes non pregnant
state
• In normal puerperium in Involution of uterus The number of muscle fibres is not decreased but
there is substantial reduction of the myometrial cell size
• In normal puerperium in Involution of uterus Weight of uterus about 60 gram at end of six weeks
• Rate of involution of an organ shown in the picture below is 1.25 cm per day
• Involution of uterus take 6 weeks
38. EPISIOTOMY
• Scar endometriosis can occur following Episiotomy, Hysterotomy or Classical Cesarean Section
• A primipara is in labor and an episiotomy is about to be cut. Compared with a midline episiotomy,
an advantage of mediolateral episiotomy is Less extension of the incision
• Most suitable method of treating 4 inch size episiotomy hematoma is by Evacuation
• The most important step in the treatment of a badly infected episiotomy is Drainage
• Episiotomy is best done Mediolaterally
• Advantages of median episiotomy over mediolateral episiotomy are Less blood loss, Easy repair
& Muscles are not cut
39. OLIGOHYDRAMNIOS
• Oligohydramnios is related to Renal Agenesis

• Oligohydramnios is the condition where the liquor amnii is deficient in amount to the extent of less
than 200 ml at term.
• Sonographically, oligohydramnios is defined when the maximum vertical pool of liquor is less than 2
cm or when amniotic fluid index (AFI) is less than 5 cm
• Oligohydramnios is seen in Renal agenesis, IUGR & Postmaturity
40. BREECH PRESENTATION
• Most common breech presentation is Left sacroanterior

• Percentage of breech at term is 3 %
• Fetal malformation , Uterine anomaly & Cornual implantation of placenta are associated with
breech presentation at normal full term pregnancy
• Prematurity is the commonest cause for breech presentation
• LEAST chances of cord prolapse are seen in Frank breech
• Causes of breech presentation are Hydramnios,Septate uterus,Hydrocephalus, Placenta praevia
& Pelvic contracture
• Recurrent breech presentation is seen In Congenital uterine anomaly
• Breech presentation is mostly mistaken for Face presentation
• In breech, engagement takes places earliest in frank
41. Placenta Previa
• Anti-D administration, Corticosteroids & Blood transfusion are included in the expectant
management of placenta praevia
• In Browne's classification of placenta previa, the placenta covers the internal os when closed but
not when fully dilated is Type 3
• The initial hemorrhage is usually painless and fatal in placenta praevia
• Per vaginal examination is contraindicated in a patient with placenta previa prior to term.
• There may be torrential bleeding if PV is done in a patient with placenta previa.
• Expectant management of placenta praevia by Macafee and Johnson method
• Placenta previa is characterized by Painless , Causeless & Recurrent bleeding
• Expectant line of management in placenta previa is contraindicated in Active labour
• Premature labour is common in placenta previa
• The best way to diagnose the degree of placenta previa is Trans vaginal sonography
• Placenta previa mouth is associated with Large placenta, Previous C. S. scar & Previous placenta
previa
• Incidence increases by two fold after LSCS
• Conservative management is contraindicated in a case of Placenta previa in Evidence of fetal
distress, Fetal malformations & Women in labour
• Termination of pregnancy in placenta previa is indicated in Active bleeding, active labour & Fetal
malformation
• Cesarean section is absolutely indicated in Type IV placenta previa
• A case of central placenta previa with anencephaly fetus should be delivered by Cesarean section
• Vaginal delivery is contraindicated in Central placenta previa
42. PRETERM BABY
• A preterm baby developed bullous lesion on the skin soon after birth. The X- ray shows periostitis
should be next investigated for VDRL for mother & baby
• Incidence of undescended testis in preterm infants is 30%
• Color, Heart rate & Muscle tone is used in a preterm infant to assess need for resuscitation
• Apnoea in a Preterm baby are Associated with bradycardia.
• Apnoea in a Preterm baby are Leads to hypoxia
• Apnoea in a Preterm baby are May cause cyanosis
• Breast feeding is best for both preterm & term
• Impedence technique is the best way to monitor the baby's breathing and detect apnaea
• Decreased subcutaneous fat and brown fat, Large surface area in relation to body weight & Less
oxygen consumption are the factors that contribute to hypothermia in preterm babies
• Blood volume in preterm neonate is 90 ml/kg
• Late metabolic acidosis is seen in Preterm baby getting cow milk
• Preterm infant is defined as Born < 37 weeks
• Physiological jaundice in preterm infant lasts upto 14 days
43. NEURAL TUBE DEFECTS
• Pre-conceptional intake of Folate results in decrease in incidence of neural tube defect

• Myelomeningocele, Anencephaly & Encephalocele are neural tube defect
• ↑Acetylcholinesterase is a marker for neural tube defects
• Acetylcholinesterase is the Most useful maternal serum test used for distinguishing open neural
tube defects and ventral wall defect in a fetus
• Sodium valproate causes open neural tube defect
• Neural tube defects are Multifactorial
• Facial presentation, Increased alpha-fetoprotein & Polyhydramnios are seen in anencephaly
• Anencephaly is best diagnosed using USG
• Most common presentation in anencephaly is Face
• Banana sign seen in the fetal brain Spina bifida
• Most common birth defect in north India is Neural tube defects (Spina bifida)
• Widened neural foramen can be seen in MRI/CT appearance of lateral meningocele
• Sonographic finding of Spina bifida Ventriculomegaly & Obliteration of cisterna magna
• Anencephaly can be diagnosed in first trimester by ultrasound
• Neural tube defect is best detected by Amniocentesis
• Commonest site of meningocele is Lumbosacral
• Accurate diagnosis of anencephaly on ultrasound can be done at 10 weeks of gestation
• Shoulder dystocia is seen predominantly in Anencephaly
44. LACTATION
• The hormone responsible for lactation is Prolactin

• Initiation of lactation is affected by Progesterone, Prolactin & HPL
• Strongest stimulus of lactation is by Suckling
• Galactokinesis means Ejection of milk
• Prolactin is Highest during pregnancy and fall during lactation
• Most common immunoglobulin secreted by mother in milk and colostrum is IgA
• Colostrum is rich in Proteins as compared to breast milk
• Daily additional requirement of protein in lactation is 25 gm
• Folic acid requirement during lactation is 150 microgram/day
• Calcium requirement above the normal during the first six month of lactation is 600mg/day
• Daily additional requirement of protein in lactation is 25 gm
45. HYPEREMESIS GRAVIDARUM
• Alert the physician to the diagnosis of hyperemesis gravidarum early in its course include Ketonuria
• Wernicke’s encephalopathy is seen in Hyperemesis gravidarum
• Hyperemesis gravidarum is associated with molar pregnancy
• Differential diagnosis of Hyperemesis gravidarum are Gastritis, UTI, Reflux oesophagitis
• Pregnancy is terminated in hyperemesis Gravidarum when Decrease in renal output
• Hyperemesis is more common in primigravida than multigravida
46. Miscarriage(abortion)
• Most common cause of abortion in first trimester is, defect in Embryo

• Commonest chromosomal anomaly leading to spontaneous abortions is Trisomy 16
• Causes of 1st trimester abortion are Rubella, Syphilis & Defective Germplasm
• Abortions in the second trimester is mostly due to Incompetent cervix
• Most common cause of Abortion Ovofetal factor
• Internationally accepted definition of abortion is the expulsion of the products of
conception Before 20th week of gestation or 500 gms (weight of foetus)
• Spontaneous abortions commonly occur during First & Second month
• Abortion is defined as expulsion of fetus Before full-term
47. Recurrent Abortion
• In cases of recurrent abortions, most common uterine malformation seen is Mullerian fusion
defects
• Lupus anticoagulant is associated with recurrent abortion and isolated prolonged APTT
• Recurrent abortion in 1st trimester is most often due to Chromosomal abnormalities
• Recurrent spontaneous abortions are seen in Uterine pathology,SLE ,Rh incompatibility & Syphilis
• Recurrent abortion in 1st trimester, investigation of choice is Karyotyping
• Hysteroscopy,Parental cytogenetics, Testing Antiphospholipid antibodies & Thyroid function tests
are investigation carried out in Recurrent abortion
• Low-dose aspirin is used to treat Antiphospholipid antibody syndrome up to 34 weeks
48. Medical Termination of Pregnancy (MTP)
• Maximum age of foetus for MTP is 20 weeks

• Under the Medical Termination of Pregnancy Act the opinion of two registered medical practitio-
ners is necessary to terminate the pregnancy Where the pregnancy exceeds 12 weeks
• The minimum age for giving consent for medical termination of pregnancy is 18 years
• Hypertonic saline methods of MTP is associated with the complication of coagulopathy
• Prostaglandin cannot be used for MTP in a patient with bronchial asthma
• Mifepristone & misoprostol is used in Ist trimester MTP
• Methotrexate, Mifepristone & Misoprostol are used in the medical termination of early pregnancy
• Pregnancy from rape, Substantial risk of delivering seriously handicapped baby & Injury to physical
and mental health of the pregnant women are indication for doing Medical Termination of
pregnancy
• Medical termination of pregnancy can be done by a registered medical practitioner if the gestation
period is less than 12 weeks
49. SEPTIC ABORTION
• The most life threatening complications of septic abortion includes Endotoxic shock
• Tricuspid valve is most likely to be involved by infective endocarditis following a septic abortion
• CT scan findings showing pockets of air within muscles of uterus indicate that she is suffering from
necrotizing endometritis caused by Clostridium species. It is caused because of incomplete
abortion.
50. MULTIPLE PREGNANCY - COMPLICATION AND MANAGEMENT
• Prematurity is the main cause of increased mortality and morbidity in twins.

• Primigravida with twin pregnancy may develop Hydramnios, Pregnancy induced hypertension
& Malpresentation
• To say twin discordance the differences in the two twins should be 25% with the larger twin as
index
• Incidence of preterm delivery in twin pregnancy is 50%
• Important factor for discordant growth between twins is Twin to twin transfusion
• In an uncomplicated twin pregnancy normal delivery should be attempted in First baby – Vertex
and second baby transverse lie
• In twin pregnancy, treatment of choice when first baby is in transverse lie is Cesarean section
• In twin pregnancy delivery by cesarean section is advocated in Monoamniotic twins & Weight less
than 1500 gm.
• Oligohydramnios is Not associated with twin pregnancy
51. Abnormalities of Placenta and Cord
• The findings of a single umbilical artery on examination of the umbilical cord after delivery is An
indicator of considerably increased incidence of major malformation of the fetus
• Velamentous insertion of the cord is associated with an increased risk for Fetal exsanguinations
before labor
• Placenta in which vessels seperate before reaching margin is Velamentous placenta
• Fetal blood loss in abnormal cord insertion is seen in Vasa previa
• Single umbilical artery is associated with diabetes in mother.
• Failure of development of one artery in later months is implicated single umbilical artery case
• Vasa previa is Associated with low lying placenta
• In vasa previa Incidence is 1:1500
• In vasa previa Caesarian section is indicated
• Single umbilical artery is associated with Polyhydramnios, Fetal growth retardation & Increased
incidence of fetal malformation
• Unilateral renal agenesis is associated with Single umbilical artery
52. ANEMIA IN PREGNANCY
• According to WHO, anemia in pregnancy is diagnosed, when hemoglobin is less than 11.0 gm%
• In pregnancy, Iron + folic acid anemia is common in India
• With oral iron therapy, rise in Hb% can be seen after 3 weeks
• Pre-eclampsia, Intercurrent infection & Heart failure complications are likely to increase in a case of
severe anemia during the pregnancy
• As per WHO, anemia is considered to exist in pregnancy, if the hemoglobin level is below
• Type of anemia in pregnancy is Microcytic hypochromic
• Cord cutting should be delayed in Sever anemia
53. Occiput-Posterior Position (OP)
• Persistent occipitoposterior is common in the Anthropoid type of pelvis

• The commonest cause of occipitoposterior position of fetal head during labor is android pelvis
• Most unfavourable presentation for vaginal delivery is / delivery not possible per vaginum is Mento
posterior
54. COURSE AND MANAGEMENT OF LABOUR - Deep Transverse Arrest (DTA)
• For Patient with occipito posterior position Wait and watch for progress of labour
• Deep transverse arrest is most commonly seen in Android pelvis,Epidural analgesia & Uterine
inertia
• In deep transverse arrest the delivery of baby is conducted by Cesarean section, Vacuum
extraction, Keilland forcep and Manual rotation and forcep delivery

• In a case of direct occipitoposterior position (Face to pubis delivery) most commonly encountered
problem is Complete perineal tears
• In deep transverse arrest with adequate pelvis, best mode of delivery will be Ventouse
• Best management in Mento-posterior presentation Caesarean section
55. Contracted Pelvis
• Naegele's pelvis is associated with a lack of single pelvic ala

• Face presentation can occur due to contracted pelvis.
• Pelvic inlet usually is considered to be contracted, when shortest anteroposterior diameter is less
than 10 cm, greatest transverse diameter is less than 12 cm & Diagonal conjugate of less than 11.5
cm
• CPD is best assessed by CT scan
• A broad flat pelvis is characteristic of Platypelloid type
• True about anthropoid pelvis, sacrosciatic notch is Wide and shallow
• Dystocia dystrophia syndrome is seen in Android pelvis
• Both alae absent in Robert's pelvis
• Symphysiotomy is indicated in Contraction of outlet
• X-ray pelvimetry is indicated in Severe CPD
• Successful trial of labour can be expected in Flat pelvis
56. Shoulder Dystocia
• In Sudden hyperflexion of thigh over abdomen (Mcrobert's procedure) Lateral cutaneous nerve of
thigh is most commonly involved
• Zavanelli maneuver,Woods Corkscrew Maneuver, Mcroberts manoeuver & Suprapubic pressure
are management of shoulder dystocia
• Shoulder dystocia result in Sternomastoid swelling, Erb's palsy & Klumpke's paralysis
• Shoulder dystocia is the most common complication during vaginal delivery in a diabetic women
• Shoulder dystocia is seen in predominantly Anencephaly
57. Endocrinology in Relation to Reproduction
• Minimum level of HCG detected by radio immunoassay is 0.001 IU/ml

• Abnormal rise of HCG in a female of reproductive age group may indicate Choriocarcinoma
• Increased free beta HCG levels are features of down's syndrome
• Human chorionic gonadotropin produced by the human placenta has LH-like activity
• Human chorionic somatotropin participates in stimulation of ductal growth in the mammary gland
during pregnancy
• HCG is glycoprotein
• hCG can be detected in the urine prior to the first missed period
• HCG titer, USG & Chest x ray are used for a diagnosis of hydatidiform mole
• Radioimmune assay is the most sensitive or gold standard test for assessing HCG in maternal
serum
• Minimum hCG level that a urine pregnancy test can detect is 5 m IU/ ml
• The corpus luteum of the ovary is maintained by the secretion of human chorionic gonadotropin
from The trophoblast cells
• HCG is secreted by Embryonal cell cancer,Yolk sac tumor, Choriocarcinoma & Polyembryoma
• Placental HCG stimulates the gonads in male at 8 week to secret testosterone
• Marker for testicular tumor is Beta hCG
• During pregnancy, maximum urinary HCG level is reached in 70 days
• Plasma levels of hCG during pregnancy doubles every 2 days
• Alpha chain of HCG is identical to
58. Amniocentesis
• Amniocentesis at 16 weeks is indicated in Anti D prophylaxis

• 12-16 weeks appropriate gestational age for performing amniocentesis
• DNA analysis of chorionic villus/amniocentesis Hemophilia A, Sickle cell disease & Duchenne
muscular dystrophy
• Hydramnios and marked respiratory distress is best treated by Amniocentesis
• Neural tube defect is best detected by Amniocentesis
• Amniocentesis is early pregnancy for genetic disorders is a kind of Secondary prevention
Gynecology
1. Asherman Syndrome
• The risk of Asherman syndrome is the highest if Dilatation and Curettage (D & C) is done for the
Post partum haemorrhage condition.
• Asherman syndrome is due to Postabortion curettage
• The presentation of Asherman syndrome typically involves Hypomenorrhea
• A 28 year old patient complains of amenorrhea after having dilatation & curettage.The most likely
diagnosis is Asherman's Syndrome

2. Endometrial Carcinoma
• Fractional curettage can be done in endometrial carcinoma

• Persistent anovulation not treated leads to Endometrial Carcinoma
• Poly cystic ovarian disease is associated with Endometrial carcinoma
• Obesity, Family History, Use of Hormone Replacement Therapy are known risk factors for de-
velopment of endometrial carcinoma
• Endometrial carcinoma is Predisposed by diabetes mellitus, hypertension and obesity
• Bleeding PV and enlarged inguinal nodes is seen in satage IV of endometrial carcinoma
• Penetration into half of myometrium, Clear cell Ca & Fundal involvement are indications of direct
lymph node dissections in endometrial carcinoma
• The most malignant endometrial carcinoma is Clear cell carcinoma
• Stage IV endometrial carcinoma, treatment is Radiotherapy, Chemotherapy and hormonal therapy
• D and C is useful in the diagnosis of endometrial carcinoma
• Most common cause of postmenopausal vaginal bleeding is endometrial carcinoma
• Use of tamoxifen for breast cancer can cause endometrial carcinoma
• The risk of endometrial carcinoma is the highest with the Complex hyperplasia with
atypia histological pattern of endometrial hyperplasia
• In Endometrial carcinoma, PTEN is the tumor suppressor gene
3. Primary amenorrhoea
• 10 year old girl with primary amenorrhoea, absent breasts, malformed uterus is diagnosed
with Turner's syndrome
• The commonest cause of primary Amenorrhoea is Ovarian dysgenesis
• Primary amenorrhoea with anosmia is seen in Kallman syndrome
• Child with primary amenorrhoea with negative progesterone challenge test but positive combined
progesterone and estrogen test. Diagnosis may be Prolactinoma
• Primary amenorrhoea, grade V thelarche, grade II pubarche and no axillary hair is seen in testicular
feminization
• Androgen insensitivity syndrome: Primary amenorrhoea normal sexual development and normal
breast but with absent public and axillary hair . B/L inguinal hernias , absent uterus & blind vagina
• PCOS, Müllerian agenesis & Congenital adrenal hyperplasia are cause of primary amenorrhoea with
eugonadism
• Primary amenorrhoea with normal breast, hirsutism and acne are features of PCOS
• Primary amenorrhoea with well developed breasts and axillary and pubic hair & missing Uterus and
vagina is diagnosed to have Mullerian agenesis
• Well-developed breasts, no hiruitism, no pubic or axillary hair with primary amenorrhea is
suggestive of Complete androgen insensitivity syndrome
4. Carcinoma occuring with oc pill consumption

• Use of oral contraceptive pills are known to protect against Ovarian carcinoma, Endometrial
carcinoma, Uterine sarcoma
• Estrogen in the OCP causes Breast carcinoma, Endometrial carcinoma & Thromboembolism
• The combined oral contraceptive pills decrease the risk of Endometrial cancer,Ovarian cancer &
Ectopic pregnancy
• Reason for hepatic involvement in oral contraceptives is Estrogen
5. EXTERNAL GENITALIA
• Bartholins duct open into Groove between labia minora and hymen
• Commonest reason of adherent labia minora in a newborn is Agglutination of labia
• The inner surface of the labia minora medial to the Hart line is lined by Squamous epithelium
• The embryonic development of the vestibule of the vagina is from Urogenital sinus
• Lymphatic drainage of clitoris is to Glands of cloquet & Deep inguinal lymph nodes
• Scrotum is analogus to Labia majora
• Clitoris develops from Genital tubercle
• Bartholin gland opening is at Inner side of labia minor external to hymen
• Triangular space between clitoris and hymen is called Vestibule
• Lymphatic drainage of Vulva is into Superficial inguinal nodes
6. Vagina
• The embryonic development of the vestibule of the vagina is from Urogenital sinus
• Levator prostatae muscle in male is equivalent for vaginal sphincter in female
• Ureter is related to lateral wall of vagina
• Mullerian duct give rise to the upper three fourth of vagina
• Lower part of vagina develops from Urogenital sinus
• Mucous membrane of vagina is lined by Nonkeratinized Stratified Squamous epithelium
• Vagina Lacks mucus secreting glands
• Least sensitive structure to radiation is Vagina
• Ligament extending from cervix and vagina to lateral pelvic wall is Transverse cervical ligament
• Epithelium of vagina arises from Mesoderm
• Angle of anteversion of uterus is between Long axis of uterus and vagina
• The urogenital triangle is the anterior part of the perineum that contains the vagina and associated
parts of the external genitalia.
• External iliac lymph nodes drain upper vagina & cervix
• Vaginal wall is derived from Endoderm and mesoderm
• Lower 2/ 3 of vagina, Fallopian tube, Uterus are derivatives of mullarian duct
• Length of Posterior vaginal wall is More than anterior vaginal wall

7. Uterus
• Size of uterus in inches is 3x2x1

• Pelvic diaphragm, Uterosacral ligament & Transverse cervical ligament are primary support of
uterus
• Paramesonephric duct forms Uterus
• Uterus develops from Mullerian duct
• External iliac , Internal iliac & Superficial inguinal recieves lymphatics from the uterus
• Uterus, before menarche, is lined by Ciliated columnar epithelium
• Blood supply of the uterus is by Ovarian & Uetrine artery
• Superficial inguinal ring in the female transmits Round ligament of the uterus
• Uterus reaches up to umbilical level at 24 weeks
• Fundus of uterus drains into Paraaortic
8. ESTROGEN
• Failure of bleeding after withdrawal of oestrogen indicates Uterine factor

• Estrogen replacement for post — menopausal symptoms causes an increase in Triglycerides
• Estrogen administration in a menopausal woman increases the Bone mass
• Oestrogen causes Weight gain, Fluid and water retention, Disappearance of comedones
• Post menopausal estrogen production is due to Peripheral aromatization of androstenedione
• Estrogen dependent conditions are Endometriosis, Endometrial carcinoma & Fibroids
• Functions of estrogen are Synthetic function on endometrium, develop secondary sexual characters
in female, Breast enlargement during puberty
• Secretion of estrogen is maximum Before ovulation
• The enzyme associated with the conversion of androgen to oestrogen in the growing ovarian follicle
is Aromatase
• Effects of estrogen are Reduces LDL,Beneficial effect on cognition,Reduced osteoclastic
activity,Increased osteoblastic activity, Increases Triglycerides & Increases HDL
• Estrogen is Used in HRT
• Estrogen causes Increased risk of breast cancer
• By estrogen administration in a menopausal woman Bone mass is increased
• Estrogen Causes cholestasis
• The success of estrogen and estrogen-like drugs in combating osteoporosis in postmenopausal
women may indicate that estrogen Inhibits osteoclastic activity
• Estradiol, Estrone & Estriol are the main form of oestrogen secreted from the ovary
• The amount of estrogen in low dose oral contraceptive pills is 20 micrograms
• Aromatase enzyme is associated with the conversion of androgen to oestrogen in a growing ovarian
follicle
• Estrogen action on carbohydrate metabolism Glycolysis increases
• Estrogen is mainly responsible for skeletal maturation
• Major estrogen in normal adult women is Estradiol
• Ethinylestradiol is synthetic estrogens
• Estrogen Causes cholestasis
• Estrogen Used in HRT
• Thromboembolism is due to Estrogen
• Ferning pattern of mucus under influence of Estrogen
• Estrogen deficiency leads to Osteoporosis
• Aromatase produces estrogen from androgen
• Estrogen Beta receptors are found on ovary
• FSH and LH both are inhibited by Estrogen
• Reason for hepatic involvement in oral contraceptives is Estrogen
• Vaginal cornification, Pubic & axillary hair growth & Cervical mucus production are pubertal change
due to estrogen
• Estrogen is secreted by Granulosa cells
• Estrogen acts on nuclear receptors
9. CORNIFICATION INDEX
• Cornification Index is maximum in Late proliferative phase

• Cornification index or eosinophilic index in the diagnosis of atrophic vaginitis indicates Estrogenic
effect
• Hypercornification of duct is one of the Causative factor for acne
10. BACTERIAL VAGINOSIS
• Bacterial vaginosis shows pH > 4.5, Fishy odour, Grey & Clue cells discharge
• Amine test is positive in Bacterial vaginosis
• Whiff test is positive in Bacterial vaginosis
• Drug of choice in bacterial vaginosis is Metronidazole
• Gardnerella is the causative agent of Bacterial vaginosis
11. TRICHOMONIASIS
• Frothy discharge with red ulceration in the vagina is seen with infection of Trichomoniasis
• Greenish vaginal discharge with severe Itching points to a diagnosis of Trichomoniasis
• Commonest genital infection in females is Trichomoniasis
• Vaginal trichomoniasis is the important cause of vaginitis in the childbearing period when the local
immunological defence is impaired.
• A woman diagnosed with Trichomoniasis should also be evaluated for Other venereal disease
• Trichomoniasis Is a sexually transmitted disease
• Trichomoniasis Produces copious thin frothy discharge
• Trichomoniasis Is most often asymptomatic
12. MULLERIAN DUCT ANOMALIES
• Complete failure of mullerian duct fusion will result in Uterus didelphys

• In complete mullerian duct aplasia Fallopian tubes, Uterus & Vagina are likely to be absent
• Mullerian agenesis shows 46 XX karyotype
• Mullerian agenesis shows Normal breast development
• The most important indication for surgical repair of a Bicornuate Uterus is Habitual abortion
• Bicornuate uterus is due to Incomplete fusion of paramesonephric duct
• MC congenital abnormality of uterus is Septate
• To diagnose uterus didelphys, procedure of choice is HSG
• Complete failure of mullerian duct fusion will result in Uterus didephys
• In cases of recurrent abortions, most common uterine malformation seen is Mullerian fusion
defects
• The most important indication for surgical repair of a double uterus, such as a septate or
bicornuate uterus, is Habitual abortion
• Androgen Insensitivity Syndrome condition is present with absence of both Mullerian and Wolffian
duct structures
• Mullerian duct anomaly type ,Uterus didelphys is associated with the presence of two cervixes
• Normal development of ovaries in a female with absent uterus and vagina indicates Mullerian
agenesis
• Mullerian fusion defects is the most common uterine malformation seen in cases of recurrent
abortions
• Structure developing from Mullerian duct in males is Prostatic utricle
13. CANDIDIAL (MONILIAL) VAGINITIS
• Vaginal candidiasis is Associated with intense pruritus

• Vaginal candidiasis shows Typical "Cottage cheese" discharge
• Vulval candidiasis is associated with Diabetes mellitus
• Vaginal candidiasis shows Buds and hyphae in KOH preparation
• Oral contraceptives causes Monilial vaginitis
• Diabetes mellitus, OCP user,Pregnancy & HIV are risk factor for vaginal candidiasis
• Commonest fungal infection of the female genitalia in diabetes is Candidial infection
• Treatment of both partners is not recomended in vaginal candidiasis
• Genital infection in females presenting with thick curdy or flaky discharge may be Candidiasis
• Candidal vaginitis is most likely to be associated with vaginal pH of 4

14. HERMAPHRODITISM
• True hermaphroditism is when Tissues of both the ovaries and testes are present
• Commonest cause of female pseudo hermaphroditism is Congenital adrenal hyperplasia
• Empty scrotum syndrome is seen in female pseudohermaphroditism
• Ovaries present in female pseudohermaphroditism
• Excessive androgen exposure is seen in female pseudohermaphroditism
• Male pseudohermaphroditism is seen in 5-a reductase & 17 hydroxylase deficiency
• 21-Hydroxylase deficiency is Autosomal recessive
15. ENDOMETRIOSIS
• Infertility is seen in Endometriosis

• Uterine fibromyoma is associated with Endometriosis
• Endometriosis is MC in 3rd or 4th decade
• Premenstrual spotting is seen in Endometriosis
• True cyst is seen in Endometriosis
• Endometriosis is Hormone dependent condition
• Endometriosis Can involve lung pleura
• Ovary is the most common site in Endometriosis
• Endometriosis is commonly associated with B/L chocolate cyst of ovary
• Pain in endometriosis correlates with Depth
• Best investigation to establish the diagnosis of endometriosis is Laparoscopy
• Medroxyprogesterone acetate,Progesterone,GnRH, OCP & Danazol are used in treatment of
endometriosis
• Scar endometriosis can occur in Classical Cesarean Section, Hysterotomy & Episiotomy
• Treatment of a cause of Endometriosis at a younger age group Progestin
• Endometriosis is explained by Sarnpson's Implantation theory & Histogenesis by induction
and Coelomic metaplasia theory both
• Endometriosis shows Metastatic epithelium
• Endometriosis is painful
• Commonest manifestation of endometriosis is pain
• Endometriosis mostly occurs in Nulliparous women
• The surgery of choice for diffuse endometriosis interna is Total hysterectomy
• Medroxy progesterone is the drug of choice to treat endometriosis
• Broad ligament (except tubes and ovaries) is the most common extrauterine site to be affected by
endometriosis
• In the etiology of endometriosis Sampson's theory is Implantation theory
• The severity of pelvic pain in endometriosis correlates best with Depth of invasion
• Treatment of endometriosis in an infertile female Clomiphene
• Cause of unilateral dysmenorrhea is Endometriosis with unilateral distribution
• CA 125 is elevated in Endometriosis
• Trans-Cervical Endometrial Resection (TCER) is used in Endometriosis
• Retroverted uterus is Associated with endometriosis
• The condition of genital organs whlch may lead to leslons in surgicalscars, rectum, lymph nodes,
lung ls endometriosis
• Pawaer burr, appearance on laparoscopy is characteristic of endometriosis
• Ectopic pregnancy is common in endometriosis
• Most common symptom of endometriosis is Dysmenorrhoea
16. ADENOMYOSIS
• Infertility is seen in Adenomyosis

• Adenomyosis is Presents with menorrhagia, dysmenorrhea and an enlarged uterus
• Symptoms of adenomyosis Menorrhagia & Dysmenorrhea
• Treatment of adenomyosis is Total hysterectomy
17. FIBROID
• All fibroids are Interstitial

• Infertility, Pelvic mass & Menstrual irregularity are seen in fibroid
• Atrophy,Calcification & Hyaline dogeneration are changes that occur in fibroid uterus
• Most common fibroid associated with malignancy is Intramural
• Least common complication of fibroid is malignancy
• Submucosal fibroid is detected by Hysteroscopy, USG & Hysterosalpingography
• Myomectomy, Embolisation of uterine artery & Laser myomectomy are methods of managing
fibroid uterus
• Decreased vascularity of fibroid is seen with GnRH agonist, Danazol & Mifepristone
• Drugs that reduce the size of fibroid are Danazol
• Red degeneration are the indications for myomectomy in a case of fibroid uterus
• True regarding fibroid uterus Estrogen dependent tumor
• Calcareous degeneration occurs most commonly in Subserous type of fibroids
• Malignant prevalence in fibroid is 0.5%
• Pressure symptom is due to Subserousfibroids
• Commonest site for fibroid is Intramural
• Treatment of choice in a perimenopausal woman with bleeding PV due to multiple fibroids Is TAH
• Sarcomatous changes is the rarest modification in a fibroid uterus
• Fibroid is Rare before 20 years
• Fibroid is Usually asymptomatic
• Fibroid is More common in nulliparous
• Commonest condition associated with menorrhagia is Fibroid
• Spasmodic dysmenorrhoea is seen in Submucous fibroid
• Cause of unilateral dysmenorrhea is One horn of malformed uterus, Endometriosis with unilateral
distribution & Small fibroid at the utero tubal junction
• A woman treated for infertility, presents with 6 week amenorrhea with urinary retention. The most
likely etiology is Impacted Cervical Fibroid
• Causes of retention of urine in reproductive age group Cervical fibroid , Retroverted gravid uterus
& Severe UTI
• Cause of secondary dysmenorrhea in a young female Subserous fibroid
• A pregnant woman presents with red degeneration of fibroid, Management is Conservative Rx
• Red degeneration, Infection & Torsion are the reasons for sudden onset of pain in an asymptomatic
case of uterine fibroid
• Nulliparous woman complains of severe menorrhagia and lower abdominal pain with 9 wks size
uterus with fundal fibroid will be treated with Myomectomy
• Pre term labour, Post partum hemorrhage & Abortion are complication of fibroid in pregnancy
• Tourniquet is used to reduce blood loss during myomectomy for fibroid uterus
• Dysmenorrhoea is the LEAST likely feature of fibroid
18. ASSISTED REPRODUCTIVE TECHNIQUES (ART)
• GIFT, ZIFT, IVF and ET are assisted reproduction technique

• Aspiration of sperms from testes is done in TESA
• In TESA sperms are aspirated from the testes
• Ovulation stimulation ,Oocyte retrieval & Transfer of unfertilized egg into the fallopian tube are
steps of GIFT
19. Anatomy Of Ovaries
• Ovary develop from Genital ridge

• The main portion of the ovarian artery, vein, and nerves are carried to and from the ovary by way
of the Suspensory ligament
• The nerve supply of the ovaries arises from T10.
• Cells found in the interstitium of the ovary that resemble steroid secreting cells and may secrete
androgens in the human ovary are Ovarian hilar cells
• Formation of primary ovary in female foetus takes place by 10th week
• Germ cells in the ovary develop from Yolk sac
• Lymphatic drainage of ovary is through Preaortic and para-aortic lymph nodes
• At birth each ovary contains about 2 million primary follicles.
• Sex cords are derived from coelomic epithelium
• Ovarian fossa is formed by Obliterated umbilical artery, Internal iliac artery & Ureter
• Posterior border of ovary is Free of ligament attachment
• Primordial Germ cell of ovary are developed from Endoderm
20. FALLOPIAN TUBE

• Narrowest part of Fallopian Tube is Interstitial portion
• Parts of fallopian tube from ovary to uterus are Infundibulum - Ampula - Isthmus - Intramural
• The length of fallopian tube is 10 - 12 cm
• Longest part of the fallopian tube is Ampulla
• Fallopian tube patency is checked by Hysterosalpingography, Laparoscopy & Hysteroscopy
• 'Peg cells' are seen in fallopian tube
• Most common site for female tubal sterilization is isthmus
• The fertilised ovum takes 3-4 days to travel through the fallopian tube and reaches the uterine
cavity by the 7th day from ovulation.
• Tubal ostium is the point where the tubal canal meets the peritoneal cavity
• MUllerian ducts develops in females into the Fallopian tubes
• Isthmus acts as a functional/anatomical sphincter.
• Maximum number of mucosal folds are found in ampulla
• Fertilization takes place in ampulla
21. BREAST ANATOMY
• Development of breast is related with Tanner scale

• Breast is a Modified sweat gland
• Lymphatic drainage of upper outer quadrant of breast is Anterior axillary
22. PELVIS MUSCULATURE
• Muscles that can cause external rotation of the hip include Obturator internus
• Pubovaginalis, External urethral sphincter & Bulbospongiosus are sphincters of lower genito urinary
tract of female
• Pelvic diaphragm is formed by Pubococcygeus,Iliococcygeus & Pubovaginalis
• Urogenital Diaphragm is made up of Sphincter urethrae , Perineal membrane & Deep transverse
Perineal muscle
• Superficial perineal muscles include Bulbospongiosus
• Lateral border of ischeorectal fossa is formed by Obturator internus
• Puborectalis is essential to maintain continence
• Sphincter urethrae is Voluntary, Arises from ischiopubic ramus and are Supplied by pudendal nerve
• Pubococcygeus supports prostate
23. Precocious puberty
• Precocious puberty may be seen in Granulosa cell tumour, Head injury & Corticosteroid intake
• The sexual development is considered is precocious if there is breast and public hair growth before
the age of 8 years
• GnRH analogue may be given in Prostate Ca, Fibromyoma – uterus & Precocious puberty
• Precocious puberty is seen with Granulosa cell tumour
• Sexual maturity is attained early in precocious puberty
• Menstruation is defined as precocious if it starts before the child reaches the age of 10 years
• Precocious puberty can be heterosexual
• 21 alpha hydroxylase deficiency males present with precocious puberty
• A male child presenting with early onset puberty and hypertension is suggestive of congenital
adrenal hyperplasia due to the deficiency of 11-β hydroxylase deficiency.
• Sexual maturity attained early in precocious puberty
• Familial male limited precocious puberty is also called Testotoxicosis
• Familial male limited precocious puberty is Autosomal dominant condition
• Flutamide can be used for treatment of Familial male limited precocious puberty
• 21 alpha hydroxylase deficiency & 11β hydroxylase deficiency can cause precocious puberty in
males
• Precocious puberty is seen in Hypothyroidism, CNS irridation & Mc cune-Albright syndrome
• Congenital 21 hydroxylase deficiency causes precocious puberty in male due to excess of
androgens.
• The diagnosis of a patient presenting with familial Polyostosis, Precocious puberty and
Pigmentation is McCune Albright syndrome
24. Menopause
• Gonadotrophins remain elevated after menopause for Rest of life

• Average age range of attaining menopause is 45 - 55
• Absence of menses for last 4 monthsin mid age women with high serum FSH and LH level & low
estradiolcan be diagnosed to have Premature menopause.
• Carcinoma vulva may be Seen after menopause and Viral predisposition
• There is a decrease in skin elasticity in menopause
• Systemic vasomotor instability may be present in meopause
• There may be an increase in FSH secretion by the pituitary gland in menopause
• The symptoms of menopause are best treated with estrogen
• The incidence of carcinoma of the breast is increased in woman who Have an early menarche and
late menopause
• Osteoporosis is seen in Menopause
25. Menorrhagia
• Myomectomy is specifically indicated in an infertiie woman or woman desirous of bearing child and
wishing to retain her uterus in severe menorrhagia
• Fundal myomas commonly present as Menorrhagia
• Intersitial myomas predispose to menorrhagia by Inhibiting uterine contractility
• Puberty menorrhagia is treated by Progesterone, estrogen & GnRH analogues
• Female presenting with dysmenorrhoea & menorrhagia most probably has Endometriosis & Fibroid
• A woman is said to be have menorrhagia if the menstrual blood loss is more than 80 ml
• Hysterectomy is the definitive treatment of adenomyosis
• NSAID's, Norethesterone & Tranexamic acid are indicated in menorrhagia
• Dilatation and curettage with blood transfusion is the primary treatment of puberty menorrhagia
with low Hb%
• Commonest condition associated with menorrhagia is Fibroid
• Retroverted uterus causes menorrhagia
• Puberty menorrhagia associated with anovulatory bleeding
• Puberty menorrhagia Routine screening for bleeding disorder is done
• Hematinics & Hormone therapy is the treatment of choice for Puberty menorrhagia
• A patient comes to you with history of frequent cycles with heavy bleeding. This condition is
called Polymenorrhagia
• Multipara, hypertensive woman with menorrhagia should be treated with MIRENA
• Adenomyosis presents with menorrhagia, dysmenorrhia, and an enlarged uterus
• lUCD of choice in women with menorrhagia Progesterone containing IUCD
26. Intrauterine Contraceptive Devices
• Mechanisms for reduce risk of upper genital tract infection in users of progestin - releasing IUDs,
include Reduced retrograde menstruation, Thickened cervical mucus & Decidual changes in the
endometrium
• Progestasert (Levonorgestrel) is used for patients with menorrhagia
• IUD Cu 7380A life span is 10 year
• Cumulative 5-year pregnancy rate for LNG-IUD (levonorgestrel intra-uterine device) is 0.5 %.
• Memory of an IUD device is important while insertion into the intrauterine cavity. Memory of
CuT380A is 5 minute
• Progesterone of choice in emergency contraception is Levonorgestrel
• Hypofibrinogenemia is most likely complication of IUD
• In calendar method of contraception, first day of fertile period is 10th day of shortest menstural
cycle
• The pregnancy rate of lippes loop and Cu-T 200 are similar
• IUD can be used for Emergency Contraception within 5 days
• Levonorgestrel releasing IUD has an effective life of 5 years
• Levonorgestrel increases the risk of ectopic pregnancy
• Levonorgestrel releases 20 µg/day of levonorgestrel
• Absolute contra indication for IUD are Pregnancy, Undiagnosed vaginal bleeding & Pelvic
infalmmatory disease
• The most common side effect of IUD insertion, which requires its removal is Pain
• Expulsion is most commonly associated side effect with Lippes loop

27. Oral Contraceptive Pills
• The first step in the management of hirsutism due to stein leventhal syndrome is OCP
• In a 45 years old lady with polymenorrhoea for 6 months duration best line of management is OCP
for 6 months
• OCP and progesterone use over long periods may contribute in Risk factors for development of Ca
cervix
• Reversible methods of contraception are OCP
• OCP is a reversible method of contraception
• Non contraceptive use of OCPs are Ca endometrium, Rheumatoid arthritis & Endometriosis
• OCP gives protection against Endometrial & Ovary cancers
• OCPs cause Hepatic adenoma, Cancer Cervix & Hepatic vein thrombosis
• OCP's are contraindicated in Smoking 35 years,Intermittent vaginal bleeding,H/0
thromboembolism, Coronary occlusion & Cerebro vascular ds
• Complication of OCP are Hyperlipidemia, Hypertension & Depression
• OCP has LEAST pregnancy failure rate
• Estrogen in the OCP causes Breast & Endometrial carcinoma and Thromoembolism
• OCP fail when used
with Ethoxsuccimide,Phenobarbital,Griseofulvin, Carbamazepine,Primidone, Phenytoin & Rifampin
• Use of OCP is associated with increased risk of asymptomatic chlamydial infection
• combined OCP decreases the risk of ectopic pregnancy,PID, Ovarian cysts & acute salpingitis &
also improves dysmenorrhea from endometriosis
• Combined OCP is the ideal contraceptive for a newly married couple who wants to plan their family
after 6 months
• Thromboembolism is due to Estrogen in OCP
• Most common cause of stroke in young women in India among OCP users is Cortical vein
thrombosis
• OCP provides protection against Fibroadenoma breast, Carcinoma ovary & Uterine malignancy
28. Progesterone
• Effects of progesterone on lipids are Lowers HDL & increases LDL

• Actions of progesterone include Increase the tone of cervical sphincter, Sodium and water
retention & Secretory hypertrophy
• Progesterone is produced by Granulosa luteal cells
• A patient with amenorrhea had bleeding after giving a trial of progesterone. This implies Sufficient
estrogen, Intact pituitary axis & Normal ovarian function and Intact endometrium
• Positive progesterone challenge test in a patient of secondary amenorrhoea, seen in PCOD
• Withdrawal bleeding with progesterone seen in otherwise amenorrhoeic woman due
to Anovulation
• Simple hyperplasia of the endometrium treated with progesterone for 21 days
• The progesterone of choice for emergency contraception is Levonorgesterel
• In a woman on subdermal progesterone implant, the menstrual abnormality seen is Metrorrhagia
• Depot medroxyprogesterone acetate is sparingly used as a contraceptive because it causes Irregular
menstrual bleeding
• Progesterone pills Acts by altering cervical mucous secretion, Break ovulation cycle &
causes Irregular bleeding
• Oral contraceptive pill containing progesterone which is given in small quantities for 30 days a
month is known as Micro pill
29. Testosterone
• High testosterone levels is a feature of testicular feminization syndrome

• Testosterone estimation is the Best investigation for hirsutism and amenorrhea
• Axillary hair growth is caused by Testosterone
• Continuous testosterone will lead to azoospermia
• Gynecomastia is associated with an estrogen / testosterone imbalance
• Most of the testosterone secreted by the testes exists in the plasma in the form of Testosterone
bound to sex-steroid-binding globulin
• Testosterone in a normal male is secreted by Leydig cells
• Spermatogenesis is maintained by Testosterone, FSH, & LH
• Placental HCG stimulates the gonads in male at 8 week to secret testosterone
• Decreased level of testosterone results in Loss of libido, Infertility & Decreased frequency of sexual
intercourse
• Pubarche is due to Testosterone
• In men LH controls secretion of Testosterone
• Testosterone hormone is responsible for acne
30. Anti-Oestrogens
• Antihormonal substance used to induce ovulation clomiphene citrate

• Anovulatory infertility can be treated by clomiphene
• Clomiphene citrate is indicated in stein- leventhal syndrome
• Clomiphene causes hyperstimulation
• Drugs used for ovulation induction Clomiphene citrate & Tamoxifen
• Clomiphene citrate is Anti estrogen
• The most serious complication of clomiphene therapy for induction of ovulation is Hyperstimulation
syndrome
• Tamoxifen is Non steroidal antioestrogenic
• Long term tamoxifen therapy may cause Endometrium Ca
• In Clomiphene citrate Risk of multiple pregnancy is 6-10%
• Clomiphene citrate can also be used for male infertility with oligozoospermia
• Gynaecomastia is caused by Clomiphene citrate

• Mechanism of action of Clomiphene Citrate is Binds estrogen receptors and prevents negative feed
back at hypothalamus
• Side effects of clomiphene citrate include Multiple pregnancy, Increase risk of ovarian ca & Multiple
polycystic ovary
• Women receiving Tamoxifen should be periodically screened with Endometrial sampling
• Use of tamoxifen in carcinoma of breast patients shows Endometrial hyperplasia,Thromboembolic
events, Endometrial Carcinoma & cataract
• Tamoxifene is SERM
• Letrozole belongs to Aromatse inhibitors
• Drug useful in breast cancer is Tamoxifen
31. Antiprogesterone
• Decreased vascularity of fibroid is seen with Mifepristone, GnRH agonist & Danazol
• Mifepristone is also called RU — 486
• Mifepristone is a 19 — norsteroid
• Mifepristone Acts on receptors
• Anti progesterone drug is Mifepristone
• Drugs used in emergency contraception is Danazol and Mifepristone
• Mifepristone is used in Abortion, Cushing syndrome,Fibroid,Ectopic pregnancy,Molar pregnancy
& Cervical ripening
• Mifepristone is used in Medical terminations of pregnancy
• Dose of mifepristone (in mg) for post-coital contraception is 10 mg
• First trimester abortion uses Mifepristone, D & C and also Suction evacuation
32. OvarianTumours of the Surface Epithelium
• Brenner tumor Resembles fibroma

• Brenner tumor Common in postmenopausal age group
• Serous cystadenoma of the ovary may be both Bilateral and unilateral
• Serous cystadenoma shows Concentric calcification
• Hob nail cells are seen in Clear cell carcinoma
• Abdomen distended, loculated masses of semi-translucent mucinous material seen in mucinous
cystadenoma.
• Ovary or appendix are the most common sites for mucinous cystadenoma.
33. Germ Cell Tumours
• The most common pure germ cell tumour of the ovary is Dysgerminoma
• Most common ovarian tumor in less than 20 years is Germ cell tumour
• Bilateral germ cell tumour is Embryonal cell carcinoma
• Choriocarcinoma is Malignant germ cell tumours of ovary
• Alpha feto protein, LDH & p HCG are the markers for malignant germ cell tumors of ovary
• Dysgerminoma, Polyembryoma & Endodermal sinus tumor are germ cell tumours of ovary
• Most common germ cell tumor of ovary is Dermoid
• The most common pure germ cell tumor of the ovary is Dysgerminoma
• Serum alpha feto protein level is raised in Teratoma, Endodermal sinus tumor
• Cryptochidism, Testicular feminising syndrome & Klinefelter's syndrome are Predisposing features
for germ cell tumour
• Extragonadal germ cell tumors occur in Sacrococcygeal region, Mediastinum & Brain
• The commonest site for extragonadal germ cell tumour is Mediastinum
• Germ cell tumours of testis are Seminoma, Teratoma
• Intratubular germ cell tumor found adjacent to Dysgerminoma
• Treatment of extragonadal germ cell tumour is Chemotherapy
• Seminomas are radiosensitive
34. Teratoma
• Most common orbital cyst in children Dermoid cyst

• Sacro-coccygeal teratoma appear as swelling over sacral region
• Maximum radio opaque shadow in ovary is seen in Teratoma
• Ovarian mass with x-ray pelvis showing radio-opaque shadow suggest Dermoid cyst
• Rokitanski protruberences are seen in Teratoma
• Dermoid cyst of ovary is teratoma
• Dermoid cyst is most prone to undergo torsion during pregnancy
• Dermoid cyst of ovary contains derivatives from Endoderm, Mesoderm & Ectoder
• Most common ovarian tumour in pregnancy is Dermoid cyst
• Dermoid cyst of ovary Has sebaceous material
• Dermoid cyst of ovary Commonly more than 10 cm
• Teratoma arises from Totipotent cells
• In Benign cystic teratoma 10% are B/L & malignant
• Testicular teratoma markers are Beta HCG, AFP & LDH
• Testicular teratoma in adults is Malignant
• Lower abdominal mass which shows a well-formed tooth on plain x-ray is sugestive of A mature
cystic teratoma
• Sacrococcygeal teratoma is associated with defect during gastrulation
• The dermoid cyst, diagnosed at 6 weeks of pregnancy should be treated At 14-16 weeks of
pregnancy
• Tumor containing cells of all three germ layers is called Teratoma

35. Ovulation
• First polar body is extruded accompanied by ovulation.

• In 40 days of menstrual cycle the ovulation occurs at 26th day.
• Ovulation occurs due to mid cycle FSH and LH surge.
• Fall of temperature at ovulation is by 0.5 degree Fahrenheit.
• Post ovulation, the cervical mucus is thick.
• Maximum function of corpus luteum occurs 9 days after ovulation.
• LH surge preceedes ovulation by 36 hours.
• Time of ovulation is detected by urine LH and urine FSH.
• Best diagnosis of ovulation is by Endometrial biopsy >Ultrasound.
• Tests for ovulation :Fern test , Basal body temperature ,LH surge , Ultrasound Monitoring
• Ovulation can be evaluated by Cervical Mucous.
• Hormonal study(Urinary LH surge) for assessment of female fertility during a menstrual cycle can
best predict the timing of ovulation.
• Hypogonadism with normal FSH and oestradiol levels belongs to type II disorders of ovulation as
per the WHO classification .
• The mid-cycle shift in the basal body temperature (BBT) after ovulation in women is caused by
Progesterone.
• Ovulation occurs 14 days prior to next menstruation.
36. Prolactin
• Prolactin secretion is tonically inhibited by the hypothalamus

• Prolactin secretion is increased by Increased FSH,Increased libido, Increased
testosterone,Sleep, Pregnancy & stress
• Prolactinoma in pregnancy is Most common pituitary tumor but rarely symptomatic
• Increase in prolactin levels worse prognosis of Prolactinoma in pregnancy
• Hyperprolactinemia is a side effect of Metoclopramide
• Initiation of lactation is affected by Progesterone ,Prolactin & HPL
• Decreased estrogen is a function of prolactin during lactation
• Prolactin Highest during pregnancy and fall during lactation
• A 30 year old woman presents with secondary amenorrhoea and galactorrhoea for 3 years is
diagnosed to have Prolactinoma
• Prolactinoma, Haloperidol & Hypothyroidism can cause hypersecretion of prolactin
• Secretion of Prolactin is affected by dopamine
• Prolactin secretion is inhibited by Bromocripitine
• Cabergoline is preferred for infertility treatment of a female with increased prolactin levels
• The most likely hormone increased in a middle aged female with a mass in sella turcica is prolactin
• Prolactinoma is the most common type of pituitary adenoma
• Prolactin secretion is stimulated by TRH
• A male presents with gynaecomastia, galactorrhoea and hypogonadism. Likely diagnosis is
prolactinoma
37. PUBERTY
• Orchidopexy for cryptorchidism is done at the age of Puberty

• 2:1 is the ratio of length of cervix and body of the uterus before puberty
• According to Tanner stages of development, Thelarche is the first sign of puberty in females
• The first sign of puberty in girls is Breast budding
• 35 gms is the approximate weight of thymus gland at puberty
• The difference in the age of onset of puberty amongst males may be explained by Increased Inhibin
levels
• Estrogen is mainly responsible for skeletal maturation of long bones during puberty
• Gamma amino butyric acid (GABA) has an inhibitory control over the GnRH neurons before the
onset of puberty
• Thelarche-puberche-growth spurt-menarche is the correct order of events at puberty in a girl
• Hormones required during puberty are LSH, Testesterone & Leptin
• First sign of puberty in female Tanner stage II
• Sign of puberty in boys is Enlargement of testes
38. UTERINE PROLAPSE
• Stress incontinence is a common symptom in Prolapse uterus

• Most common genital prolapse is Cystocoele
• Cause of decubitus ulcer in uterine prolapse is Venous congestion
• For Multipara with uterine prolapse the management of choice is Fothergill's repair with tubal
ligation
• Indication of Manchester operation in prolapse is Women of < 35 yrs age, Congenital elongation of
cervix & Patient who wants child bearing function
• Birth trauma is a risk factor for Prolapse uterus
• Most important structure preventing uterine prolapse is Cardinal ligament
• Purandare's cervicopexy is done in Congenital prolapse of uterus
• Pregnancy with prolapse : Pessary treatment
• Uterine prolapse in a nulliparous : Shirodkar sling operation
• Prolapsed pouch of Douglas : Posterior colpoperineorrhaphy
• Genital prolapse is best repaired after 6 months of child birth
• Fothergill's, Ward Mayo & Le Forte operations are used for genital prolapse
• Urinary incontinence in uterovaginal prolapse is mostly is due to Stress incontience
• Treatment of choice in a multiparous female with 2nd degree uterovaginal prolapse is Fothergill's
operation with tubal ligation
• The best way to treat decubitus ulcer in a case of genital prolapse is by Reduction with tampoon
• Presence of decubitus ulcer in prolapse indicates Circulatory disturbances
• In Early pregnancy a rubber — ring passary is an appropriate management for a woman who
is having utero — vaginal prolapse
• According to shaw's classification, IIIrd degree of uterine prolapse is Cx outside the introitus
• Broad ligament doesn't prevent prolapse of uterus
39. Secondary amenorrhea
• In a case of secondary amenorrhea who fails to get withdrawl bleeding after taking E and P, the
fault lies at the level of Endometrium
• In secondary amenorrhea the cause could be Stein leventhal syndrome & Premature ovarian
failure
• Commonest cause of secondary amenorrhea is Pregnancy
• Female with secondary amenorrhea with serum prolactin level 75 ng/ml is to be treated
with Cabergoline
• Secondary amenorrhea and galactorrhea with tumour of < 10mm diameter in the pituitary fossa
can be treated by Bromocriptine
40. POLYCYSTIC OVARIAN SYNDROME (PCOS) OR DISEASE (PCOD)
• Elevated LH hormone is seen in PCOD

• PCOD Can cause infertility
• PCOD May be associated with abnormal glucose tolerance test
• Polycystic ovaries is characterized by obesity,Theca cell hyperplasia and Hyperandrogenism
both,Amenorrhoea or Oligomenorrhea, infertility and hirsutism/Alopecia
• Increased LH / FSH ratio & DHEAs are seen in PCOD
• Polycystic ovary disease is the most common cause of Hirsutism
• Poly cystic ovarian disease is associated with Endometrial carcinoma
• High LH, low FSH and low Estradiol are the hormonal changes seen in PCOD
• Positive progesterone challenge test in a patient of secondary amenorrhoea, seen in PCOD
• Sample for testing LH and FSH are best taken on 8-10 days of menstrual cycle in suspected case of
PCOS
• Ovarian carcinoma, Endometrial carcinoma,Adrenal hyperplasia & Insulin Resistance are associated
with PCOD
• GnRH analogue is used in treating PCOD
• Metformin is used in treatment & control of Diabetes & PCOD
41. IMPERFORATE HYMEN
• Cryptomenorrhea occurs due to Imperforate hymen

• Acute pain in the lower abdomen & tense bulge in the region of hymen in 13 year old with absence
of menarche suggests Imperforate hymen
• Heamatocolpos is seen in Imperforate hymen
42. PELVIC INFLAMMATORY DISEASE
• Mycobacterium can be grown from menstrual blood in PID due to TB

• PID due to TB is Associated with infertility
• Ectopic pregnancy is common in PID due to TB
• Salpingitis / Endosalpingitis is best confirmed by Hysteroscopy + Laparoscopy
• Most comon cause of pelvic inflammatory disease in virgin girls is Tubercular
• Surest sign of salpingitis is Seropurulent discharge from the fimbria/ part of the tube
• Incidence of sterility is maximum in pelvic inflammatory disease caused by Gonococci
• Backache is a characteristic symptom of chronic pelvic inflammatory disease
• PID is caused by Schistosomiasis, Crohn's disease & Syphilis
• Pelvic Inflammatory Disease occurs least common with Condom
inflammatory disease is Fallopian tubes
• Pelvic inflammatory disease (PID) predispose to ectopic pregnancy
• Fitz-Hugh-Curtis syndrome is a complication of PID in which Pain and discomfort in the right
hypochondrium is due to concomittent perihepatitis
• Abdominal pain of rapid onset in the right lower quadrant showing tubal pregnancy is suggestive of
history of PID
• Sequence of events, after salpingitis, in gonorrhoeal pelvic infection is Pyosalpinx, hydrosalpinx,
pelvic abscess
43. Genuine stress incontinence
• Bonney's test is used to demonstrate Stress incontinence

• Stress incontinence is repaired by Marshall Marchatti Krantz repair
• Stress incontinence is a common symptom in Prolapse uterus
• Kelly's suture is done in Stress incontinence
• Treatment of genuine stress incontinence are Anterior colporrhaphy, Pelvic floor exercise
& Colposuspension
• Bead cystogram is used for the diagnosis of Stress incontinence
• The recommended non surgical treatment of stress incontinence is Pelvic floor muscle exercises
• Tension Free Vaginal Taping (TVT) is the treatment of choice for genuine stress incontinence
• To differentiate between stress incontinence and detrusor instability investigation done
is Urodynamic study

44. VAGINAL PROLAPSE
• Shirodkar's abdominal sling is the treament of choice for nulliparous woman who has 3rd degree
uterovaginal prolapse without any cystocele or rectocele.
• Treatment of choice in a multiparous female with 2nd degree uterovaginal prolapse is Fothergill's
operation with tubal ligation
• Cystocele is formed by base of the bladder
• The most common type of genital prolapse is Cystocele
45. Perineal Lacerations
• Commonest cause of recto vaginal fistula is Improper repair of perineal tear

• Prolonged labour, H/O difficult vaginal delivery incontinence of loose stools and flatus from the day
of delivery is suggestive of Complete perineal tear
• Perineal hematoma after trauma is due to Rupture of bulbar urethra
• The muscle that is most often injured by a tear of the perineum is innervated by Pudendal nerve
• Tear involving the perineal muscles but sparing the external and internal anal sphincters are kept
under 2nd degree perineal tear
• During childbirth, Pubococcygeus is most often injured by a tear of the perineum
• In a case of direct occipitoposterior position (Face to pubis delivery) most commonly encountered
problem is Complete perineal tears
• In a patient with third degree perineal tear, presenting after 1 week, repair should be done After 12
weeks
• III degree perineal tear is involvement of Anal sphincter
46. DYSFUNCTIONAL UTERINE BLEEDING (DUB)
• Treatment of DUB in young female is Hormones

• Causes of dysfunctional uterine bleeding can be Irregular ripening of endometrium
• The most common histological finding of endometrium in DUB is Hyperplastic
• Treatment for 32 years old multipara with dysfunctional uterine bleeding (DUB) is Progesterone
• In DUB, there is Increased oestrogen
• Dysfunctional uterine bleeding is associated with Metropathia-haemorrhagica
• Dysfunctional uterine bleeding is defined as abnormal bleeding due to Anovulatory cycle
• In a case of dysfunctional uterine bleeding thehormone which is usually deficient is Progesterone
• The progestogen with the greatest haemostatic effect used in dysfunctional uterine bleeding (DUB)
is Norethisterone
• D and C is useful in the diagnosis of DUB
47. Acute Pelvic Pain
• The severity of pelvic pain in endometriosis correlates best with Depth of invasion
• Acute pelvic /abdominal pain is seen in PID
• Pelvic pain is mediated by Autonomic nerves
48. SEMEN ANALYSIS
• Sperm count - 15 million/ml ; pH - 7.5 ; volume - 2 ml ; no agglutination is seen. Morphology shows

60% normal and 60% motile sperms suggest diagnosis of Oligospermia
• Sperm count > 20 million / ml, Sperm with normal morphology (strict criteria) > 15% & Motility >
25% with rapidly progressive motility are essential criteria according to WHO for normal semen
analysis
• A specimen obtained by masturbation near the laborator & colitus interuptus into a wide-vessel
is best specimen for semen analysis
• The most useful imaging modality to evaluate the cause of low volume, fructose negative ejaculate
with azoospermia infertility case is Transrectal ultrasonography
• First test for a couple presenting with infertility is Husband's semen analysis
• Azoospermia diagnosed on semen CFTR gene mutation analysis
49. SPERM ANATOMY
• Daily sperm production is 120 million per day

• Mitochondria of a sperm is seen in Body
• With respect to the spermatozoa tail structure Axoneme is the unit that is essential for motility
• Spermatogenesis occurs at Temperature lower than core body temperature
• Length of a mature human spermatozoon is 50-60 microns
• Sperm after formation is stored in Epididymis
• Acrosome cap of sperm is derived from Golgi body
50. MALE INFERTILITY
• Male infertility occurs if the sperm count is less than 20 million / ml

• Infertility is a common feature in Sertoli cell only syndrome, because There is no germ cells in this
condition
• Transrectal ultrasound and seminal vesicle aspiration are investigations which help in confirmation
of the diagnosis of Ejaculatory Duct obstruction
• Degeneration of the epithelium of seminiferous tubules is the cause of infertility in patient
with failure of testes to descend down in the scrotum
• Patient with Kartagener's syndrome is diagnosed to have Immotile sperm
• Liver dysfunction causes increased estrogen and decreased testosterone leading to testicular
atropy leading to infertility
• Kartagener's syndrome includes Male infertility, Situs inversus & Bronchiectasis Sinusitis
• Most common cause of surgically treatable male infertility is Varicocele
51. FEMALE INFERTILITY
• Lady with infertility with bilateral tubal block at cornua : best method of management is IVF
• Treatment for Cervical infertility can be Condom for 3 month, Gamete Intrafallopian transfer IUI
• Salpingitis, PID & Submucosal myomata are cause of infertility
• LH, GnRh and Clomiphene are used in treatment of infertility
• Endometrial biopsy for infertility is taken on 23 to 26 day
• In endometriosis, cause of infertility is Immobility of tubes, Anovulation & Tubal block
• A woman treated for infertility, presents with 6 week amenorrhea with urinary retention. The most
likely etiology is impacted Cervical Fibroid
• For infertility without significant clinical problem, most likely diagnosis is T.B. endometrium
• Laparoscopic and dye test are done doing secretory phase of the cycle for finding out the tubal
factors of infertility.
• To test ovarian reserve, FSH is measured
• MOST common cause of ovarian hyperstimulation FSH/LH therapy
• PCOS shows oligomenorrhoea, infertility and hirsuitism
• Both Bromocriptine and cabergoline can be used as both decrease prolactin levels, however,
cabergoline is better tolerated.
• Gold standard investigations for female infertility is Laparoscopy and hysteroscopy
52. TESTS FOR OVULATION
• Luteal phase defect is best diagnosed by Endometrial biopsy

• Perforation of the uterus while doing endometrial biopsy in a case of suspected genital tuberculosis
needs Laparascopy & Observation
• Inadequate secretion of Progesterone may cause luteal phase defect
• 20 - 22 days is the right time in menstrual cycle to do endometrial biopsy in case of infertility.
• Fern test is due to Presence of NaCI under estrogenic effect
• The hormone responsible for a positive "Fern test" is Estrogen
• Ovulation is associated most commonly with LH surge
• Investigation of choice in post-menopausal bleeding is Endometrial biopsy
• Endometrial biopsy best diagnostic method for finding out ovulation
• The best method of assessment of female fertility that allows accurate prediction of ovulation is the
measurement of urinary LH surge (Hormonal Test).
• Hysteroscopy is not a documentation test for ovulation in women of reproductive age
• The best time to do an endometrial biopsy in a patient with suspected endometrial cancer is 26th
day

53. MALE STERILIZATION-VASECTOMY
• After vasectomy aspermia will become evident in 10 to 12 weeks

• Failure of the husband to use a condom soon after vasectomy may lead to pregnancy of his wife.
• When sperms are absent from two consecutive samples of semen, the vasectomy is considered
complete for contraception
• 1 in 2000 men can become fertile again after vasectomy
• Sperm granuloma is a common complication in vasectomy
• Reversal is most successful within 10 years of initial surgery
• Take about 3 months before the sperm stores are used up
• There is a risk of chronic testicular pain
• Ductus deferens is ligated in vasectomy
• Done under local anaesthesia
• Antibodies against sperms may develop after vasectomy
54. FEMALE STERILIZATION
• Method of sterilization which is least effective is Hysteroscopic tubal occlusion

• Minilaparotomy is the safest method of sterilization in immediate post partum period
• The success rate following tubal recannalisation is low after Fimbriectomy
• Methods used for Laparoscopic sterilization include Electrocoagulation, Falope ring & Filchie clip
• Pomroy , Aldridge’s & Madlener are reversal methods of sterilization surgery
• Shoulder pain post laparoscopy is due to CO2 retention
• Gas commonly used in laparoscopy is CO2
55. FIBROID MANAGEMENT
• Methods of managing fibroid uterus include Myomectomy, Embolisation of uterine artery & Laser
myomectomy
• Drugs that reduce the size of fibroid are Danazol and GnRH analogues
• Treatment of choice in a perimenopausal woman with bleeding PV due to multiple fibroids Is Total
abdominal hysterectomy (TAH)
• Conservative surgical therapy is Indicated in a pregnant female with red degeneration of fibroid
56. VAGINAL CANCER
• Most common type of vaginal carcinoma is Squamous cell carcinoma

• Ingestion of Diethyl stilbestrol during pregnancy increase the risk of vaginal adenocarcinoma in a
female offspring
• Vaginal adenocarcinomas in children is caused by Adminstration of DES to pregnant mothers
57. PAPANICOLAOU TEST
• Pap smear is useful in the diagnosis of Trichomonas vaginalis, HPV & Inflammatory changes
• Women > 20 years,Pregnant female, Sexually active female are all indicaed for pap smear
• Pap smear in pregnancy is Routine, as a part of screening
• Pap smear can detect CIN
• Pap smear reduces incidences of Ca cervix
• Koilocytes with perinuclear halo on pap smear is pathognomic of HPV infection
• Pap smear most commonly demonstrates protozoal parasites Trichomonas vaginalis in women
• A female presented with post coital bleeding can be managed by Pap smear and colposcopy
• Pap smear is an example of Secondary level of prevention
• Screening of cervical cancer at PHC level is done by PAP smear
• Sensitivity of conventional PAP smear in picking up cervical cancer is 80%
58. CARCINOMA CERVIX
• Intravenous pyelography, Cystoscopy & Proctoscopy investigations are used in FIGO staging of
carcinoma cervix
• A case of carcinoma cervix is found in altered sensorium and is having hiccups, likely cause is
uremia
• CA cervix is Common at squamocolumnar junction
• Post coital bleeding is a common symptom of CA cervix
• HPV 16 and 18 are associated with high risk of carcinogenesis
• In Carcinoma of cervix lymphatics drain to Hypogastric , External iliac & Obturator lymph nodes
• Adenocarcinoma cervix is associated with HPV 16, 18 & 51
• Post coital bleeding would be the earliest symptom of Ca cervix
• Carcinoma cervix involving upper 2/3 of vagina without parametrial involvement are classed as IIA
• Carcinoma cervix is the Commonest cause of pyometra
• Ca cervix can be prevented by screening
• Complication, which results in mortality, in carcinoma cervix is Renal failure
• Carcinoma cervix involving upper 2/3rd of vagina. The stage would be Stage II a
• Risk factor of CA cervix Smoking
59. Management of CA of cervix
• A case of carcinoma cervix who earlier received radiotherapy, relapses with new lesion should be
treated with Pelvic exenteration
• Management of stage IIB cancer cervix is Radiotherapy with combination with chemotherapy
• Ca cervix of stage between II - III should be treated with Radiotherapy and chemotherapy
• Ca cervix stage III B is treated with Intracavitary brachytherapy with external beam radiation
• Point B in treatment of Ca cervix corresponds to Obturator Lymph node
• Treatment of carcinoma Cervix stage IIIB include Concurrent chemoradiation
• 80-85 and 85-90 gy. is the maximum radiation dose to point A for early and advanced Ca cervix
60. Hirsutism
• Polycystic ovaries shows obese woman presenting with Oligomenorrhea, infertility and hirsutism
• Most common cause of Hirsutism is PCOD
• Commonest cause of hirsutism in a teenage girl is Ovarian disease
• The first step in the management of hirsutism due to stein leventhal syndrome is OCP
• Spironolactone, Finasteride & Flutamide are used for hirsutism in female
• Hirsutism and amenorrhea with change in voice can be estimated by Testosterone tests
• Hirsutism is seen in Stein leventhal syndrome , Cushing syndrome & Congenital adrenal hyperplasia
• Hirsutism can be caused by Steroidogenic enzyme defects, Minoxidil & Acromegaly
• Primary overproduction of ACTH shows hirsutism, hyperglycemia, obesity, muscle wasting, and
increased circulating levels of ACTH.
• Spironolactone, Flutamide & Cyproterone are used in treatment of hirsutism
• Oligomenorrhea ,hirsutism and virilisation with enlarged left ovary & testosterone levels 4 ng/ml is
suggestive of Ovarian tumor
• Hirsutism is a Complications of cyclosporine
• Phenytoin causes hirsutism
• MC cause of hirsutism in females is Stein Leventhal syndrome
61. Gartner's cyst
• Cystic swelling at the junction of lower 1/3rd and upper 2/3rd of anterior wall of vagina at 10 0'
Clock position is diagnosed as Gartner's cyst
• Gartner's cyst can be a congenital cyst
• Gartner's cyst arises from Remnant of mesonephric duct
• Swelling enlarges and becomes more painful with approaching menses in case of Gartner's cyst
• Gartner’s cyst is a cystic remnant of Wolffian duct
• Gartner's cyst is seen in Vagina
62. Testicular Feminization syndrome
• 46XY, Primary amenorrhea & Vagina may be present in testicular feminization syndrome
• High testosterone levels is seen in testicular feminization syndrome
• In Testicular Feminization syndrome Gonadectomy is indicated At puberty
• Androgen insensitivity syndrome the Phenotype may be completely female
• Androgen Insensitivity Syndrome is present with absence of both Mullerian and Wolffian duct
structures
• Short vagina and absent ovaries may be seen in Testicular Feminization syndrome
• Primary Amenorrhea with absent uterus, normal breasts and scanty pubic hair is seen in Androgen
Insensitivity Syndrome
63. Pearl index
• Calculation of pearl index is No. of pregnancies X 1200/( Number of women X number of months)
• Pearl Index is a measure of Potency of contraceptives
• Pearl index is Failure rate/100 women years
• Total accidental pregnancy is important in calculaton of pearl index
64. Barrier Methods of contraceptions
• Spermicidal jelly acts through Disruption of cell membrane

• Nonoxynol & Menfegol are Spermicidal agents
• Best mode of contraception for a newly married lady with rheumatic heart disease Condom
• Pelvic Inflammatory Disease occurs least common with Condom
• Condom is Unrolled over erect penis
• Air should be squeezed out of tip of Condom
• K-Y jelily may be used for lubrication of Condom
• Contact dermatitis is associated with the use of condom
• Condoms has the least risk of ectopic pregnancy
• Contraceptive failures with condoms are MOST often due to Incorrect use
• Condom or diaphragm is the safest contraceptive method for a woman with sickle-cell anaemia
• 10-20 percent is the failure rate in use of condoms.
• Dutch cap is a Diaphragm
• Best protection from STD and Syphilis is by Condom
• Condoms are more preferred because Reduced side effects
• Conventional contraception is Condom
• Failure rate of female condom 5-20 per 100 women years

65. Sheehan's syndrome
• Empty sella in skull x-ray,amenorrhea & failure of lactation following delivery are seen
in Sheehan's syndrome
• Amenorrhoea, Failure to lactate & Absence of secondary sexual characteristics are seen with
Sheehan's syndrome
• Cortisone is essential in Sheehan's syndrome
66. Dysmenorrhea
• Dysmenorrhea & Menorrhagia are Symptoms of adenomyosis

• Treatment of choice in a young patient with primary dysmenorrhea is Symptomatic
• One horn of malformed uterus, Endometriosis with unilateral distribution & Small fibroid at the
utero tubal junction are Cause of unilateral dysmenorrhea
• Cause of secondary dysmenorrhea in a young female are TB, Subserous fibroid & Endometriosis
• Secondary dysmenorrhea is Present just before menstruation
• In Secondary dysmenorrhea The pain may persist for 12 - 24 hours
• Dyspareunia is seen in Secondary dysmenorrhea
• Hysterectomy is definitive treatment of adenomyosis
67. Endometrial Hyperplasia
• Endometrial hyperplasia is seen in PCOD cervix

• Treatment of choice in a postmenopausal lady with atypical endometrial hyperplasia
is Hysterectomy
• Atypical endometrial hyperplasia undergoes malignant transformation in 25%
• Endometrial hyperplasia is indication for using endogenous progesterone
• Estrogen causes endometrial hyperplasia
• The risk of endometrial carcinoma is highest with Complex hyperplasia with atypia
• Tamoxifen causes Endometrial hyperplasia
68. Laparoscopy
• Best gas used for creating pneumoperitonium at laparoscopy is CO2

• Laparoscopy is best avoided in patients with COPD
• Best tubal function test is Laproscopy
• Laproscopy detects Endometriosis
• Primary amenorrhea and absent vagina can be diagnosed with Laparoscopy
inflammatory disease is Fallopian tubes
• Pawaer burr, appearance on laparoscopy is characteristic of Endometriosis
• Best investigation to diagnose ectopic pregnancy is laparoscopy
• Pressure needed for abdominal insufflation in laparoscopy is 10 mm Hg
• Advantage of carbon dioxide in laproscopy are Non-irritant, Non-inflammable & No tissue reaction
• Shoulder pain post laparoscopy is due to CO2 retention
• Anorchia best diagnosed by Laparoscopy
69. Laparotomy
• Minilaparotomy is the safest method of sterilization in immediate post partum period

• Mini laparotomy is done in Internal sterilisation, Uterus elevations & Tubectomy
• Necrotizing pancreatitis with secondary infection can be treated with Exploratory laparotomy
• Death from untreated chronic adrenal insufficiency may occur within hours of laparotomy surgery
• In blunt trauma abdomen laparotomy is done Always via midline incision
• Immediate laparotomy and clamping of the bleeding vessels may be the only means of saving the
life of a moribund patient
• Gravimetric method gives the best estimation of blood loss in prolong laparotomy surgery.
• Prolonged postoperative ileus is best treated by Laparotomy and exploration
• An ovarian cyst is detected in a pregnant woman, management is Laparotomy
• Most common site for infra abdominal abscess following laparotomy is Sub hepatic
• Serous discharge from the wound following Hemicolectomy can be treated with urgent Laparotomy
• Most common indication for laparotomy in intestine T.B is Intestinal obstruction
• Aims of abbreviated laparotomy Hemostasis
70. Hysteroscopy
• Hysteroscopy can diagnose Asherman's syndrome,Uterine synechiae, AUB,Infertility, Septate

uterus & TB endometritis
• Hysteroscopy means visualization of Uterine cavity
• Fallopian tube patency is checked by Hysteroscopy, Laparoscopy & Hysterosalpingography
• Submucosal fibroid is detected by Hysteroscopy, USG (Transabdominal) & Hysterosalpingography
• The method to diagnosis misplaced intra uterine device is Hysteroscopy,Ultrasound & X-Ray
abdomen (Erect view)
• Gold standard IOC for female infertility is Laparoscopy and hysteroscopy
• Treatment of choice for Asherman's syndrome Hormones, Hysteroscopy and adhesiolysis & IUCD
• Media commonly used for distension in hysteroscopy is Carbon dioxide
71. Red degeneration of fibroid

• Fibroid uterus with acute abdominal pain ,low grade fever and mild leucocytosis is suggestive
of Red degeneration of fibroid .
• Red degeneration in uterine fibroid is most common in Second trimester
• Treatment of Red degeneration of fibroid during pregnancy include Analgesics
• Red degeneration of fibroid is due to Thrombosis of the veins
• Red degeneration of uterine fibroid Is aseptic infarcation
• Red degeneration of fibroid is associated with Pregnancy
72. Cervical intraepithelial neoplasia (CIN)
• CIN II have risk of malignancy as of 5%

• CIN grade III followed by pap smear should be confirmed by Colposcopy directed biopsy
• Treatment of choice of stage III CIN is Hysterectomy
• Time taken for conversion of CIN cervix to invasive carcinoma is 10 years
• Cervical intraepithelial neoplasia III with no colposcopy activity treatment of choice Conisation
• HPV-related cervical intraepithelial neoplasia can be diagnosed by the presence of Cytoplasmic
vacuolization and nuclear enlargement of cells
• Human papillomavirus (HPV) is most commonly associated with cervical intraepithelial neoplasia,
grade II (CIN II)
• Cervical intraepithelial neoplasia associated with a previous viral infection shows E6 and E7 proteins
• Abnormal cervical cytology on PAP smear suggestive of CIN III (HSIL) should be managed
with Colposcopy and LEEP
• Treatment modality In CIN patients can be Cryotherapy, LEEP and Cold knife conization
73. MYOMECTOMY
• Myomectomy is a method of managing fibroid uterus

• Sub-serosal fibroids of on anterior wall of uterus and fundus, can be best treated
with Myomectomy
• Cesarean section should be done in Myomectomy scar after 2 years
• Tourniquet can be used to reduce blood loss during myomectomy for fibroid uterus
Orthopedics

1. Lesions of radial nerves
• Injection palsy(Tetracycline injection)

• Injury to radial nerve in lower part of spiral groove results in Anconeus muscle paralysis.
• If lesion occurs in radial groove long head of triceps are spared & thus it leaves extensions at elbow
joint intact.
• Radial nerve palsy produces an inability to extend the metacarpophalangeal joints, owing to
paralysis of the extensor digitorum communis muscle.
• In radial nerve injury triceps(Nerve supply to the triceps is proximal to the mid shaft level) are
spared.
• Low radial nerve palsy occurs when the radial nerve is injured at the level of elbow, so that the
muscles supplied by the radial nerve in the distal arm (Brachioradialis and Extensor Carpi radialis
longus ) are not affected. The muscles affected are finger extensors, extensor carpi radialis brevis &
sensation on dorsum of hand.
• Radial nerve injury cause anaesthesia over anatomical snuff box
• Radial nerve injury only weakens (affects) abduction & extension movements of thumb and spares
flexion, adduction & opposition
• Cock-up splint is used for radial nerve palsy (extensors of wrist and metacarpophalangeal joints
paralyzed)
• In radial nerve injury Below the elbow low radial nerve palsy occurs.
• Wrist drop- fracture is seen in radial nerve injury.
• radial nerve injury is most common incase of # of middle 3rd of shaft of humerus.
2. ULNAR NERVE INJURY
• Ulnar nerve commonly seen involved In injuries at the elbow are usually associated with fractures
of the medial epicondyle.
• Ring & little fingers are not capable of being markedly flexed
• The patient is unable to adduct and abduct the fingers and consequently is unable to grip a piece of
paper placed between the fingers.
• It is impossible to adduct the thumb in ulnar nerve palsy
• The metacarpophalangeal joints become hyperextended in ulnar nerve palsy
• In case of lesion of ulnar nerve, paralysis of interosseous muscles occurs which leads to clumsiness
• claw deformity is seen in long standing case of ulnar nerve palsy
• Loss of skin sensation will be observed over the anterior and posterior surfaces of the medial third
of the hand
• TARDY ULNAR NERVE PALSY is seen in lateral condyle # of humerus resulting in ulnar nerve injury
• Cubitus valgus deformity and tardy ulnar nerve palsy is seen as the late complication of ulnar
nerve injury
• Hypothenar atrophy is seen in ulnar nerve injury.
• Ape thumb deformity is associated with ulnar nerve palsy.
• It is the most common nerve involved in Hansen's disease(leprosy)
• Froment sign is test use to detect ulnar nerve palsy
• Knuckle bender splint is used in palsy of ulner nerve
3. Erb's paralysis
• Erb's point (upper trunk of brachial Plexus) Six nerves meet here(C5 ,C6)
• Nerve roots involved in erb's palsy are Mostly C5 & partly C6
• Arms: Medially Rotated (Hangs by side) owing to paralysis of teres minor & infraspinatus.
• Policeman's tip hand (or) Porter's tip hand seen in erb's palsy
• Abduction & lateral rotation of the arm
• Flexion & Supination of the fore-arm at elbow
4. KLUMPKE'S PARALYSIS
• Lower trunk of brachial plexus is the site of injury leading to brachial plexus
• Mainly T1, Partly C8 nerve roots are affected in klumpke's palsy
5. Foot Drop
• Classic sign of lead induced peripheral neurotoxicity is Foot drop

• A previously healthy 45 yrs old laborer suddenly develops acute lower back pain with right-leg pain
and weakness of dorsiflexion of the right great toe showing foot drop is indicated for early surgical
intervention
• Foot drop is features of common peroneal nerve injury
• Foot drop with weakness of the anterior tibial, posterior tibial, and peroneal muscles with Sensory
loss demonstrated over the anterior shin and dorsal foot suggest a radiculopathy at L5
• Foot drop occurs due to the involvement of Sciatic nerve, Direct injury to the dorsiflexors, Common
peroneal nerve palsy
6. Rickets
• Defect in proximal tubular reabsorption is seen in vitamin D resistant rickets

• Craniotabes, Bow legs & Increase alkaline phosphatase are findings of rickets
• Rickets in infancy is characterised by Craniotabes,Rachitic rosary, Wide open fontanelles
• Radiological examination of long bones are investigations showing the earliest evidence for healing
in treatment of rickets
• Flaring of anterior ends of the ribs is characteristically seen in Rickets

• A child presented with clinical features of rickets but low level of serum alkaline phosphatase is
seen in Hypophosphatasia
• Any child with rickets also has osteomalacia while the reverse is not necessarily true
because Osteomalacia is found within the same spectrum of rickets, but occurs in persons of any
age group, not only in children.
• vitamin D-resistant rickets X-linked dominant showing Defect in skeletal ossification & Reduced
serum phosphorus
• Triradiate pelvis is seen in Rickets
• Serum marker of rickets is Alkaline phoshpatase
• Rickets is due to Loss of calcium in urine,Increased mobilisation of calcium from bone
• Basic pathology in rickets is Defect in mineralization
• Cupping of metaphysis & Defective Mineralization is seen in rickets
• Craniotabes & Widening of wrist are seen in nutritional rickets
• Bow legs,Pot belly & Craniotabes is seen in Rickets
• Most common cause of genu valgum in children is Rickets
• Wind swept deformity is seen in Rickets
• Costochondral junction swelling is seen in Rickets
• Prominent fontanelle,Hot cross bun sign & Caries teeth is seen in active rickets
• Cupping of metaphysis,Ricketic rosary are the radiographic feature of rickets
• Quant's sign (a T-shaped depression in the occipital bone) may be present in rickets
• Hypophophatemia is seen in Rickets
• Wormian bones are seen in rickets
7. Shoulder Dislocation
• In Inferior shoulder dislocation nerve most common injured is Axillary nerve

• Velpeau bandage and Sling and Swathe splint are used in Shoulder dislocation
• Hill Sachs lesion' is a consequence of Anterior dislocation of shoulder joint
• Inferior dislocation of shoulder is referred to as Luxatio erecta
• Attitude in subcoracoid dislocation of shoulder includes Limb on side of body
• The position of arm in posterior dislocation of shoulder is In internal rotation
• Loss of the normal contour of the shoulder and a abnormal-appearing depression below the
acromion.
• Recurrent dislocation are common in Shoulder
• Commonest type of shoulder dislocation Subcoracoid
• Recurrent dislocation of shoulder occurs, because of Crushed glenoidal labrum
• Hill sachs defect ,Bankart lesion,Lax capsule are related to recurrent shoulder dislocation
• The most common complication of dislocation of shoulder joint is Injury to circumflex nerve
• A patient with anterior dislocation of shoulder will most likely give a history of Abduction and
external rotation
• The easiest way to reduce dislocation of shoulder is by simple pressure with the patient under
general anesthesia with muscle relaxation
• Dugar's test is helpful in Anterior dislocation of shoulder
• Traumatic anterior dislocation of shoulder with sensory loss in lateral side of forearm and weakness
of flexion of elbow joint, most likely injured nerve is Musculocutaneous nerve
• Head of humerus usually dislocates forward from shoulder joint
• Injury is produced by forced extension & external rotation of abducted arm
• Posterior dislocation is often over-looked & Radiography may be misleading
• Fixed medial rotation in posterior dislocation
• Kocher's manoeuvre is effective in anterior dislocation
• Stryker's view is used in shoulder joint to visualise Recurrent subluxation
• Commonest shoulder dislocation is Preglenoid
8. HUMERUS FRACTURE
• Fracture shaft of humerus damages Radial nerve

• Fracture of surgical neck of humerus leads to loss of abduction movement of the corresponding
shoulder joint due to injury of Axillary nerve
• Fracture of lateral condyle of humerus is seen in age group of 5-15 years
• Most common nerve involved in supracondylar fracture of humerus is Anterior Interosseous nerve
• In supracondylar fracture of the humerus in children Admission to hospital is essential following
reduction
• Displaced fracture of the surgical neck of humerus as well as a fracture of the medial epicondyle of
his distal humerus with pain swelling & abnormal motor functions of arm suggest sustained nerve
injury causing trouble in Extensor carpi radialis longus action
• Ulnar nerve is injured in fracture of the medial epicondyle of humerus
• Periosteum is responsible for producing the majority of the new bone that will reunite the two
fragments
• Fracture neck Humerus is common in Elderly woman
• Treatment of choice for fracture neck of humerus in a 70 year old male Analgesic with arm sling
• Hanging cast is used in fracture humerus
• "Cubitus-valgus" deformity is complication of # Lateral condyle of humerus
• Tardy ulnar nerve palsy seen in Lateral condyle #humerus
• Tingling sensation and numbness in the little finger with history of fracture in the elbow region 4
years back is suggestive of Lateral condyle fracture humerus
• Ideal treatment for a displaced fracture lateral condyle of the humerus is Open reduction and
internal fixation
• The most common injury in a 7 years old child due to fall on outstretched hand is Supracondylar
fracture of humerus
• The most common elbow injury in children is Extension type of supracondylar fracture of humerus
• The most common deformity seen in supracondylar fracture of humerus is Varus
• Gunstock deformity is due to Supracondylar fracture of humerus
9. Fat Embolism
• Multiple injuries develops fever, restlessness, tachycardia, tachypnea and periumbilical rash is
diagnosed with Fat embolism
• Fracture femur followed by breathlessness is seen in fat embolism
• Fracture mobility is a risk factor, Thrombocytopenia & On ABG PaO2 is seen in fat embolism
• Tachypnea,Systemic hypoxia, Fat globules in urine,Petechiae in anterior chest wal &
Manifestation after several days of traumais the features of fat embolism
• The management of fat embolism includes Oxygen, Heparinization, Low Molecular weight dextran
• Tachypnoeic, and conjunctival petechiae seen after femur fracture may be due to fat embolism
• After an operation on femur bone, chest X-ray shows widespread mottling throughout the lung
field like a snowstorm. It is diagnostic of Fat embolism
• Fat embolism is characterized by Petecheal haemorrhages, Closed fractures of femur & Aggregation
of chylomicrons
• Laboratory findings in fat embolism consist of Thrombocytoenia, Fat globules in urine &Anemia
10. Osteochondritis
• Kienbock's disease - lunate

• Freiberg's disease is a recognised osteochondritis which affects Head of 2nd and 3rd Metatarsal
• Perthe’s disease Osteochondritis of femoral head, Presents at 5 – 10 years of age & Management is
conservative
• Locking of knee joint can be caused by Osgood shalter
• Osgood schlatter disease is osteochondritis of Tibial tuberosisty
11. ELBOW DISLOCATION
• Pain around elbow which is held in pronation with extension and normal X ray is diagnosed with
pulled elbow
• Most common type of Elbow dislocation is Posterior
• Most common associated injury of fracture medial epicondyle is Elbow dislocation
• Three point relationship is reversed in Elbow dislocation, Medial & lateral epicondyle fracture
• A child is spinned around by holding his hand by his father. While doing this the child started crying
and does not allow his father to touch his elbow. The diagnosis is Pulled elbow
• Myositis ossificans follows either a posterior dislocation or a spuracondylar fracture of elbow joint
• Pulled Elbow is Subluxation of proximal radio ulnar joint or Dislocation of head of radius
• Vascular injury,Median nerve injury, Myositis ossificans are the Complications of elbow dislocation
12. FRACTURE CLAVICLE
• Most common Complication is Malunion of Fracture of clavicle

• In treating a fractured clavicle in a 14 month old child, the best procedure is Figure - of - eight
bandage
• Fracture of clavicle is commonest at Junction of medial 2/3rdand lateral 1/3rd
• Clavicle fracture result from a violent force
13. GENU VALGUM
• Genu valgus deformity seen when Long axis of tibia & fibula moves lateral to the long axis of femur
• Pappu, 7 yrs old young boy, had fracture of lateral condyle of femur. He developed malunion as the
fracture was not reduced anatomically. Malunion will produce Genu valgum
• Most common cause of genu valgum in children is Rickets
• Genu valgum deformity is seen in Rickets, Bone Dysplasia & RA
14. Compartment Syndrome
• Indication for surgical compartment release in compartment Syndrome in any compartment is

absolute pressure greater than 30 mm Hg
• Dorsiflexion of foot causes pain in deep posterior compartment syndrome
• Fasciotomy, Splitting of tight pop cast & Reexploration are relevant in compartment syndrome
• Fractures is the commonest cause of anterior compartment syndrome
• Foot inversion causes weakness in deep posterior compartment syndrome
• Pain on passive stretch is reliable sign of compartment syndrome
• Fasciotomy is earliest management in compartment syndrome
• Interstitial pressure > capillary pressure in compartment syndrome
• Hyperesthesia is seen in compartment syndrome
• If A patient develops compartment syndrome (Swelling, pain and numbness) following
manipulation & plaster for fracture of both bones of leg the best treatment is operative
decompression of fascial compartment
• Characteristic features of the acute compartment syndrome in the lower leg includeAcute pain on
employing the stretch test, Normal pulses & Venous occlusion
• In posterior compartment syndrome Toe dorsiflexion can cause pain
• Intra abdominal pressure > 15 cm H2O in intra abdominal compartment syndrome
• Abdominal compartment syndrome is characterized by Oliguria due to ureter obstruction
• Most common cause of acute compartment syndrome in children is Fracture supracondylar
humerus
• Hyperbaric oxygen is useful in compartment syndrome
15. Genu Varum

• Blount's disease is associated with Genu varum
16. Pulled elbow
• A 4 year boy complaining of pain around elbow which is held in pronation with extension and
normal X ray is diagnosed to have Pulled elbow
• A child is spinned around by holding his hand by his father. While doing this the child started crying
and does not allow his father to touch his elbow. The diagnosis is Pulled elbow
• Pulled Elbow is Subluxation of proximal radio ulnar joint
• Pulled elbow is Dislocation of head of radius
• Pulled elbow Occurs due to sudden axial pull on extended elbow
• Pulled elbow Most commonly occurs between 2-5 years of age
• Forearm is held in pronation and extention in Pulled elbow
17. Green stick fracture
• A green-stick fracture is Part of cortex is intact and part is crumpled
18. OSTEOMYELITIS
• Salmonella osteomyelitis is common in Sickle cell disease

• Commonest site of bone involvement in hematogenous osteomyelitis Metaphysis
• Microorganism which causes pyogenic osteomyelitis is Staphylococcus aureus
• Sequestrum is a piece of dead bone seen in osteomyelitis
• In osteomyelitis Involvement is dense sclerotic bone overlying a sequestrum
• Tubercular osteomyelitis is a type of secondary osteomyelitis
• Sequestrum is uncommon in tubercular osteomyelitis
• Inflammation is minimal in tubercular osteomyelitis
• The most common site of infection in osteomyelitis in a 10 year old child is rapidly growing and
highly vascular metaphysis of growing bones
• The apparent slowing or sludging of blood flow, as the vessels make sharp angles at the distal
metaphysis, predisposes the vessels to thrombosis and the bone itself to localized necrosis and
bacterial seeding making metaphysis most common site of infection in osteomyelitis
• Pott’s puffy tumor , a complication of frontal sinusitis, is due to osteomyelitis of frontal bone
• Garre's osteomyelitis commonly involve Jaw bone
• Acute osteomyelitis can best be distinguished from soft tissue infection by MRI
• Secondary amyloidosis occurs in Chronic osteomyelitis
• Periosteal reaction in a case of acute osteomyelitis can be seen earliest at 10 days
• Commonest cause of hematogenous osteomyelitis Staph. aureus
• Earliest radiological change to appear in case of acute osteomyelitis is Loss of plane between soft
tissue and muscle
• Chronic discharging sinus with bone particle is seen in Chronic osteomyelitis
• Ewings sarcoma clinically mimics Osteomyelitis
• Reactive new bone formation occurs in chronic Osteomyelitis
• Cloaca is an opening in involucrum seen in chronic Osteomyelitis
• Brodie's abscess is present in chronic Osteomyelitis
19. Scoliosis
• Risser Localiser cast is used in the management of Idiopathic scoliosis

• Progression of congenital scoliosis is least likely in Block vertebra
• Scoliosis is the most common skeletal manifestation in Type-1 Neurofibromatosis
• Increased RV/TLC is seen in a preoperative pulmonary function test, done in a patient with severe
kyphoscoliosis
• Spastic quadriplegia is commonly associated with scoliosis and other orthopedic problems
• Musculo skeletal abnormality in neurofibromatosis is Scoliosis , Cafe au lait spots & Hypertrophy of
limb
• Unilateral elevation of diaphragm is commonly due to Scoliosis
• Vertebral rotation in scoliosis is checked in Forward bending
• Milwalkee brace is used in treatment of Scoliosis
• Turn-buckle cast is used for Scoliosis
20. COLLE'S FRACTURE
• Colles fracture is fracture at cortico-cancellous junction of the distal end of the radius with dorsal
tilt
• Colles fracture is common in women because of postmenopausal osteoporosis.
• Carpal tunnel syndrome, Reflex sympathetic dystrophy (RSD), Frozen hand shoulder syndrome are
the complications of Malunited Colles fracture
• Colles fracture best describes the patient's wrist fracture
• Stiffness of wrist, Stiffness of shoulder & Carpal tunnel syndrome are complication of colles fracture
• Dinner fork deformity is the characteristic of colles fracture
• Deformities present in colles fracture is Dorsalt tilt
• Proximal impaction , Lateral rotation & Dorsal angulation is seen in colles fracture
• Colles fracture is common in old age
21. Galeazzi fracture
• Galeazzi fracture is fracture of the distal third of the radius with dislocation of the distal radio-ulnar
joint
• Galeazzi fracture is fracture of Lower end of radius
• Galeazzi fracture is Fracture of the distal radius with inferior radio ulnar joint dislocation
• Fracture distal 1/3 radius with DRUJ subluxation
22. MONTEGGIA FRACTURE DISLOCATION
• Monteggia fracture is fracture of the proximal third of the ulna with radial head dislocation
• In Monteggia fracture Both ulnar fracture and head of radius is displaced anteriorly
• Posterior interosseous nerve is injured in Monteggia fracture dislocation
23. VOLKMANN'S ISCHEMIA
• The muscle which is affected by Volkmann's ischaemia most commonly is Flexor digitorum
profundus
• The first sign of Volkman's ischemia is Pain on passive extension of fingers
• In Volkman's ischemia, surgery should be done Immediately
• Split open the plaster of Paris cst and bandage, Decompression by fasciotomy, Exploration are done
to manage Volkmann's Ischaemia
• In Volkmann's ischaemia, surgery should be done within 1hour
• The most important sign in Volkman's ischemia is Stretch pain
24. VOLKMANN'S ISCHEMIC CONTRACTURE
• The most common nerve involved in volkmann’s ischemic contracture or forearm includes Median
• The most common cause of Volkmann's ischaemic contracture (V.I.C) in a child is Supracondylar
fracture of humerus
• The most important sign in Volkmann's ischaemic contracture is Pain
• Volkmann's ischaemic contracture mostly involves Flexor digitorum profundus
• Volkmann's contractrue Follows Ischaemia of the forearm
• Volkmann's Ischaemic Contracture is due to Ischaemic vascular injury to the muscle
• Volkmann's ischaemic contracture is commonly due to Tight palster or Tight splint
25. Bone graft
• Irradiation can be used to sterilize Bone graft

• Autologous bone graft is commonly taken from Iliac crest
• Treatment of choice for old non-united fracture of shaft of femur Compression plating with bone
grafting
• Treatment of Non-union of # shaft femur Bone grafting with internal fixation with K-Nail
• Best treatment of 3 weeks old, fracture shaft femur with nonunion is Bone graft with internal
fixation
• Cancellous bone graft taken from Femoral condyles, Pelvis & Greater trochanter
• Iliac crest is ideal site for harvesting bone graft
• Bone marrow aspirate bone grafts have osteogenic properties
• X-ray shows soap bubble appearance at lower end of radius, treatment of choice is Excision & Bone
grafting
26. Non union and Mal-union
• Fracture lower half of tibia, neck of femur & scaphoid are known for nonunion
• Pappu, 7 yrs old young boy, had fracture of lateral condyle of femur. He developed malunion as the
fracture was not reduced anatomically. Malunion will produce Genu valgum
• Periosteal injuries, Absence of nerve supply & Chronic infection fascilitate non union
• The most common cause of non union is Inadequate immobilization
• Non - union is a complication of Scaphoid #
• The most common complication of clavicle fracture is Malunuion
• The most important cause of Nonunion of fracture of - humeral shaft is Distraction at fracture site
• Fracture shaft of humerus is known for Non union in children, if left untreated
• Growth disturbance, nonunion, elbow instability & late ulnar nerve palsy is commonly seen
in Fracture lateral condyle
• A 10-year-old boy presenting with a cubitus varus deformity and a history of trauma 3 months back
on clinical examination, has the preserved 3 bony point relationship of the elbow. The most
probable diagnosis is Malunited supracondylar fracture of humerus
• The malunion of supracondylar fracture of the humerus most commonly leads to Cubitus varus
• The most common complication of supracondylar fracture is Malunion with gun stock deformity
• Commonest complication of Colles' fracture is Malunion
• In nonunion of scaphoid vescularized muscle pedicle graft is taken from Pronator quadratus
• Nonunion is a very common complication of intracapsular fractures of the neck of femur most
commonly caused by Inadequate immobilization, blood supply or Inhibitory effect of synovial fluid
• Commonest complication of extra capsular intertrochanteric fracture of neck of femur is Malunion
• The most common complication of intracapsular fracture neck of femur is nonunion
• Treatment of Non-union of # shaft femur Bone grafting with internal fixation with K-Nail
• Best treatment of 3 weeks old, fracture shaft femur with nonunion is Bone graft with internal
fixation
• Non union is a common feature of fracture of Lower tibia
• Common sites of fracture non union are Waist of scaphoid, Neck of femur & Distal 1/3 tibia fibula
• Mc Murray's osteotomy is done for Nonunion transcervical neck fracture of femur
• Fracture neck femur cause of non-union is Injury to blood supply with shearing stress
27. osteoporosis
Teriparatide
• Drug used in osteoporosis

• Inhibit resorption Bisphosphonates, donesumab, cinacalcet, calcitonin, estrogen, SERMS, gallium
nitrate.
• Stimulate formation :-Teriparatide, calcium, calcitriol, fluorides.
• Both actions Strontium renelate.
• The pain in right thigh in a 70 years old female, who is on treatment with alendronate for 7 years
for osteoporosis might be due to femoral shaft fracture.
• Plain X-rays showed a characteristic picture consisting of a transverse or short oblique fracture line,
lateral cortical thickening, and medial spiking.
Spontaneous femoral shaft fracture after long-term alendronate:
• Alendronate is used as first-line treatment for osteoporosis in postmenopausal women worldwide.

• The evidence supporting its benefit in reducing the risk of fragility fracture among this high-risk
group is well established.
• Due to its mechanism of action, there were concerns about potential reduction in bone turnover,
repair of microdamage and hence reduced bone toughness and increased risk of fractures with
long-term use.
Plain X-rays:
• Plain X-rays showed a characteristic picture consisting of a transverse or short oblique fracture
line, lateral cortical thickening, and medial spiking.
• he gold standard for diagnosis of osteoporosis is dual energy X-ray absorption scan (DEXA scan).
The test is performed by passing low energy X-rays through a bone (e.g. spine, hip or wrist). The
test takes about ten minutes, is painless, and is associated with very limited radiation exposure.
The values generated by the test can then be compared to both:
• Young adult population : called a "T score", this test measures the variance between the patient
and the young adult baseline. A score above -1 is considered normal; a score between -1 and -2.5 is
considered osteopenia; and a score below -2.5 is considered osteoporosis. For each -1 standard
deviation in T score there is a 3 times increased risk of hip fracture and a 2.5 times risk of spine
fracture.
• Age-and gender-matched control groups : a "Z score" measures the variance between the patient's
and control groups' amount of bone. The control group consists of other people in the patient's
age group of the same size and gender. An unusually high or low score may indicate the need for
additional tests.
28. FIBROUS DYSPLASIA
• McCuneAlbright syndrome includes

• Polystotic fibrous dysplasia ( maxilla most commonly involved).
• Cafe au lait pigmentation with rough border ( coast line of Maine).
• o Precocious puberty ( most common presentation).
• o Other endocrinopathies are hyperthyroidism, increased GH (pituitary adenoma) and primary
adrenal hyperplasia. o Involvement of facial bones usually presents as radiodense lesions, which
may create a leonine appearance (leontiasis osea).
Fibrous dysplasia:
• It is characterized by the replacement of normal lamellar cancellous bone by an abnormal fibrous

tissue that contain small, abnormally arranged trabeculae of immature woven bone. It may affect
one bone (monostotic form) or several bones (polyostotic form)
• The monostotic form is the most common and is usually diagnosed in patients between 20 and 30
years of age without associated skin lesions. The polyostotic form typically manifests in children
• Monostotic fibrous dysplasia most commonly affects the femur particularly the femoral neck as
well as the tibia and ribs. Polyostotic fibrous dysplasia most commonly affects the maxilla and other
craniofacial bones, ribs, and metaphyseal or diaphyseal portions of the femur or tibia.
Radiological findings:
• In the long bones, the fibrous dysplasia lesions are typically well-defined, radiolucent areas with
thin cortices and a ground glass appearance. The articular ends are usually spared.
• Involvement of the facial bones usually presents as radiodense lesions, which may create a leonine
appearance ( leontiasis sea).
29. Simple / solitary / unicameral bone cysT
• Fallen leaf (fragment) sign is pathognomic manifestation

• Curettage and bone grafting is done for enlarging lesions (even after steroid injection), large cyst at
high risk of fracture and if pathological fracture develops or cyst in the proximal femur.
30. Aneurysmal bone cyst
Regarding the location of the aneurysmal bone cyst, any bone may be affected. Approximate
frequencies by site are:
• Skull and mandible (4%)

• Spine (16%)
• Clavicle and ribs (5%)
• Upper extremity (21%)
• Pelvis and sacrum (12%)
• Femur (13%)
• Lower leg (24%)
• Foot (3%)
• Short tubular bones are less frequently affected and are involved in about 10% of cases.
• Spinal involvement demonstrates a predilection for the posterior elements. In decreasing order of
frequency, the following parts of the spine are involved: cervical, thoracic, lumbar. Contiguous
vertebrae may be involved in 25% of cases.
• The cyst involves the diaphysis in isolation in about 8% of cases
31. Chondrosarcoma
• The orthopaedic disorder shown in the picture above represents paget’s disease.
• The tibia is the bone affected most commonly.
• It is also seen in other bones like ilium, femur, skull, vertebrae, humerus, pelvis, spine and skull.
• It is rarely diagnosed in people < 40 years of age.
• Men are more commonly affected than females.
An elevated level of alkaline phosphatase in elderly patients are suggestive of paget’s disease.
• Serum calcium and phosphate levels are normal in paget’s disease.
A variety of tumor and tumor like conditions develops in paget’s disease.
• The benign lesions include: giant cell tumor, giant cell reparative granuloma and extraosseous mass
of hematopoiesis.
• The most dreaded is the conversion to sarcoma, which occurs in 0.7% to 0.9% of cases.
• The sarcomas are usually osteosarcoma, malignant fibrous histiocytoma, orchondrosarcoma, and
they arise in long bones, pelvis, skull and spine.
Chondrosarcomasdeveloping in patients with The tibia is the bone affected most commonly.
ollier's and maffucci syndrome is called
secondary chondrosarcoma. It is also seen in other bones like ilium, femur,
skull, vertebrae, humerus, pelvis, spine and skull.
Secondary chondrosarcoma
It is rarely diagnosed in people < 40 years of age.
It is the chondrosarcoma arising in benign
precursor either osteochondroma and Men are more commonly affected than females.
enchondroma. An elevated level of alkaline phosphatase in
elderly patients are suggestive of paget’s disease.
There are no reliable figures about the risk of
developing secondary chondrosarcoma in Serum calcium and phosphate levels are normal in
benign precursors. paget’s disease.
A variety of tumor and tumor like conditions
The risk of chondrosarcoma in solitary develops in paget’s disease.
osteochondroma is 2% and that for
osteochondromatosis is 5 - 25%. The benign lesions include: giant cell tumor, giant
cell reparative granuloma and extraosseous mass
Patients with ollier's disease and maffucci
syndrome have a 25 - 30% risk of developing of hematopoiesis.
chondrosarcoma.
The most dreaded is the conversion to sarcoma,
which occurs in 0.7% to 0.9% of cases.
The sarcomas are usually osteosarcoma,

malignant fibrous histiocytoma,
orchondrosarcoma, and they arise in long bones,
pelvis, skull and spine.
Ref: Maheshwari 3/e, Page 269; Robbins 7/e, Page

1286; Harrison 17/e, Page 2410.
32. Ewing sarcoma
Commonest site
• Ivory osteoma → Frontal sinus

• Osteoid osteoma → Tibia
• Admantinoma (Ameloblastoma) → Mandible
• Chordoma → Sacrum and cervical spine
• Osteoclastoma → Lower end of femur
• Ewing's sarcoma → Femur diaphysis > tibia diaphysis
• Osteosarcoma → Distal femur (45%), Proximal tibia (25%)
• Simple bone cyst → Proximal humerus
• Aneurysmal bone cyst → Bones around knee (Femur, tibia)
• Osteochondroma → Bones around knee (distal femur > proximal tibia)
• Fibrous dysplasia → Proximal femur > Tibia
• Enchondroma → Phalanges of hand
• Multiple myeloma → Vertebrae
• Metastasis → Vertebrae
33. osteogenesis imperfecta
• Differential expression of same gene depending on parent of origin is referred to as genomic

imprinting.
• Germline (Gonadal) mosaicism results from a mutation only affecting cells destined to form gonads
- postzygotically during early embryonic development. So the individual (parent) is phenotypically
normal but can transmit the disease to offsprings through mutant gametesQ. And because the
progenitor cells of gametes carry mutation, there is a high possibility that more than 1 child of such
parent would be affected.
• Collagen is a fibrous protein composed of 3 chains which form the collagen triple helix.
• Several different types of collagen exist which vary in the types and combinations of the 3 chains
forming the collagen helix.
• Each collagen chain is the product of separate genes.
• For example, the type of collagen found in skin, arteries, bone, and tendons, Type I Collagen, is
composed of 2 a1(I) chains and 1 a2(I) chain. Every third amino acid residue of all of the collagen
chains is glycine.
• This allows the chains to intertwine with glycine at the center. Osteogenesis imperfecta is a disease
consisting of at least 4 clinically, genetically, and biochemically distinguishable disorders.
• All are characterized by multiple bone fractures which result in bone deformities. Mutations leading
to shortened a1(I) chains cause many of these variants. The short a1(I) chain associates with normal
a1(I) chains and a2(I) chains which prevents normal helix formation. Defective molecules are
degraded leading to weakened collagen structures.
• Other forms of osteogenesis imperfecta are due to mutations in which glycine residues are changed
to other amino acids. This leads to destabilization of the collagen helix because of the larger amino
acid forced to the center of the helix structure. A decrease in hydroxyproline occurs in scurvy. This
occurs because ascorbic acid (vitamin C) is necessary to form the hydroxyproline.
• With decreased amounts of hydroxyproline in the collagen molecule, the helix is less stable. The
result is deficient growth and poor wound healing in the individual with scurvy. The disease Ehlers-
Danlos VI is characterized by a decrease in the enzyme lysyl hydroxylase, the enzyme responsible
for the formation of hydroxylysine. The decrease in hydroxylysine in collagen results in less stable
cross-linking of the collagen molecules.
34. ACHONDROPLASIA
• Achondroplasia is an autosomal dominant condition.

• Let 'a' represent the normal allele and A represent the achondroplasic allele.
• Given that both parents have achondroplasia, the most favourable inheritance would be
• 3 out of 4 children would be affected or 75% of children will be affected
• 1 out of 4 i.e. 25% children will be unaffected.
• zv
• irst see general features of autosomal dominant disorders ?
• Autosomal dominant disorders are manifested in heterozygous state.
• So, at least one of the parent should be affected to transmit the disease to child.
• Homozygous state does not exist as it is not compitable with life, i.e. homozygous fetus usually dies
in utero. o So, all the affected individuals will be heterozygous.
• If an affected person marries an unaffected one, i.e. if one of the parents is affected than every
child has 50% of chance of having the disease and 50% of chance not having the disease.
• In this situation it is tricky to calculate the percentage of having affected baby.
• Most of you must be thinking 75% (very easy).
• But, it is not the case, as already explained homozygous state is not compitable with life and fetus
dies in utero. So, the chances of having affected baby will be 50% because 25% (AA) will die in
utero.
• Now see the question
• Achondroplasia is an autosomal dominant condition.
• Both the parents are affected.
• So, chances of having an unaffected baby are 25%.
35. VOLKMANN'S ISCHEMIA
• Volkmann’s ischemic contracture most commonly involve flexor digitorum profundus muscle and
median nerve.
• Volkmann's ischaemia is an ischemic injury to the muscles and nerves of the flexor compartment of
the forearm.
• This occurs due to the occlusion of the brachial artery following a supracondylar fracture.
• The muscles supplied by the anterior interosseous artery are most susceptible to ischemic damage
because this artery is an end artery. Most commonly affected muscles are the flexor pollicis longus
and flexor digitorum profundus (medial-half). Severe pain will be present over forearm usually over
the flexor aspect of the forearm when the fingers are extended passively. Ischemic pain is much
severe than the pain due to the fracture.
36. SHOULDER DISLOCATION
• Anterior dislocation of the shoulder is the most common type of shoulder dislocation. Head of the
humerus comes out of the glenoid cavity and lies anteriorly. Anterior dislocation of shoulder could
be :?
• Preglenoid - It is the most common type of anterior dislocation and head lies in front of glenoid.
• Subcoracoid - The head lies below the coracoid process.
• Subclavicular (infraclavicular) - The head lies below the clavicle.
• Intrathoracic - It is very rare.
37. MONTEGGIA FRACTURE DISLOCATION
• Monteggia fracture-dislocations are classified by the Bado system Bado type I injuries are
characterized by a proximal ulnar fracture with anterior dislocation of the radial head. This is due to
a forceful pronation injury of the forearm and is the most common type. Bado type II injuries are
"reversed" Monteggia fracture-dislocation injuries. Here, there is posterior angulation of the ulnar
fracture site and posterior dislocation of the radial head. Bado type III and IV are rare injuries.
38. COLLE'S FRACTURE

• The fracture is dorsally displaced and may be comminuted. The fracture pattern is often described
as a silver or dinner-fork deformity.
Two classification systems are used:
• The Association for Osteosynthesis (AO) system

• The Frykman system.
A.Complications of the Colles fracture include:
• Post-traumatic stiffness
• Mal-union
• Subluxation of the inferior radio-ulnar joint
• Acute carpal tunnel syndrome
• Sudeck's osteodystrophy.
• Rupture of the extensor pollicis longus tendon
B. An impact to the dorsum of the hand or a hyperflexion or hypersupination injury results in

Smith's fracture. A Smith fracture is usually called a reverse Colles fracture because the distal
fragment is displaced volarly. It is often described as a garden-spade deformity.
C. Barton fractures are classified as dorsal or palmar (always intra-articular), and they always
involve carpal subluxation. The volar Barton fracture is thought to occur with the same mechanism
as the Smith fracture, with more force and loading on the wrist.
• The dorsal Barton fracture is caused by a fall on an extended and pronated wrist, increasing
carpal compression force on the dorsal rim. The salient feature is a subluxation of the wrist.
• By definition, this fracture has some degree of carpal displacement, which distinguishes it
from a Colles or Smith fracture. The palmar variety is more common than the dorsal type.
D. The chauffeur's fracture derives its name from injuries that were acquired, in the days when
motor vehicles were cranked, when a vehicle backfired.
• The force is described as a direct axial compression of the scaphoid into the radial facet.
• The radial styloid is fractured, with associated avulsion of the radial collateral ligament.
• A chauffeur's fracture represents an avulsion related to the attachment sites of the
radiocarpal ligaments or of the radial collateral ligament.
E. Galeazzi fracture results from a FOOSH mechanism with the forearm hyperpronated or from a
direct impact to the dorsal radial wrist.
• The radial diaphysis at the distal and middle third junction is fractured, with associated
subluxation of the distal radioulnar joint.
• On PA views, the radius is shortened and the radioulnar joint is disrupted.

• On the lateral view, the distal radius is angulated either volarly or radially as a result of the
pull of the brachioradialis muscle with more than 3 mm of ulnar displacement.
F. The Essex-Lopresti fracture consists of a comminuted and displaced radial head fracture along
with disruption of the distal radioulnar joint and interosseous membrane.
39. KILOH—NEVIN SYNDROME
• The muscles supplied by the anterior interosseous nerve are flexor pollicis longus, lateral half of
flexor digitorum profundus and pronator quadratus.
• Anterior interosseous nerve arise as median nerve leaves the cubital fossa and soon join company
with anterior interosseous artery and the two descend on the anterior surface of interosseous
membrane. It passes posterior to the pronator quadratus muscle and end in front of the wrist. Its
articular branches supplies the distal radioulnar, radiocarpal and intercarpal joints.
• Radial nerve is the largest branch of the posterior cord of the brachial plexus with a root value of C5
- C8 and T1. The radial nerve is commonly injured in the region of the spiral groove. this result in
the wrist drop and sensory loss over a narrow strip on the back of forearm, and on the lateral side
of the dorsum of the hand.
• Posterior interosseous nerve is the branch of radial nerve given off in the cubital fossa while
anterior interosseous nerve is a branch of the median nerve given off in the upper part of the
forearm.
• Skin of the back of the forearm (i.e. extensor compartment) is supplied by the posterior cutaneous
nerve of the forearm which is a branch of radial nerve.
40. bursitis
• Prepatellar bursitis, also known as Housemaid's knee, is a common cause of swelling and pain
above the patella, and is due to inflammation of the prepatellar bursa.
• This structure is a superficial bursa with a thin synovial lining located between the skin and the
patella.
• The bursa develops within the first years of life as a result of mechanical pressure and friction, and
it serves the purpose of reducing friction on underlying structures and allowing maximal range of
motion in the knee.
• Aseptic prepatellar bursitis is commonly caused by repetitive work in a kneeling position, hence the
name "housemaid's knee
41. PES PLANUS
• May be exacerbated by walking, sports, high level of activity, or traumatic event

• Abnormal shoe wear pattern
• Increasing severity is associated with forefoot abduction and the ?œtoo many toes?€? sign when
the patient is viewed from behind.
Rigid flatfoot:

• Loss of the normal longitudinal arch of the foot at all times
• Restricted motion of the hindfoot
Flexible flatfoot:
• Loss of arch only on standing on the affected foot, with reconstitution of the arch when the foot is
dependent or when the patient toe-stands.
• Normal motion of the hindfoot.
42. LUMBAR DISC HERNIATION (Herniated nucleus pulposus,slipped dics Ruptured disc, Sciatica)
• Painis the usual presenting symptom.

• May affect the back only, leg only, or both
• Pain often is aggravated by forward flexion of the lumbar spine and relieved by extension.
43. THORACIC DISC HERNIATION
• Patients may present with

• Axial pain (localized from the middle to lower thoracic spine)
• Radicular pain (T10 dermatomal is most common)
• Myelopathy (bowel and bladder dysfunction)
44. SPONDYLOLISTHESIS
• Spondylolisthesis is a forward slip of one vertebrae upon another; so it is best viewed (or seen
earliest) in sagittal images of spine i.e. lateral and oblique X rays of spine and saggital & axial views
of CT & MRIQ. AP views of X ray can only be used to demonstrate indirect evidences (eg. inverted
Napoleon's hat sign) of late/ severe spondylolisthesis.
• Oblique view of spine display the lamina and articular processes more clearly than the classical
anteroposterior & lateral views. The shadow of neural arch resembles that of Scottish terrier dogQ.
• Spondylothesis is forward slip of one vertebrae upon another. Majority of cases are due to stress
fracture of pars interarticularis leading to broken neck or presence of collar on the Scottie
doe. More displacement will lead to Beheaded (without head) Scottie terrier sign(2.
• Spondylolisthesis : ventral slipping or gliding of all or part of one vertebrae on a stationary vertebra
beneath it. Most common is between L5 - S1 and between L4 — L5.
• "Inverted Napoleon's HatQ" sign: A severe degree of spondylolisthesis at L5 - Si can be identified on
A-P view by ventrocaudal displacement of L5 over sacrum and creates curvilinear densities.
45. BLOUNT'S DISEASE
• Blount’s disease is characterized by varus and internal tibial torsion and genu recurvatum, with varus of
the proximal tibia being the primary deformity. It is not associated with external tibial torsion.


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NEET PG High Yield Topic Synopsis NEET 2019 PDF Version - Final

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Anatomy

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• Congenital elevation of scapula is called Sprengel shoulder.

• First bone to ossify.

• Humerus ossifies from 1 primary & 7 secondary centers.

• Radial nerve is Derived from C5,6,7,8, T1

6. MOVEMENTS OF SHOULDER JOINT

9. MUSCLES OF PECTORAL REGION

• Pectoralis major Forms anterior axillary fold

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10. TRIGEMINAL (V) NERVE

• Spinal nuclei is nuclei of trigeminal nerve.

11. TRIGEMINAL NEURALGIA

TRIGEMINAL NEURALGIA Or TIC DOULOUREUX Or TRIFACIAL NEURALGIA Or FOTHERGILL’S NEURALGIA

• Trigeminal neuralgia characterized by intermittent, shooting pain in the face.

• From a well taken history

• First line of treatment is CARBAMAZIPINE ( anticonvulsant)

• LONG ACTING ANESTHETIC AGENTS

12. MAXILLARY NERVE

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13. MANDIBULAR NERVE

• Mandibular nerve exits skull from foramen ovale.

14. OPHTHALMIC (V1) NERVE

15. SCALP & SUPERFICIAL TEMPORAL REGIION

• Subcutaneous tissue is the highly vascular layer of scalp.

SCALP: Soft tissue which covers the clavira of skull.

LAYERS OF SCALP: CONSISTS OF FIVE LAYERS

• Thick and hairy.

2. Close network of Connective tissue (superficial fascia):

• Contain vessels and nerves; highly vascular layer.

3. Aponuerosis (galea aponeurotica) with occipitofrontalis muscles:

4. Loose areolar (Subaponuerotic) tissue:

5. Pericranium (outer periosteum of skull):

• BEHIND THE AURICLE-

• Supratrochlear+ supraorbital→ angular vein→ FACIAL VEIN.

• Scalp supplied by ten nerves on each side.

IN FRONT OF AURICLE(SENSORY) BEHIND THE AURICLE(SENSORY)

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TEMPORAL BRANCH OF FACIAL NERVE POSTERIOR AURICULAR BRANCH OF

4. Hemostasis in scalp wound is best achieved by pressure over wound.

8. Lacerated wound appears as incised wound in scalp.

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• Facial muscles develops from mesoderm.

17. BELL'S PALSY

• Bell's palsy is due to paralysis of LMN VII nerve.

18. MUSCLES OF MASTICATION

• PRIMARY MUSCLES OF MASTICATION:

1. Temporalis: fan shaped & fills the temporal fossa

MUSCLE ORIGIN FIBERS INSERTION NERVE ACTION

Temporalis 1. Temporal Converge & 1. Margins 2 deep 1. Elevat

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Medial 1. Superficial Down, back & Roughened Nerve to 1. Elevat

19. EXTRAOCULAR MUSCLES

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20. FACIAL (VII) NERVE