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GIT
ANATOMY
SYLLABUS
Gross Anatomy: (p .7)
Regions and quadrants of abdomen, Umbilicus: Normal position, umbilical hernia
Oral cavity:(p .8)
Adult tooth: Dental Formula, Microscopic Structure, palate: Development, gross features, tongue:
Development, gross features, blood supply, Microscopic Structure, salivary glands: Development, Microscopic
Structure, gross features
Pharynx:(p .14)
Gross features, parts, relations, innervation.
Peritoneum and subdiaphragmatic spaces
Oesophagus:(p .21)
Extent, normal constrictions, blood supply, lymphatic drainage, microscopic structures
Stomach (p. 23) and Duodenum (p. 26):
Gross features, vasculature, relation, innervation, lymphatic drainage, microscopic structure, applied aspects.
Jejunum and ileum: (p .29)
Gross features, Regional differences, parts, blood supply, microscopic structure
Large intestine: (p .30)
Parts, cardinal features, Differences between small and large intestines, blood supply, nerve supply
Appendix, Caecum:(p . )
Position, gross features, applied anatomy, microscopic structures of appendix V
Colon :parts, gross features, nerve supply, Blood supply, lymphatic drainage
Pancreas:(p. 38)
Parts, position, relations, blood supply, lymphatic drainage, development, applied anatomy, microscopic
structures
Rectum and Anal Canal:(p .34)
Parts, gross features, nerve supply, blood supply, lymphatic drainage, applied anatomy
Anterior Abdominal Wall:(p. 43)
Flat Muscles
Rectus sheath:(p. 44)
Formation, boundaries and contents, Rectus abdominis, nerves, blood supply, rectus sheath.
Inguinal canal-Boundaries, contents in males and females, Inguinal hernias
Posterior Abdominal Wall: (p .47)
Muscles and fascia-thoracolumbar fascia
Abdominal aorta: (p. 48)
Extent and branches
Inferior venacava: (p. 48)
Formation and tributaries
Lumbar plexus: (p. 48)
Formation and branches
Cisterna chyli (p. 49)
FAST TRACK BASIC SCIENCE MBBS -5-

Anatomy
-6- FAST TRACK BASIC SCIENCE MBBS

GIT
ANATOMY
GROSS ANATOMY Embryological importance:

Regions and quadrants of Abdomen - Meeting point of:
• Four folds of embryonic plate (2 lateral
folds, head folds and tails folds)
• 3 systems:
1. GI-Vitellointestinal duct
2. Excretory→Urachus
3. Vascular - umbilical vessels
Applied Aspects:
1. Raspberry red tumor: or cherry red tumor
Remnant of Vitello intestinal duct may form a
tumor at umbilicus.
2. Fecal Fistula: Persistence of patent vitello
intestinal duct.
♦ Abdomen is divided into nine regions by four 3. Urinary fistula/urachal fistula: Persistance of
imaginary planes, two horizontal and two vertical. entire urachus.
♦ Transpyloric (L1) and Transtubercular plane (L5)→ 4. Urachal cyst, urachal sinus: Persistance of some
Horizontal planes part of urachus.
V
♦ Right lateral and left lateral → Vertical planes 5. Omphalocele or Exomphalos (Umbilical hernia):
(Passing through Mid clavicular line and Mid - Herniation of abdominal viscera through
inguinal point) enlarged umbilical ring.
♦ Regions are as shown in figure. - Viscera are covered by amnion.
Umbilicus - Due to failure of bowel to return to the body
♦ Normal scar in Anterior Abdominal wall formed by cavity from its physiological herniation during
remnants of the root of the umbilical cord. 6th to 10th week.
♦ Variable in position, lower in infants and person 6. Gastroschisis:
with pendulous abdomen. - Protrusion of Abdominal contents through body
♦ In healthy adult: Lies in Anterior median plane, at wall, directly into the Amniotic cavity.
the level of disc between L3 and L4. - Occurs lateral to umbilicus, usually on right.
Anatomical Importance: - Due to abnormal closure of body wall around
- Level of umbilicus is watershed (see special connecting static.
points for MCQs). - Viscera are not covered by peritoneum or
- Skin around it supplied by T10 segment of Amnion.
spinal cord. - Survival rate more than omphalocele.
- Site of portocaval anastomosis, forms caput - Not associated with chromosome abnormalities.
medusae in portal hypertension.

Anatomy
ORAL CAVITY - In man: Teeth replaced only once so called

Past Questions: Diphyodont.
- Dental formula for milk/deciduous teeth
1. Give an account on development of tongue.
2102
Mention its lymphatic drainage (4)[11 July] =2102
2. Mention the sensory and motor nerves supply of
2123
the tongue. Explain in brief the source of For adult/permanent= 2123
development in relation to the nerve supply.
(2+2=4) [10 July] - It represents number of tooth in each half of
each jaw in order – Incisor, canine, premolar
3. Name the extrinsic muscles of tongue. Mention
and molar.
their nerve supply. (3+1= 4) [09 Dec]
4. Name the extrinsic muscles of the tongue. - In milk teeth: 2 incisor, 1 canine, no premolar
Mention their actions and nerve supply. and 2 molars : Total = 20
(3+3+2) [05 June] - In permanent teeth: 2 incisor, 1 canine, 2
5. Describe the tongue under the following premolar and 3 molar in each half of each jaw.
headings: (2 + 2 = 4) [09 July] Total = 32
a. Sensory nerve supply Microscopic structure of adult tooth [07 July]
b. Lymphatic drainage
6. Give an account of the development of the
tongue, with reasons according to the sources of
nerve supply. (3 + 1 = 4) [05 Dec]
7. Name the extrinsic muscle of tongue. Give their
nerve supply. Which muscle is called the safety
V muscle and why? (2 + 1 + 1 = 4) [05 June]
8. a. Mention the sensory and motor nerve supply
of the tongue. (4) [04 Nov]
9. Write briefly about the tongue under the
following headings: (2 +2 = 4) [03 Nov]
a. Sources of the development
b. Nerve supply-sensory and motor.
10.Draw a neat labelled diagram to show the parts
of an adult tooth. Add a note on the dental
formula. (2 +2 = 4) [07 July]
11.Describe the parotid gland under the following
headings. (1+1+2=4)[08 Dec] - Each tooth has 3 parts:
a. Location
1. Crown
b. Structure present within the gland
2. Neck, surrounded by gum
c. Nerve supply
3. Root
Tooth - Structurally: (1) Pulp in centre (2) Dentine
Dental formulae [07 July] surrounding the pulp, (3) Enamel (4)
- Way of representing the number of different Cementum (5) Periodontal membrane
types of teeth.
GIT
1. Pulp: Contains vessels, nerve and ↓

lymphatics; enter the pulp through apical Which forms primary palate.
foramen. ↓
Covered by a layer of tall columnar cells Two shelf like outgrowths from maxillary prominence
called odontoblasts: From dentine. called palatine shelves
2. Dentine: Calcified material, No blood ↓
supply, No nerve supply.
Fuses and forms the secondary palate.
3. Enamel: Hardest substance in the body, No
blood supply, No nerve supply. Primary palate
(From intermaxillary segment)
4. Cementum: Resembles bone in structure,
No blood supply, No nerve supply.
5. Periodontal membrane: Acts as
periosteum.
Incisive foramen
Applied Aspects: Secondary palate
(From palatine shelves)
1. Scurvy:
– Gums swollen and spongy, bleed on touch. Hard palate
– Vit 'C' deficiency
2. Pyorrhoea alveolaris: Chronic pus discharge at
Gross features
margin of gums. - Its anterior two thirds are formed by palatine
process of maxilla and its posterior one third
3. Dental caries: Decalcification of enamel and
by horizontal plates of palatine bones.
dentine.
- Arteries: Greater palatine branch of maxillary V
4. Apical abscess: Infection of Apex of root creating
artery.
abscess.
- Venous drainage: Pterygoid plexus of veins.
5. Hutchinson's teeth: Notched teeth occuring in
congenital syphillis. - Nerve supply: Greater palatine and
nasopalatine branch of pterygopalatine
6. Natal teeth: Erupted by the time of birth.
ganglion.
7. Tetracyalines: Discolored tooth
- Clinical correlation: Partial or complete lack of
8. Rickets: Deficient in enamel.
fusion of maxillary prominence with the medial
Development: nasal prominence on one or both sides: Cleft
1. Enamel: Ectoderm palate.
2. Dentine, Pulp: Mesoderm Soft palate:
3. Cementum: Periodontal membrane Development
Palate - Epithelium from: Ectoderm of maxillary
Hard palate: process.
Development: - Muscles from: 1st, 4thand 6th branchial arches.
Two medial nasal prominences margining at deeper level - It is unossified posterior part of fused palatal
process. (Note: ossified part forms: Part of
↓
hard palate)
Forms intermaxillary segment

Anatomy
Gross features:
Muscles of soft palate:
Muscles Arrangement Nerve supply Actions
1. Tensor veli palatine - It is flattened tendon i.e. palatine - Mandibular nerve - Tightens soft palate
aponeurosis forms fibrous base of
soft palate
2. Muscular uvula - Near the median plane palatine - Pulls up uvula

aponeurosis splits enclose this
muscle
3. Levator veli palatine - Superior surface of palatine - Elevates soft plates

aponeurosis - Cranial part of accessory
- Opens auditory tube
nerve through vagus
4. Palatopharyngeus - Superior surface of palatine - Pulls up wall of
aponeurosis pharynx
5. Palatoglossus - Inferior surface of palatine - Pulls up root of

aponeurosis tongue
Note: - Epithelium:
a. Of anterior 2/3rd: From two lingual
- Levator veli palatini→ Closes pharyngeal isthmus.
swellings and tuberculum impair, which
- Palatoglossus→ Closes oropharyngeal isthmus. arises from first branchial arch, so it is
supplied by: lingual and chorda tympani.
V Blood Supply:
- Greater palatine branch of maxillary artery, b. Posterior 2/3rd: From hypobranchial
eminence, i.e. from 3rd brancial arch, so it is
ascending palatine branch of facial artery,
supplied by Glossopharyngeal nerve.
palatine branch of ascending pharyngeal
artery.
Congential anomaly:
- Ankyloglossia (Tongue tie)
- Venous drainage:
- Macroglossia
• To pterygoid and tonsilar plexus.
- Microglossia
Clinical correlation:
Gross feature:
- Paralysis of soft palate in vagus nerve lesions: Muscles of tongue:
• Produces nasal tone, fattening of palatal 1. Intrinsic muscles: Originate and terminate in the
arch. tongue itself and is responsible for changing the
Tongue shape of tongue.
Four on each side:
Development and relation to nerve supply
a. Superior longitudinal
(11 July, 05 Dec )
b. Inferior longitudinal
- Muscles of tongue: From occipital myotomes
c. Transverse
- Connective tissue: From local mesenchyme d. Vertical

GIT
2. Extrinsic muscles [05 June]

Extrinsic muscles of tongue
Muscle Origin Insertion Action
Pulls up the root of tongue,
Descends in the palatoglossal arch
Oral surface of approximates the palatoglossal
Palatoglossus to the side of tongue at the junction
palatine aponeurosis arches and thus closes the
of oral and pharyngeal parts
oropharyngeal isthmus
Whole length of
Side of tongue between styloglossus Depresses tongue, makes dorsum
greater cornua and
Hyoglossus and inferior longitudinal muscle of convex, retracts the protruded
lateral part of hyoid
tongue tongue
bone
Tip and part of
Pulls tongue upwards and back
Styloglossus anterior surface of Into the side of tongue
wards
styloid process
Retracts the tongue
Genioglossus (fan- Upper fibres into the tip of tongue Depresses the tongue
Upper genial tubercle
shaped bulky Middle fibres into the dorsum Pulls the posterior part of tongue
of mandible
muscle) Lower fibres into the hyoid bone forwards and protrude the tongue
forwards. It is a life saving muscle
Arterial supply: - Tip of the tongue:
- Lingual artery; branch of external carotid • Bilaterally to the submental nodes.
- Tonsilar branch of facial artery.
- Right and left halves of the remaining part of
- Ascending pharyngeal branch of external
carotid. the anterior two thirds of the tongue:
Venous drainage: • Unilaterally to the submandibular nodes.
- Lingual vein → Internal Jugular vein. - Posterior one-third of the tongue: V
Lymphatic drainage [9 July, 11 July] • Bilaterally to the jugulo-omohyoid nodes.
- Posterior most part:
• Bilaterally into the upper deep cervical
lymph nodes.
Nerve supply [10, 09, 09, 05, 04, 03]
- Motor nerves:
• All Intrinsic and extrinsic muscles except
palatoglossus supplied by hypoglossal
nerve.
• Palatoglossus supplied by: cranial root of
accessory nerve through pharyngeal plexus.
- Sensory nerves:
Sensory nerves by:
a. Lingual nerve
b. Glossopharyngeal nerve
c. Internal laryngeal branch of vagus

Anatomy
Parts of the tongue

Posterior most part of
Nerve supply Anterior two - thirds Posterior one-third
vallecula
Sensory Lingual (post-trematic Glossopharyngeal Internal laryngeal branch of
branch of 1st arch) vagus
Taste Chorda tympani except Glossopharyngeal including Internal laryngeal branch of
vallate papillae (pre- the vallate papillae vagus
trematic branch of 1st arch)
Development of epithelium Lingual swellings of I arch. Third arch which forms Fourth arch which forms
from endoderm Tuberculum impar which large ventral part of small dorsal part of
soon disappears hypobranchial eminence hypobrachial eminence
Applied Aspects: • Capsule and stroma from mesenchyme.
- Genioglossus: Life saving muscles. Note:
- Under surface of tongue: Site for observation of - Parotid: Largest
Jaundice. - Sublingual: Smallest salivary gland
- Carcinoma of tongue: Spread via lymphatics, - Submandibular and sub lingual glands:
carcinoma of posterior 1/3rd is more dangerous Endodermal in origin – from oral mucosa.
because of bilateral lymphatic spread. - Capsule and stroma from Mesenchyme
Salivary glands Gross features of parotid gland:
♦ 3 parts: Parotid, submandibular and lingual. - Resembles pyramid, 15g in wt.
Development: Location [08 Dec]
- Parotid gland [08 Dec] - Situated below external acoustic meatus.
• Ectodermal in origin. - Between ramus of mandible and
• From Buccal epithelium lateral to angle of sternocledomastoid.
V mouth. - Gland overlap these structures.
• Outgrowth branches repeatedly form duct - Capsule of parotid gland: formed by investing
system and acini. layer of deep cervical fascia.
Relations:

GIT
Structure within parotid gland [08 Dec]
V
Blood supply: ↓
- Arterial supply: External carotid artery and its Relay in otic ganglion
branches. ↓
- Venous drainage: External Jugular vein and Postganglionic fibres through auriculotemporal nerve
Internal Jugular vein. ↓
Nerve supply [08 Dec] Parotid gland
1. Para sympathetic nerves: are secretomotor 2. Sympathetic nerves
- Reach parotid through the Auriculotemparal - Vasomotor
nerve. - Derived from plexus around middle meningeal
artery.
Inferior salivatory nucleus
3. Sensory nerves: From auriculotemporal nerve.
↓
Note: Parotid fascia by sensory fibers of great
IX nerve
auricular nerve (C2, C3)
↓
Tympanic branch Applied Aspects:
↓ 1. Parotid swellings are very painful due to
unyielding nature of parotid fascia.
Tympanic plexus
2. Parotid abscess: Caused by spread of infection
↓ from opening of parotid duct in mouth cavity.
Lesser petrosal nerve Best drained by Hilton's method.

Anatomy
3. Malignant changes of mixed parotid tumor is ♦ Division: The interior of pharynx is divided into
indicated by: pain, rapid growth, fixity with three parts namely:
hardness, enlargement of cervical lymphnodes. i. Nasophanyx
4. Frey syndrome/Auriculotemporal syndrome ii. Oropharynx
occurs at times after parotidectomy. iii. Laryngo-pharynx
- Characterized by: Increased sweating in Relation
regions supplied by auriculotemporal nerve on
♦ Superiorly: supported by body of sphenoid and
chewing.
basilar part of occipital bone.
♦ Inferiorly: Oesophagus opposite the C6 vertebra.
PHARYNX ♦ Anteriorly:
Communicates with:
Past Questions:
- Nasal cavity through choanae
1. Name the boundaries of the tonsillar fossa and
- Oral cavity through oro-pharyngeal isthmus
mention the arterial supply of palatine tonsil.
- Larynx through laryngeal inlet.
(2) [04 Nov]
♦ Posteriorly
2. Mention the extent of pharynx and name its
- Supported by upper six cervical vertebrae with
subdivisions. Write in brief the important
intervertebral discs, pre & para-vertebral muscle.
features present in the interior of pharynx.
- Prevertebral fascia
(1 +3 = 4) [03 June]
- Retro-pharyngeal space and its contact.
3. Give an account of the interior of the pharynx. -
♦ On each sides:
Enumerate nerves supplying the inferior
V pharyngeal constrictor. (3 +1 = 4) [06 June] - Styloid process of temporal bone
- Styloid group of muscle
4. Mention shape, extent, length and
communications of pharynx (2+2+2+4) [08 Nov] - Carotid sheath
- Lateral lobe of thyroid gland
Definition ♦ Lateral wall of naso-pharynx communicates with
♦ The pharynx is a musculo–membranous tube tympanic cavity via the auditory tube.
which is lined internally by the mucous
Gross features of each part of pharynx
membrane.
1. Naso-pharynx (Epipharynx)
♦ It acts as a common channel for both deglutition
- Location: Behind nasal cavity and above the
and respiration, because the food and air passage,
soft plate.
cross each other in this region.
- Boundaries:
♦ Extent:
• Anterior wall: Deficient and communicates
If extends from the base of skull to level of 6th with nasal cavity via choanae
cervical vertebra there onwards, continued as • Roof and posterior wall: Form continuous
esophagus. surface that slopes downwards backward
♦ Situation: It is situated behind the nasal and oral supported by body of sphenoid, occipital
cavities and behind the larynx. bone (basilar part) and anterior arch of
atlas.

GIT
• Features: Roof and posterior wall → Extend between levator veil palatini
a. Naso-pharyngeal tonsil and longus capitis.
→ Formed by aggregation of lymphoid 2. Oro-pharynx (Mesopharynx)
tissue beneath the mucus membrane. - Location:
b. Pharyngeal bursa (Pouch of luschka) • Behind the oral cavity
→ It is mucus diverticulum extending → Supported dorsally by bodies of C2 and C3
upward into substance of naso- vertebrae and by content of retro-
pharyngeal tonsil. pharyngeal space.
c. Pharyngeal hypophysis - Communication:
→ Some cell of nasopharyngeal roof • Anteriorly with oral cavity through oro-
resembles histologically to pharyngeal isthmus.
adenohypophysis. • Inferiorly with laryngo pharynx at level of
→ Cells are derived from backward upper border of epiglottis.
extension of Rathke's pouch.
- Features:
• Floor
• Palatine tonsil lodged in tonsilar fossa.
a. Communicates with oro-pharynx via
pharyngeal isthmus. • The tonsil presents on lateral wall of
oropharynx on each side.
b. Bounded in front by posterior surface
and free margin of soft plate. 3. Laryngo-pharynx (Hypopharynx):
Behind by mucous elevation of - Extent:
passavant's ridge • From upper border of epiglottis to the V
c. On each side: palato-pharyngeal arch lower border of cricoid cartilage.
contain muscle palato-pharyngeus. - Support: Behind by
• Lateral wall: Features are:
• Bodies of C4 to C6 vertebrae
a. Pharyngeal opening of auditory tube
• Prevertebral fascia
→ It is situated 1.25cm behind and
slightly below the posterior end of • Retropharyngeal space
inferior nasal choncha. - Features:
b. Tubal elevation • Anterior wall of laryngo-pharynx presents
→ Guards the upper and posterior pharyngeal inlet.
margin of auditory opening. • Laryngeal inlet is bounded:
→ Acts as guide for the introduction of a → Above and infront: By upper margin of
catheter. epiglottis
→ Tubal tonsil overlies the elevation.
→ Below: Inter-arytenoids fold of mucus
c. Pharyngeal recess (Fossa of Rosenmuller) membrane.
→ It is a mucous covered deep • Lateral wall of laryngo-pharynx presents
depression behind the tubal pyriform fossa
elevation.

Anatomy
Comparison between nosopharynx, oropharynx and laryngopharynx

Particulars Nasopharynx Oropharynx Laryngopharynx
a. Situation Behind nose Behind oral cavity Behind larynx
b. Extent Base of skull (body of Soft palate to upper border Upper border of epiglottis to
sphenoid) to soft palate of epiglottis lower border of cricoid cartilage
c. Communications Anteriorly with nose I. Anteriorly with oral Inferiorly with oesophagus
cavity
II. Above with nasopharynx
III. Below with
laryngopharynx
d. Nerve supply Pharyngeal branches of IX and X nerves IX and X nerves
pterygopalatine ganglion
e. Relations: Posterior nasal aperture Oral cavity I. Inlet of larynx,
i. Anterior II. Posterior surface of cricoid
III. Arytenoid cartilage
ii. Posterior Body sphenoid bone Body of second and third Fourth and fifth cervical
cervical vertebrae vertebrae
iii. Lateral wall Opening of auditory tube Tonsillar fossa containing Piriform fossa
palatine tonsils
f. Lining epithelium Ciliated columnar epithelium Stratified squamous Stratified squamous
nonkeratinised epithelium nonkeratinised epithelium
V g. Function Passage for air (Respiratory Passage for air and food Passage for food
function)
Muscles of pharynx - But stylo-pharyngeus is supplied by the
- Muscular coat of pharynx are arranged in outer glossopharyngeal nerve.
circular layers and inner longitudinal layer. - In addition, inferior constrictor is supplied by
- Circular layer consists of recurrent laryngeal and external laryngeal
i. Superior constrictor muscle nerve.
ii. Middle constrictor muscle Sensory innervations:
iii. Inferior constrictor muscle i. Naso-pharynx: By pharyngeal branch of
- Longitudinal layer consist of 3 paired muscle pterygopalatine ganglion/converging fibres of
maxillary nerve.
i. Stylo-pharyngeus
ii. Oro-pharynx: By glossopharyngeal nerve.
ii. Palato–pharyngeus
iii. Laryngo-pharynx: By internal laryngeal nerve.
iii. Salpino-pharyngeus
Innervations of pharynx: Note: Pharyngeal plexus:
Motor innervations: Formed by pharyngeal branch of
- All pharyngeal muscles are supplied by the i. Vagus carrying fibres of accessory nerve
cranial part of accessory nerve via the ii. Glossophapyngeal nerve
pharyngeal plexus. iii. Superior cervical ganglion of sympathetic trunk.

GIT
- It is loosely attached to the walls by extra-

PERITONEUM peritoneal connective tissue.
Past Questions: - Developmentally, it is derived from somato-
1. Discuss the greater omentum under the pleuric layer of lateral plate mesoderm.
following heading: (1 + 1 + 1) [06 June] - Blood supply and nerve supply are the same as
a. Development those of overlying body wall.
b. Structures present within it - Because of somatic innervations, parietal
peritoneum is pain-sensitive.
c. Clinical importance V
2. Short notes on: ii. Visceral peritoneum
a. Epiploic foramen (2, 3)[07 July, 05 June] - It lines the outer surface of viscera to which it
is firmly adherent and cannot be stripped.
b. Lesser omentum (3) [3 June]
- Developmentally: it is derived from the
Definition
splanchno-pleuric layer of the lateral plate
♦ Peritoneum is a large serous membrane lining the mesoderm.
abdominal cavity. - Blood supply and nerve supply are the same as
♦ Histologicaly, it is composed of: those of underlying viscera.
i. Fibrous tissue (outer layer): provides strength • Because of autonomic innervation, visceral
ii. Mesothelial cells (inner layer): Secrete fluid. peritoneum evokes pain when viscera is
♦ Peritoneum is in form of closed sac which is stretched, ischemic or distended.
invaginated by number of vicera. Functions of peritoneum
♦ Division of peritoneum - Movements of viscera
i. Parietal peritoneum - Protection of viscera
ii. Visceral peritoneum →Suspends the viscera - Absorption and dialysis
i. Parietal peritoneum - Healing power and adhesion
- It lines inner surface of abdominal and pelvic - Storage of fat
wall and lower surface of the diaphragm.

Anatomy
Peritoneal folds
♦ The peritoneal folds are
1. Greater omentum
2. Lesser omentum
3. Mesoappendix
4. Transverse mesocolon
5. Sigmoid colon
6. Mesentery
1. Greater omentum [06]
Definition:
- The greater omentum is a large fold of
peritoneum
- It hangs down from the greater curvature of
the stomach like apron and covers the loops of
intestines to varying extent.
- It is made up of 4 layer of peritoneum fused 2. Lesser omentum (03)
together to form fenestrated membrane with Definition:
varying amount of fat, small arteries and veins. - This is a fold of peritoneum which extends
Attachment: from the lesser curvature of stomach and first
- The anterior 2 layers descend from the greater 2cm of the duodenum to the liver.
curvature of the stomach to a variable extent, Modification:
V which fold upon themselves to form the i. Hepato-gastric ligament: The portion of lesser
posterior two layers that ascend to the anterior omentum between stomach and liver.
surface of head and anterior border of the
ii. Hepato–duodenal ligament: The portion
body of the pancreas.
between duodenum and liver.
- The folding is such that 1st layer becomes 4th
Structures related to lesser omentum:
layer and 2nd layer becomes 3rd layer.
i. Lesser sac: Behind the lesser omentum
Content:
ii. Epiploic foramen: Behind the free right margin
i. The right and left gastroepiploic vessels and its
of lesser omentum.
anastomoses
Attachment:
ii. Fat
- Inferiorly, the lesser omentum is attached to
Functions:
the lesser curvature of the stomach and to the
i. It is a storehouse of fat upper border of first 2cm of duodenum.
ii. Provides protection against infection because - Superiorly: It is attached to the liver and line of
of presence of macrophages patches (milky attachment is "L" shaped.
spots).
- Vertical limb of "L" is attached to bottom of
iii. Limit the spread of infection by moving to site fissure for the ligamentum venosum.
of infection and sealing it off from the adjacent
- Horizontal limb of "L" to margin of porta-
area. So, greater omentum is called policeman
hepatis.
of the abdomen.

GIT
Content: Contents:
a. Hepatic artery proper a. Jejunal and ileal branches of superior
b. The portal vein mesenteric artery.
c. The bile duct b. Accompanying veins
c. Autonomic nerve plexuses
d. Lymph nodes and lymphatics
d. Lymphatics or lacteals
e. Hepatic plexus of nerves.
e. 100-200 lymph nodes
Along lesser curvature of stomach and along upper f. Connective tissue
border of adjoining part of duodenum contain
Epiploic foramen (07, 05)
i. The right gastric vessels
♦ Also known as
ii. The left gastric vessels - Foramen of Winslow
iii. The gastric group of lymph nodes and - Aditus
lymphatic's - Opening of lesser sac
iv. Braches from gastric nerve Definition:
3. Mesoappendix: - It is vertical slit like opening through which the
lesser sac communicates with the greater sac.
- It is small triangular fold of peritoneum which
suspends the vermiform appendix. Posterior Location:
Surface of lower end of mesentery is close to - Located behind the right free margin of lesser
omentum at level of 12th thoracic vertebra.
the ileocaecal junction.
Boundaries:
4. Transverse mesocolon: - Anteriorly: Right free margin of lesser
- Broad fold of peritoneum which suspends the omentum containing the portal vein, hepatic
transverse colon from upper part of the artery proper and common hepatic duct.
posterior abdominal wall. - Posteriorly: IVC, right suprarenal gland and T12 V
Content: vertebra.
- Inferiorly: 1st part of duodenum and the
- Middle colic vessel
horizontal part of hepatic artery.
- Nerves, lymph nodes - Superiorly: Caudate process of the liver.
- Lymphatics of transverse colon.
Applied Aspects:
5. Sigmoid mesocolon - Passage of internal hernia into lesser sac take
- This is a triangular fold of peritoneum which place via the aditus.
suspends the sigmoid colon from the pelvic
wall.
Content:
- Sigmoid vessel (in Lt. limb of inverted "V")
- Superior rectal vessel (in Rt. limb of inverted
"V")
- Lymph nodes and lymphatics
6. Mesentery
- It is broad, fan shaped fold of peritoneum
which suspends the coils of jejunum and ileum
from post abdominal wall.

Anatomy
Lesser Sac or omental bursa Boundaries:

♦ This is a large recess of the peritoneal cavity Anteriorly
behind the stomach, lesser omentum and caudate - Inferior surface of right lobe of liver.
lobe of liver. - Gall bladder
♦ Communication: It communicates with greater sac Posteriorly
via epiploic foramen. - Right suprarenal gland
Boundaries - Upper part of right kidney
Anterior walls is formed by: - Second part of duodenum
i. Caudate lobe of liver - Hepatic flexure of colon
ii. Lesser omentum - Transverse mesocolon
iii. The stomach - A part of head of pancreas
iv. Anterior two layer of greater omentum Superiorly
Posterior wall is formed by: - Inferior layer of coronary ligament
i. Posterior two layer of greater omentum Inferiorly
ii. Transverse mesocolon - Opens into general peritoneal cavity
iii. Duodenum Applied Aspects:
iv. Pancreas i. It is the most dependent part of abdominal cavity
Upper border is formed by: proper when body is supine.
i. Reflection of peritoneum to diaphragm from ii. Collection of fluids, pus
oesophagus. iii. Commonest sit of sub phrenic abscess caused by
ii. Upper end of fissure for the ligamentum spread of infection from organs in this region.
V venosum.
iii. Upper border of the caudate lobe of the liver.
Lower border is formed by:
i. Continuation of the 2nd with 3rd layers of
greater omentum
Sub division of lesser sac
i. Inferior recess
ii. Superior recess
iii. Splenic recess
Note: The portion of lesser sac behind lesser
omentum is known as vestibule of lesser sac.
Applied Aspects: Recto uterine pouch of Douglas

i. Pus collection ♦ This most dependent part of peritoneal cavity
ii. Internal hernia (Strangulated type) when body is upright in position.
Hepatorenal pouch (Morison's pouch) Boundaries
Anteriorly
♦ It is called as right subhepatic space.
- Uterus
♦ Location: Lies below right half of visceral surface
of liver. - Posterior fornix of vagina

GIT
Posteriorly Development:
- By rectum Peritoneal folds Source of developments
Inferiorly
i. Greater omentum Dorsal mesogastrium
- By recto-vaginal fold of peritoneum
(Greater part)
Clinical importance
ii. Lesser omentum Dorsal part of ventral
- Pus collection
mesogastrium
Note:
iii. Gastro-splenic Ventral part of dorsal
i. The pouch can be drained either via rectum or
ligament mesogastrium
posterior fornix of vagina.
ii. In supine position Hepatorenal pouch is most iv. Lineorenal ligament Dorsal part of dorsal
dependent part of pelvic cavity. mesogastrium
v. Gastro-phrenic Cranial most part of dorsal
Sub-diaphragmatic space
ligament mesogastrium.
♦ It is also called sub-phrenic space
vi. Mesentry (ileum and Dorsal mesentery
♦ Location: It is just below the diaphragm in relation
to the liver. jejunum)
mesoappendix,
Classification
transverse-
A. Intra-peritoneal spaces are
mesocolon, sigmoid
i. Left anterior space colon
ii. Left posterior space
iii. Right anterior space Note: The mesentries of duodenum, ascending colon,
iv. Right posterior space and rectum are lost during development.
B. Extra peritoneal spaces are Development of lesser sac:
i. Right extra-peritoneal space i. Superior recess is developed from right V
ii. Left extra-peritoneal space pneumoneteric recess.
iii. Midline extra-peritoneal space (= bare area of ii. Inferior recess is developed from the
liver) invagination of dorsal mesogastrium
Note: downwards.
i. Left posterior space is lesser sac.
ii. Midline extra-peritoneal space corresponds to OESOPHAGUS
bare area of the liver. Past Questions:
1. Constrictions of esophagus with vertebral levels
and causes. (2)[08 July]
Extent
- Thoracic part: From lower border of cricoid
cartilage (C6) to opening in diaphragm
(Esophageal hiatus T10)
- Abdominal part: From Esophageal hiatus up to
cardiac end of stomach (T11/7th costal cartilage
level)
- Length: 25cm, (1.25cm is abdominal part)
- Curvatures: Two, side to side curve and one
anteroposterior curvature.

Anatomy
Constrictions: 4 constrictions normally [08]

Distance from incisor in inches (1 inch =
Sites and Causes of constriction Vertebral level
2.5cm)
1. At its beginning C6 6 inches, (15cm)
2. Where it is crossed by Aortic arch T4 9 inches (22.5cm)
3. Where it is crossed by left bronchus T5 11 inches (27.5cm)
4. Where it pierces diaphragm T10 15 inches (37.5cm)
Blood supply and lymphatic drainage:
Cervical part Thoracic part Abdominal part
Arterial supply Inferior thyroid Esophageal branch of Esophageal branch of left gastric
artery Aorta
Venous Interior thyroid Azygous, Hemiazygous Left gastric vein (portal), Azygous vein (Systemic)
drainage vein vein Hence, site of portosystemic anastomosis
Lymphatic Deep cervical Posterior mediastinal Left gastric nodes
drainage lymph nodes lymph nodes
Development: - Lumen: Irregular
th
- At 4 week - Mucosa:
- Part of foregut caudal to pharyngeal gut.
• Stratified squamous non keratinized
- Congential anomaly:
• At lower end, abrupt transition to columnar
• Esophageal atresia: Tracheoesophageal fistula
lining.
V • Esophageal stenosis
• Lamina propria with few lymphocytes,
• Congenital hiatal hernia
lymphatic nodules.
Applied Aspects:
• Few tortuous mucus secreting glands near
- Esophageal varices: Occurs due to portal HTN upper and lower ends.
- Achalsia cardia: Can occur during chagas disease • Muscularis mucosa with few smooth
- Barrett's esophagus: Complication of GERD muscles.
Histological features: - Submucosa: Tubuloacinar mucus secreting
glands.
- Muscularis externa:
• Upper 1/3rd has skeletal muscle
• Middle 1/3rd has both skeletal and smooth
muscles
• Lower 1/3rd has only smooth muscle
- Serosa:
• In the abdominal part
• Rest have Adventitia

GIT
STOMACH These structures are:

Past Questions: 1. Diaphragm
1. Write briefly on the relations of posterior surface 2. Left kidney
of stomach. (2) [KU2013] 3. Left suprarenal gland
Gross features 4. Pancreas
♦ Location: Lies obliquely in upper & left part of abdomen 5. Transverse mesocolon
- Occupies epigastric, umbilical and left 6. Splenic fexure of colon
hypochondriac region
7. Splenic artery
External features:
Anterior relations:
- 2 orifices: Cardiac and pyloric
- 2 curvatures: Lesser and greater 1. Liver
- 2 surfaces: Anterior and posterior 2. Diaphragm
- 2 parts: Subdivided into four 3. Anterior abdominal wall
Blood supply
Arterial supply:
Arteries Branch of
Along 1. Left gastric Coeliac trunk
lesser artery
curvature 2. Right gastric Hepatic artery proper
artery
Along 1. Right gastro Gastroduodenal
greater epiploic
V
Parts:
curvature 2. Left Splenic
1. Cardiac part: Fundus, body
2. Pyloric part: Pyloric antrum, pyloric canal gastroeplpolic
Relations Fundus 1. 5-7 short Splenic artery
Posterior relations of stomach/stomach gastric arties
bed [KU 2013]

Anatomy
Venous drainage: Nerve supply

1. Portal vein ♦ Sympathetic nerves: T6 – T10
2. Superior mesenteric ♦ Parasympathetic nerves: Vagus nerve
3. Splenic vein
Development
Lymphatic drainage:
♦ Stomach appears as fusiform dilation of foregut
in the fourth week.
♦ Positional changes occurs by rotation around
longitudinal and an Anteroposterior axis.
♦ Stomach rotates clockwise 90° around its
longitudinal axis, causing its left side to face
anteriorly and right side to face posteriorly.
♦ Left vagus nerve, initially innervating left side of
stomach now innervates anterior wall and vice
versa.
♦ Original posterior wall grows faster than anterior,
forming greater and lesser curvatures.

GIT
Congenital anomaly: d. Nerve supply is more abundant, with large

- Pyloric stenosis ganglia.
Applied Aspects: e. Because of Gastric canal, it receives most of
1. Gastric ulcer – Most common on lesser curvature. insult from irritating drinks.
2. Gastric carcinoma – Most common on lesser f. Being shorter in length the wave of contraction
curvature. stays at particular point.
This is possibly due to following reasons: 3. Metastasis of gastric carcinoma can occur to left
supraclavicular lymph node called Troisier's sign.
a. Mucosa is not freely movable over muscular
coat. 4. Gastric pain is felt in epigastrium because the
stomach is supplied from same segment of spinal
b. Epithelium is comparatively thin.
cord which also supply the upper part of
c. Blood supply is less abundant and there are
abdominal wall.
fewer anastomosis.
Histological features
1. Mucosa: Simple columnar epithelium iii. Pyloric glands:

a. 3 types of glands: - In pyloric antrum and canal
i. Cardiac glands: Simple tubular glands, - Open into deep gastric pits
posses majority of mucus secreting cells,
- Coiled tubular
few parietal and zymogen cells.
- Mainly mucus secreting cells
ii. Fundic glands:
- Lie is fundus and body b. Lamina propria and Muscularis mucosa
- Simple tubular, open into shallow gastric pits 2. Submucosa: With auerbach's plexus, blood vessels
- 5 types of cells → Chief cells, parietal 3. Muscularis externa: Outer longitudinal, middle
cells, mucus cells, stem cells, entero circular and inner oblique layer.
endocrine cells.

Anatomy
SMALL INTESTINE ♦ 6m long

Past Questions: ♦ Extends from pylorus to ileocaecal junction
1. Mention the extent and relations of second part Duodenum:

of duodenum. Name the structures opening into ♦ 25cm long
it. Add a note on its development. ♦ 4 parts:
(2+1+1=4) [04 Nov] Length level
2. Describe the relations of the second part of First part – 2 inches L1
duodenum with diagrams. What is its correlation
Second part – inches L2
with the development of hepatobiliary system.
Third part – 4 inches L3
[2+1 = 3] (KU2013) Fourth part – 1 inch L2
Relation of various parts:
First part Second part [04 013] Third part Fourth part
Peritoneal - Proximal half is attached - Retroperitoneal, - Retroperitoneal, - Retroperitoneal,
relations: to lesser omentum fixed. anterior surface is covered with
above and greater - Anterior surface is covered with peritoneum only
omentum below. covered with peritoneum except anteriorly
- Distal half is covered peritoneum, except in median plane.
with peritoneum only near the middle.
anteriorly
Visceral relations:
Anterior - Quadrate lobe of liver - Right lobe of liver - Superior mesentric - Transverse colon
V - Gallbladder - Transverse colon vessels, - Transverse
- Root of transverse - Root of mesentry mesocolon
colon - Lesser sac
- Small intestine - Stomach
Posterior Gastroduodenal artery - Anterior surface of - Rt. Ureter - Lt. sympathetic
Bile duct right kidney - Rt. psoas major chain, Lt. psoas
- Right renal vessels - Rt. gonadial vessels major
- Right edge of - IVC, Abdominal - Lt. testicular
inferior venacava aorta vessels
- Rt. Psoas major - Inferior mesentric
vein
Medical - Head of the - Attachment of
relation – pancreas – upper part of root
- The bile duct of mesentery
Lateral - Right colic flexure - Left kidney, ureter
– –
relation
Superior Epiploic foramen Head of pancreas with Body of pancreas
–
relation uncinate process
Inferior Head and neck of pancreas – Coils of Jejunum –

GIT

Anatomy
- Venous drainage: Splenic, superior mesentric

and portal vein.
- Nerve supply:
• Sympathetic →T9– T10
• Parasympathetic → Vagus nerve
Development
- Duodenum develops from two sources
- Part proximal to opening of hepatopancreatic
duct: from foregut
- Since foregut is supplied by celiac artery and
the midgut is supplied by superior mesentric
artery duodenum is supplied by branches of
both arteries.
Relation of second part with development of
hepatobiliary system: [KU 2013]
Blood supply - At distal end of foregut (i.e. in second part),
Arterial supply: liver bud arises.
- Upto level of opening of hepatopancreatic duct - The rapidly proliferating cells penetrate
is supplied by superior pancreaticoduodenal, septum transversum.
below it: By inferior pancreaticoduodenal. - The connection between hepatic diverticulum
V - First part also receives from: and foregut (duodenum) narrows forming bile
1. Right Gastric artery duct.
2. Supraduodenal artery of wilkie - Small outgrowth is formed by the bile duct, this
3. Retroduodenal branches of gastro duodenal outgrowth gives rise to gallbladder and cystic
artery duct.
Applied Aspects:
- In skiagrams taken after giving a barium meal, the
first part of duodenum is seen as a triangular
shadow called duodenal cap.
- Annular pancreas can cause duodenal obstruction.
Microscopic structure:
1. Villi: Numerous and leaf like
2. Crypts of liberkhun and Goblet cells are
present in epithelium (Few in number)
3. Submucosa has numerous mucus glands called
Brunner's gland.
4. Serosa is incomplete.

GIT
JEJUNUM AND ILEUM 2. Describe the differences between the jejunum

and the ileum, both in macroscopic and
Past Questions:
microscopic features. (3 +3 = 6) [03 Nov]
1. Give in tabular form the differences between the
3. Differences between jenjunum and ileum (4) [8 July]
gross features and microscopic anatomy of
4. Meckel's diverticulum (2) [10 July] (2) [05 Dec]
jejunum and ileum. (3 + 3 = 6) [09 July]
5. Intestinal villi (2) [07 July]
Differences between Jejunum and ileum [09 July, 03 Nov]
Features Jejunum IIeum
1. Location Occupies upper and left parts of the Occupies lower and right parts of the
intestinal area intestinal area
2. Walls Thicker and more vascular Thinner and less vascular
3. Lumen Wider and often empty Narrower and often loaded
4. Mesentery a. Window present a. No windows

b. Fat less abundant b. Fat more abundant
c. Arterial arcades, 1 or 2 c. Arterial arcades, 3 or 6
d. Vasa recta longer and fewer d. Vasa recta shorter and more numerous
5. Circular mucosal folds Larger and more closely set Smaller and sparse
6. Villi Large, thick (leaf-like) and more abundant Shorter, thinner (finger-like) & less abundant V
7. Peyer's patches Absent Present
8. Solitary lymphatic Fewer More numerous

follicles
Microscopic structure
Jejunum Ileum
- Villi are taller and - Villi are shorter and

tongue shaped fewer
- Crypts of liberkuhn - Lymphatic follicles in
longer than duodenum lamina propria
- Globlet cells are more - Peyer's patches
- Peyer's patches absent formed By
collescence of
- Submucosa is thin
lymphatic nodules in
- Serosa is almost complete
lamina propria

Anatomy
Blood supply: - This rotation is counter clockwise, Aprox. 270°

- Is by Branches of superior mesenteric artery when complete.
and are drained by corresponding veins. - 90° during herniation and 180° during return to
Development: abdominal cavity.
- From midgut - Retraction of loops occurs during 10th week.
- Development of midgut is characterized by Congenital anomaly:
rapid elongation of the gut and its mesentery, 1. Omphalocele (Described earlier)
resulting in formation of the primary intestinal 2. Gastroschisis (Described earlier)
loop (Apex of loop via vitellointestinal duct
3. Gut rotation defects → Results in abnormal
V communicates with yolk sac)
positioning of portions of gut.
- The cephalic limb of loop develops into the
4. Meckel's Diverticulum [10 July]
distal part of the duodenum, the jejunum and
part of the ileum. Persistent proximal part of vitellointestinal
- The caudal limb of loop becomes lower portion duct (it normally disappears during 6th week of
of ileum, the cecum, the appendix, ascending intrauterine life)
colon and the proximal 2/3rd of the transverse a. Occurs in 2% subjects.
colon. b. Usually 2 inches long.
Physiological herniation/ Physiological umbilical c. Situated 2 feet proximal to ileocecal valve.
herination 5. Apple peel atresia: Atresia in proximal jejunum.
- Development of primary intestinal loop is
characterized by rapid elongation, particularly LARGE INTESTINE
of cephalic limb.
Past Questions:
- As a result of rapid growth and expansion of
1. Differences between large and small gut
liver, abdominal cavity temporarily becomes
smaller to contain the umbilical cord during the (2) [11, July]
sixth week of development (physiological 2. Positions of vermiform appendix (2)
umbilical herination) 3. Micro-anatomy of vermiform appendix with a
Rotation of midgut labelled diagram (3) [03 June]
- Primary intestinal loop rotates around an axis 4. Draw a labelled diagram showing micro anatomy
formed by the superior mesenteric artery. of vermiform appendix. [4](2013 KU PBQs)
GIT
Parts 2. Fixed except Appendix, transverse colon and

- Extends from ileocecal junction to anus. sigmoid colon
- 1.5m long 3. Taeniae coli present
- Caecum, Ascending colon, the transverse 4. Appendices epiploicae [Small bags of peritoneum
colon, the descending colon, the sigmoid colon, filled with fat, found over large intestine except:
rectum and anal canal, vermiform appendix. Caecum, Appendix, Rectum (@CAR)]
Cardinal features 5. Blood supply by marginal artery
1. Wider in callibre 6. Sacculated and puckered.
Differences between small intestine and large intestine [11 July]
Feature Small intestine Large intestine
1. Appendices epiploicae Absent Present
2. Taeniae coli Absent Present
3. Sacculation Absent Present
4. Distensibility Less More
5. Fixity Greater part is freely mobile Greater part is fixed
6. Villi Present Absent
7. Transverse mucosal folds Permanent Obliterated when longitudinal muscle coat relaxes
8. Peyer's patches Present in ileum Absent
9. Common site for a. Intestinal worms a. Entamoeba histolytica
b. Typhoid b. Dysentery organisms
c. Tuberculosis c. Carcinoma V
10.Effects of infection and irritation Diarrhoea Dysentery
Caecum
♦ Situated in right iliac fossa
♦ Above the lateral half of Inguinal ligament.
Dimension:
- 6cm long , 7.5cm broad
Note: Breadth > Length
Other organs whose b > l are:
i. Pons ii. Prostate iii. Pituitary
Relations:
- Anterior: Coils of intestine and anterior
abdominal wall.
- Posterior:
a. Muscles: Right psoas and Iliacus
b. Nerves: Genitofemoral, femoral and lateral Vermiform appendix
cutaneous nerve of thigh. (All of right side) ♦ Arising from posteromedial wall of caecum.
c. Vessels: Testicular or ovarian
♦ 2cm below ileocecal orifice.
d. Appendix in retrocecal recess.
♦ Length: 9cm (average)
Anatomy
Position [04 July] 3. Splenic 1. Upward to left

- Lies in Rt. iliac fossa. 2. Points toward spleen
- Base is fixed but tip direction is variable. 3. 2 o'clock position
4. Can be preileal or post ileal
Types of
Comments 4. Promontroic 1. Horizontally to left toward
appendix
sacral promontory
1. Paracolic 1. Pass upward to right 2. 3 o'clock position
2. 11 o'clock position 5. Pelvic 1. Second most common (30%)
2. Descending into pelvis
2. Retrocecal 1. Commonest position (65%) 3. 4 o'clock position
2. Lies behind caecum/colon 6. Subcecal or 1. Below caecum
mid inguinal 2. Point towards inguinal ligament
3. 12 o'clock position
3. 6 o'clock position
Parts of Large
Blood Supply Nerve Supply
Intestine
1. Caecum a. Cecal branch of Ileocolic Sympathetic: T11 – L1
b. Venous drainage into superior mesenteric vein Para-sympathetic: Vagus
2. Vermiform a. Appendicular branch of lower division of Sympath: T9–T10through celiac plexus
appendix Ileocolic artery Parasympth: Vagus
b. Venous drainage into appendicular, mesenteric
vein into portal vein
Lymphatic drainage
3. Colon a. Ileocolic, right colic & middle colic artery 1. Ascending colon: Epicolic and paracolic
(branches of superior mesenteric artery) & left colic Lymph nodes.
& sigmoid arteries (branches of inferior mesenteric 2. Transverse colon: Middle colic L.
artery) anastomose & forms marginal artery Nodes.
b. Vasarecta arises from marginal artery and 3. Descending colon and Sigmoid colon:
supply colon. Epicolic and paracolic lymph nodes.

GIT
Blood supply Ascending colon:

- Arterial supply: Appendicular artery which is a - Caudal limb of primary intestinal loop (i.e.
branch of the lower division of the ileocolic from mid gut)
artery. Transverse colon:
- Venous drainage: Blood from the appendix is - Proximal 2/3rd from caudal limb of primary
drained by the apendicular, ileocolic & superior intestinal loop. (i.e. from mid gut)
mesenteric veins, to the portal vein. - Distal 1/3rd from Hind gut.
V
Note: Appendicular orifice which situated on the Descending colon and sigmoid colon:
posteromedial aspect of the caecum 2cm below the - From Hindgut
ileocaecal orifice is guarded by an indistinct semilunar Microscopic Features of Appendix
fold of the mucous membrane, known as the valve of
[03 June, PBQ 2013 KU]
Gerlach.
Development
♦ Large intestine develops from both midgut and
Hindgut.
Caecum:
- From cecal bud (i.e. from midgut)
- As small conical dilation of caudal limb of
primary intestinal loop.
- Is last part of gut to reenter abdominal cavity
so lies in right side.
Appendix:
- Distal end of cecal bud form narrow diverticulum
called appendix. (i.e. from midgut)
- Since it develops during descent of colon. Its
final position is mostly Retrocecal.
Anatomy
1. Lumen small, Irregular outline. RECTUM AND ANAL CANAL

2. Villi absent. Past Questions:
3. Crypts of liberkuhn few.
1. Describe the rectum under the following
4. Epithelium is of columnar cells and few goblet
headings: (1+1+2+2=6) [08, July]
cells.
2. Short notes on rectum: (2 + 3 + 3 + 2) [05]
5. Lamina propria has lymphatic follicles
a. Extent with curvatures
6. Muscularis mucosa → Incomplete.
b. Posterior relations
7. Submucosa is thick with blood vessels and
nerves. c. Venous drainage
8. Muscularis externa→ Thin d. Peritoneal relations
9. Serous coat → Complete 3. Discuss anal canal under the following headings:
(4+1+1=6) [09, Dec]
Applied Aspects:
a. Interior
Caecum
1. Caecum is involved in: b. Arterial supply
i. Amoebiasis c. Sources of development
ii. Intestinal tuberculosis. 4. Interior of anal canal (2) [10, July]
iii. Carcinoma 5. Peritoneal relation of rectum (2) [11, July]

2. Inflammation of caecum is called a 6. Structures related anteriorly to the rectum in
caecitis/Typhilitis female (2) [05, Dec]
V Appendix
1. Inflammation of appendix is called appendicitis.
Rectum [05]
2. Removal of appendix is called appendectomy. ♦ Distal part of the large gut.
3. Pain is first felt in region of umbilicus; this is ♦ Between sigmoid colon above and anal canal
referred pain (because of innervations by same below.
spinal segment (T10) of the spinal cord) ♦ Curved in an anteroposteior direction and from
4. With increasing inflammation pain is felt in right side to side i.e. -It is not straight.
Iliac fossa. This is caused by involvement of ♦ Three cardinal features of large gut (sacculation,
parietal peritoneum. appendices epiploices and taeniae ) are absent.
5. MC Burney's point is site of maximum tenderness Gross features
in appendicitis.
Situation:
Colon
- In posterior part of lesser pelvis.
1. Congenital megacolon (Aganglionic megacolon or
- Infront of the lower three pieces of the sacrum
Hirschsprung disease):
and coccyx.
- Due to absence of parasympathetic ganglia in
Extent [05]
bowel wall.
- Begins as continuation of sigmoid colon at the
- These ganglia are derived from neural crest
level of third sacral vertebrae (S3).
cells.
[MCQ 2013 KU)

GIT
- Ends by becoming continuous with anal canal

at the anorectal junction.
- the anorectal junction lies 2 to 3 cm in front of
and a little below the tip of the coccyx .
Curves [05]
- The beginning and end of the rectum lies in the
median plane.
- However, it shows two types of curvatures in its
course:
1. Two anteroposterior curves:
- Sacral flexure
- Perineal flexure
2. Three lateral curves:
- Upper lateral curve
- Middle lateral curve
- Lower lateral curve Visceral
Males Females [05]
relations
Upper
Anterior - Upper 2/3rd - Upper 2/3rd
Sacral flexure Right relation related to related to
rectovesical rectouterine
pouch with coils pouch with coils V
Perineal flexure Lower Middle of intestine and of intestine and
Right Left
sigmoid colon. sigmoid colon.
Anal canal
- Lower 1/3rd to - Lower 1/3rd of
base of Urinary rectum is related
(a) (b) bladder, to lower part of
Curvatures of rectum terminal part of the vagina.
ureter, seminal
Relations vesicles, vas
Peritoneal relations: [05] deferens and
1. Upper 1/3 : rd prostate.
• Covered with peritoneum in front and on Posterior relation:
the sides. Same in male and female.
2. Middle 1/3rd: 1. Lower three pieces of the sacrum, the coccyx
• Covered only in front. and the anococccygeal ligament.
2. pyriformis, the coccygeus and the levator ani.
3. Lower 1/3rd:
3. The median sacral, the superior rectal and
• Devoid of peritoneum.
lower lateral sacral vessels.
4. The sympathetic chain with the ganglion impar.

Anatomy
Blood supply Anal canal [09]

Arterial supply: Situation:
1. Superior rectal artery: Continuation of inferior - Below level of the pelvic diaphragm.
mesenteric artery. - Lies in anal triangle of perineum in between
2. Middle rectal arteries. right and left ischioanal fossa.
3. Median sacral artery. Relations of anal canal:
Venous drainage: Both sex Males Females
V 1. Superior rectal vein pains into inferior mesenteric
1. Membranous
vein. Anteriorly Perineal 1. Lower end of
urethra
2. Middle rectal vein opens into internal iliac vein. body the vagina
2. Bulb of penis
3. Median sacral vein joins left common iliac vein.
Nerve supply: Posteriorly:
- Sympathetic: L1, L2 ⇒ Vasoconstrictor, inhibit 1. Anococcygeal ligament
rectal musculature and motor to internal 2. Tip of coccyx
sphincter. Laterally:
- Parasympathetic: S2, S3, S4 through superior - Ischioanal fossae
rectal or inferior mesentric and inferior
All round:
hypogastric plexus ⇒ motor to musculature of
- By sphincter muscles
rectum and inhibitory to the internal sphincter.
Interior of anal canal [10]
Note: Sensations of distension of rectum passes
through the parasympathetic nerves, while pain Divided into 3 parts:
sensations carried by both sympathetic and 1. Upper part:
parasympathetic nerves. - 15 mm long
Lymphatic drainage: - Lined by mucusmembrane, Endodermal origin.
1. Inferior mesenteric lymph nodes - 6–10 vertical folds called 'Anal columns of
2. Internal iliac lymph nodes morgagni'.

GIT
- Anal columns united at lower ends by anal valves.

- Depression in mucosa above each valve called
anal sinus.
- Line formed by anal valves together called
pectinate line.
2. Middle part/Transitional zone or pecten
- 15mm, lined by mucos membrane
- No anal columns
- Bluish appearance because of dense venous
plexus between mucosa and muscle coat.
- Lower limit has white line called white line of
Hilton.
3. Lower cutaneous part
- 8mm long, lined by true skin containing sweat
and sebaceous glands.
Note:
1. Conjoint longitudinal coat is formed by fusion of
puborectalis with longitudinal muscle coat of
rectum at anorectal junction.
2. Anorectal ring is formed by fusion of puborectalis
with uppermost fibers of external sphincter and
the internal sphincter.
Arterial supply Venous drainage Lymphatic drain V
age
- Above pectin 1. Internal rectal - Above
ate line by venous plexus pectinate line
superior in submucosa into internal
rectal artery of anal canal. iliac nodes
Musculatures of Anal canal - Below 2.External rectal - Below into
Anal sphincters: pectinate line venous plexus superficial
by inferior outside inguinal nodes
Internal anal sphincter:
rectal artery muscular coat
- Involuntary, circular muscle of rectum and
- Surrounds upper 3/4th of anal canal. anal canal;
- Ends at level of white line of hilton. communicates
with internal
External anal sphincter:
plexus.
- Voluntary 3. Anal veins
- Made of striated muscle
Nerve supply
- Surrounds whole length of anal canal.
1. Above the pectinate line
- 3 parts:
i. Subcutaneous - Supplied by autonomic nerves. Both sympathetic
(inferior hypogastric plexus: L1, L2) and
ii. Superficial
parasympathetic (pelvic splanchnic :S2, S3, S4)
iii. Deep

Anatomy
2. Belowpectinate line PANCREAS

- By somatic nerves.
Location:
- Inferior rectal: S2, S3, S4 - More or less transversely across the posterior
3. Sphincters: abdominal wall.
- Internal sphincter: - At the level of first & second lumbar vertebrae.
Sympathetic and parasymphathetic Parts:
↓ - From right to left:
Causes contraction and relaxation respectively - Head, Neck, Body, Tail
- External Sphincter: Inferior rectal nerve and Parts External features
perineal branch of S4.
Head - 3 borders: Superior, inferior & right lateral
Applied Aspects: - 2 surfaces: Anterior and posterior
Piles/Haemorrhoids: - 1 process: Uncinate process
i. Internal piles/True piles: Neck - 2 surfaces: Anterior and posterior
- Dilation of internal rectal venous plexus. Body - 3 borders: Anterior, superior, inferior
- Occur above pectinate line; painless. - 3 surfaces: Anterior, posterior, inferior
- Bleed profusely during straining.
Relations:
a. Primary piles:
Head of
in 3, 7 and 11 o'clock position Relations
pancreas
viewed on lithotomy position.
1. Superior - Overlapped by first part of
b. Secondary piles: In other position. border: duodenum.
V ii. External piles - Related to superior pancreaticoduodenal
- Occur below pectinate line artery
- Very painful, don't bleed. 2. Inferior - Third part of duodenum
Factors responsible for causing internal piles: border: - Inferior pancreaticoduodenal artery
1. Poor support to veins from surrounding connective 3. Right - Second part of duodenum
tissue. lateral - Terminal part of bile duct
border - Anastomosis between 2-
2. Absence of valves in superior rectal and portal
veins. pancreaticoduodenal arteries
3. Portal hypertension. 4. Anterior From above downwards:
4. Compression of veins at sites where they pierce surface: 1. First part of duodenum
muscular coat of rectum. 2. Transverse colon
2. Fissure in Ano: 3. Jejunum
- Rupture of one of anal valves. 5. Posterior 1. Inferior venacava
surface 2. Terminal part of renal veins
- Due to passage of dry, hard stools.
3. Right crus of diaphragm
3. Fistula in Ano:
4. Bile duct
- Track connecting two cavities.
6. Uncinate - Anteriorly to superior mesenteric vessels
- Due to spontaneous rupture of abscess around
process - Posteriorly to Aorta.
the anus.

GIT
Neck of Body of
Relations Relations
pancreas pancreas
1. Anterior - Attachment to root of transverse
1. Anterior 1. The peritoneum covering posterior
border mesocolon.
surface wall of lesser sac.
2. Superior - Coeliac trunk, Hepatic artery and
2. Pylorus
border splenic artery V
2. Posterior 1. Termination of sup. mesenteric 3. Inferior - Superior mesenteric vessels.
surface vein border
2. Begining of the portal vein. 4. Anterior - Related to lesser sac and to the
surface stomach
5. Posterior - Aorta with origin of sup.
surface mesenteric artery.
- Left crus of diaphragm
- Left supra renal gland
- Left kidney
- Left renal vessels
- Splenic vein
6. Inferior - Duodenojejunal flexure
surface - Coils of jejunum
- Left colic flexure
Note: Splenic vein in relation with posterior surface
but splenic artery in relation with superior border of
body of pancreas.

Anatomy
Tail of pancreas: - Opens into minor duodenal papilla (6–8cm

- Lies in Lienorenal ligament together with from pylorus)
splenic vessels. - The opening of the accessory duct lies cranial
and ventral to that of the main duct.
Note:
- Maximum amount of insulin is produced in tail of Note:
pancreas.(KU, MCQ) - The two ducts remind the doubled origin of
- Carcinoma of head of pancreas causes obstructive pancreas from the ventral and dorsal pancreatic
jaundice. (KU, MCQ) buds.
V
Ducts of pancreas a. Main duct: Development from whole of ventral
bud and distal part of duct of dorsal bud.
♦ Exocrine pancreas is drained by two ducts, main
b. Accessory duct: From proximal part of duct of
and accessory.
dorsal bud.-
1. Main pancreatic duct of whirsung
- Begins at tail, runs towards right through body Blood Supply
and bends at neck. Arterial 1. Mainly by pancreatic branches of
- Lumen is 3mm. supply: splenic artery.
- Herring bone pattern. 2. Superior pancreaticoduodenal.
- Joins with bile duct 3. Inferior pancreaticoduodenal.
- Enters wall of second part of duodenum Venous 1. Splenic
- Opens on summit of major duodenal papilla drainage: 2. Superior mesenteric
(8–10 cm from pylorus) 3. Portal veins
2. Accessory pancreatic duct of santorini:
Lymphatic 1. Pancreaticosplenic
- Begins in lower part of head. drainage: 2. Coeliac
- Crosses the front of main duct with which it
3. Superior mesenteric group of lymph
communicates.
nodes.

GIT
Development ♦ Ventral bud ⇒ Forms [MCQ 13 KU]

♦ Formed by 2 buds: Dorsal and ventral i. Uncinate process
♦ Buds originate from endodermal lining and ii. Inferior part of head
duodenum. ♦ Dorsal bud ⇒ Forms: Remaining part
♦ Ventral bud rotates as duodenum rotates to the ♦ Main pancreatic duct/(Wirsung): By entire ventral
right. pancreatic duct and distal part of dorsal
pancreatic duct. V
♦ Ventral bud moves dorsally and lies below and
behind dorsal bud. ♦ Accessory duct/(Santorini): By proximal part of
dorsal bud.

Anatomy
Congenital anomaly: Microscopic structure:

i. Annular pancreas:
• Right portion of ventral bud migrate along
normal route but left portion in opposite
direction.
ii. Accessory pancreatic tissue:
• May be present at wall of duodenum,
jejunum, ileum and Meckel's diverticulum.
V
iii. Inversion of pancreatic ducts
Applied Aspects:
i. Pancreatic cancer: Has exocrine and endocrine portion
– Common in head Exocrine part
– Causes extra hepatic obstruction of biliary - Tubuloacinar gland.
ducts. - Acini are tubular or pear shaped with narrow
– Can–cause obstructive Jaundice, Ascitis. lumen and is surrounded by basal lamina and
ii. Pain from pancreatitis is referred to rich capillary network.
– Epigastrium - Myoepithelial cells are not present.

- In between acini, there is connective tissue
– Posterior paravertebral region
containing blood vessels, lymphatics, nerves
iii. Rupture of pancreas: and excretory ducts.
– Can result from sudden, severe, forceful - Cytoplasm near base of acinar cells is strongly
compression of abdomen. basophilic while supranuclear part is
– Like in automobile accident. acidophilic.
iv. Pancreas is prone to hemorrhage because of rich • Acidophilic → Zymogen granules
blood supply. • Basophilic → RER

GIT
Duct system: Past Questions:

- Has intralobular and interlobular part 1. What is the conjoint tendon (falx inguinale) of
Endocrine part the inguinal canal? Mention its clinical
- Formed by islets of langerhans importance
- Scattered throughout the pancreas but more in (2) [04 Nov]
tail. 2. Mention the boundary and contents of inguinal
canal. (2 +1 = 3) [03 Nov]
- Enclosed by fine capsule of reticular fibers.
3. Mention the location and boundaries of inguinal
- Compact mass polyhedral cells pervaded by canal. (1 +2 = 3) [06 June]
network of fenestrated capillaries. 4. Mention the boundaries and the contents of the
- Four types of cells differentiated inguinal canal. What is Hesselbach's triangle?
• α-cells: 20% of islet cells, usually at Give its clinical importance. (3 +1 + 2 = 6) [08 Dec]
periphery 5. Inguinal ligament (2) [10 July]
• β-Cells: 60–80% islet cells, mostly in center. 6. Formation of rectus sheath at the level of
umbilicus (2)[05 Dec]
• δ -Cells: Small, Scattered
7. Contents of rectus sheath (2)[04 June]
• PP cells: Scattered, few in numbers.
8. Superficial inguinal ring. (2) [07 July]
ANTERIOR ABDOMINAL WALL
Flat muscles
Muscle Origin Insertion Innervation Main Action
External External surfaces of 5th - Linea alba, pubic Thoraco-abdominal
oblique (A) 12th ribs tubercle, and anterior nerves (T7–T11)spinal
half of iliac crest nerves) & subcostal
Compresses and
V
nerve
support abdominal
Internal Thoracolumbar fascia, Inferior borders of viscera, flexes and
oblique (B) anterior two thirds of iliac 10th-12th ribs, linea rotates trunk
crest, and connective tissue alba, and pecten
deep to lateral third of pubis via conjoint
inguinal ligament tendon Thoraco-abdominal
nerves (anterior rami
Transversus Internal surfaces of 7th - 12th Linea alba with of T6-T12 spinal nerves) Compresses and
abdominis (C) costal cartilages, aponeurosis of and first lumbar nerves supports abdominal
throacolumbar fascia, iliac internal oblique, viscera
crest, and connective tissue pubic crest, and
deep to lateral third of pecten pubis via
inguinal ligament conjoint tendon
Rectus Pubic symphysis and pubic Xiphoid process and Thoraco-abdominal Flexes trunk (lumbar
th th
abdominis (D) crest 5 - 7 costal nerves (anterior rami vertebrae) and
cartilages of T6-T12 spinal nerves) compresses
abdominal viscera,
stabilizes and
controls tilt of pelvis
(antilordosis)

Anatomy
Conjoint Tendon or Falxinguinalis ♦ Medially, it is continuous with anterior wall of

♦ Formed by fusion of lowest aponeurotic fibers of rectus sheath and laterally it is free.
internal oblique and of transversus muscle. Function:
♦ Is attached to pubic crest and to the medial part - Strengthens the abdominal wall at site where it
of the pecten pubis. is weakened by the superficial inguinal ring.
Rectus sheath
Formation [05 Dec]
Above costal margin Anterior wall: External oblique Aponeurosis.
Posterior wall: Deficient , rests directly on 5th, 6th, 7th costal cartilage.
Between costal margin and arcuate Anterior wall:
line 1. External oblique aponeurosis.
2. Anterior lamina of aponeurosis of the internal oblique.
Posterior wall:
1. Posterior lamina of aponeurosis of internal oblique.
2. Aponeurosis of transversus muscle.
Below arcuate line/At the level of Anterior wall:
umbilicus [05 Dec] 1. Aponeurosis of all 3 flat muscles of abdomen.
Posterior wall:
– Deficient
– Rectus muscle rests on fascia transversalis (MCQ 2013 KU )
Boundaries
Anterior – Complete
wall: – Composition is variable (described
V above)
– Is firmly Adherent to the tendinous
intersection of the rectus muscle.
Posterior – Incomplete
wall: – Deficient above costal margin and
below arcuate line.
– Uniform composition (described above)
– Is free from rectus muscle.
Contents [04 June]
Muscles: – Rectus abdominis
– Pyramidalis
Vessels: Arteries:
– Superior epigastric artery
– Inferior epigastric artery
Veins:
– Superior epigastric vein
Note: Midway between umbilicus and the pubic
– Inferior epigastric vein
symphysis, the posterior wall of rectus sheath ends in
Nerves: – Terminal parts of lower 6 thoracic nerves.
the arcuate line or line a semicircularis or fold of
– Lower 5 intercostal and subcostal nerves
Douglas.
GIT
Note: Posterior 1. In whole extent:

– Superior epigastric artery is branch of internal wall: – Fascia transversalis, extraperitoneal
thoracic artery. tissue, parietal peritoneum.
– Inferior epigastric artery is branch of external iliac 2. In lateral 1/3rd:
artery. – Interfoveolar ligament
3. In medial 2/3rd:
Inguinal canal – Conjoint tendon, reflected part of
Boundaries [03 Nov,06 june,08Dec] inguinal ligament
Roof – Arched fibers of internal oblique and

Anterior 1. In whole extent: Skin, superficial
transversus abdominis
wall: fascia, ext. oblique aponeurosis.
2. In lateral 1/3rd: Fleshy fibers of internal Floor – Upper surface of Inguinal ligament
oblique – Lacunar ligament
Content of canal [03 Nov, 06 June, 08 Dec] 3. Vein: Pampiniform plexus of veins.
In males: In females: 4. Nerves: Genital branch of genitofemoral, sympathetic
nerves around artery of ductus deferens.
1. Spermatic cord 1. Round ligament of 5. Lympatics: Lymph vessels from testis
uterus
6. Remnant of processus vaginalis.
2. Ilioinguinal nerve 2. Ilioinguinal nerve Inguinal ligament [10 July]
Contents of spermatic cord: - Formed by lower border of external oblique
1. Ductus deferens aponeurosis.
2. Arteries: Cremastric, Artery of ductus deferens - Extends from Anterior superior iliac spine to
and Testicular (@ CAT) pubic tubercle.

Anatomy
- Extensions: i. Congenital vaginal

1. Pectineal ligament of cooper ii. Congenital funicular
2. Pectineal part of inguinal ligament or iii. Bubonocele
lacunar ligament. Direct inguinal Indirect inguinal
3. Reflected part of Inguinal ligament. hernia hernia
1. Aetiology Weakness of Performed sac
posterior wall of
inguinal canal
2. Precipitating Chronic -
bronchitis
3. On standing comes out Does not come
out
4. Direct of the It comes out of Sac comes
sac Hesselbach's through the deep
triangle inguinal ring
Inguinal hernias: 5. Obstruction not common Common, as neck
- Abnormal protrusion of abdominal contents because neck is is narrow
into the inguinal canal. wide
- More likely by chronic cough, work involving 6. internal ring The swelling is Not seen
frequent lifting of heavy weights etc. occlusion seen
V
Types: test
1. Direct: Hesselbach's triangle [08 Dec]
– Contents of hernia enter inguinal canal, not - Triangular gap at posterior wall of Inguinal
through deep ring but through posterior canal.
wall (medial to inferior epigastric artery).
Boundaries:
(i.e. through Hesselbach's triangle)
- Medially: Lateral border of rectus abdominis.
– Can be either medial direct or lateral direct
- Lateral: Inferior epigastric artery
divided by obliterated umbilical artery.
- Below: Inguinal Ligament
2. Indirect:
Significance
– Contents enter inguinal canal through deep
inguinal ring. 1. Direct inguinal hernia pass through this
triangle.
– And pass through inguinal canal, superficial
inguinal ring into the scrotum. 2. Obliterated umbilical artery, divides this
triangle into medial and lateral parts.
– Can be either:

GIT
POSTERIOR ABDOMINAL WALL

Muscles
Muscle Superior Attachment Inferior Attachment Innervation Main Action
Psoas major Transverse processes of By a strong tendon to Anterior rami Acting inferiorly with iliacus,
lumbar vertebrae; sides of lesser trochanter of of lumbar it flexes thigh; acting
bodies of T12-L5 vertebrae and femur nerves L1, L2, L3 superiorly it flexes vertebral
intervening intervertebral column laterally; it is used to
discs balance the trunk; when
sitting it acts inferiorly with
iliacus to flex trunk
Illiacus Superior two thirds of iliac Lesser trochanter of Femoral nerve Flexes thigh and stabilizes
fossa, ala of sacrum, and femur and shaft (L2-L4) hip joint; acts with psoas
anterior sacro-iliac ligaments inferior to it, and to major
psoas major tendon
Quadratus Medical half of inferior border Illiolumbar ligament Anterior Extends and laterally flexes
lumborum of 12 ribs & tips of lumbar and internal lip of iliac branches of T12 vertebral column, fixes 12th
th
transverse processes crest and L1-L4 nerves rib during inspiration

Fascia
Thoracolumbar fascia:
External oblique
Internal oblique V
Transversus abdominis
Fascia transversalis
Renal fascia
Kideny
Psoas fascia
Thoracolumbar fascia
- Also called lumbar fascia

- Fascia enclosing deep muscles of back
- Consists of 3 layers: Posterior, middle and
anterior.
Extent:
- Posterior layer: Covers loin and continue
upward on back of thorax and neck.
- Anterior and middle layer: Confined to lumbar
region.

Anatomy
Abdominal aorta Tributaries:

1. Common Iliac [Median sacral vein joins
♦ Extent: T12– L4
common iliac] vein.
♦ From aortic opening of diaphragm to L4 where it 2. Third and fourth lumbar veins.
divides into right and left common iliac arteries. 3. Right testicular or ovarian vein.
Branches: 4. Renal veins
5. Right Supra renal vein.
Vertebral
Arteries 6. Hepatic veins.
level
Ventral 1. Coeliac trunk T12
branches 2. Superior mesenteric L1
3. Inferior mesenteric L3
Lateral 1. Inferior phrenic T12
branches 2. Middle suprarenal L1
3. Renal L1
4. Testicular or ovarian L2
Dorsal 1. Lumbar L1 – L4
branches 2. Median sacral
Terminal Pair of common Iliac L4
branches
Lumbar plexus
♦ Formation and braches:
Inferior venacava
Formation:
- Formed by union of right and left common Iliac
veins on the right side of the body of vertebra L5.
- Ascends in front of vertebral column, on the
right side of the aorta, grooves the posterior
surface of liver → Pierces central tendon of
diaphragm (T8) and opens into lower and
posterior part of right atrium.

GIT
♦ Formed by ventral rami of upper four lumbar ♦ Situated in front of first and second lumbar
nerves. vertebrae, immediately to the right of abdominal
♦ First lumbar nerve receives contribution from the aorta.
subcostal nerve. ♦ Upper end is continuous with thoracic duct.
♦ Fourth lumbar nerve gives contribution to the ♦ It is joined by right and left lumbar and intestinal
lumbosacral trunk. lymph trunks.
Branches Root value ♦ Intestinal trunk brings lymph from:
1. Stomach
Iliohypogastric nerve L1, Anterior ramus
2. Intestine
Ilioinguinal nerve L1, Anterior ramus
3. The pancreas
Genito femoral nerve L1, L2 ventral division 4. The spleen
Lateral Cutaneous nerve L2, L3 dorsal division 5. Anteroinferior part of the liver.
of thigh ♦ Lumbar trunk brings from:
Femoral nerve L2,L3, L4 dorsal division 1. Lower limbs
Obturator nerve L2, L3, L4 ventral division 2. The pelvic wall and viscera
Lumbosacral trunk L4, L5 ventral rami 3. The kidneys

4. Supra renal glands
Cisterna chyli
5. Testes or ovaries.
♦ Elongated lymphatic sac
6. Deeper parts of the abdominal wall.
♦ 5-7 cm long.
V

Anatomy
SPECIAL POINTS FOR MCQs

1. Umbilicus:
- Level of umbilicus is watershed.
- Lymph and venous blood flow upwards above the plane of umbilicus and downward below
this plane.
- Lymphatic drainage of umbilicus is to both axillary and inguinal lymphnode.
- Above the level of umbilicus drain into axillary lymph nodes and below the level of umbilicus
drain into superficial inguinal lymph nodes
- Cutaneous venous drainage:
• In venacaval obstruction, the Thoracoepigastric vein open up, connecting the great
saphenous vein with axillary vein.
→ In superior V.C. obstruction, direction of flow is downwards breaking barrier of
water shed line.
→ In IVC obstruction, direction of flow is upwards crossing the water shed line
- Supplied by T10 segment of spinal cord
2. Fascia
- Superficial fascia anterolateral abdominal wall
Superficial fatty layer /campars fascia Deep membranous layer/scarpas fascia
In Perineum: In perineum:
i. Superficial fascia of surrounding region. i. Colles fascia
V
ii. Investing or gallaudet's fascia
In penis: In penis:
Devoid of fat i. Bucks fascia
ii. Fundiform ligament (More superficial than
suspensory ligament)
iii. Suspensory ligament
In scrotum:
- Dartous fascia
- Holden's line is related with attachment of scarpa's fascia of abdomen and colle's fascia of
perineum and prevents passage of extravasated urine.
3. Hesselbach's triangle
i. Lateral border: Epigastric artery
ii. Medial border: Lateral border of rectus abdominis where it is attached to pubic crest
iii. Base: Inguinal ligament
4. Epiploic foramen/foremen of winslow
- It is a vertical slit like opening through which the lesser sac communicates with the greater
sac.
- It is situated behind right free margin of lesser omentum at T12 vertebra level
- Mostly boundaries are asked in MCQs (study from theory)

GIT
5. Peritoneal folds of intestine

Peritoneal folds of intestine
Mesentery proper Mesoappendix Transverse Sigmoid

Mesocolon Mesocolon
Border Contains:
i. Root: i. Root:
i. Root/Attached boarder: i. Vessels - Attached to anterior - Inverted V
- 15 cm long (Appendicular surface of the head shaped
- Directed obliquely downwards & artery) and anterior border - contains sigmoid
to the right ii. Nerves & of body of pancreas & superior rectal
- From dudenojejunal flexure on the lymphatics - Upward inclination vessels, nerve and
left side of vertebra L2 to upper supplying towards left lymphatics of
part of the right sacroiliac joint appendix - Contains middle sigmoid colon.
- It crosses colic vessels &
• 3rd part of deodenum nerves and
• Abdominal aorta lymphatics of
• IVC transverse colon.
• Right ureter, Right psoas major,
Right gonadal vessels
ii. Free/intestinal border
- 6 meter longs
- thrown into pleats
6. Lesser Sac/Omental Bursa:
- Subdivision:
• Divided into superior and inferior recess by right and left gastropancreatic folds formed due to
downward and forward course of hepatic artery and upward course of left gastric artery
V
• Superior recess lies behind lesser omentum and liver.
• Inferior recess lies behind stomach and with the greater omentum.
7. Blood supply of soft palate:
- Greater palatine artery (branch of descending palatine artery which is branch of maxillary
artery)
- Lesser palatine artery (branch of descending palatine artery which is branch of maxillary
artery)
- Ascending palatine artery (branch of facial artery)
- Palatine branch of ascending palatine artery
8. Waldeyr's ring is formed by palatine, lingual, pharyngeal and tubual tonsils
9. Inguinal canal:
- Superficial inguinal ring is triangular gap in external oblique aponeurosis.
- Deep inguinal ring is oval opening in fascia transversalis.
- Inguinal canal is about 4cm is length but larger in males than in females.
- Testicular vein is not constituent of spermatic cord.
- Spermatic cord is covered from within outwards: internal spermatic fascia, cremastericfascia,
external spermatic fascia
- Triangle of Doom:
• Vas deferens medially • Gonadial vessels laterally

Anatomy
- Circle of death (Vascular ring):

• Common iliac artery • Internal iliac • External iliac
• Obturator • Accessory obturator • Inferior epigastric artery
10. Fascia Derived from
a. Internal spermatic fascia - Fascia transversalis
b. Cremasteric fascia - Internal oblique + transversus abdominis
c. External spermatic fascia - External oblique aponeurosis
11. Abdominal Wall:
- Conjoint tendon is formed by internal oblique and transverses abdominis.
- Cremaster muscle is supplied by genital branch of genitofemoral nerve.
- Cremastric artery is branch of inferior epigastric artery.
- The inner surface of abdominal muscles is lined by fascia. This part of fascia which lines inner
surface of transversus abdominis muscle is called 'fascia transversalis'.
• It forms anterior wall of femoral sheath.
- Over 75% strength of intact abdominal wall is in aponeurosis.
- Main antagonist muscle of rectus abdominisis: "Erector spinae"
- Pyramidalis is supplied by: Subcostal nerve.
- Linea alba and external oblique poorly formed in lower 1/4th anterior abdominal wall.
12. Tongue:
- Tip of tongue drains to submental lymphnodes.
- Pain due to cancer of base of tongue is also referred to ear through glossopharyngeal nerve.
V
- Pain in posterior 1/3rd of tongue after tonsillectomy is due to injury to IX nerve.
- Circumvallate papillae of tongue are supplied by glossopharyngeal nerve.
- Ipsilateral deviation of tongue (on lower motor neuron lesion of hypoglossal nerve) is due to
unaltered action of genioglossus.
13. Esophagus:
- Esophagus enters through muscular part of diaphragm at level of level of T10 vertebra.
- Esophagus is lined by stratified squamous non keratinized epithelium.
- Upper 1/3rd of esophagus has skeletal muscle.
- Esophagus is accompanied by vagus nerve, esophageal branch of left gastric artery.
- Esophagus enters through muscular part of diaphragm
14. Stomach:
- Gastroduodenal artery ruptures during duodenal ulcer while bleeding left gastric artery
during gastric ulcer.
- "Prepyloric vein of myo" lies in front of pyloric constriction.
- Mucus secreting cells are more abundant in pylorus of stomach.
Chief cells abundant in fundus.
- Nerve of literate of vagus is seen in stomach.
- Gastric rugae are temporary i.e. not permanent mucosal folds.
1
- Mean capacity of stomach is 30ml at birth, 1 litre at puberty, 1 2 to 2 liters or more in adult.

GIT
15. Duodenum:
- Duodenal cap is due to first part of duodenum.
16. Pancreas:
- Pancreas is at level of L1 – L2
- Posterior surface of pancreas is devoid of peritoneum
- Most common site of ectopic pancreatic tissue are stomach and diverticulum.
- Islets of langerhans are more common in 'tail of pancreas'. [KU, MCQ]
17. Raspberry/cherry red tumor is in remnants of vitellointestinal duct.
18. Structures corresponding to transpyloric plane :
- Region close to hila of the left and right kidneys
- Level of the emergence of superior mesenteric artery from the abdominal aorta
- Level of L1 vertebra
- Level of the pylorus
- Level of the point at which the lateral border of the rectus abdominis meets the costal margin
- Level of the first part of the duodenum
- Neck of pancreas
19. The angle between the last rib and border of erector spinae is known as renal angle. (MCQ 2013 KU)
20. Dartos muscle in scrotum is replacement of superficial fatty layer (fascia of camper)
21. "Stave cells" line splenics inusoides.
22. Tortuous arteries:
Facial artery Lingual artery Splenic artery
PICA Uterine artery Vaginal artery
Opthalmic artery
V
23. Gland
Gland Duct Type of gland Duct of opening
Parotid Stensons duct Serous acini only Vestibule of mouth , opposite
to second upper molar
Submandibular Wharton's duct Mixed: predominantly serous On floor of mouth on summit
of sublingual papilla on side of
frenulum of tongue
Sublingual Bartholins duct Mixed: predominantly mucus On the floor of mouth , on
summit of sublingual papillae
24. Meckel's diverticulum (2) [10 July]
- Rule of 2's in meckel's diverticulum:
• 2% (population)
• 2 feet (from ileocaecal valve)
• 2 inches (in length)
• 2% are symptomatic
• 2 types of common ectopic tissue (gastric and pancreatic)
• Most common age at clinical presentation is 2.
• Males are 2 times as likely to be affected.
- Meckels diverticulum arises from antimesenteric border of ileum.
25. Plica circularis, spiral valve of Heister, Transverse rectal folds are permanent fold.

Anatomy
26. Superior rectal artery is branch of inferior mesenteric but middle rectal is branch of internal iliac
artery.
27. Anal continence is not contributed by Houston valve.
28. Posteriorly perforating ulcer is pyloric antrum of stomach is most likely to produce initial localized
peritonitis or abscess formation in "omental bursa".
29. Common structure in Heselbach's triangle and femoral triangle is inguinal ligament.
30. Greater superficial petrossal nerve supplies lacrimal gland and lesser petrossal supplies parotid.
31. Anal Canal
Anal canal above pectinate line Anal canal below pectinate line/ dentate line
- Endodermal - Ectodermal
- Cuboidal epithelium - Stratified squamous
- Superior rectal artery, vein - Inferior rectal artery, vein
- Internal iliac group lymph nodes - Superficial inguinal group
- Pain insensitive - Pain sensitive
- Internal anal sphincter is part of internal circular fibers.
- Anal canal zones:
Middle (Transitional or Pecten)
Upper Mucous Zone Lower (cutaneous) zone
zone
- 15 mm (1.5 cm) - 15 mm (1.5 cm) - 8 mm( 0.8cm)
- Simple columnar mucous - Non Keratinized staratified - Non Keratinized staratified
membrane showing anal squamous epithelium squamous epithelium with
columns of morgagni, anal without sweat and sebaceous sweat and sebaceous gland
valves, anal sinus, anal gland and hair follicle and hair follicle
papilla.
V - Pain insensitive - Pain sensitive - Pain sensitive
- Dentate/Pectinate line lies between upper and middle part
- Anal glands open at the dentate line
- White line of Hilton lies at lower limit of middle (transitional) part
• Upper mucous zone
→ 15 mm (1.5 cm)
→ Simple columnar mucous membrane
32. Cystic artery arises from right hepatic artery. (MCQ 2013 )
33. Colon is supplied by marginal artery.
34. Cutting and cauterisation don't produce visceral pain.
35. Hiatus hernia is most common type of diaphragmatic hernia.
36. Ascending colon ⇒ Length = 12.5cm
Transverse colon ⇒ 50cm
Descending colon ⇒ 25cm
Sigmoid colon ⇒ 37.5 cm
Rectum ⇒12cm
Anal canal ⇒ 3.8cm
i.e. Shortest colon ⇒ Ascending colon
Longest part of colon ⇒ Transverse colon
37. Iliac crest at the level L4.

GIT
biochemistry
SYLLABUS
Biochemical principles to nutrition: (p. 57)
BMR: Factors affecting, energy expenditure related to BMR, specific dynamic action and respiratory quotient. caloric
value of carbohydrate, fat, protein, ethanol. Proximate principles of diet, RDA. Energy requirement: with age, for physical
activity. Nutritional importance of protein, protein requirement, protein energy undernutrition
Digestion and absorption: (p. 59)
Digestive enzymes, secretagouges, NaCl absorption and secretion, cystic fibrosis, diarrhea, NaHCO3 secretion by pancreas,
composition of pancreatic, gastric and bile secretion
Carbohydrate Digestion: (p.60 )
Dietary carbohydrates.
Enzymatic digestion of carbohydrates: Salivary, pancreatic, intestinal enzymes.
Intestinal absorption of monosaccharides: glucose, galactose, fructose.
Mechanism of absorption of glucose.
Lactose intolerance.
Dietary fiber: types, requirement, advantages, disadvantages.
Proteins Digestion: (p. 63) V
Enzymatic digestion of proteins-gastric, pancreatic, intestinal enzymes.
Intestinal absorption of amino acids-carrier systems for absorption of amino acids.
Proteins intolerance.
Lipids Digestion: (p. 65)
Dietary lipids.
Enzymatic digestion of lipids- pancreatic, role of bile
Intestinal absorption of lipids
Maldigestion, malabsorption, steatorrhoea.
Starvations and Obesity: (p. 67)
Biochemical aspects of starvation and obesity.

Biochemistry

GIT
BIOCHEMISTRY
BIOCHEMICAL PRINCIPLES OF 8. Fever: Elevation by more than 10% in BMR occurs

NUTRITION for every 1o C rise in body temperatures
9. Disease states: BMR increases in infections,
BMR
leukemia, polycythemia, cardiac failure and
♦ Basal metabolic rate is the minimum amount of
hypertension, whereas decrease marginally in
energy required by the body to maintain life at
adrenal insufficiency.
complete physical and mental rest in the post
10. Racial variations: BMR is higher in Eskimos and
absorptive state.
less in Oriental women of USA than American
♦ Several bodily function continuously occur at total women.
rest such as working of the heart, conduction of
Energy expenditure related to BMR
nerve impulse, reabsorption by renal tubules,
gastrointestinal motility and Na+ - K+ pump (the - Total energy expenditure depends on BMR,
pump consumes 50% of basal energy) energy required for physical activity and the
energy required for synthesizing reserves, in
Factors affecting BMR:
the fed state.
1. Surface area: BMR is directly proportional to
- Working of heart, conduction of nerve impulse,
surface area. Surface area is related to weight and
gastrointestinal motility consumes basal
height.
energy. 50% of basal energy is consumed by
2. Sex: Men have marginally higher (5%) BMR than ions transport across membranes (Na+ - K+
women due to higher proportion of lean muscle pump)
mass in men. Women's body contain V
- The most useful method of expressing energy cost
proportionally more adipose tissue.
of physical activities is as a multiple of BMR.
3. Age: BMR is higher in children with lean muscle
- Sedentary Activities: 1.1 -1.2 × BMR
mass. BMR decrease at a rate of about 2% per
- Vigorous exertion: 6-8 × BMR
decade of life.
4. Physical activity: BMR is increased with regular Specific dynamic action
exercise mostly due to increase in body surface ♦ The phenomenon of extra heat production by the
area. body, over and above the calculated caloric value,
5. Hormones: Thyroid hormones have stimulatory when a given food is metabolized by the body is
effect on the metabolism of body. BMR is known as specific dynamic action.
elevated by about 70% in hyperthyroidism and ♦ SDA for protein, fat and carbohydrate are 30%,
lowered by about 40% in hypothyroidism thus 13% and 5% respectively. For a mixed diet, SDA is
used to assess thyroid function. Other hormones around 10%.
like epinephrine, cortical, growth hormone and ♦ The higher SDA for protein indicates that it is not a
sex hormones increase BMR. good source of energy. Fat is the good source of
6. Environment: BMR is higher in cold climate than energy due to its lowering effect on SDA. However,
warm climate. excessive utilization of fat leads to ketosis.
7. Starvation: BMR decreases up to 50% it may be an ♦ SDA of foods is due to energy required for
adaptation by the body. digestion, absorption, transport, metabolisms and
storage of foods in the body

Biochemistry
♦ SDA for proteins Is to meet requirements for Functions of proteins:

deamination, synthesis of urea, biosynthesis of 1. Proteins are the fundamental basis of cell
proteins, and synthesis of triacylgycerol. structure and its function.
♦ SDA of carbohydrates is attributes to the energy 2. All enzymes, hormones, immunoglobulin are proteins
expenditure for conversion of glucose to
glycogen. 3. Proteins maintain osmotic pressure, clotting of
blood, muscle contraction.
♦ For fat, SDA may be due to its storage,
mobilization and oxidation. 4. During starvation, amino acids serve as the major
♦ Due to high SDA of proteins, consumption of a supplier of energy.
protein rich diet makes us feel warm and Requirement of proteins:
comfortable in cold weather. - Protein requirement is dependent on its
Respiratory quotient (R.Q) nutritive value, caloric intake and physiological
♦ R.Q is the ratio of the volume of CO2 produced to states (growth, pregnancy, lactation) of the
the volume of O2 utilized in the oxidation of individual. For an adult, 0.8-1.0 g protein/ 1 kg
foodstuffs. body weight / day is adequate; which should
♦ Carbohydrates are completely oxidized and their be nearly double for growing children,
R.Q is close to 1. pregnant and lactating women.
E.g. Glucose Protein energy under nutrition:
C6H12O6 + 6O2 → 6CO2 + 6H2O Features Marasmus Kwaskhiorkor
CO2 6 Clinical Always present
R.Q. for carbohydrate = O = 6 = 1
2 Sometimes hidden
Muscle wasting Obvious
♦ Fats have lower R.Q. since they have low oxygen by oedema and fat
content. Severe loss of Fat often retained
Fat wasting
E.g. Tristearin subcutaneous fat but not firm
V
2C57H110O6 + 163 O2 → 114 CO2 + 110H2O Present in lower
CO2 114 Oedema None legs, and usually in
R.Q for fat = O =163 = 0.7 [MCQs 2013 KU] face and lower arms
2
♦ Proteins have a highly variable chemical formula, Weight for

Very low
Low but may be
by individual measurements, the R.Q of protein is height masked by oedema
found to be around 0.8. Sometime quiet Irritable, moaning,
Mental Change
♦ Mixed diets have an R.Q. around 0.8. and apathetic apathetic
Calorific values of foodstuffs (Atwater Clinical Sometimes present
factors) Appetite Usually good Poor
Often (current Often (current and
Foodstuff Energy value (Kcal /g) Diarrhoea
and past) past)
Carbohydrate 4
Diffuse
Fat 6 pigmentation,
Protein 4 Skin changes Usually none
sometime 'flaky
Alcohol (ethanol) 7 paint dermatosis'
Nutritional Importance of proteins Sparse, silky, easily
Hair changes Seldom
pulled out
♦ Proteins are regarded as 'body-building foods'.
Also, 10-15 % of total body energy is derived from Hepatic Sometimes, due to
None
proteins. enlargement accumulation of fat

GIT
Biochemical ii. In an Individual with light work, about 60% of

Normal or calories are spent towards BMR, about 30% for
Low (<3g/100ml physical activity and about 10% to take care of SDA.
Serum albumin slightly
blood)
decreased
Proximate principles of diet
Urinary urea per Normal or ♦ Macronutrients like protein, fats and
Low
gm creatinine decrease
carbohydrates which are often called "Proximate
Hydroxyproline/ Principles" because they from main bulk of food.
Low Low
creatinine ratio In Nepalese diet, they contribute to total Energy
Plasma/amino intake in following proportions.
Normal Elevated
acid ratio Proteins: 7-15%
Note: Fats: 10-30%
- Flag sign ⇒ Kwashiorker Carbohydrate: 65-80%
- Baggy pant, Monkey face ⇒ Marasmus.
DIGESTION AND ABSORPTION
Recommended dietary allowances (RDA) ♦ Digestive enzymes: Described later in
♦ The RDA represents the quantities of nutrient to carbohydrate, protein and lipid digestion.
be provided in the diet daily for maintaining good ♦ Secretagogues: Those which causes a flow of
health and physical efficiency of the body. secretion - Refer physiology, GI hormones.
Factors Affecting RDA: E.g. Cholecystokinin is secretagogue of pancreatic
1. Sex: enzyme and bicarbonate.
- RDA for men is about 20% higher than in NaCl absorption and secretion
women. Absorption of Na+: V
- Requirement is greater for pregnant and - Absorbed along entire length of intestine
lactating women. - Na+ absorption is mainly secondary active
2. Age: transport in which, Na+ K+ ATPase is present on
- Nutrient requirement is higher in growing age. the basolateral surface, pumps sodium out of
3. With physical activity: enterocytes, which creates low concentration
of sodium in the cell.
- Energy requirement also depends on duration
- Therefore sodium enters enterocytes by
and intensity of muscle activity.
facilitated diffusion and via SGLT.
- As per some rough calculations, caloric
- Na+ glucose reabsorption are facilitatory to
requirements of adults per day (Kcal/day) are each other; this process is utilized in oral
in following ranges. rehydration therapy.
Light work → 2,200-2,500 Absorption of CL– ions:
Moderate work → 2,500-2,900 - Cl- is reabsorbed mainly in Jejunum.
Heavy work → 2,900-3,500 - In ileum, HCO3- is secreted and Cl- is absorbed.
Very heavy work → 3,500-4,000 - Cl- absorption occurs through special Cl-
Note: channels in enterocytes.
i. 3 Factors: Physiological significance:
- BMR, SDA and physical activity determine the Diarrhea:
energy needed by the body. - In acute diarrhea like cholera (secretary diarrhea)
Cl-, Na+ and water are secreted into lumen.

Biochemistry
The cholera toxin produced by Vibrio cholera - Because the pancreatic ducts are permeable to
activates adenylate cyclase, therefore water H2O moves into the lumen to make the
increases cAMP concentration in mucosal cells. pancreatic secretion isosmotic.
- This facilitates the secretion of Na+ and water Composition of pancreatic, gastric and bile secretion:
resulting in profuse diarrhea.
& Refer: Physiology
Cystic fibrosis:
- Autosomal recessive disorders.
CARBOHYDRATE DIGESTION
- Defective gene for chloride channel causes Past Questions:
reduction in these channel in mucosal cells of
1. Lactose intolerance. (3, 2) [07 July, 05 June]
intestinal epithelium.
2. Role of fibre in diet. (1) [05 June]
- Therefore, such patients suffer from less
severe secretory diarrheas as compared to Dietary Carbohydrates
normal individual.
♦ Polysaccharides - Starch and glycogen.
Note:
♦ Disaccharides-Sucrose (cane sugar), lactase (milk
Major Clinical manifestation of cystic fibrosis:
sugar).
i. Recurrent pulmonary infections.
♦ In small amounts monosaccharide - fructose,
ii. Defect in digestion and absorption.
pentose.
iii. Sterility.
Process of Digestion
NaHCo3 secretion by pancreas
a. Digestion in the mouth: During the process of
mastication, salivary α-amylase (ptyalin) cleaves
Blood Ductule cells Lumen
α-1,4 glycoside bonds. The products formed
V include α-limit dextrins, maltotriose and maltose.
b. In the stomach: The enzyme salivary amylase is
Na+ Na+ Na+
H + H+ HCO3- HCO3- inactivated by high acidity (low PH) in the
(Active (Active stomach, so no digestion of carbohydrate in
transport) H2CO3 transport) stomach.
(Carbonic anhydrase)
H2O c. Digestion in small intestine: The acidic dietary
+
CO2 CO2 contents of the stomach on reaching the small
H2O H2O intestine are neutralized by bicarbonate produced
by pancreas. The pancreatic α-amylase acts on
starch and continues the digestion process. The
resultant products are disaccharides (maltose,
Secretion of isosmotic sodium bicarbonate
solution by the pancreatic ductules & ducts isomaltose) and oligosaccharides.
In upper jejunum:
a. Acinar cells:
disaccharidases
- Produce a small volume of initial pancreatic - Disaccharide→ Monosaccharides
-
secretion, which is mainly Na+ and Cl . oligosaccharidases
- Oligosaccharides → Monosaccharide
b. Ductal cells:
sucrase
- Modify the initial pancreatic secretion by - Sucrose→ Monosaccharides
secreting HCO3- and absorbing Cl- via Cl- HCO3–
exchange mechanism in luminal membrane.
GIT
Absorption of monosaccharide • Sodium therefore moves into the cells

♦ The absorption of sugars mostly takes place in the along its concentration gradient and
duodenum and upper jejunum of small intestine. simultaneously glucose is transported
into intestinal cells.
♦ Hexoses are more rapidly absorbed than
pentose. Further, among the monosaccharide; 2. The GLUT-5 Na+ independent facilitative
galactose is more efficiently absorbed followed by
transporter allows fructose, as well as V
glucose and galactose, to be transported
glucose and fructose.
down their concentration gradients.
Mechanism of absorption
Galactose:
Glucose: - The mechanism of absorption of galactose is
- Absorption occurs by 2 separate mechanisms: similar to the of glucose
1. Transported into the mucosal intestinal cells Fructose:
by carrier mediated and energy requiring
- Absorption is relatively simple.
process:
- Does not require energy and is independent of
• Glucose and Na+ share the same
sodium transport.
transport system (symport) which is
referred to as sodium dependent - Fructose is transported by facilitated diffusion
glucose transporter. [@F for f]
• The enzyme Na+/K+ ATPase is involved in Note:

the transport of sodium in exchange of - Glucose & galactose are absorbed by Na-
potassium against the concentration dependent process.
gradient. (On basolateral surface) - They're carried by same transporter protein (SGLT-
• Now, the concentration of sodium is 1) and compete with each other for intestinal
higher in the intestinal lumen as absorption.
compared to mucosal cells.
Biochemistry
Pentose: ♦ Lactic acid is produced → abdominal cramps, pain

- Absorbed by process of simple diffusion. ♦ Lactose → acts as irritant
Glucose from the intestinal cells enters into ♦ Diagnosis
circulation passively - H2 breath test
Glucose Glucose
- Oral dose of lactose
fructose galactose SGLT-1 - Stool acidity test
galactose transporter
protein ♦ Prevention and treatment
GLUT-5 Brush
border - Feeding of lactose free diet
- Take yeast-contains enzyme lactase
Dietary Fibers [05 June]
3Na+
ATP
3Na+ ♦ Dietary fibers are indigestible and unabsorbable
Glucose Na+-K+ carbohydrates in the diet that are not digested by
pump
fructose 2K+ intestinal digestive enzymes but can be partially or
galactose ADP+Pi
completely fermented in small intestine by
normal flora.
GLUT - 2
To capillaries ♦ Daily requirement: 20-30 g
♦ Types:
Lactose intolerance [07 July, 05 June] 1. Water soluble: Occurs within plant cells. E.g.
♦ Disorder caused due to absolute or relative pectin, mucilage.
deficiency of lactase enzyme in intestine resulting 2. Water insoluble: Occurs in plant cells
in failure of digestion, absorption and consequent membrane, cell wall. E.g. cellulose,
intolerance to dietary lactose.
V hemicelluloses.
Small intestine Advantages:
Lactose 1. Prevents constipation: Helps to maintain normal
motility of gastrointestinal tract.
(–) Lactase deficiency
2. Eliminates bacterial toxins: Adsorbs large
Galactose + Glucose quantities of water and toxic compounds
Large intestine produced by intestinal bacteria that lead to
increased fecal mass and its easier expulsion.
Lactose
3. Decreases GIT cancers: Colon and rectum cancers are
↓
lower in vegetarians as compared to non-vegetarians.
Bacteria
↓ 4. Improves glucose tolerance: Diminishes rate of
glucose absorption from the intestine.
2-Carbon Co2 3-Carbon H2 (measured 5. Reduces plasma cholesterol level
Metabolites metabolites in breath) - Decreases absorption of dietary cholesterol
H2O
from the intestine.
Bloating, Diarrhoea,
- Fiber binds with bile salt and reduces their
Dehydration
enterohepatic circulation causing increased
♦ Accumulation of lactose → Osmotic diarrhea degradation of cholesterol to bile salts and its
disposal from the body.
♦ Bacterial fermentation release H2, CH4, Co2,
lactate → flatulence
GIT
6. Satiety value Pepsin

- Proteins →Proteases and peptones
- Adds to weight of food stuffs ingested Rennin
- Milk proteins (casein)→ calcium paracaseinate
- Gives a sense of stomach fullness
gelatinase
Disadvantages: - Gelatin →Polypeptides
1. Digestion and absorption of protein are adversely c. In intestinal lumen
affected. - Pancreas secretes trypsinogen, chymotrypsinogen,
procarboxypeptidase, proelastase & collagenases.
2. Intestinal absorption of certain minerals (Eg. Ca, P,
Mg) is decreased. - Enterokinase/ enteropeptidases activates
trypsinogen to trypsin.
3. Intestinal bacteria ferment some fibers, causing
- Trypsin further can activate trypsinogen (Auto
flatulence and often discomfort.
activation), chymotrypsinogen, pro-elastase &
PROTEIN DIGESTION pro-carboxypeptidases.
Past Questions: Peptides Amino acids
1. How is protein digested and absorbed in the CCK Intestine

body? Mention the steps and names of two CCK, secretin
endopeptidase and two exopeptidase and their Pancreas
mechanism of action. (4) [08 Jan]
2. List the steps and enzymes involved in protein Trypsinogen
Enteropeptidase
digestion. (4) [05 Dec]
3. What aromatic essential amino acids obtain Trypsin
during protein digestion? (2) [08 Jan]
Chymotrypsinogen Chymotrypsin
Digestion of protein [08 Jan, 05 Dec] Proelastase Elastase
V
♦ Proteins are degraded by a class of enzymes Procarboxypetidases Carboxypetidases
namely hydrolases/peptidases i.e. exopeptidase (A & B) (A & B)
and endopeptidase. Formation and activation of pancreatic proteases
♦ Endopeptidase: Attacks internal peptide bond and (CCK-Cholecystokinin)
releases the peptide fragment. E.g. pepsin, trypsin. - The activated form of enzymes act on proteins
♦ Exopeptidase: Attack peptide bonds of terminal and releases free aminoacids and small
amino acids. E.g. Carboxypeptidase, peptides.
aminopeptidase.
- Result of protein digestion by these enzymes is
Digestion in various parts free amino acids and small peptides.
a. In mouth
d. In intestinal brush border
- No digestion occurs
- Aminopeptidase
- Absence of proteolytic enzymes
b. In stomach • Hydrolyze polypeptides up to dipeptide
- 3 enzymes are present • Breaks peptide bond through amino
Pepsinogen, prorenin (chymosin) and terminal of polypeptide.
gelatinase • Cannot act on proline/hydroxyproline
- These are activated to their active forms by containing polypeptide
action of HCl (PH 2-3) - Tri and dipeptidase
HCl
Pepsinogen→ Pepsin (Active) • Acts on villous membrane or inside the cells
HCl
Prorenin → Rennin (Active) • Requires Mg++, Co+, Zn++ etc.

Biochemistry
Mouth Stomach Small intestine
Pepsin
Trypsin
Proteins Polypeptides Chymotrypsin Aminoacids
Amino acids Elastase Oligopeptides
Unchanged
Aminoacids Carboxypeptidases
Dipeptides Aminopeptidases
Dipeptidases
Digestion of proteins
Note: - Cyclic pathway in which glutathione is

- Carboxypeptidase are formed in intestinal lumen regenerated again by the use of three ATP for
from procarboxypeptidase released by pancreas. the transport of single amino acid.
- Aminopeptides are intestinal brush border Hartnup's disease (Neutral amino aciduria)
enzymes secreted by intestinal mucosal cells. - Hartnup is the name of the family in whom,
this disease was first discovered.
Absorption of protein - It is the inability of intestinal and renal
V ♦ L-Amino acids are more rapidly absorbed than D- epithelial cells to absorb neutral amino acids
Amino acids. - Tryptophan absorption is most severely
♦ L-Amino acids occurs by an active process affected.
♦ D-Amino acids takes place by simple Diffusion - Symptoms of pellagra are observed i.e.
[@D for D] Diarrhoea, dementia and dermatitis (3D's).
- There is impairment in the conversion of
♦ Amino acids like D-glucose, are absorbed by a Na+
tryptophan to NAD+ and NADP+, the coenzymes
dependent active process linked with the
of niacin.
transport of Na+.
Note:
♦ A Na+ independent system of amino acid transport
i. Absorption of intact proteins and polypeptides
across intestinal cells is also present.
causes food allergy. In normal adult intact proteins
♦ Another transport system known as γ-glutamyl and polypeptides are not absorbed. Food allergy is
cycle also plays some role in absorption. due to the antibody formed against those intact
Gamma Glutamyl cycle/ Meister cycle proteins.
- Involves glutathione (tripeptide) ii. For short period, immediately after birth, the small
- Active group translocation of L amino acids intestine of infants can absorb intact proteins and
(except L-proline) into the cells of small polypeptides.
intestine, kidneys, seminal vesicles, peptides iii. Deficiency of pancreatic section such as
and brain. pancreatitis, cystic fibrosis or surgical removal
cause defect in protein digestion.

GIT
LIPID DIGESTION Trypsin

- Procolipase → Colipase → Binds at lipid
Past Questions: aqueous interface and helps to anchor and
stabilize lipase.
1. Write short notes on:
2. Degradation of cholesteryl esters
a. Digestion and absorption of neutral fat
Pancreatic
(4) [03 Dec] - Cholesterylesters → cholesterol +
cholesterolesterase
b. Process of fat digestion. Indicate role of bile free fatty acids
salts, state the functions of lipase and
3. Degradation of phospholipids
colipase. (4) [09 July] Phospholipase-A-2
c. Role of bile salts in lipid digestion. (2) [04 June] - Phospholipids → Lysophospholipid
+free fatty acid
2. What is steatorrhoea? Show the role of bile salts
in the digestion of lipid. Also mention the role of Role of bile [10, 09, 04]
lipase and co-lipase. (2+4=6) [10 July] 1. Bile salts aid in digestion of fats by:
3. List the process of digestion of fat and role of bile - Activation of bile salt dependent lipase
salts (mention enzyme and co-enzyme involved). - Emulsifications of fat
(5+2=7) [04 Dec] • Increases surface area
Dietary lipid • Decreases interfacial area between
♦ Animal fats: More saturated fats aqueous and lipid phase
♦ Vegetable fats: More PUFAs, antioxidants 2. Bile salts aid in absorption of fats by
♦ Dietary lipids are triacylglycerol, phospholipids, • Micelles formation
cholesterol, cholesteryl esters and free fatty acids 3. Helps in absorption of fat soluble vitamin A, D, E, K
Enzymatic digestion of lipids 4. Stimulates secretion of more bile form liver
(choleretic action) V
[03 Dec, 09 July, 04 Dec]
5. Keeps cholesterol in solution
Lipid digestion in mouth and stomach 6. Bile also helps in absorption of some metals,
- In mouth, actual digestion of lipid doesnot excretion of some drugs, hormone, metabolites,
occur; but lingual lipase is believed to originate dyes etc.
from the glands at back of tongue. 7. Bicarbonate in bile helps neutralize acidic chyme
- This lingual lipase acts on lipid substrates in from the stomach to some extent
acidic medium in stomach. Lipid absorption [03 Dec]
- Stomach contains a separate gastric lipase ♦ Three theories are described for absorption of
which can degrade fat with short chain fatty lipids. These are:
acids at neutral PH but digestion in stomach is i. Lipolytic theory put forth by Verzar
almost negligible, possibly due to low PH. ii. Partition theory proposed by Frazer
- In infants, milk fat can be hydrolyzed by gastric iii. Bergstrom theory
lipase to some extent because stomach PH of ♦ Bergstrom theory is the most recent and
infants is close to neutrality. comprehensive theory to explain lipid absorption.
Pancreatic enzymatic digestion of lipids Bergstrom theory
1. Digestion of triacylglycerols (fat) - Bile salts form mixed micelles with lipids.
pancreatic-lipase - Bile salt micelles exert a solubilizing effect on
- Triacylglycerol →
lipids, they transport lipids from intestinal
2-Monoacylglycerol + free fatty acids
lumen to membrane of intestinal mucosal cells.

Biochemistry
- Absorption is almost complete for Secretion of lipids from intestinal

monoacylglycerols and free fatty acids which
mucosal cells
are slightly water soluble.
- Short and medium chain fatty acids are not ♦ Lipids that are re-synthesized are put together,
dependent on micelle formation for the surrounded by a thin layer consisting mostly
absorption. apolipoproteins A1 and B48 and phospholipids;
- Long chain fatty acids are activated by these particles are known as chylomicrons.
thiokinase in intestinal cells. The acyl-CoA
♦ Chylomicrons migrate to the plasma membrane of
derivatives so formed combine with 2-
monoacylglycerols to produce triacylglycerols; intestinal mucosal cells and released into the
catalysed by acyltransferases. lymphatic vessels by exocytosis → Enters the
- Further, within intestinal cells, cholesterol is Lymphatic system → Thoracic duct → Large veins
converted to cholesteryl ester; phospholipids are → Heart → Blood → Peripheral tissues → Liver.
regenerated from absorbed lysophospholipids.

GIT
Steatorrhea [10 July] - Grade I obesity or overweight = 25-30 kg/m2

- Condition characterized by loss of lipids in - Grade II or clinical obesity = >30 Kg/m2
feces. - Grade III or morbid obesity = > 40 kg/m2
- Cause: Biochemical aspects of obesity
1. Defect in secretion of bile or pancreatic Ob gene
juice into the intestine ↓
2. Impairment in lipid absorption by intestinal Leptin polypeptide
cells.
↓
- Seen in disorders associated with pancreas,
Acts as lipostat
biliary obstruction severe liver dysfunction;
conditions such as pancreatitis, surgical ↓
removal of pancreas, cystic fibrosis etc. - Restricts feeding behavior
- Limit fat deposition
STARVATION AND OBESITY - Stimulates lipolysis
Past Questions: - Inhibits lipogenesis
1. Sketch the diagram showing the change in - When there is mutation in 'ob' gene and or in
metabolism during long term starvation and receptors in hypothalamus, body weight
short term fasting. Show the change in various regulation is impaired resulting in obesity.
hormone and their roles. (3+3=6) [10 July]
Orlistat and olestra
2. What is obesity? Draw an explanatory diagram
- Orlistat is a non-hydrolysable analogue of
showing the change taking place in obese person.
triacylglycerol and is a powerful inhibitor of
(5) [11 July]
pancreatic lipase preventing fat digestion and
3. Metabolic changes taking place during starvation & V
absorption.
formation of ketone bodies. (4) [09 July, 06 July]
- Olestra is a synthetic lipid, produced by
4. Metabolic changes taking place during starvation
esterification of natural fatty acids with
(4) [03 Dec]
sucrose instead of glycerol that tastes like
5. Biochemical changes in starvation with
natural lipid; it cannot be hydrolysed and
explanatory diagram. (4) (6) [06 Dec]
therefore gets excreted.
6. Obesity (4) [08 July]
Starvation
Obesity [08 July, 11 July] ♦ Starvation is a metabolic stress which imposes
♦ Accumulation of excess body fat due to disorder certain metabolic compulsions on the organism.
The metabolism is reorganised to meet new
of body weight regulatory systems.
demands of starvation.
♦ The person is considered obese if their weight due
Metabolic changes during starvation [10, 06, 03]
to fat exceeds more than 20% and 25% of body
Liver:
weight.
1. Carbohydrate metabolism: Increased
Assessment of obesity gluconeogenesis and glycogenolysis.
- Body mass Index (BMI) 2. Lipid metabolism: Increased fatty acid oxidation
wt. in kg with elevated synthesis of acetyl Co A that enters
BMI = ht. in m2 TCA cycle. Excess acetyl-CoA is diverted for ketone
- Normal BMI = 18.5-25 kg/m2 synthesis.

Biochemistry
Adipose tissue: 3. Protein metabolism: Muscle proteins are

1. Carbohydrate: Decreased glucose uptake degraded to liberate amino acids which are
metabolism. effectively utilized by liver for gluconeogenesis.
2. Lipid metabolism: Increased degradation of Brain:
triacylglycerol leading to increased release of fatty 1. During first days of fasting, brain continues to use
acids and glycerol. Glycerol again serves as glucose exclusively as a fuel. [Blood glucose is
precursor for glucose synthesis in liver. maintained by a hepatic gluconeogenesis from
Skeletal muscle glucogenic precursors, such as aminoacids
1. Carbohydrate metabolism: Decreased glucose provided by rapid breakdown of muscle proteins].
uptake and metabolism. 2. In prolonged fasting (>2-3 wks) plasma ketone
2. Lipid metabolism: Fatty acids and ketone bodies bodies are significantly elevated and are used in
are utilized by muscle as fuel source. On addition to glucose as fuel by brain.
saturation beyond 3 weeks, muscle adapts to
exclusively utilize fatty acids.

GIT

1. Vitamin B12 is absorbed in terminal ileum [MCQ 2013]
2. Specific dynamic action is greatest of protein (30%)
3. Short chain fatty acid, medium chain fatty acid and ethanol are absorbed from stomach
4. Ouabain and phlorhizin inhibit absorptive mechanism of glucose and fructose
5. Cholesterol is not saturated or precipitated when the composition of bile is 5% cholesterol, 15%
phosphatidyl choline and 8% bile salt.
6. Protein digesting enzymes are secreted as zymogens
7. Pepsin is acid protease
8. GLUT 2 is Dependent on insulin action
9. Elastase, chymotrypsin and trypsin are serine proteases
10. Lignin is not fermented by gastrointestinal microorganisms
11. Benedict reagent can detect minimum of 0.1% glucose
12. Winslow test is used to estimate serum or urinary amylase
13. 1 liter of oxygen consumed, accounts for 20 KJ of energy
14. Alpha-amylase acts on alpha 1-4 glycosidic bond
15. The brush border bound hydrolase linked with sucrase is alpha dextrinase
16. Indican in urine is tested by Obemeyer's test
17. True blood sugar level measures the levels of both glucose and fructose
18. Certain protease preferentially cleaves peptide bonds formed by certain amino acids
Enzyme Amino Acids
Pepsin A Tyr, Phe, Leu
Trypsin, Carboxypeptidase B Arg, Lys V
Carboxypeptidase A Ala, Ile, Leu, Val
Chymotrypsin Trp, Tyr, Phe, Leu, Met
19. Cytochalasin B inhibits Na+- independent transport system of amino acids
20. Intact proteins and polypeptides are not absorbed in small intestine but their macromolecular
absorption in certain individuals is responsible for "food allergy".
21. Colipase, secreted by pancreas as procolipase and converted to active form by trypsin. Colipase
binds at the lipid-aqueous interface and helps to anchor and stabilize lipase.
22. Raffinose containing galactose, glucose and fructose is a predominant oligosaccharide found in
leguminous seeds causing the occurrence of flatulence.
23. Essential fatty acid deficiency leads to phrynoderma or toad skin, characterized by scaly
dermatitis on the posterior and lateral parts of limbs and buttocks. Poor wound healing and hair
loss is observed in EFA deficiency
24. In an individual with light work, about 60% of the calories are spent towards BMR, about 30%
for physical activity and about 10% to take care of SDA.
25. The BMR is determined either by the apparatus of Benedict and Roth (Closed circuit device) or
by Douglas bag method (open circuit device).
26. Triacylglycerols constitute 90% of dietary lipids
27. Rice and wheat proteins are limiting in lysine and threonine
28. Fish is limiting in tryptophan
29. Soya bean, Red gram, Bengal gram, Meat and milk are limiting in sulphur containing amino
acids

Biochemistry
30. Well fed state

- ↑ Ingestion of glucose → ↑ Blood glucose →↑ Insulin release →↑ Phosphatase activity →↑
fructose 2,6bisphosphatase
31. Fasting stage
- ↓ Ingestion of glucose→↓Blood glucose→↑Glucagon release →↑cAMP→↓ Fructose 2,
6bisphosphatase
32. Fat Absorption
- Major fat absorption takes place in upper small intestine except (mainly jejunum &
duodenum) short chain fatty acids which is absorbed in colon.
- Normal fecal fat excretion is less than 6gm/day, more than 6gm/day indicates malabsorption.
- Steatorrhea is defined as fatty stool > 7gm/day.
- Daily fecal fat averages 15-25 gm/d with small intestinal disease & exceeds 40gm/d with
pancreatic exocrine insufficiency.
- Evaluation of fat malabsorption:
a. Quantitative estimation of fecal fat : Gold standard test
b. Sudan III : Qualitative test, Best for screening
c. Oral glycine – I[14C] glycolate test: Shows bile acid malabsorption
33.
Effects of Starvation on Metabolism
Ist Stage IInd Stage IIIrd – Stage
(First 2 to 3 days i.e. 48-72 hours) (Last for longest period, usually
over 2 weeks)
- Glycogenolysis: Liver glycogen is - 90% of energy requirement will - When the fat stores are
first metabolized but d/t its be derived from fat & almost exhausted
limited storage it cannot last long remainder 10% from protein energy is derived from
- Gluconeogenesis: Initially from - Since the adipose tissue breakdown of tissue
V glucogenic amino acids (alanine represents largest amount of protein.
glutamate) and then by glycerol stored fat, 2 stage will last for
nd - Digestive enzymes,
& lactate longest period followed by muscle
- Glucagon secretion increases - Adipose tissue is broken into protein are first to be
during starvation. It reaches a peak FFA which is oxidized for utilized, as these are
on 3rd day of fast at the time of energy production and used for least required
maximal gluconeogenesis. There ketone body formation. - This stage last for less
after glucagons level declines as the - The burning of fat is reflected than one week & leads
ketones & fatty acids become the by a lower RQ (~0.73)↓ to death.
major source of energy.
34. Limiting amino acids
Source of protein Limiting amino acid (s)
Egg Nil
Milk S-containing amino acids (cysteine, methionine)
Fish Tryptophan
Meat S-containing amino acids
Rice, Wheat Lysine, threonine
Pulses (Bengal gram, Red gram) S-Containing amino acids
Groundnut Lysine, threonine, Sulphur containing amino acids
Soyabean S-containing amino acids
Maize Tryptophan, lysine

GIT
microbiology
SYLLABUS
Normal Flora; GI Infections: (p. 73)
Terminology, causative agents of gastroenteritis, diarrhoea, dysentery, Pseudomembraneous colitis
(enterocolitis), Acquisition and transmission of infections, host defenses, laboratory diagnosis,
Pathogens:
a. Bacteria: E. coli (p. 74), S. typhi (p. 76) and paratyhi, Shigella (p. 79), V. cholerae,(p. 80) H. pylori, (p. 83)
Clostridium difficle.(p. 84)
b. Virus: Viral diarrhea (p. 85) (Rota virus, Norwalk virus, adenovirus etc).
c. Parasite (p. 87): Parasites- protozoa in the small intestine (p. 87): morphology, life cycle, pathogenicity
laboratory diagnosis of G. lamblia, C. parvum
Worms (p. 93) - Ascaris lumbricoides, Ancylostoma duodenale, Necator americanus, Strongyloides
stercoralis, Taenia solium, Taenia saginata, Trichinella Spiralis, D. latum, E. vermicularis, Trichuris trichura
Parasites - Protozoa in the large intestine: morphology, life cycle.
Pathogenicity, laboratory diagnosis of E. histolytica.
Food poisoning (p. 105)
V

Microbiology

GIT
MICROBIOLOGY
NORMAL FLORA 2. Gastroenteritis (09)

Past Questions: - Is an infection of gastrointestinal tract which may
1. Enumerate bacterial causes of diarrhoea (3)[06 Dec] be acute or chronic, characterized by diarrhoea
and symptoms of Gastric irritation (eg. Nausea,
2. Pseudomembranous colitis (3) [07 Dec]
vomiting, epigastric pain) common etiologic
3. Short notes on normal flora (3) [05]
agents are: Bacteria and viruses.
4. Short notes on diarrhoea associated viruses.
(3) [07 July]
3. Enterocolitis:
- It is an infection of the lower GI tract which
Terminology
doesn't produce symptoms of gastric irritation.
1. Normal flora:
- Is found on body surfaces contiguous with the 4. Diarrhoea:
outside environment. - Defined as passage of loose, liquid or Watery
- Is semipermanent, varying with major life changes. stools usually more than 3 times a day.
- Can cause infection if misplaced. e.g. Causative agents of diarrhoea (07)
• Fecal flora to urinary tract or abdominal cavity. 1. Viruses 2. Bacteria: 3. Others
• If person becomes immunocompromised,
- Rota virus - Campylobacter - E. histolytica
normal flora may overgrow.
jejuni
- Contributes to health:
- Astro virus - Escherichia coli - Giardia
eg. Protective host defense by maintaining
intestinalis
conditions such as other organisms may not grow.
- Adenovirus - Shigella - Trichuriasis
• Serves nutritional function by synthesizing: Vit. K V
Normal flora of GIT (05) - Calci virus - Salmonella - Crypto-
sporidium
Site Organisms
- Corona virus - Vibrio cholerae - Intestinal
1. Mouth Anaerobic micrococci, microaerophilic &
worms
anaerobic streptococci, vibrios, fusiform
- Norwalk - Vibrio para-
bacilli, corynebacterium sp.,
group viruses hemolyticus
actinomyces, leptothrix, mycoplasma,
neisseria, bacteroides. - Entero - Bacillus cereus
viruses
2. Esophagus, - Lactobacilli
stomach Dysentery:
3. Small - Lactobacilli, streptococci, - A clinical entity characterized by the frequent
bowel enterobacteria, bacteroides sp. passage of blood-stained mucopurulent stool, can
4. Large Anaerobes: be classified as amoebic & bacillary dysentery.
bowel - Bacteroides, Bifidobacteria, clostridia, Causative agents (06)
lactobacillus Bacteria Protozoa
Aerobes:
- Shigella - Entamoeba histolytica
- Escherichia coli
- Enteroinvasive E. coli (Causes amoebic
- Klebsiella species
- Campylobacter dysentery)
- Streptococcus fecalis Pseudomonas
- Proteus, enterobacter - V.Parahaemolyticus

Microbiology
Pseudomembrane enterocolitis (07) ESCHERICHIA COLI

- Is a severe form, life threatening disease of Past Questions:
colon with fulminant diarrhoea.
1. What are the types of E. coli? Describe
- An accumulation of inflammatory exudates pathogenesis of each them. (1+4=5) [04]
composed of polymorphonuclear leucocytes,
Morphology:
fibrin and mucin is attached to mucosal surface
that gives a membrane like appearance when - Gram negative, nonsporing non capsulated
viewed via colonoscopy. bacilli
- Causative agent: Clostridium difficile - Measures 1-3 µm × 0.4 - 0.7 µm
(MCQs 013 KU) - Motile - Peritrichous flagella
Acquisition and transmission of infections: - Some strains possessing a polysaccharide
1. Fecal oral transmission: capsule are non motile.
a. Direct person to person transmission: usually Cultural character:
seen in overcrowded places and with poor 1. Nutrient ager:
personal hygiene. - At 37°C in 8-24 hours → colonies are large (2-3
b. Contamination of certain food products such as mm), thick, colorless, moist
meat, poultry products, sea foods.
2. MacConkey's agar:
c. Contamination of food during or after cooking.
- Pink, circular, convex, smooth, non viscous,
d. Contamination of water sources in unhygienic colonies with clear cut margin.
environment.
Biochemical test:
2. Food borne transmission:
1. Fermentation: Ferment most of the sugars (lactose,
- May involve distribution of infected food
glucose, mannitol, maltose) with production of acid
V product (Eg. meat, poultry product, sea food or
and gas.
vegetables) which gets contaminated before
processing (eg. by zoonotic bacteria) - do not ferment sucrose
Lab diagnosis: 2. IMViC→ + + - -
A. Specimens: - Indole - Positive
1. Fecal sample is examined for detection of - V.P - Negative
offending agent. - Methyl red - Positive
2. Enzyme immunoassay of fecal samples is - Citrate utilization-Negative
useful in rapid detection of organism.
Antigenic structure:
3. Blood cultures are indicated only with
1. Somatic antigen (O antigen)
constitutional symptoms.
2. Surface antigen (K antigen): Capsular polysaccharide.
B. Microscopy: Saline and iodine preparations when
examined microscopically, causative parasitic 3. Flagellar antigen (H antigen)
agents can be detected. 4. Fimbrial antigen (F antigen)
C. Culture: Specimen is inoculated in macConkey's Virulence factors:
agar (or in TCBS in suspected cases of cholera) and 1. Adhesion factors:
incubated overnight.
i. AFA-I, AFA-II and Dr.adhesions→ Responsible
D. Identification: By biochemical and agglutination
for UTI
test.
ii. O-antigen: Adhesion to bladder-epithelium.

GIT
2. Enterotoxins ↓
- Enterotoxigenic E. coli (ETEC) produce plasmid A1 subunit transfers ADP ribose from NAD to
mediated enterotoxins. GTP binding protein.
- Heat labile enterotoxin (LT) ↓
- Heat stable enterotoxin (ST) Activation of Adenylyl cyclase
3. Verotoxin ↓
- Enterohemorragic E. coli (EHEC) produce Increase in cAMP
verotoxin. ↓
- It is also called shiga like toxin due to similar Hypersecretion of Cl and inhibition or Na+
-
biological, physical and antigentic properties of reabsorption.

shiga toxin. ↓
4. Antiphagocytic capsule Osmotic secretion of H2O
- KI strain of E. coli cause neonatal meningitis ↓
due to antiphagocytic capsule. Produce watery diarrhoea
Clinical features: b. Heat stable enterotoxin

• Mechanism is similar except guanylyl
1. Urinary tract infection (60-80% of UTI)
cyclase is activated which increases
2. Septic infection of wound. cGMP concentration.
3. Septicaemia, pneumonia, neonatal meningitis and ii. Enterohemorrhagic E. coli (EHEC)
abscess formation in variety of organs. - Disease: Bloody diarrhoea (but not dysentery),
4. Gastro intestinal disease. hemorrhagic colitis, hemolytic uremic
Based on gastro intestinal manifestations, syndrome, no fever
E. coli are classified as: (04) Note: Clinically, enteroinvasive E. coli resembles
shigellosis. V
i. Enterotoxigenic E. coli (ETEC)
- Diseases: Traveller's diarrhoea, infant Pathogenesis:
diarrhoea in developing countries, watery EHEC produce cytotoxin/ shiga like toxin/
diarrhoea, nausea, vomiting, cramps, low grade verotoxin
fever. (@t for T) ↓
Pathogenesis: Consists of A and B subunit
- ETEC produces two types of Enterotoxins: ↓
a. Heat labile enterotoxin (LT) B subunit binds to the host cells of large intestine
and facilitates transfer of subunit A
• Resembles cholera toxin (CT) and is
plasmid mediated enterotoxin. ↓
Subunit A disrupts protein synthesis.
Enterotoxin is composed of 2 subunits, A and B
Damage vascular endothelium → bloody
↓
diarrhoea.
A subunit is enzymatically active, whereas B
subunit helps in binding to the GM1 iii. Enteroinvasive E. coli (EIEC)
ganglioside at the brush border of epithelial Disease:
cells of the small intestine - Dysentery with scanty blood stools; fever,
↓ cramping, more prevalent in developing
After binding, A subunit dissociates to the A1 countries.
and A2 - Resembles shigellosis clinically

Microbiology
Pathogenesis: SALMONELLA
First attach to the surface epithelium of large Past Questions:
intestine 1. Write short notes on:
↓ a. Enteric fever (3) [05 June]
Invasion and destruction of colonic epithelium b. Widal test (3) [05 June]
↓ 2. Define Gastroenteritis. Describe pathogenesis
Dysentery and laboratory diagnosis of Salmonella typhi.
(1 +4 +5 = 10) [09 July]
iv. Enteropathogenic E. coli (EPEC)
3. Describe the pathogenesis of Salmonella typhi.
Disease: Write in detail the laboratory diagnosis of Enteric
- Infant diarrhoea (Paediatric diarrhorea) (P@P) fever. (6 +4 = 10) [05 Dec]
- Vomiting, nausea, non bloody stools. 4. Describe the laboratory diagnosis of Salmonella
Pathogenesis: typhi infection. (10) [04 June]
- Plasmid mediated adherence and destruction ♦ Produces 3-main types of disease in man but
mixed forms are frequently observed.
of epithelial cells of small intestine.
1. Enteric fever:
v. Enteroaggregative E.Coli (EAEC)
- Salmonella typhi → Typhoid fever
- Disease: Infant diarrhea in developing
- S. Paratyphi A, B & C → Paratyphoid fever
countries
2. Enterocolitis:
Laboratory diagnosis: - S. typhimurium
1. Specimen collection: - S. enteritidis
V - Collection depends on the type of lesion - S. Thompson
• Faces or rectal swab in acute diahorrea - S. Newport
- S. Dublin
• mid-stream urine in UTI
3. Septicemia: S. Choleraesuis
• Pus from wound in sterile cotton swab
Note: Salmonella enteritidis can cause osteomyelitis
• C.S.F. in pyogenic meningitis. in patients with sickle cell anaemia.
2. Microscopy
Salmonella typhi & paratyphi
- Centrifuged deposit of the collected sample is
Virulence factors:
stained with Gram staining technique
1. Endotoxin: Bacterial (lipopolysaccharide (O Ag)
- On Gram staining: Gram negative bacilli. activates TLR4 on host cells.
3. Culture: Refer cultural characteristic. - TLRs play essential role in cellular response to
4. Biochemical test: Refer biochemical reaction. bacterial lipopolysaccharide.
2. Invasins: Proteins that mediate adherence to and
5. Agglutination test:
penetration of intestinal epithelial cells.
- Colonies are confirmed by agglutination tests 3. Factors involved in resistance to phagocytosis:
with group-specific polyvalent and type a. Catalase and superoxide dismutase: protect
specific antisera of E. coli. bacteria from intracellular killing by
- Important for identification of neutralizing oxygen radicals.
enteropathogenic strain of E. coli. b. Other factors neutralise defensins (that
facilitate killing of bacteria by phagolysosomes)
GIT
4. Factors involved in resistance to acidic pH: Enteric fever (05)

- Acid tolerance response (ATR) gene. Includes: Typhoid fever and paratyphoid fever.
5. Vi (virulence) antigen: A. Typhoid fever: Caused by S. typhi
- Surface Ag of salmonella typhi - Incubation period = 7 - 14 days usually
- Has antiphagocytic property • Clinically, it may vary from a mild
6. Flagellin: undifferentiated pyrexia to rapidly fatal
- The core of bacterial flagella disease.
- Activates TLRS on host cells and increase the • Typical features are step ladder pyrexia,
local inflammatory response. with relative bradycardia and toxaemia.
Pathogenesis [ 09, SAQ 2013 KU] • Onset is usually gradual with headache,
3 6
- Infective dose (ID50) = 10 to 10 bacilli malaise, anorexia, constipation or
diarrhoea.
- Incubation period = 7-14 days
• A soft, palpable spleen is a constant finding.
Infection is acquired by ingestion of contaminated
food, milk, water • Hepatomegaly is also common.
↓ • "Rose spots" that fade on pressure appear
On reaching gut, attach themselves to microvilli of on skin during second or 3rd weeks.
ileal mucosa Complications:
↓ - Intestinal perforation
Taken up by and invade M cells - Hemorrhage
↓
- Circulatory collapse
Penetrate to lamina propria and submucosa
- Bronchitis or bronchopneumonia
↓
Organisms are engulfed by mononuclear cells in
- Psychoses, deafness or meningitis V
underlying lymphoid tissue - Cholecystitis, Arthritis, abscesses, periostitis,
↓ nephritis, thrombosis, peripheral neuritis,
Resist intracellular killing and multiply within these osteomyelitis.
cells B. Paratyphoid fever: Caused by S. paratyphi A
↓ and B
Enter mesenteric lymphnodes - Milder form of febrile illness.
↓ - Shorter duration and incubation period.
They multiply and enter blood stream - Transient diarrhoea is commonly seen.
↓ Lab diagnosis of enteric fever (04,05,09)
Transient bacteremia 1. Specimens: Blood, feces, urine, bile and serum
↓ - Samples to be collected depends on stage of
Bacilli are seeded in liver, gallbladder, spleen, illness.
bonemarrow, lymphnodes, lungs and kidneys
Stage: Examination:
↓
1st week Blood culture
Further multiplication nd
2 week Widal test (Antibody test)
↓
Massive bacteremia 3rd week Stool culture
↓ 4th week Urine culture
Onset of clinical disease [@ BASU]
Microbiology
2. Culture: d. Bile culture: To detect chronic carrier in whom

st
a. Blood culture: In 1 week organism are present in biliary tract.
• Bacteremia occurs early in disease so blood Identification:
cultures are positive in 90% cases in first - In macConkey's agar or DCA, salmonella grow
week of fever, 75% in second week, 60% in as non lactose fermenters.
3rd week and 25% after that.
- When they are further studied by Gram
• Blood is to be collected before antibiotic staining, motility preparation and biochemical
therapy is given. reactions:
• Collected by venepuncture method with all
• Gram staining: Gram negative, non sporing,
aseptic precautions.
bacilli
• 5-10 ml of blood is collected from median
• Motility preparation: Motile
cubital vein.
• Biochemical reactions:
• This blood is transferred directly into a
blood culture bile broth. → IMVIC: - + - + (citrate negative in
• Alternatively, clot culture may also be done in salmonella typhi, S. paratyphi A)
which, 5-10 ml of collected blood is allowed to → H2S +ve (Except S. paratyphi A)
clot; serum is seperated out. Clot is broken up → Urease - Ve
with sterile glass and added to blood culture
3. Serology:
medium containing streptokinase.
- Widal test
Note: Clot culture offers a higher rate of isolation
4. Demonstration of Ag:
than blood culture as, bactericidal activity of serum is
obviated in the technique. - Sensitized staphyloccal coagglutination test.
V • After incubation overnight at 37°C, sub
5. Indirect evidence:
culturing is done on MacConkey agar or - Blood for Total Leucocyte Counts (TLC) and
DCA; colourless colonies (NLF) appear. Differential Leucocyte Counts (DLC)
Note: Castaneda's method of blood culture may be - Progressive Leucopenia with relative
adopted to eliminate risk of introducing lymphocytosis.
contamination during repeated subcultures. Widal test (05)
• The method provides both liquid and solid - Agglutination test that detects antibodies
media in one bottle (Eg. brain heart produced against S. typhi, S. paratyphi A & B.
infusion medium) it is biphasic media. Principle:
b. Stool culture: In 3rd week - When patient's serum is tested with 'O' & 'H'
• Salmonella are shed in feces throughout the suspension of S. typhi and S. paratyphi, there
course and even in convalescence with occurs Ag-Ab reactions and agglutination is
varying frequency, so stool culture is also visible.
valuable.
Antigens used:
• Media: MacConkey's agar, DCA, tetrathionate.
- H & O of S. typhi
c. Urine culture: In 4th week
• Salmonella are shed infrequently in urine - H of S. paratyphi A and B
so, urine culture is less useful as compared Note: Paratyphoid O isn't used as they cross react
to blood and stool cultures media: with typhoid 'O' Ag by sharing factor XII.
MacConkey's agar.
GIT
Procedure: SHIGELLA
- Widal track with four rows of test tubes for 4 Past Questions:
Ags is used.
1. Discuss the aetiology and laboratory diagnosis in
- Serial two fold dilution of serum (1/10, 1/20, a case of bacillary dysentery. (3 + 7 = 10) [07 July]
1/40) is added to all the test tubes and equal 2. Write short notes on laboratory diagnosis of
volumes of Ag are then added to respective bacillary dysentery. (5) [09 July]
rows.
♦ Causative agent of bacillary dysentry.
- Incubated at 37°c for 4 hrs and then at 4°C
Classification (07)
overnight.
Antigenically classified as:
Observations:
1. Group A (S. dysenteriae)
- H agglutination: Loose cotton woolly clumps.
2. Group B (S. flexneri)
- O angulations: Granular disc like at bottom.
3. Group C (S. boydii)
Interpretation:
4. Group D (S. sonnei)
- No single titre is diagnositic
Morphology:
- Rising titre is important: A fourfold rise is said - Gram negative bacilli
to be diagnostic.
- Non motile, non and flagellated, non capsulated.
- In a single test, a titre of 100 of 'O' or more and
- Measures: 1-3 × 0.54m
titre of 200 of 'H' agglutinin signifies presence
- Fimbrae may be present.
of active infection, but that has to be
interpreted taking into following factors. Culture characteristic:
- Aerobes or facultative anaerobes with a growth
- Local titre, immunizations, Anamnestic
temperature range of 10-40°C and pH 7.4.
reaction, non specific Ag's, antibiotic
1. Nutrient agar:
treatment, carriers. V
• Colonies are 2mm in diameter, circular,
Note: Anamnestic reactions are due to 'H' Ags. convex, smooth and translucent.
Identification of carriers: 2. MacConkey's agar: Colorless colonies except
- Carriers can be convalescent carriers or Sh. sonnei which is a late lactose (beyond 24
healthy carriers. hours) fermenter
- They can excrete the organisms in feces, less Selective media:
commonly in urine for about 2 months to a 1. Deoxycholate citrate agar (DCA) media
year. • Same as MacConkey's agar.
i. Repeated stool culture. 2. Salmonella shigella agar
ii. Bile aspiration and culture, duodenal • Contains high concentration of bile salt →
drainage cultures. inhibit gram +ve bacteria and coliforms.
iii. Detection of Antibody to Vi Ag (1:10 or • Colourless colonies are formed.
above) in serum. Biochemical reaction:
Enteric fever: Control measures: 1. Fermentation:
a. Sanitation measures and personal Hygiene - Ferment glucose with acid production. (except
b. Immunization: flexneri)
i. Killed S. typhi vaccine: TAB vaccine - Mannitol is fermented by all except sh.
dysenteriae.
ii. Live oral typhoid vaccine: TY 21a
- Lactose is not fermented except S sonnei.
iii. Purified Vi polysaccharide vaccine.

Microbiology
2. IMViC: - + - - ↓ ↓
3. Catalase: Positive, except Sh. dysentria type I. Severe diarrhoea Bleeding from
Virulence factors: and toxaemia mucosa
1. Invasion plasmid antigen:
↓
- Mediate attachment and penetration of
Ulcer is covered by pseudomembrane formed by
mucosal epithelial cell or colon.
fibrin, leucocytes, cell debris, necrosed epithelia and
2. Toxins:
bacteria
a. Endotoxin
• Release after autolysis Clinical syndrome:
• Triggers inflammation 1. Dysentry: frequent painful passage of low volume
b. Exotoxin stools containing blood, pus and mucous with
abdominal cramps.
• Also called shiga toxin.
• Released by sh deysentraie type I. 2. Complications: Polyneuritis, myocarditis, joints-
• Toxin consists of binding (B) and active (A) effusion, hemolytic uraemic nephritis.
subunits. Laboratory diagnosis (07,09)
• It has 3 types or toxicity: Enterotoxicity, 1. Specimen collection: Fresh stool, mucous flakes,
neurotoxicity, and cytotoxicity. rectal swabs.
Pathogenesis: 2. Stool examination:
- Shigella is highly acid resistant: 10 - 100 bacilli i. Macroscopic: Odourless stool mixed with
are able to produce clinical features. blood and mucous.
Food or drink contained with shigella ii. Reactivity: Alkaline
↓
iii. Microscopic: Abundant cellular exudates,
Reach terminal ileum and colon as they resist gastric pH
bright red RBCs, epithelial cells, macrophage.
V ↓
3. Culture: Refer cultural characteristics
Attach themselves to the epithelial cells and
gradually taken by the epithelial cells where they 4. Biochemical test: Refer biochemical reactions.
multiply 5. Detection of endotoxin: Limulus test
↓ 6. Slide agglutination test: Done by using polyvalent
Colonization of the bacilli occurs laterally in adjacent antisera of three groups (A, B and C) of shigella
cells and in lamina propria and antiserum of group D (S. sonnei), one by one
↓ against the isolate.
↓ ↓
Liberate shiga toxin Autolysis of bacilli and release of
VIBRIO CHOLERA
which has 2 subunits: endotoxin Past Questions:
A&B ↓ 1. Describe the laboratory diagnosis of Vibrio
↓ Trigger acute inflammatory cholera. (5) [10 Jan]
B subunit helps in reaction 2. Describe etiology, mode of infection clinical
binding to host cells ↓ features and laboratory diagnosis of cholera.
whereas A subunit Micro-abscess formation with (1+2+2+5=10) [08 July]
disrupt protein capillary thrombosis
3. Describe the morphology and cultural
synthesis ↓
characteristics of Vibrio cholera. Write the
↓ Necrotic epithelia is soft and friable
pathogenecity and laboratory diagnosis of
Damage vascular and is sloughed out in patches
cholera. (2+2+3=10) [07 Dec]
endothelium forming Serpiginous ulcers

GIT
4. Enumerate bacterial causes of diarrhoea. - Very actively motile, single polar flagellum and the
Elaborate the mechanism involved in case of movement is of "darting type" [MCQs 2013 KU]
Vibrio cholera. (3+7=10) [06 Dec] - Is stained mucous flakes or cholera stool, the
5. Differences between classical and EI Tor Vibrios. vibrios are derranged in parallel rows; described
by Koch as "fish in stream" appearance.
[04 Dec]
Pathogensis (07)
Classification: - IP = 6 hrs-3days
VIBRIO - Faeces & vomitus of human cases or carriers
are the main sources of infection.
Group A (Cholera & Group B: Unrelated to - Infection occurs by ingestion of contaminated
cholera like vibrios) cholera vibrios, food and water.
Common H Antigen biochemically & Mechanism:
(Vibrio cholera) Antigenically - Cholera toxin has entirely main role in cholera.
(on the basis of 'O' Ag)
- Potent enterotoxin.
O subgroup I (V. O subgroups II, III, IV, - Very much similar to heat stable toxin of E. coli.
cholera 01) V & VI - It has two parts:
(Non -01 V. i. A subunit with biologic activity:
cholera)(01-0139) • A subunit has 2-fragments A1& A2.
Subtype O Antigens • A1 helps in binding of A2 and B
Biotypes • A2 helps in prolonged activation of ATP.
Ogawa AB
Inaba AC ii. B subunit that facilitates binding of A
Classical El tor Hikojima ABC subunit to intestinal cell.
Contaminated → Pathogen reaches the small
(On the basis of minor Ags)
food/water ingestion intestine by escaping acid
barrier of stomach
Ogawa Inaba Hikojima V
↓
Pathogens multiply ← In an alkaline medium, in
Difference between classical & El. tor rapidly & become the presence of nutrient &
vibrios (04) actively motile bile salts
↓
Features Classical El-tor Organism liberates
1. Haemolysis of sheep RBC - + their potent exotoxin Binding of 'B' subunit of
→
known as GM1 on cell surface
2. Haemagglutination of chick - +
enterotoxin
RBC
↓
3. V.P. reaction Usually Usually (ATP → ↑ cAMP) ← Entry of 'A' subunit into the
weak or - strong + ↓ target cell
4. Susceptibility to + - Secretion of
chloride, water,
polymyxin B
bicarbonate &
5. Sensitivity to phage V - + inhibition of
Morphology (07) reabsorption of
Na, K, Cl
- Gram negative, nonsporing, non capsulated,
↓
curved or comma shaped rod with rounded or
Rice watery
pointed ends.
diarrhoea (cholera)
- Also called 'Comma' vibrio.

Microbiology
Clinical features of cholera (08) iii. Microscopy:

- Cholera is an acute intestinal infection caused 1. Rapid diagnosis by direct fluorescent antibody
by V. cholera characterized by massive watery staining of smears from liquid stool.
diarrhoea and recurrent vomiting occurring in 2. Hanging drop preparation: shows typical
severe form resulting in rapidly progressive "Shooting star"
dehydration and death if not promptly and 3. Gram staining: Typical morphology of vibrios.
adequately treated. iv. Culture:
a. Stage of evacuation: 1. Stool sample is directly plated into one or more
V • Profuse, painless effortless, watery selective media like BSA, TCBS or Monsur's
diarrhoea, followed by vomiting. GTTA medium.
2. Specimens received on holding transport medium
• The patient may pass as much as 40 stools
are first inoculated into enrichment media such as
in a day which is Rice watery in nature
alkaline peptone water and incubated for 6-8 hrs
b. Stage of collapse (Due to dehydration) before plating on a selective media.
• Sunken eyes, hollow cheeks v. Identification: Can be done by:
• Loss of skin elasticity a. Cultural characteristic in Media (07)
• Shallow & quick respiration Media Characteristics
• Restless and intense thirst 1. MacConkey's - (Pale, non lactose fermenting)
• Cramps in leg. media Which may turn pink on
• Hypovolemic shock → death if not treated. prolonged incubation because
Lab diagnosis (06,07,08,10) of late lactose fermentation.
i. Specimens: 2. Blood agar - Hemolysis (+) in EL TOR vibrios
media Hemolysis (-) in classical
1. Watery stool and mucus flakes from stool.
3. TCBS - Colonies are large yellow due
2. Rectal swabs from contact & carriers.
(Thiosulphate to sucrose fermentation by V.
ii. Transport media:
citrate bile cholera strains (Bromothymol
1. Venkataraman - Ramakrishnan medium sucrose agar) blue as indicator)
2. Cary - Blair medium 4. Alkaline Bile - Colonies become 1-2mm
3. Bile peptone transport medium salt agar (BSA) diameter in size in 24 hrs.

GIT
b. Biochemical tests: i. Campylobacter media (37° for 3-5 days)

1. Fermentation: • Colonies appears: Circular, convex and
• Non lactose fermenter translucent and less than 2mm in
• Ferments glucose mannitol, sucrose, diameter.
maltose & mannose catalase & oxidase (+) Biochemical Reactions:
• Form indole and reduce nitrates to form - Oxidase, urease and catalase positive.
Nitrites.
- Also produce DNAase, alkaline phosphatease
2. Cholera red reaction: +ve and glutamyl amino peptidase.
3. V.P. reaction:
Virulence factors:
• El-tor → (+)
1. Urease activity:
• Classical → (-)
- Urease dissociate urea to NH3 and CO2.
4. Hemolytic reactions:
- NH3 neutralize gastric acidity facilitating initial
• El-tor → (+)
colonization of the organism.
• Classical → (-)
2. Motility
vi. String test:
3. Autoimmune response: Bacterial antigens cross
- When a drop of 0.5% sodium deoxycholate is
placed on a clean slide and colonies of V. react with antral antigens stimulating
cholerae mixed with drop on slide, they autoimmune response.
produce viscous suspension that can be drawn 4. Protease and other enzymes like mucinase and
into a string when inoculating loop is slowly lipopolysaccharidase.
raised from the slide.
Pathogenesis:
vii. Serological test:
Infection of the H. pylori as transmitted from person
- Indirect haemagglutination assay
to person
- ELISA. V
↓
HELICOBACTER PYLORI Bacilli secrete an enzyme urease which cleaves urea
Past Questions: to release NH3 and CO2
1. Laboratory diagnosis of H. pylori (4) [06, 07] ↓
2. Write short notes on: H. pylori (3) [06, 07] Ammonia neutralize the gastric pH and makes
Morphology favourable environment for H-pylori
- Gram- negative rods ↓
- Spiral or curved bacilli With the help of flagella, bacilli move to the mucosa
- After long culture, form spheroid or coccoid and is attached with epithelial cells
bodies. ↓
- Motile due to multiple monopoloar sheathed Bacilli secrete enzymes like proteases, mucinase,
flagella polysaccharidases
- Non capsulated and nonsporing. ↓
Note: Other helicobacter posse unipolar flagella These enzymes digest and degrade gastric mucosa
Cultural characteristic creating ulcer
- Strictly microaerophilic (5% O2) & capnophilic (5- ↓
10%, CO2) There is also a superficial infiltration of
- Require high humidity for growth. polymorphonuclear leucocytes causing gastritis

Microbiology
Clinical syndrome: d. Antigen detection:

- Often it causes no problems, but it can cause • Faecal antigen is detected by commercial
i. Duodenal ulcer (90%) antigen detection kit.
ii. Gastric ulcer (60%) CLOSTRIDUM DIFFICILE
iii. Increase risk of adenocarcinoma of stomach
Past Questions:
Laboratory diagnosis (06)
1. Short notes on:
- Can be done by both invasive & non invasive tests. a. Clostridium difficle. (5) [08 Jan]
1. Invasive test b. Pseudomembranous colitis (3) [07 Dec]
- Gold standard approach to the diagnosis ♦ First isolated by hall and 'O' tool from faeces of
- Involves gastric intubation, endoscopy and newborn infants.
biopsy
Habitat
i. Endoscopy
- Found in feces of 3-5% healthy adults.
• Reveals pathological change - 40-50% in feces of healthy infants.
• Character & location of ulcer can be found out. - Colonization is favored by preexisting GI
ii. Biopsy: disease and environmental contamination
• Mucosa is taken out which can be tested by: Morphology:
a. Rapid urease test: - Gram (+)ve rod
1. Biopsied tissue is placed into a small - Oval & subterminal spore
quantity of urea-containing broth to Toxins:
which pH indicator has been added.
1. Enterotoxin (toxin A) → Causes gut symptoms
2. Urease released by bacilli increases gastric
pH, which is detected by indicator. 2. Cytotoxin (toxin B) → Causes cytopathic effect
in cell cultures.
V 3. Most rapid and dependable
- Both toxins important in pathogenesis of
b. Microscopy
clostridium difficle associated disease
1. Gastric mucosa is stained by Gram stain
Pathogenesis (07)
or Giemsa stain or Warthin - starry silver
staining - It can cause:
2. Gram staining - Gram negative rods 1. Antibiotic associated diarrhoea:
c. Culture: (Refer to cultural characteristics) Use of antibiotics (Amphicillin, tetracycline,
Usually not done for diagnosis chloramphenicol, lincomycin, clindamycin)
d. Molecular tests: DNA hybridization, PCR ↓
Alter the balance of normal flora of gut
2. Non-invasive tests:
↓
a. Serology:
It favors colonization and multiplication of C. difficile
ELISA: detection of antibody
↓
b. Urea containing an isotope or carbon (Carbon14) Production of toxin in colon of carriers
is fed to the patient → Urease break it into C14O2
↓
and NH3→ expired C14O2 is detected.
i. Diarrhoea (Watery & profuse, sometimes
c. Urine test: bloody)
• Radioactive isotope of nitrogen (N15) is ii. Colicky abdominal pain
incorporated to urea. Urea after broken iii. Body temperature is > 39°C
yields N15H3 which dissolves in H2O to form
N15H4OH. This is passed in urine which can Note: In most cases, the imbalance of normal flora
be detected by mass spectrometry. subside after therapy.

GIT
2. Pseudo membranous colitis: VIRAL DIARRHOEA

Enterotoxin
Past Questions:
↓
Accumulation of inflammatory exudates 1. Diarrhoea associated viruses. (3) [07 July]
composed of polymorphonuclear leukocytes, 2. Discuss pathogensis and laboratory diagnosis of
fibrin & mucin is attached to mucosal surface
Rota virus. (2+3=5) [11July,10 July]
↓
Gives membrane like appearance when viewed via 3. Write short notes on morphology of Rota virus.
colonoscopy (3) [07 Dec]
Note: Lincomycin and clindainycin are most
♦ Virus responsible (07)
important offending agents of colitis
- Rota virus
Lab-diagnosis:
1. Colonoscopy: Pseudo membrane can be seen - Norwalk virus
2. Direct demonstration of toxin in feces and - Adenovirus
patient: By inoculation of cell cultures of
- Calcivirus
difficile toxin
3. Isolation of organism: From feces by - Astrovirus
inoculating in selective media with subsequent - Sapovirus
test for toxigenecity
Primary age (great Clinical
Virus Family Genome Size Symmetry Envelope
risk) severity
1. Rota virus Reoviridae dsDNA Children < 5yrs +++ 70nm Icosahedral Absent
segmented
V
2. Norwalk virus Calciviridae ssRNA All ages ++ 27 nm Icosahedral Absent
3. Sapoviurs Calciviridae + ssRNA Children <5 yrs + 30 nm Icosaheadra Absent
4. Adenovirus Adenoviridae dsDNA Children <5 yrs + 80 nm Icosamedral Absent
(Type 40 & 41)
5. Astrovirus Astroviridae +ve ssRNA Children < 5yrs + 38 nm Icosahedral Absent
6. Calcivirus Calciviridae ssRNA Children + 35 nm Icosahcdral Naked
Rota virus - Rota virus group is most common, causes 90%
of infection.
Morphology (07)
- Member of Reoviridae family
Pathogenesis (10,11)
Mode of transmission:
- Non enveloped, dsRNA virus with icosahedral
symmetry. - By fecal oral route
- RNA consist of 11 segment - Season: winter
- Electron microscopy shows two type of rota - Age Group:
viruses, complete and incomplete particles. • <5 yr of age
- The virus has the characteristic wheel like Note: By age of 6 yr, majority of children have
appearance. antibodies to at least one serotype.

Microbiology
- Incubation period: 2 - 4 days ♦ Only the virus with a fibre protruding from each of
Ingestion of Rota virus the 12 vertices of the capsid.
↓ ♦ The fibre is the organ of attachment and is a

Bind to lactose receptor in brush border in small haemagglutinin.
intestine ♦ There are 41 known antigenic serotypes.
↓ ♦ The fibre protein is main type specific antigen.
Infection of mature enterocyte ♦ Type 40 and 41 cause infantile gastroenteritis.
↓ Laboratory diagnosis:
Cell death and villous atrophy I. Adenovirus antigen detection in patients stool.
↓ II. Isolation of the virus in cell culture
↓ ↓
III. Detection 4-fold or greater rise in Ab titre
Reduced digestion and Crypt hyperplasia
Astrovirus
absorption of nutrient ↓
♦ Linear, positive sense ssRNA virus
↓ Hypersecretion of water
Primary malabsorption into lumen ♦ The surface of the icosahedral capsid has five or
six pointed star appearance.
↓ ↓
♦ Causes outbreak of diarrhoea in children under 5 yr.
Non absorptive diarrhea Watery diarrhea
♦ Mild gastroenteritis.
Note: No inflammation occur and the diarrhoea is ♦ Transmission: By fecal oral

non bloody ♦ Diagnosis: Detection of viral antigen.
V Norwalk virus
Clinical feature:
- Nausea, vomiting and watery, non bloody ♦ Membrane of calciviridae
diarrhoea ♦ Genome: Positive sensed SSRNA
- Dehydration: main complication ♦ Viral size: 27 nm
Laboratory diagnosis (10,11) Pathogenicity

I. Specimen - Mode of transmission: By fecal oral route.
a. Stool collected in dry container, emulsified in - Incubation period: 24 - 48 hrs

buffered saline - It is cause of epidemic viral gastroenteritis in
adults, rapid onset diarrhoea, vomiting, nausea
b. Rectal swab (for unconscious patient)
etc.
II. Electron microscopy: demonstrates virus
Laboratory diagnosis:
III. Viral antigen: By CFT, ELISA
- Demonstration of virus: Electron microscopy
IV. Antibody titre: Is measured by ELISA
- Viral antigen detection: by ELISA
V. Viral genome detection: RT - PCR
- Antibody detection by ELISA
Adenovirus • 4 fold rise of Ab-titre in paired sera
♦ Non enveloped DNA virus with icosahedral capsid indicates recent infection.

GIT
PARASITES (GIT PARASITOLOGY) - Parabasal bodies: Two curved median bodies

posterior to sucking disc.
PROTOZOA (GIT) - Division: Longitudinal, following duplication of
Past Questions: all cell organelles.
1. Describe the life cycle, pathogenesis and
laboratory diagnosis of Amoebiasis caused by
Entamoeba histolytica. (3+3+4=10) [10 July]
2. Describe etiology, mode of infection, clinical
features and laboratory diagnosis of amoebic
dysentery. (1+2+2+5=10) [08 Jan]
a. Entamoeba histolytica. (3) [05 Dec, 04 June]
b. Intestinal protozoal parasites. (3)[08 July]
Giardia lambia
♦ Habitat: Duodenum and upper part of jejunum of
man.
♦ Morphology: Exists in two phases:
II. Cyst:
I. Trophozoite - Shape: Oval, football shaped
II. Cyst - Size: 12 × 7 µ
I. Trophozoite/vegetative form - Nucleus: 4 nuclei in cluster or lie in pairs at
opposite pole. V
- Shape: Tennis or badminton racket, or heart
shaped - Cyst wall: Tough, hyaline.
- Size: 14 × 7 µ
- Motility: Actively motile with the help of 4
pairs of flagella.
- Nucleus: Two nuclei, one on each side, nucleus
has large central endosome with no chromatin
granules on the nuclear membrane.
- Axostyle: Slender rod like structure, two in
number formed by the fusion of axonemes of
flagella and associated group of microtubules.
- Symmetry: Bilaterally symmetrical
- Dorsal surface: Convex
- Ventral surface: Concave
- Anterior end: Broad, posterior end: pointed
- Sucking disk: Present on ventrally concave
surface.

Microbiology
Life cycle: • Indefinite abdominal pain, nausea, vomiting

- Definitive host: Human beings • Steatorrhoea: Passage of yellowish and
- Intermediate host: Not required, passes life greasy stool with excess fat
cycle in one host • Malabsorption
Mature cyst - passed in feces of contaminated food • Severe flatulence
and drinks • Children: Develop chronic diarrhoea,
↓ malabsorption, wt. loss
Infection occur by ingestion of contaminated food or • Cholecystitis and jaundice occasionally
drink Laboratory diagnosis:
↓ I. Specimen:
Cyst hatches out in 2 trophozoites within 30 minutes. - Faeces should be collected in clean, wide,
↓ mouthed container and transported immediately
Multiply in intestine by longitudinal binary fission within 30 min to laboratory for examination.
↓ II. Microscopy:
When condition in duodenum become unfavourable - Saline preparation: Demonstration of motile
for survival of trophozoite form; trophozoite
↓ - Iodine preparation
Encystment occur in large intestine • To demonstrate trophozoite in killed state
↓ • Cyst in stained state
Mature cyst are passed in faeces to repeat the cycle • Only cyst are seen in asymptomatic carriers.
Pathogenicity: - Demonstration of cyst in concentrated stool
V - Mode of transmission: Fecal-oral route sample when cysts are less in number
- G. Lambia is not tissue invader. - Demonstration of trophozoites in bile
Pathogenesis aspirated duodenum (bile A) or removed from
bile duct (bile B).
Trophozoite - Colonize in the duodenum and attach
to epithelial cells with the help of sucking disk III. Serology:
↓ a. Ag-detection: By ELISA, fluorescent method

using monoclonal antibodies.
Because of tight association with epithelial cells of
duodenum b. Ab-detection: ELISA and indirect
immunofluorescence tests.
↓
Causes disturbance of intestinal function and Balantidium coli
abnormalities in villus ♦ It occur in following form
↓ I. Trophozoite/vegetative form
This leads to mechanical interference to absorption - Shape: Oval
of fat, fat soluble vitamin & haematinic factors. - Size: 60 - 70 µ × 40 - 50 µ
Clinical feature: - Motility: Motile with the help of cilia covered
- Disease caused by it: Giardiasis all over the body.
- Giardiasis → Is characterized by - Nucleus: Two nuclei, one large kidney shaped
• Diarrhoea → 5-6 stools per day - explosive (Macronucleus), one small round (micro
watery stool. nucleus)

GIT
- Anterior end: Narrow, show cytosome (mouth) ii. Intermediate host: Not required, passes life
& cytopharynx. cycle in one host.
- Posterior end: Broad, show small pore iii. Transmission: Pig to pig, pig to man, man to
(Cytopyge - anus) man, and man to pig
- Two contractile vacuoles: One in middle and Infection occurs by ingestion of cyst
other at posterior end ↓
- Many food vacuoles, tissue debris, white blood Cyst hatches out in trophozoite in large intestine
cells and red blood cells are present in ↓
cytoplasm. Multiply in intestine by binary fission and form large
II. Cyst number of trophozoites
- Shape: Oval ↓
After a period of growth and multiplication, when
- Size: Smaller than trophozoite → 50-60µ in
conditions become unfavourable for survival of
diameter
trophozoite form, encystment occur
- Nucleus: Two nuclei → Macronucleus and ↓
micronucleus
Mature cyst are passed in faeces & repeat cycle
- Cyst wall: Thick, transparent, double layered
wall.
Pathogenecity
- B. coli feeds mainly on starch, but also ingest
bacteria, RBC & epithelial cells.
- Clinical disease occurs when trophozoite
invade intestine mucosa.
- The factors that play role in pathogenesis are
i. Malnourishment V
ii. Concurrent infection
Clinical feature:
- Disease caused by it is called Balantidiasis→
characterized by
• Mucosal ulcer and submucosal abscess
- Diarrhea or dysentery with abdominal pain,
tenesmus, nausea and vomiting
- Occasionally, intestinal perforation with peritonitis
and involvement of genital and urinary tract.
Laboratory diagnosis:
i. Specimen: Stool collection
ii. Microscopy
- Demonstration of parasite in stool sample
by saline and iodine preparation
iii. When stool examination is negative, scraping
or biopsy specimen obtained by sigmoidoscopy
Life cycle: is useful in suspected cases.
i. Definitive host: Pig is the natural host, man is iv. Culture: B. Coli can also be cultivated in vitro
accidental host. like E. histolytica
Microbiology
Entamoeba histolytica (04,05) - Contain small dot like structure, central in

position called karyosome, which is surrounded
Habitat:
by clear halo.
- Trophozoite of E. histolytica inhabit in the - Nucleus is surrounded by a nuclear membrane
mucous and submucous layers of the large lined with a single layer of uniformly
intestine of man. distributed chromatin granules.
Morphology: II. Pre cystic stage
- It occur in 3 stages - It is a transitory stage, formed during the
I. Trophozoite form conversion of trophozoite to cyst.
II. Pre cystic - Shape: Round or oval with blunt pseudopodium.
III. Cystic - Size: 10-20µ
I. Trophozoite/vegetative form - Endoplasm: Free of red blood cells and other
- Is feeding stage of E. histolytica ingested particles.
- Shape: Irregular, constantly changing → No - Nucleus: Retains the features of trophozoite
fixed shaped stage.
- Size: 10-40µ (Avg. 20-30µ) III. Cyst state
- Motility: Actively motile with the help of - Shape: Spherical
pseudopodium - Size: 10-15µ
- Cytoplasm: Differentiated into Nucleus:
a. Ectoplasm: Thin, clear, translucent outer layer - Each cyst contains a single nucleus and a mass
b. Endoplasm: Granular inner layer containing of glycogen and 1-4 cigar shaped or oblong
nucleus, food vacuoles, RBCs, occasionally retractile rods is called chromatoid bodies.
WBCs and tissue debris. - As it matures, the glycogen mass and
Nucleus chromatoid bodies disappear.
- Spherical - The nucleus undergoes two successive mitotic
V - Size 4-6µ division to form 2 and finally 4 nuclei (mature
cyst-quadrinucleate)

GIT
Life cycle (10) Pathogenesis of amoebiasis (10)

- Definitive host: Human beings Ingestion food and water contaminated with
- Intermediate host: Not required, passes life quadrinucleated cyst
cycle in one host - the man ↓
Mature cyst passes in faeces of convalescents and The cyst wall resistant to Gastric juice so, the cyst
carrier contaminate food & drink wall is damaged in caecum or lower ileum by action
↓ trypsin causing excystation
Infection occur by ingestion of contaminated food or ↓
drink Releases tetranucleate amoebae followed by
↓ metacystic trophozoites
Cyst passes through the stomach undamaged and ↓
enter the small intestine Metacystic trophozoites invade the mucous
↓ membrane of large intestine due to proteolytic
Excystation occurs in the caecum or lower part of the ferment and active motility
ileum. During this period, the cytoplasm gets ↓
detached from the cyst wall, then causing a tear in Proteolytic ferments secreted
the cyst wall a tetranucleate amoeba (metacyst)
comes out Cysteine Lectin Histolysin Amoebapore
↓ Digest ECM Binds to Causes Form pore in
Nuclei and cytoplasm of metacyst divide to form 8 and degrade carbohydrat necrosis & plasma
amoebulae, which lodge in the submucous tissue of Fibronectin, e on surface destruction membrane
the large intestine where they grow and multiply by Laminin, of colonic of tissue
binary fission type I epithelial V
collagen cells
↓
Produce characteristic lesions of amoebiasis (flask
shaped ulcer) Damage mucosal epithelium and reach submucous
↓ coat, where they multiply and ↑in number and form
colonies
When condition becomes unsuitable for survival in
↓
trophozoite form, some of them get converted into Destroy the tissue in their vicinity and utilize
precystic stage and finally into cystic state cytolysed material as their food. Thus spread rapidly
↓ in various direction and dissolve surrounding tissue
and bring about coagulative necrosis by histolysin
Cysts are passed in faeces to repeat the cycle
↓
Pathogenecity Form abscess, which breaks down to form a
- Trophozoites in lumen do not cause any illness, characteristic flask shaped ulcer with a narrow neck
until they invade the intestinal tissue. and broad base
- This happens in 10% cases, 90% cases are Clinical feature (08)
asymptomatic. Disease produce is called Amoebiasis
Mode of transmission (08) a. Intestinal amoebiasis: Also called primary
amoebiasis
- Faeco-oral route
b. Extra-intestinal amoebiasis: Also called
- Infective stage: Quadrinucleated cyst
secondary or metastatic amoebiasis

Microbiology
a. Intestinal amoebiasis: 2. Diagnosis in Asymptomatic carrier (Cyst passer)

It is characterized by - Important in epidemiological surveys
- The passage of blood and mucous in stool - Demonstration of E. histoytica
• Repeated stool examination for
- Stool - foul smelling and brownish black in color
trophozoites and cysts.
- The patient is usually acerbate and nontoxic
• Concentration method: to demonstrate cysts.
- Sometime only diarrhoea and vague abdominal - Culture: Microscopically, negative stool may
symptom. give positive result by culture.
b. Extra - intestinal amoebiasis - Serology: May be positive in invasive amoebiasis.
- Hepatic amoebiasis: Difference between Amoebic and Bacillary
• Occurs in tropics in 2-10% cases of intestinal dysentery (03)
amoebiasis S.
Feature Amoebic dysentery Bacillary dysentery
• The pain and tenderness in rt. hypochondrium N.
Clinical
• Wt. loss, fever with chills
1. Onset - Gradual - Acute
- Pulmonary amoebiasis 2. Fever, - No - Fever & usually
- Cutaneous amoebiasis vomiting vomiting
- Cerebral amoebiasis 3. Frequency - 6 to 8 time per - Over 10 times/
day day
- Splenic abscess
Macroscopic
- Amoebic vaginitis
1. Odour - Offensive - Odourless
Laboratory diagnosis (08, 10) 2. Nature - Blood & mucus - Often water &
1. Intestinal amoebiasis (symptomatic pattern) bloody
I. Specimen Collection 3. Reaction - Acidic - Basic
V - Stool are collected & transported immediately
4. Color - Dark red -
(altered blood)
Bright red (fresh
blood)
II. Examination: 5. Amount - Relatively - Small
1. Stool copious
a. Naked eye 6. Consistency - Do not adhere - Adhere to
to the container bottom of
Colour: Dark brown container
Odour: Offensive Microscopic
Bloody mucus: Present 1. RBC - In clump - Discrete or in
rouleaux
Consistency: Semi fluid
2. Pus cells - Scanty - Numerous
b. Microscopy
3. Macrophages - Nil or very few - Numerous &
• Saline preparation: To demonstrate large
motile trophozoites 4. Ghost cells - Nil - Numerous
• Iodine preparation: To demonstrate 5. Eosinophils - Present - Scarce
killed trophozoites and stained cyst 6. Pyknotic - Very common - Nil
bodies
• RBC: Rouleax formation
7. Trophozoite - Present of E. - Nil
2. Blood: histolytica
Moderate leucocytosis 8. Charcot- - Present - Nil
III. Serology: Leyden
Causative E. histolytica Bacteria (Shigella)
- Negative in early cases and in the absence
agent
of deep invasion.

GIT
Complication of E. Histolytica infection - Anterior end: Thin, has mouth surrounded by 3

I. Pulmonary complication finely toothed lip.
- Empyema - Freshly passed worms: Light brown or pink in
- Pneumonia color that changes gradually to white.
- Hepatobronchial fistula - Body cavity: Present and contains ascarase or
ascaron, a toxic fluid
II. Hepatobiliary complication
Male worm:
- Hemobilia & Jaundice
- Length: 15-25cm and 2-4mm in diameter
III. Septic shock
- Has curved posterior end (tail) and two
IV. Peritonitis, ascitis
copulatory spicules
V. Cerebral amoebiais
- Life span: About 6 months.
VI. Skin: Granulomatous ulceration
Female worm:
VII. Splenic: Abscess
- 25-40cm in length and 5mm in diameter,
VIII. Amoebic Pericarditis
stouter than male with straight and conical
posterior end
WORMS (HELIMINTHOLOGY)
- The vulva is situated at the junction of anterior
Past Questions:
and middle third of the body which is narrow
1. Life cycle, pathogenesis and laboratory diagnosis and is called vulvar waist.
of ascaris lumbricoides. (3+3+4=10) [05] - It is oviparous -mature female can liberate
2. Describe the life cycle pathogenesis and about 2,00,000 egg daily.
laboratory diagnosis of hook worm. - Life span about 1yr.
(4+3+3=10) [10 Jan] - Unfertilized female is also capable of laying
3. Distinguish nematodes from cestodes. eggs. V
(5) [11 July] Eggs: Two types
4. Describe the life cycle and laboratory diagnosis of I. Fertilized egg
hook worm. (7+ 3=10) [05 June] - Shape: Round or oval
- Size: 60 - 70 µ× 40 - 50 µ
a. Taenia solium (5) [05 Dec]
- Colour: Yellowish - brown - bile stained
b. Morphological differences between taenia
- Egg shell: Thick smooth, translucent with an
solium and taenia saginata (5) [06 June]
uneven outer albuminous coat
c. Bile stained ova. (5) [06 June] (rugosities/corticated) this albuminous coat
d. Ascaris lumbricoides (5) [08 July] is sometimes absent (decorticated egg
e. Complication of Ascariasis (5) [04 Dec] ie.egg without an outer coat)
f. Hook worm (5) [07 July] - Ovum: Large, unsegmented ovum
g. Laboratory diagnosis of Enterobiasis (5) [04 Dec] - There is clear, crescentric area between the
Ascaris lumbricoides (08) ovum and the egg shell at each pole.
- It floats in saturated solution of common
Morphology:
salt.
Adult worm
- Covering - 3 (i) outer mamillated layer (ii)
- Shape: cylindrical with tapering ends.
middle transparent (iii) Inner lipoidal
- Size: Upto 40cm in length it is the largest
vitelline.
intestinal nematode.
Microbiology
II. Unfertilized eggs: Pathogencity (10)

- Shape: Narrower, longer and more elliptical - The disease caused by it called ascariasis
than fertilized egg.
- Most of infection (85%) are asymptomatic,
- Size: 80 - 90 µ × 45-55µ
however mild infection is clinically manifested
- Color: Brownish - Bile stained.
by intestinal disorder, malnutrition etc.
- Egg-shell: Thinner, with irregular outer
albuminous coat. - Symptom is caused by both migrating larvae
- Ovum: Small, highly refractile granules of and adult worms.
various sizes. A. Symptoms due to larvae
- It does not float in saturated solution of I. Ascaris pneumonia (Loeffler's syndrome)
common salt
• It occurs in heavy infection, which is
Life cycle (10)
characterized by fever, non-productive
- Definitive host: Human beings
cough and dyspnoea.
- Intermediate host: Not required
• The pulmonary infiltration with eosinophilia
Fertilized eggs with unsegmented ovum passed in
(eosinophils count > 20/cumm is called
faeces develop in soil, unsegmented ovum develops
Loeffler's syndrome)
into rhabditiform larva (ripe egg)
st
↓(1 moulting in soil) II. Hypersensitive reaction
Infection occurs by ingestion of food, drink or raw • Urticaria, asthma
vegetables contaminated with eggs containing
B. Symptoms due to adult worms
rhabditifom larva.
↓ - Incubation period is 60-75 days.
V Eggs are subjected to the action of digestive juice in - Infection may be asymptomatic.
the duodenum and the motile rhabditiform larvae are
- The adult worms produce pathogenic effect in
released in the upper part of the small intestine.
following ways.
↓
Rhabdiform larvae penetrate the intestinal mucosa,enter i. Nausea & vomiting
the portal circulation and reach the liver. ii. Spoliative action: Absorbs nutrition by
↓ robbing the host causing malnutrition.
After a period of 3 or 4 days in liver, the larvae enter iii. Toxication: Body fluid of Ascaris when
the systemic circulation and reach the lung via right absorbed in blood causes toxic effect and
heart.
gives rise to typhoid like fever and
↓(II & III moulting in lungs)
nd rd
hypersensitivity reaction such as fever,

From alveoli they ascend the bronchi and trachea urticaria, edema of face.
larynx and pharynx and are swallowed with saliva
iv. Mechanical effect:
↓
Finally, they reach the upper part of small intestine • Causes obstruction and perforation of
th
(IV moulting) where they grow into adult worm in 6-10 intestine
weeks and after mating, the females lay fertilized • Occasionally, obstruction of bile duct
eggs which pass out in faeces and pancreatic duct.
↓ v. Ectopic ascariasis: Can cause liver abscess
The cycle is repeated and appendicitis.
GIT
Laboratory diagnosis (08, 10) Male worm:

A. Direct evidences - Size: Smaller, 8-11 yr and 0.45mm
I. Demonstration of adult worm - Posterior end: Its posterior end has umbrella
like copulatory bursa with two copulatory
a. Adult worm can be seen when adult worm
spicules.
is spontaneously passed in stool.
- The bursa has 3 lobes: 1 dorsal and 2 lateral.
b. Administration of an anti-helminthic may
result in expulsion of worm and defecation. - These lobes are supported by 13 chitinous rays:
dorsal lobe with 3 and lateral lobes with 5 each.
II. Detection of egg
Female worm:
a. Direct wet mount: By direct saline preparation
- Size: Larger, 10-13 × 0.6mm
b. Concentration technique: Is applicable
- Posterior end: Its posterior end is tapering and
when parasitic infestation is light.
no expanded bursa is present like male worm.
c. Duodenal aspirate: Show egg
- The vulva opens ventrally at the Junction of
III. Demonstration of larva in sputum: posterior and middle third of body. It is oviparous
Can be observed in Loeffler's syndrome along with mature female can lay 10,000 - 25,000 eggs.
eosinophils and Charcot Leyden crystals Egg: (13)
B. Indirect evidences - Shape: oval or elliptical
i. Blood examination: ↑ed eosinophils count in - Size: 60µ × 40µ
early phase of infection. - Colour: Colorless, non bile stained
ii. Skin test - Egg shell: Transparent hyaline
- Content: Segmented ovum generally with 4 V
ii. Serological test
blastomeres
• Used for Ascaris pneumonia
- Floats in saturated solution of common salt
• ELISA, IHA & micro precipitation
Ancylostoma duodenale (Hook worm) (07)
Morphology
Adult worm:
Egg shell
- Shape: Small, grayish white and cylindrical
- Anterior end: Bent dorsally, hence the name
hookworm.
Blastomere
- Freshly passed worm: Is reddish brown
because of ingested blood in its intestine
- Mouth: Has 6 teeth, 4 hook like on the ventral
surface and 2 knob-like on dorsal surface.
Esophageal gland secretes an anticoagulant
ferment.
- Life span: 6-8 yr
Life cycle (10)
i. Definitive host: Human beings
Microbiology
ii. Intermediate host: Not required. B. Symptoms due to adult worms

rd
Infective stage: Filariform larva (3 state) i. Gastrointestinal symptoms:
Egg with segmented ova containing 4 blastomeres • In early phase of infection
which are passed in stool • Includes: abdominal pain, body diarrhea.
↓ ii. Chronic infection: Iron deficiency anemia,
They develop in soil to form 1st stage rhabditiform
pallor, nutritional defects.
larva
↓ 1 moulting
st
Causes of anemia
2nd stage Rhabditiform larva
Sucking of Secretion of ↑ed worm burden
↓ 2 moulting
nd
blood by anticoagulation ↓
Filariform larva (infective form)
worm at containing Deplete iron store
↓ multiple site secretary and folic acid
Infection occurs by penetration of filariform larva in gut mucusa material ↓
via the skin. Filariform larva on reaching causing ↓ Interference with
subcutaneous tissue, enter into lymphatics of bleeding Leads to iron absorption
small venules continuous from intestinal villi
↓ Via right heart bleeding from
Enter venous circulation punctured site
↓
Reach pulmonary capillaries and enter the Anemia
alveolar spaces
↓ Note:
Migrate to bronchi, trachea, larynx and pharynx - A single adult of worm of A. duodenal sucks 0.2ml
epiglottis and are swallowed in oesophagus
of blood/day
V (IIIrd moulting)
- N. americanus sucks 0.03 ml blood/day
↓
Finally they reach small intestine where they grow Laboratory diagnosis (10)
into adult worms, after IVth moulting in 3 or 4 1. Direct evidence
weeks, They sexually mature and after mating,
Examination of stool
the females lay eggs and pass in faeces
↓ a. Macroscopic examination
The cycle is repeated • Adult worm demonstration
Pathogenecity (10) b. Microscopic examination
- Disease: Ancylostomiasis (hookworm disease) • To demonstrate characteristic hookworm
- The symptoms are produced by both larvae egg.
and adult worms. • Concentration method: For light infestation
- Portal of entry: Skin penetration • <5ggs/mg of faeces → indicates light
A. Symptoms due to larvae infection.
i. Ground itch or dermatitis • >20egg/mg of faeces → indicates heavy
• Characterized by pruritic maculopapular infection.
dermatitis c. Study of duodenal contents material obtained
ii. Creeping eruption by duodenal intubation (Ryle's tube) may
• Characterized by reddish itch papule along sometimes reveal either egg or adult worm.
the path. 2. Indirect evidences
iii. Bronchitis or bronchopneumonia a. Blood examination: Shows eosinophila, anemia
GIT
b. General examination of stool: Necator Americanus

• Occult blood loss → indicates positive ♦ N. americanus is similar to A. duodenal in many aspects
• Charcot-Leyden crystals → often present with some morphological differences as follow.
Features (Adult worm) A. duodenale N. americanus
1. Size - Adult worm large and thicker - Adult worms smaller and more
slender
2. Anterior end - Bend in the same direction - Bend in opposite direction to the
body curvature
3. Buccal capsule - 6 teeth - 4 hook like teeth on ventral surface - 4 chitinous plates - 2 on ventral
& 2 knob - like teeth on dorsal surface. surface and 2 on dorsal surface
4. Copulatory Bursa - Dorsal ray is single fold number of rays - 13 - Dorsal ray is split from base. Total
two spicules, separate no. of rays - 14. Two spicules,
fused at the tip.
5. Posterior end of female - A spine is present - No spine
6. Vulval opening - Behind the middle of body - In front of middle of body.
7. Shape of buccal capsule - Elongated, pear - shaped - Almost spherical
rd
8. 3 stage larva - Longer - Shorter
9. Pulmonary reaction - More common - Less common
10. Peripheral eosinophilia - More pronounced - Less pronounced
♦ Life cycle, morphology, pathogencity and diagnosis - The posterior end is pointed
of N. americanus are similar to A. duodenale. - It is ovo-viviparous V
♦ But N. americanus is comparatively less pathogenic Eggs:
than A. duodenale. - Shape: oval
Strongyloides stercoralis - Size: 55µ × 30µ
♦ Smallest pathogenic nematode - Egg shell: Thin and transparent
♦ Habitat: Upper part of small intestine - Contain a larva ready to hatch
Morphology - Egg: Laid in the tissue and immediately
Adult worm: rhabditiform larva hatches out, and makes its
- Only female worms are demonstrated in way from the mucous membrane into the
human as male worms are unable to lumen from where it is passed in faeces.
penetrate intestinal wall and hence remain in Larvae:
the lumen of the bowel.
- These are of following two types
- Male are eliminated from the bowel by the
1. Rhabditiform larvae
time females start laying eggs.
Male worms: • Size: 200µ - 250µ in length and 16µ in
- Shorter and broader than females breadth
Female worms: • Motility: Actively motile
- 2.5mm long and 0.04 - 0.05mm brand • Mouth: Small mouth and a double bulb
- It has a small buccal cavity surrounded by 4 lips oesophagus
and 2 uteri with 5-10 eggs in each.
Microbiology
2. Filariform larvae: Infective stage Clinical manifestation

• Size: Larger and more slender than 1. Cutaneous lesions
rhabditiform larvae • Uritcarial rash
• Mouth: Short mouth, cylindrical • Erythematous urticarial wheal reaction
esophagus around the anus
Life cycle: • Larva currens
- Definitive host: Human beings. 2. Pulmonary lesions
- Intermediate host: Not required • Hemorrhages in the lungs by migrating
- Infecting stage: Filariform larvae larvae
- Portal of entry: Skin penetration • Bronchopneumonia
3. Intestinal lesion:
Entry occurs by penetration of filariform larvae in
contaminated soil through skin or mucous membrane • Intractable bloody diarrhoea with mucus
and mild epigastria pain
↓
4. Eosinophilia and moderate leucocytosis
Filariform larva reach the lungs through the blood
stream via heart and break into alveoli In Immuno-Compromised host → cause
I. Hyper infection syndrome: Represents an
↓
acceleration of normal life cycle of S.
From alveoli, they migrate to the bronchi trachea,
stercoralis leading to excessive worm burden
larynx and epiglottis, and are swallowed
without spread of larvae outside the usual
↓ migration pattern (GI tract, lungs)
Finally they reach the small intestine where they II. Disseminated strongyloidiasis: Involve wide
grow into adult worms spread of dissemination of larvae to CNS,
V
↓ heart, urinary tract which are outside the
The female lays eggs either by parthenogenesis realm of the parasite's ordinary life cycle.
(laying eggs without fertilization) or after fertilization Auto infection:
with male - It occurs when non infective rhabdiform larvae
↓ prematurely transform into infective filariform
larvae.
Egg hatch out immediately to form rhabditiform
I. Endoauto infection
larvae in intestinal mucosa and migrate into the
lumen of intestine • The larvae penetrate the mucosa of the
colon and the upper small intestine and
↓
causes endoauto infection.
The rhabtidiform larvae either pass with the faeces to II. Exo-auto infection: The larvae penetrate
soil where they develop into infective filariform the perianal skin and cause exoauto
larvae or develop into filariform larvae in the lumen infection.
and cause autoinfection (hyperinfection) in same Laboratory diagnosis:
host by penetrating mucosa or perianal skin
1. Direct evidence
Pathogenecity: a. Direct wet mount of stool: Reveals
- Disease: Strongyloidiasis rhabditiform larvae
- Most cases are asymptomatic or mild • Presence of egg: Strong evidence of
cutaneous or abdominal symptoms infection.

GIT
b. Concentration method: In case flight infection Egg:

by formol - ether method - Shape: Spherical and brown colour (bile
c. Duodenal aspiration: stained)
• Larvae can be detected in duodenal - Size: 33-43 µm
aspirates or in sputum in heavy infection. - Covering: Thin outer transparent membrane
2. Culture: Not routinely done - Thick brown radially striated wall
3. Indirect evidence (embryophore surround the embryo)
a. Serology: - Within the egg there is a embryo with 3 pairs
of hooklets, the oncoshpere.
• Ab detection: By ELISA, Immunoblotting
Life cycle:
b. Blood examination:
i. Definitive host: Man → harbours the adult
• Peripheral blood eosinophilia
worm.
Taenia saginata ii. Intermediate host: Cattle (Cow/buffalos) →
♦ Common name: Beef tapeworm/unarmed tape worm. harbours larval stage.
♦ Habitat: Small intestine (Jejunum) Acquisition of infection by eating inadequately cooked
Morphology beef containing larval stage cysticercus bovis
Adult worm: ↓
- Length: 5 - 10 m Evagination of scolex and develops into adult worm in
small intestine and attain sexual maturity, fertilization
- Color: Whitish in color and semitransparent.
occur in segment and egg develop
- Largest helminth infecting man
↓
- It is divided into (i) Head (ii) Neck (iii) strobilla
Eggs are passed in feces after rupture of gravid
Head: segment
- Pear shaped, quadrate in cross section
V
↓
- Bear 4 circular sucker, no rostellum or hooks, Cow/buffalo ingest while grazing (human may be
so called unarmed tapeworm. infected by ingestion of vegetable or by water
Neck: contamination.
- Fairly long, fragile and narrower ↓
- Strobila: Strobila consists of 1000-2000 Reach systemic circulation by penetrating the gut
segments. The mature segments are 3-4 times wall and filtered in muscle tissues
longer as they are broad. ↓
- A mature segment contains male and female In muscle, the embryos develops into infective
reproductive organs. cystic larvae called cysticercus bovis
↓
- Testes are numerous
The cycle is repeated when human consume beef
- The gravid uterus consists of central
containing cysticerci bovis larva
longitudinal stem with 15-30 lateral branches
Cysticerus bovis
on each side of lobes.
- Is larval form (bladder form) of T. saginata
- Ovary → two - Develops in muscle of cow/buffalo
- Genital pore → situated marginally at the hind - It consist of 0.5-1cm diameter cyst containing a
end of each segment, alternating irregularly single invaginated scolex.
between right and left margin. - Is infective to man
- Gravid segment has vaginal sphincter. - Life span: 8 month (approximately)

Microbiology
Pathogenecity: • Gravid uterus: Consist of longitudinal

- Mode of infection: By ingestion of stem with 5-10 compound lateral
undercooked beef. branches on each side.
- Disease produced is called: Intestinal taeniasis • Ovary: Two with an accessory lobe.
(tape worm infection) which is characterized by: • Vaginal sphineter: Absent
abdominal discomfort, chronic indigestion, anemia, • Common genital opening: Mid-lateral
crawling segments rupture around perianal area. • Testes: 150-200
Laboratory diagnosis: Egg: Similar to T. sagniata (see T.sagniata)
A. Direct evidence Larva:
I. Examination of stool: to demonstrate gravid Cysticercus cellulosae:
segment and egg. - Measurement: 8 - 10mm and 5mm
II. Microscopy - The long axis of the cyst lies parallel with
a. Stool microscopy muscle fibre.
• Egg with characteristic thin shell and 6 - There is a dense milk-white spot at the side,
hooked on oncosphere are diagnostic. where scolex with its hooks and suckers
b. Segment microscopy remains invaginated.
• Applicable for the differentiate T. - The cyst contain a fluid rich in salt and
Saginata from T. solium albuminous material.
• Micro-examination of gravid segment - Life span: 8 months
pressed between two slide show 15-20 Life cycle:
lateral branch of uterus - Definitive host: Man
B. Serology - Inter mediate host: Pig, Occasionally man
- Used for detection of T. saginata coproantigen.
Note: Life cycle is similar to T. saginata except
- Serodiagnosis by IHA, ELISA intermediate host is pig and larval stage is cysticercus
V C. Diagnosis in animal cellulosae. See life cycle T saginata
- ELISA & CIEP using oncosphere as antigen have
been used with some success Pathogencity:
Mode of infection (MOI) (i) ingestion of uncooked
Taenia solium (05) pork (ii) Autoinfection
♦ Common name: Pork tapeworm or Armed tapeworm. Disease:
♦ Habitat: Small intestine (upper jejunum) - Taeniasis, cysticercosis, neurocysticercosis
Morphology: - Intestinal taeniasis
Adult worm: - Usually asymptomatic
- Length: 2-3 meter - Occasionally there may be abdominal pain with
- Life span: 25 yrs intestinal disturbances, anorexia, chronic
- Divided into (i) Scolex (ii) Neck (iii) Body indigestion, diarrohea, eosinophilia.
i. Scolex: Cysticercosis
• Measures 1mm diameter (pin head size) - It is fatal systemic condition
• Globular possess a rostellum with double - Caused by the cysticerci cellulosae living in
rows of hooklets and 4 circular suckers. human tissues.
ii. Neck: - The manifestations vary with number of
• Short, 5.1cmlong cysticerci and tissues and organs involved.
iii. Body/strobila: - Cysticercois is divided into
i. Subcutaneous type:
• Number: 800-900
• Usually found in head, limbs, neck abdomen.
• Measurement: 12mm × 6mm twice as
long as wide • Movable and painless

GIT
ii. Ocular type: B. Human cysticercosis

• Usually found in vitrous body or subretina a. Biopsy of subcutaneous nodules → show
• Visual disturbance often occur presence of suckers and hooklets on scolex.
• Dead worm may provokes local
b. Radiology: Calcified intramuscular cyst can be
inflammation causing blindness.
detected.
iii. Brain type (Neuro cysticerosis)
• Symptoms are: related to site of infection. c. Find needle aspiration cytology (FNAC)
• Manifested by headache, nausea, • Useful and cost effective since it eliminates
vomiting, epilepsy, mental disorder. the biopsy
• Epilepsy is most frequent symptom. d. Blood picture: Eosinophilia
Laboratory diagnosis: e. Serology: IHA,CFT, ELISA
A. Intestinal taeniasis
- Diagnosis is made by f. CT scans or MRI: Indicates presence of
a. Identification of gravid segmented in faeces cysticerci in brain
b. Detection of eggs in faeces.
Difference between T. sagniata & T. solium (06)
Feature T. Saginata T. Solium
1. Common name Beef tape worm/ unarmed tapeworm Pork tape-worm or armed tapeworm
2. Habitat Small intestine (jejunum) Small intestine (upper jejunum)
Morphology
1. Adult worm Tape like, 5-10m in length white, semi transparent Tape like, 2-3 meter in length white,
semi-transparent
2. Scoloex Quadrate with four sucker (pigmented) Globular pin head size with four
sucker. V
3. Head Head without rostellum and hooklets Head provided with rostellum armed
with double row of alternating large
and small hooklets
4. Neck Long, thin & fragile Short & thick, 5-6 mm long
Proglottides
1. Number 1000-2000 800-900
2. Size 20 × 5 mm 12 × 6 mm
3. Expelled Singly In chains of 5 or 6
4. Uterus Longitudinal stem with 15-30 lateral branches on Central longitudinal stem with 5-10
each side compound lateral branches on each side
5. Common genital Posteriorly, on lateral margin of each segment Mid lateral
opening
6. Testes 300-400 150-200
7. Life span 10 year 25 year
Larvae Cysticercus bovis Cysticercus cellulosae
Size 5-10 mm × 3.4mm 8-10mm ×5mm
Location Found in muscle of cow, buffalo Found in muscle of pig

Microbiology
Diphylobothrium latum II. Procercoid larva

♦ It is the longest parasite in the intestine of human • Elongated
being • 500-600µm long
Adult worm • Has 3 pair of hooklets
- Yellowish gray with central marking III. Plerocercoid larva
- Size: 3-10m in length • Glistening white, unsegmented with
- If has head/scolex, neck and strobilla wrinkled surface
Scolex • 1-2cm long with rudimentary scolex
- Spoon shaped - possess false grooves called • Remain in bent or twisted form.
bothria one on ventral & another on dorsal surface. Life cycle:
- No rostellum and hooklets - Definitive host: Human beings or other fish
Neck eating animals.
- Thin, unsegmented and longer than head. - Intermediate host: Need two intermediate
Strobilla host
- Consist of 3000-4000 segment i. First: Cyclops or diatoms
- Mature segment measure 2-4mm in length and ii. Second: Fresh water fish (trout, salmon etc)
10-20mm in breadth and has 3 genital opening Infection occurs by ingestion of raw or inadequately
on mid ventral aspect and opening are formed cooked fish containing plerocercoid larvae
as vas deferens, vagina and uterus in the order ↓
from front, on middle ventral surface. Plerocercoid larvae develop into adult worms in the
- Mature segment consist of bilobed ovary intestine of human beings
centrally coiled uterus. ↓
V Adult worms liberate eggs in lumen, which pass out
- After discharge of eggs through uterine pore,
with faeces of definitive host onto the soil and
dried up segment breaks off and is passed in
further eggs gain entry into water
chains in host's faeces.
↓
Egg:
Eggs develops in water forming coracidium - ciliated
- Shape: Oval embryo with 6 hooks (1st stage larva), which escapes
- Size: 70-45 µm from the egg through opercular end.
- Colour: Brown (bile stained) ↓
Coracidum is ingested by Cyclops and develops into
- Ovum: Unsegmented and surrounded by yolk
procercoid larva (2nd stage larva)
granules.
↓
- Operculated at one and have one knob at Infected Cyclops in swallowed by fish and
opposite side. plerocercoid (3rd stage larva) develops
- It doesn't float in saturated salt solutions. ↓
- Freshly passed eggs are not infective Human beings ingest plerocercoid larva in fish and
Larvae: cycle is repeated
I. Coracidium Pathogenecity:
• Spherical ciliated embryo - Disease produced by it is called Diphyllobothriasis
• 40-55 µm is diameter - Mode of infection: By ingestion of improperly
cooked infected fish or fish containing
• Has 3 pair of hooklets.
plerocercoid larvae.

GIT
- It causes: Eggs:
i. Gastrointestinal disturbances - Shape: Planoconvex →flattened on ventral
• Abdominal discomfort side and convex on dorsal side.
• Nausea, vomiting, diarrhea - Size: 50-60µ× 30µ

- Color: Colorless → non bile stained
• Loss of appetite and wt. loss
- Egg shell: Transparent
• Abdominal pain due to intestinal
- Ovum: Fully developed, a coiled tadpole like
blockage by worm
larva.
ii. Anemia by absorbing Vit. B12:
- Floats in saturated solution of common salt.
Bothriocephalus anaemia.
- Infective to man.
iii. Eosinophilia in early phase.
Life cycle:
Laboratory diagnosis
i. Macroscopic examination
- Intermediate host: Not required
a. Stool: for segments of adult worms
ii. Microscopic examination Egg with a tadpole like larva laid on perianal skin
iii. Serology: ELISA, latex agglutination completes its development in 24-36 hrs and becomes
mature
Enerobius vermicularis
↓
♦ Common: Pinworm, threadworm
Infection occur by ingestion of mature eggs
♦ Habitat: Caecum, vermiform appendix and
↓
adjacent parts of ascending colon.
Egg hatch in intestine to release the larvae
Morphology:
↓ V
Adult worm
The larvae develop into mature worms
- Shape: Small, white spindle - shaped, resemble
a piece of white thread. The male worm fertilizes the female worms & dies
- There are wing like expansions at the anterior ↓
end called cervical alae. The gravid female migrates out of the anus during
- No buccal cavity night and lays up to 10,000 on perianal skin
Male worm: ↓
- Measurement: 2 - 4 × 0.1× 0.2 mm The cycle, repeated
- The posterior end is curved and has a coiled tail Pathogenicity:
with a single spicule. - Mode of infection: Person to person by
- It dies after fertilization of the female. ingestion of eggs.
Female worm: - Disease caused by it: Enterobiasis
- Measurement: 8-13 × 0.3×0.5mm - It is common in children
- The posterior third of the body is pointed like a - Familial infection is common.
pin. So, called pin worm. - The egg deposited on perianal skin,
- Oviparous: mature female lays eggs and after contaminated night clothes and bed linens of
oviposition dies in 2 or 3 weeks. infected persons.

Microbiology
- Infection can be transmitted due to ♦ Habitat:

contamination of hands by handling night • In large intestine → in caecum and also in
clothes and bed linens. vermiform appendix.
- Autoinfection (Re-infection) is also possible in
Morphology
following way.
Adult worm:
i. By hand to mouth
- Shape: Pinkish white resembles a whip
ii. Retrograde infection:
- The anterior 3/4th is thin, hair like and coiled.
• The egg laid on perianal skin hatch out
- The posterior 2/5th is thick and stout →
into larvae, which migrate back through
the anus upto caecum and develop into resemble handle of whip.
adult worms. - The anterior portion contain a long capillary
Clinical features oesophagus
- Perianal pruritus and an eczematous condition - The posterior part contains the intestine and
around the anus and perineum reproductive organs.
- Nocturnal enuresis - It lives in intestine for many years.
- Inflammation of the vermiform appendix may Male worm:

also occur. - Length: 3-4 cm long
- Vulvovaginitis - The posterior end is coiled and has a single
- Salpingitis spicule.
- Pelvic or perineal granulosus rarely occurs. Female worm:

- Length: 4-5 cm long
V Laboratory diagnosis (04)
i. Enterobiasis should be suspected in children and - The posterior end is blunt and rounded.
adult who show perianal itching relieved only by - It is oviparous: Fertilized female lays eggs
vigorous scratching. 5,000 egg every day.
ii. Demonstration of adult worm Eggs:
- On the surface of stool sample - Shape:
- On the perianal skin • Barrel - shaped with projecting mucous
iii. Demonstration of eggs plug at both poles.
- As they are seldom excreted in faeces, stool - Size: 50µ × 25µ

sample is not useful for diagnosis. - Color: Brown → Bile stained
- So, diagnosis is made by collecting egg in - Egg shell: Double shell
morning sample collected from perianal skin by - Content:
adhesive pad cellophane tape/NIH (National • Unsegmented ovum which is not infective.
institute of Health, USA)
- It floats in saturated solution of common salt.
- Scotch tape swab
Life cycle
- Dirt from finger nails.
Trichuris trichura - Intermediate host: Not required
♦ Common name: Whipworm
GIT
Egg released in faeces, complete development occurs Laboratory diagnosis

slowly in water or damp earth I. Heavy infection
↓ Examination of stool: By saline preparation
Rhabditiform larvae develop in 3-4 weeks - Indicates characteristics Barrel - shaped, bile
↓ stained egg
Infection occurs by ingestion of embryonated egg - Adults may occasionally present.
with food or water II. In light infection
↓ - Concentration technique
Egg hatch in intestine to release the larvae, which - Routine wet mount of stool → for detection of
migrate to the caecum and appendix eggs.
↓ Eggs [06]
The larvae develop into adult worm. 1. Bile stained eggs
↓ i. Egg of A. lumbricoides
The anterior portion of adult worm lies embedded in ii. Egg of Trichuris trichuria
the mucous membrane and posterior end project in
iii. Egg of taenia species
the lumen
iv. Egg of Echinococcus granulosus
↓
2. Non bile stained egg
The mature sexually & fertilized female, lays eggs
which passes in faeces i. H. nana
ii. A. duodenale
↓
The cycle is repeated FOOD POISONING V
Pathogenecity: Definition:
- The diseased caused by it → Trichuriasis - Acute illness usually of sudden onset, brought
about by eating contaminated food poisonous
- Usually, worms donot produce any pathogenic
food like
effect.
• Bacteria or their toxins
- Light infection are asymptomatic
• Chemicals including metals
- Heavy infection
• Plants, fish, viruses, mycotoxins
Characterized by - It causes different clinical manifestations such as :
• Abdominal pain • Nausea and vomiting
• Bloody or mucoid diarrhoea • Abdominal cramps
• Wt. loss • Diarrhoea
- It may lead to: • Fever
• Anemia Note:
• Malnutrition - Food poisoning due to clostridium botulinum
• Growth retardation. causes constipation.
- Rarely, prolapsed of rectum in massive - Food poisoning associated with undercooked or
infection and appendicitis occur. raw seafood is due to vibrio parahaemolyticus.

Microbiology
Bacterial Food Poisoning

Incubation
Bacteria Source Mechanism of action Sign and symptoms
period
- Meat Heat stable enterotoxin - Vomiting, abdominal cramps,
1. Staphylo-
- Daily product 1-6 hours ingestion preformed in diarrhoea
cocus aureus
- Poultry food → GI symptoms - Last for 6 - 24 hours
Adsorb to epithelial cell
2. Salmonella - Raw meat - Chills fever, headache,
in small intestine → PMN
typhimurium, - Poultry of eggs 12-24 abdominal pain and profuse
and PG response → in
S. Cholerasuis - Raw unwashed hours watery diarrhoea
cAMP → watery
S. Enteritidis vegetable - Last for 2 - 5 days
diarrhea
- Reheated fried 2 different types of - Nausea, vomiting, abdominal
rice preformed enterotoxin cramps
3. Bacillus cereus 1-6 hours
- Meat, seafood, → one emetic form, - Last for less than 24 hours of
salad, potatoes other diarrhoeal form onset.
- Dysphagia, diplopia drooping
- Home canned eyelids
meat, vegetables
Preformed toxin → - Constipation
and fish
4. Clostridium 12-36 inhibit release of - Muscle weakness
- Pickle & home
botulinum hours acetylcholine in NM - Frequently fatal (1mg = 200
made cheese
junction million death) within 4-8 days
preserved at low
pH due to respiratory or cardiac
V failure.
Spores survive cooking
- Beef poultry, meat - Diarrhoea and abdominal
5. Clostridium → germinate → multiply
products 6-24 hours cramps
perfrigens rapidly between 30-50°C
- Reheated food - Nausea and vomiting rare
→ produce toxins
- Meat - Invasion →
- Diarrhoea, abdominal pain,
6. Campylo- - Poultry epithelium of small
2 - 11 days malaise: fever
bacter jejuni - Unpasteurized intestine
- Last for 2 - 7 days
milk - Heat stable toxin
- Meat, milk and - Abdominal cramps

Cytotoxin absorbed from
vegetables - Diarrhoea with blood
7. E-coli (EHEC) 3 - 8 days gut → damage vascular
contaminated by - Hemolytic uremic syndrome
endothelial cells
faeces - Can lead to death
- Milk
- Water Terminal ileum →- Fever
8. Yersinia contaminated enlargement of - Diarrhoea (frequently with
2-7 days
enterocolitis with wild, mesenteric lymph nodes blood and WBC)
domestic animals → necrosis - Abdominal pain
faeces.

GIT
Mycotic Poisoning • Amanita Virosa

♦ Poisoning due to the intake of fungus containing • Amanita versa
toxins. - Major toxins in mushroom are:
Mycotoxins: 1. Alpha amanitin
- Toxins formed by the hyphae of many fungi • Deadly
growing in contaminated foods and other
• Causes liver damage within 1 - 3 days of
substrate.
ingestion
- It causes mycotoxicosis which results from
• Principle toxin in Amanita
ingestion of food contaminated with
mycotoxins (fungal toxins). 2. Phallotoxin
Mycetismus: • Also found in Amanita
- Ingestion of toxins along with fungus • Causes GI upset
- Examples: 3. Muscarine
• Claviceps species – ergot poisoning • Sometimes deadly
• Coprine species – coprine poisoning • Acts as muscarine receptor against and
• Inocybe species – muscarine poisoning brings about different mucarinic symptoms
- Amanita species of mushroom most common • Death may occur due to respiratory failure
in poisoning are: 4. Ibotenic acid: Causes neurotoxicity
• Amanita phalloides (major)

Microbiology
Bacteriology:
Normal flora of GTI
1. The empty stomach is sterile due to gastric acid
2. But stomach may have scanty organism soon after eating.
3. In gastric carcinoma and pyloric stenosis, Gram positive cocci and bacilli proliferate in stomach
due to stagnation of food–stuff.
4. Normal flora increase progressively beyond duodenum to colon.
Part of intestine Bacterial count
i. Duodenum 103-106 per gram of content
ii. Jejunum and proximal ileum 105-108 per gram of content
iii. Lower ileum and caecum 108-1010 per gram of content
iv. Colon and rectum 1011-1013 per gram of content
5. The normal for a of adult colon contain 96-99% of anaerobes and only 1-4% aerobes. Bacteroides
(fragilis mainly) are predominant anaerobes followed by Bifidobacterium.
6. Anaerobic condition of colon is maintained by aerobes that utilize free oxygen. Enterococci are
predominant aerobes.
Clostridium difficle:
V 7. Causative agent of pseudomembranous enterocolitis (KU, 2013)
8. Is a normal gut commensal
9. Is Gram positive rod with oval and sub-terminal spore but has tendency to become Gram-
negative in old culture.
10. Noninvasive C. difficle produces 2 toxins
i. Enterotoxin (toxin-A) →produces symptoms
ii. Cytoxin (toxin-B → produces cytopathic effects.
11. Almost all antibiotics even the once used in treatment of pseudomembrane enterocolitis can cause
the disease.
12. Enterotoxin produced by C. difficle causes antibiotic associated pseudomembrane enterocolitis.
13. persons above 50 years of age are most susceptible to C. difficile infection.
14. C-difficle toxin is neutralized by C. Sordelli antitoxin.
15. Metronidazole is DOC
16. Vancomycin is also used
17. In severe cases, IV metronidazole is recommended
18. Cytotoxin say in stool is the best test.
Salmonella:
19. Are gram negative, motile bacilli
20. Have peritrichate flagella.

GIT
21. Need tryptophan as growth factor.

22. Selenite F is used as growth medium.
23. Affect payer’s patches in intestine.
24. H antigen is the most immunogenic.
25. Vi agglutination detects carrier.
26. Vi antigen is not seen in normal population
27. Blood culture is the gold standard for diagonosis
28. Diazo-reaction is also used of diagnosis
29. Causes 3 types of clinical syndrome human:
i. Enteric fever, ii. Septicaemia, iii. Gastroenteritis
Salmonella Species Diseases produces
S. typhi Typhoid fever
S. paratyphi A,B &C Paratyphoid fever
S. cholerae suis, S. paratyphic Septicaemia
S. typhimurium Food poisoning (Gastroenteritis)

30. Wilson and Blair bismuth sulphide medium is selective medium for salmonellae.
31. Jet black colonies with metallic sheen are formed due to formation of H2s.
32. S. typhi is anaerogienic, produces only acid and no gas.
33. Kauftmann – White scheme:- is diagnostic scheme based on ‘O’ & ‘H’ antigen identification by
agglutination test.
34. Enteric fever (Typhoid fever) is characterized by step-ladder pyrexia, relative bradycardia and rose spots. V
35. Rose spots is red macules , appear on chest and abdomen in 2nd and 3rd week.
36. Blood culture is very important specimen in first week of enteric fever.
37. In third week, widal test is best.
38. In fourth week, widal test(mainly) and stool and urine culture yields best result.
39. Stool culture is mainly done for detecting the carries.
Widal test: It is test of blood serum based on agglutination reaction to diagnose typhoid fever.
40. Presumptive serological test for enteric fever.
41. It is demonstration of agglutinating antibodies against antigen(in salmonella infection)
42. For brucellosis, only ‘O’ somatic Ag. Is used.
43. The antigen used in test the ‘H’ and ‘O’ antigen of S. typhi and H antigen of S. paratyphi.
44. The paratyphoid are not employed as they cross react with S. typhi ‘O’ due to variant of factor 12.
45. A single test of O titer of 1:100 or more and H titer of 1:200 or more is significant .
46. A rising titer of 4 fold or higher of 7-10 days is more meaningful than one test.
47. TAB vaccine →used for prophylaxis.
i. Is heat killed whole cell vaccine,
ii. Contain S. typhi 1000million + S. paratyphi A and B 750million/ml.
48. Live oral (Ty21a) is another typhoid vaccine.

Microbiology
Vibrio-Cholera:
49. 1st isolated by Robert Koch.
50. Most cases are subclinical.
51. Gram-negative nonsporing, non capsulated curved or comma shaped bacilli.
52. Very actively motile with a single polar flagellum.
53. The movement is of darting type Darting Motility.
54. Slective Medium for V. Cholera.
i. TCBS (Thiosulphate .Citrate Bile Sucrose agar)
ii. BSA(Alkaline Bile Salt agar)
55. Transport Medium.
i. Venkataraman-Ramakrishan (V.R) medium
ii. Cary –Blair medium.
56. Toxin action is CAMP mediated
57. Humans are the reservoir
58. Survive boiling for 30 seconds and cold temperature (ice for 4-6 weeks)
59. Causes Rice water stools/Pea soup diarrhea.
60. Non halophilic.
61. V. cholera has 2 biotype→classical and EI. tor.
62. V. cholera has 3 serotypes (1) Ogawa(AB) Inaba (AC) and Hikojima (ABC) on the basis of minor ‘O’
antigens.
63. Non-01 V. cholera is K/A →Non –agglutinating vibrios (NAG)
V Escherichia Coli:
64. E. coli, kleb. , serratia,citrobacter porteus,morganella belong to Enterobacteriaciea.
65. E. coli, klebsiella, Enterobacter are Lactose fermenter.
66. Salmonella, shigella, proteus, pseudomonas→Non lactose fermenter.
67. Gram negative, non-sporing , non-capsulated.
68. Is divided into six pathotypes,of intestinal pathogens. which are:
i. Enterotoxigenic E. coli (ETEC) →commonest causes for Traveller’s diarrhea.
ii. Enterohemorrhagic E. coli (EHEC) →Also called Shiga like toxin producing E. coli.
→ Shiga like toxin also called →Verotoxin.
iii. Enteropathogenic E. coli (EPEC) →Important cause of Infant diarrhea.
iv. Enteroinvasive E. coli (EIEC)
→ Shares may feature with shigella infection
→ Unlike shigella. EIEC causes disease only at high inoculums(108to 1010CFU
→ Penetrate Hela cells in tissue culture.
v. Enteroaggregative E. coli (EAEC)
vi. Primarily found in developing countries and mostly affect young children.
vii In vitro, the organism exhibit a diffuse or stacked –brick” adherence pattern.
69. Toxins produced by E. coli are
i. Enterotoxin, ii. Hemolysin, iii. Vero cytotoxin.
GIT
70. Nephrotoxigenics strain of E. coli are 09, 02, 04, 06, 07, 018, and 075.
71. Most strains of Eschaerichia are motile due to peritrichate flagella.
72. E. blattae→non motile
73. Enterotoxigenic E. coli (ETEC) produce one or both of two enterotoxins, a heat-labile toxin (LT)
and a heat-stable toxin(ST).
Shigella:
74. Gram-negative, aerobic, non-motile, non flagallete, non capsulated
75. Non Lactose fermenter.
76. S. sonnei is late lactose fermenter.
77. Ferment mannitol ,except S. dysentriae.
78. Most virulent type is S. dysenteriae.
79. Stool culture is best test.
80. Subdivided on the basis of Mannitol fermentation.
81. In shigella-Salmonella agar, the colonies of shigella are colourless.
82. Causes superficial snail. Tract of serpiginous ulcers.
Helicobacter Pylori:
83. Is a Gram-negative, spiral flagellate bacillus,
84. Non Invasive, lives Gastric mucus.
85. Its spiral shape, flagellae render H. pylori motile in the mucus environment.
86. Its efficient urease protects it against by catalyzing urea hydrolysis to produce buttering ammonia.
87. In vitro , H. pylori is microaerophilic and slow- growing and requires complex growth media.
88. Complete genomic sequence has been studied. V
89. Causes duodenal ulcer (stronger relation) and gastric ulcers.
90. Transmitted from man to man, feco-orally and orogastric route.
91. The test of choice for documenting eradication is the urea breath test (UBT).
92. Rapid urease test is most rapid and dependable test for defection of H. pylori.
93. Urea breath test:- Isotope of carbon(C14) is fed to patient.
94. Urine test :- Isotope of nitrogen-15 N15 is used as urea.
Campylobacter:
95. Are motile
96. Non-spore-forming
97. Curved gram-negative rods,
98. Microaerophilic
99. The principal pathogen is C. Jejuni
100. Skirrows medium is culture medium
101. Butzlers medium is culture medium
Food Poisoning:
102. Food kept at 50c-630c has active bacterial multiplication, so intake of such food is the danger.
103. E. coli 0157 causes food poisoning.
104. Aflatoxin is produced by Aspergillus flavus and parasiticus

Microbiology
105. Aflatoxin B1 is highly carcinogenic and widespread occurrence in foods.

106. Ochatoxins is produced by A. ochraceus, which is a nephrotoxin.
107. Fusarium species produces
i. Trichothecenes, ii. Zearalerone
108. Patulin is produced by penicillium, Aspergillus
109. Alternaria-tenuazonic acid→detected in commercial tomato paste.
110. Amanita phalloides→Major cause of mushroom poisoning
111. Major mushroom toxins are α−amanitin, phallotoxin, muscarine and ibotenic acid
112. Ibotenic acid causes neurotoxicity.
113. Food poisoning due to reheated rice is due to Bacillus cereus.
114. In food poisoning due to clostridium botulinum , constipition occurs not diarrhoea.
Parasitology:
Giardia Lambia
1. It is bilaterally symmetrical protozoan.
2. Trophozoite has 2 axostyl, 2 nuclei and 4 pairs of flagella.
3. Cyst has 4 nuclei which may remains of the flagella and the margins of sucking disc.
4. Acid environment causes the parasite to encyst.
5. Cyst is bile stained.
6. G. lambia doesnot causes invasion of tissue but causes intestinal disturbance leading to
malabsorption of fat i.e. steatorrhoea.
7. It does not cause bloody diarrhoea with mucus.
V 8. Trophozoite show slow oscillation motility along its long axis, which is comparable to falling leaf.
9. It divides by longitudinal binary fission.
10. Mode of transmission is few oral route.
11. In heavy infection, it causes disaccharidase deficiency leads to lactose intolerance that undergoes
resolution after treatment.
12. Giardia lambia attaches to small intestine mucosa with sucking disc.
Balantidium coli:
13. Definitive host - pig, man is accidental host
14. No intermediate host
15. Infection form: Binucleate cyst
16. Clinical disease is manifested when trophozoite eroide intestional mucosa unlike G. lambia
17. It causes mucosal ulcer and submucosal abscess.
Entamoeba histolytica:
18. Infection stage: Mature cyst (Quadrinueleate) or cyst.
19. About 90% of infection are asymptomatic, but remaining 10% produce a spectrum of clinical
syndromes ranging from dysentery to abscesses of liver or other organs.
20. Both trophozoite and cyst are found in the intestinal lumen, but only one trophozoites of E.
hisotolytica invade tissue.
21. Cyst has glycogen mass, chromoidal bar, eccentric nucleus.

GIT
22. The most common type of amoebic infection is asymptomatic cyst passage.
23. Amoebic liver abscess is an extra intestinal infection by E. histolytica.
24. Pleuropulmonary involvement (20%-30% of patients), is the most frequent complication of
amoebic liver abscess.
25. Primary amoebic encephalitis is caused by → Nagleria flowerie
26. Fulminant amoebic meningoencephalitis is cause by Nagleria flowerie
27. Granulomatous amoebic enceptialitis is caused by → Balmuthia mandralliy.
28. VIrulence is related to secretion of potent cysteine proteinase.
29. Cystein proteinase produced by invasive strains of E. histolytica inactivates complement factor
(C3) and thus resistant to complement mediated lysis.
30. Cystein protein cleaves ECM, fibtonectin, laminin and Type - I collagen.
31. Best way to distinguish amoebic liver abscess from bacterial liver abscess in serological evidence of
E. histolytica.
32. E. Histlytica can be cultivated in
i. Boeck and Drhohalv's medium ii. Diamond's axenic medium
iii. Balamutub's medium
33. E. histolytica multiplies by Binary fission
34. Bundle of crystalline ribonucleic acid is called chromatoidal bodies.
35. Pathogenic E.histoloytica strains are best distinguished from non pathogenic strains by Isoenzyme
analysis.
36. Anchovy sauce 'pus' of amoebic liver abscess is mainly contributed by Degenerated nepatocytees.
37. Nagleria fowleri infection is usually transmitted by swimming.
38. Charcot - leyden crystals are derivative of Eosinophils.
V
39. Isospora belli is only protozoan which is consistently associated with eosinophilia.
40. Pentamidine isethionate is used to prevent pneumonia due to pneumocystis carini in AIDS patients.
Worms (Heminthology):
41. Common names of parasites:
Tape worm Worm/ Parasites Common names
- Diphyllobotherium → Fish tapeworm
- Taenia saginata → Beef tapeworm
- T. solium → Pork tapeworm
- H. nana → Dwarf tapeworm
- H. diminuta → Raw tapeworm
- E. granulosus → Dog tapeworm
- Clonorchis sinesis → Chinese liver fluke
- Fasciola hepatica → Sheep liver fluke
- Fasciola buski → Giant intestinal fluke
- Paragonimus westermanii → Lung fluke
- E. Granulosus → Hydatid cyst
- E. mutilocularis → Alveolar hydatid

Microbiology
42. Parasites causing autoinfection

i. T. solium ii. S. stercotralis
iii. H.nana iv. E. vermicularis
v. Cryptosppridium parvum vi. Capillaria philippinensis
43.
Parasites Infective form Transmission
A. Lumbricoides Embryonated egg Ingestion
E. vermicularis Embryonated egg Ingestion
S. stercoralis Filariform larva Penetration of skin
T. trichiuris Embryonated egg Ingestion
A. duodenale Filariform larva Penetration of skin
N. americana Filarifom larva Penetration of skin
44. Bile stained egg
i. Egg of A.lumblicoides ii. Egg of Trichuris trichura
iii. Egg of taenia species iv. Egg of Echinococcus granulosus
45. Non bile stained egg
i. H.nana ii. A.duodenale
Ascaris lumbricoides:
46. Because of its resemblance to earth wrom(Lumbricus teres), the name for common earthworms.
The parasite is called Ascaris lumbricoides.
V 47. The parasite maintain position by muscle tone and show spinal movement.
48. Female is larger than male.
49. Has two types of egg liberated (i) fertilized (ii) unfertilized egg both are bile stained.
50. Infective form: Embryonated egg.
51. The larva of A. lumbricoides undergoes 4 times moulting.
One → outside, two in lung, and last in (4th) in intestine.
52. Ascariasis in pregnancy should be treated in 1st trimester.
53. Egg becomes infective in 21 days after passing in stool.
A. Duodenale:
54. Female adult worm is larger than male worm.
55. Adult worm looks reddish brown due to ingested blood.
56. Eggs are laid in an unsegmented stage during their passage through the bowel. It become of 4
celled stage i.e.4 blastomere.
57. Egg is non bile stained.
58. No intermediate host is required.
59. It is also called old world hookworm.
60. Larva undergoes 4 moulting.
1st and 2nd moulting → in soil
3rd moulting → in oesophagus.
4th moulting in → small intestine

GIT
61. Mode of infection is: By penetration of skin.

62. Infective form → 3rd stage filariform larva.
63. Anemia is most chronic clinical manifestation manifested by it.
64. N. americanus is new world hookworm.
65. N. americanus is less pathogenic to A.duodenale.
66. For further information: Refer text
Strongyloides stercoralis:
67. Smallest nematode inhabits in upper part of small intestine.
68. Only female adult worm is demonstrated in human.
69. Female adult worm → ovo viviparous.
70. Has two larvae
i. Rhabditiform → Activiely motile, double bulb oesophagus.
ii. Filariform → Infective form has cylindrical oesophagus.
71. It causes internal autoinfection.
72. In immunocopromised patients, it causes hyper infection syndrome and disseminated
strongyloidosis.
T. Saginata:
73. Called beef tapeworm/ unarmed tapeworm.
74. Strobilla consist of 1000-2000 proglottids
75. Has two ovary
76. Testes: 300-400
77. Egg: bile stained V
78. Larvae: Cysticerus bovis → life span 8 month.
79. Mode of infection: Ingestion of under cooked beef.
80. Definitive host: Man
81. Intermediate: Cattle (Cow, buffalo)
T. Solium
82. Pork tape wrom /armed tapeworm
83. Strobilla: 800-900 proglottids
84. Testes: 150-200
85. No vaginal aphineter.
86. Same egg as that of T. saginata.
87. Larvae: Cysticercus cellulosae.
88. Definitive host: Man
Intermediate host: Pigs
89. Cuases subsutaneous cysticerosis
Ocular cysticercosis
Neuro cysticercosis
90. Causes Auto infection

Microbiology
D. Latum:
91. K/A → Fish tapeworm
92. Liver in small intestine
93. Longest intestinal parasite of man
94. Bile stained operculated egg (not infective to man)
95. Human → definitive host
96. Infective stage for man: plerocercoid larva from fish.
97. Inhibits dietary absorption of vitamin B12, So can cause megaloblastic anemia.
98. Length of parasite: 10 meter
Enterobius vermicularis:
99. Commonly called → pinworm, thread worm
100. Has not buccal cavity but has cervical alae.
101. Female oviparous
102. Male dies after fertilized the female.
103. Egg-non bile stained and contain a coil tadpole like larvae.
104. Causes autoinfection, retrograde infection
105. Diagnosed by cellophane tape
Trichuris trichuria:
106. Commonly called whipworm.
107. Adult worm → within resemble a whip
108. Eggs → Bile stained, barrel shaped with a projecting mucous plug at each pole.
V 109. Infection by ingestion of embryonated egg.
110. After ingestion of egg, it hatches in small intestine but there is no migratory phase.
Rota - virus
111. Rota virus is non cultiviable virus
112. Main cause of infantanile diarrhoea.
113. Causes destruction of mature enterocytes.
114. Double walled, wheel like appearance in electron microscope.
115. "SPLIT GENOME" is feature of rota virus.
Norwalk virus:
116. Causes epidemic viral gastroenteritis in adults.

GIT
Pathology
SYLLABUS
Oral Pathology- premalignant Lesions: (p. 119)
List, morphology
Squamous Cell Carcinoma: (p. 119)
Aetiopathology, morphology
Pleomorphic Adenoma: (p. 120)
Classification, gross and morphology of pleomorphic adenoma.
Barret's oesophagus (p. 121)
Carcinoma of the Oesophagus: (p. 122)
Aetiopathogenesis, gross and microscopic features.
Peptic Ulcer: (p. 122)
Definition and sites of occurrences, pathogenesis, gross and microscopic features and complications.
Carcinoma of the Stomach: (p. 125)
Benign and malignant; Classification; aetiopathogenesis, gross and microscopic features
Tuberculosis of Intestine: (p. 126)
Pathogenesis, gross and microscopic features, complications.
Typhoid of Intestine: (p. 127)
V
Appendicitis: (p. 127)
Amoebic Colitis: (p. 128)
Aetiology, gross and microscopic features, complications.
Necrotizing enterocolitis: (p. 129)
Pathogenesis and morphology
Ulcerative Colitis and Crohn's Diseases: (p. 129)
Aetiology, gross and microscopic features, complications.
Polyps of large Intestine: (p. 133)
Classification, comparison of morphology of tubular and villous adenomas
Carcinoma of the Colon: (p. 131)
Pathogenesis, gross and microscopic features.
Acute pancreatitis: (p. 134)
Aetiopathogenesis, morphology and complications.
Carcinoma of the pancreas: (p. 135)
Morphology and complications.

Pathology

GIT
PATHOLOGY
ORAL PATHOLOGY Histologically:

Premalignant lesions - Superficial erosions with dysplasia, carcinoma
insitu or already developed carcinoma in
1. Leukoplakia
surrounding margins
2. Erythroplakia
- Subepithelial inflammatory infiltration
3. Speckled leukoerythroplakia
- Vascular dilation
Leukoplakia: Speckled leukoerythroplakia:
- "A white patch or plaque that cannot be - Characteristics of Both leukoplakia and
scraped off and cannot be characterized erythroplakia
clinically or pathologically as any other disease"
Note:
Note: If a white lesion in oral cavity can be given a
- All leukoplakias must be considered precancerous
specific diagnosis, it is not leukoplakia. So, white
until it is proved otherwise via histological
patches caused by entities such as lichen planus and
evaluation.
candidiasis are not leukoplakias.
- Premalignant changes may be seen in adult at any
Morphology: age but usually between ages 40 and 70.
Site: - Male: female occurrence = 2:1
- Buccal mucosa - Etiology: Tobacco use.
- Floor of mouth Alcohol, spicy foods, jagged teeth, ill fitting
- Ventral surface of tongue, palate and gingival dentures. V
or, anywhere in oral cavity
Gross: SQUAMOUS CELL CARCINOMA OF
- Solitary or multiple white patches or plaques. ORAL CAVITY
- Sharply demarcated borders. ♦ Among of head and neck, 95% occurs in oral
cavity.
- Lightly thickened, wrinkled, fissured or smooth.
Etiopathogenesis:
- May appear raised, corrugated, verrucous
plaques. Strong association:
Microscopy: - Tobacco smoking/Chewing.
- Hyperkeratosis. - Chronic alcohol abuse
- Dysplastic changes. - HPV 16, 18, 33
- Sometimes carcinoma insitu. Weak association:
- Lymphocytic infiltration - Chronic irritation (jagged teeth, ill fitting
dentures)
Erythroplakia:
- Submucosal fibrosis
- A red, velvety, possibly eroded area within the
oral cavity - Poor nutrition.
- Usually remains in level with or may be slightly - Actinic radiation

depressed in relation to surrounding mucosa. - Plummer - Vinson syndrome.

Pathology
Molecular biology: PLEOMORPHIC ADENOMA

- Activation of oncogenes Classification of tumors of salivary
- Inactivation of tumor suppressor genes. gland
Morphology: Histological classification:
Sites:
Benign Malignant
- Ventral surface of tongue, floor of mouth,
- Pleomorphic - Mucoepidermoid
lower lip, soft palate, gingival
adenoma/mixed carcinoma (15%)
Gross:
( 50%)
- Early stages, possibly mistaken for leukoplakia.
- Warthin tumor - Adenocarcinoma (10%)
Types: (5- 10%)
1. Ulcerative: Ulcerated protruding mass,
- Oncocytoma (1%) - Acinic cell carcinoma (5%)
Irregular and indurated borders
2. Papillary/verrucous type: Soft, wart like, - Other adenomas - Adenoid cystic carcinoma
(5% to 10%) (5%)
growth
3. Nodular type: Firm, slow growing, - Basal cell adenoma - Malignant mixed tumor
submucosal nodule. (3-5%)
4. Scirrhous types: Infiltration into deeper - Canalicular - Squamous cell carcinoma

structures. adenoma (1%)
• Cervical LN involvement. - Ductal papilloma - Other carcinoma (2%)
V Note:
@ PWOO BCD @ MAAAMS
i. Most common sites of distant metastasis:
- Mediastinal lymphnodes, Lungs, Liver and
Note: Carcinoma arising in pleomorphic adenoma is
bones
referred to variously as a "Carcinoma ex pleomorphic
ii. Site of local metastasis → cervical lymphnodes adenoma" or malignant mixed tumor.
Microscopy: Pleomorphic adenoma:
- Dysplastic lesions ♦ 60% of tumors in parotid gland.
- May or may not progress to full thickness ♦ Are less common in submandibular glands and
prior to invasion rare in minor salivary glands.
- Ranges from well differentiated keratinising Morphology:
neoplasm to Anaplastic semisarcomatoid
Gross:
tumors.
- Rounded, well demarcated masses, < 6cm
Note: - Encapsulated but expansile growth produces
- In cervical cancer: full thickness invasion occurs tongue like protrusion into surrounding gland.
prior to invasion - Cut surface:
- Relative degree of keratinization is not related • Gray-white with myxoid and blue
with behavior. translucent chondroid area.

GIT
Microscopy: BARRET'SOESOPHAGUS
- Posses both epithelial and mesenchymal Past Questions:
component 1. Short notes on Barret’s oesophagus [10 Jan]
1. Epithelial component: ♦ Complication of chronic GERD that is
• Epithelial elements resembling ductal characterized by intestinal metaplasia within the
cells or myoepithellal cells are present. esophageal squamous mucosa
• These cells are arranged in duct ♦ It confers increased risk of esophageal
formations, acini, irregular tubules, adenocarcinoma
strands or sheets of cells. ♦ Sequence of progression is:
• These cells are dispersed within Barrets epithelium
mesenchyme like background. ↓
2. Mesenchymal component (product of Dysplasia
myoepithelial cells): ↓
• Islands of chondroid tissue and rarely Carcinoma insitu
foci of bone. ↓
• Simulates cartilage Invasive adenocarcinoma
♦ Pathogenesis:
- Unclear, appears to result from alteration in
differentiation of stem cells of esophageal mucosa.
Morphology:
Gross:
- One or several tongues or patches of red
velvety mucosa extentending upward from V
gastroesophageal junction.
- Metaplastic mucosa alternates with residual
smooth, pale squamous mucosa
- Long segment barret's esophagus → in which 3
cm or more involved.
- Short segment → If less than 3 cm involved.
Microscopy:
1. Intestinal metaplasia:
• Contains: Gastric glands, Intestinal
epithelium with goblet cells, inflammatory
infiltrates, Dysplastic changes
Clinical Features:
• Dysplasia may be:
- Painless, slow growing, mobile discrete mass
within parotid, submandibular or buccal Low grade High grade
glands. - ↑ed epithelial proliferation - More severe
- Recurrence after surgery because of - Atypical mitoses cytological
incomplete removal: - Nuclear hyperchromasia & and
stratification architectural
1. Proximity to facial nerve
changes
2. Multiple foci of tumor - Irregularly clumped chromatin
3. Pseudoencapsulation. - ↑ N/C ratio

Pathology
CARCINOMA OF ESOPHAGUS PEPTIC ULCER

Squamous cell carcinoma: Past Questions:
♦ Most common carcinoma in esophagus.
1. Define peptic ulcer. List the sites of occurrence and
♦ Male: female = 2 -20:1
discuss its pathogenesis. Enumerate the complication
Etiopathogenesis:
1. Dietary factors: of peptic ulcer. (1 +2 +5 +2 = 10) [09 July]
- Deficiency of Vitamin A, C, B1, B6 2. Describe the etiopathogenesis, gross and
- Deficiency of trace elements: Zn, Mb microscopic feature and complications of peptic
- Fungal contamination of food stuffs. ulcer. (3 +5 +2 =10) [08 Jan]
- High nitrite/Nitrosamine 3. Define peptic ulcer. Describe aetiopathogenesis.,
- Betel chewing gross and microscopic features of peptic ulcer. Name
2. Life style the various complications. (2 +6 + 2 = 10) [07 July]
- Hot beverage, food
4. Describe the etiopathogenesis, gross and
- Alcohol consumption
microscopic features and complications of peptic
- Tobacco use
- Urban environment. ulcer. (4 +4 +2 = 10) [07 Dec, 06 Dec]
3. Esophageal disorders: 5. Define peptic ulcer. Explain its aetiopathogenesis
- Long standing esophagitis. and complications. (2 +6 +2 = 10) [05 Dec]
- Ectodermal dysplasia ♦ Chronic, most often solitary lesions that occur in
- Achlasia any part of GI tract exposed to aggressive action
- Plummer Vinson syndrome of acid/peptic juices.
4. Genetic predisposition:
Sites of Occurrence [09]
- Loss of tumor suppressor genes: P53, P16, INK
V 4a. In descending order of frequency:
Morphology: 1. First part of duodenum
Gross: 2. Stomach, usually antrum
- Site:
• Middle 2/3rd (50%) 3. Gastroesophageal junction, in setting of
• Lower 1/3rd (30%) gastroesophageal reflux or Barrett esophagus.
• Upper 1/3rd (20%) 4. Within the margins of gastro jejunostomy.
- Early lesions: Small, gray - white, plaque like 5. In duodenum, stomach and or jejunum of
thickening.
patients of zollinger Ellison syndrome.
- Over month to years: Polyploid/ exophytic/
protruded (60%), Flat (15%), ulcerated (25%) 6. Within or adjacent to meckels diverticulum
Microscopy: that contains ectopic gastric mucosa.
- Moderate to well differentiated
Note: 4 times more common in proximal duodenum
- Several histological patterns: verrucous,
spindle cells, basaloid. than in stomach.
- Individual cell keratinisation and intercellular Pathogenesis: [05, 06, 07, 08, 09]
bridges called desmosomes are seen.
- Prickle cells, keratin formation, epithelial keratin Cause:
pearls formation, undifferentiated forms. - Imbalance between gastroduodenal mucosal
Note: Adenocarcinoma usually occur in distal third of defense mechanism and damaging forces.
esophagus.

GIT
Note: 5. Bacterial PAF promotes thrombotic occlusion of V

Role of H pylori: surface capillaries.
6. Bacterial Ag recruits inflammatory cells to the
1. - Induces intense inflammatory and immune
response causing increased production of pro- mucosa.
inflammatory cytokines such as IL - 1, IL- 6, TNF 7. Damage to mucosa permits leakage of Nutrients
and most notably IL - 8 into surface microenvironment, thereby sustaining
- Secretes urease that converts urea into the bacillus.
ammonia, Ammonia thus released forms Role of NSAIDS:
ammonium chloride with the help of chloride
salts 1. ↓ PGs→ direct chemical irritation by cigarettes
and Alcohol → ↓ Blood flow and healing.
↓
Myeloperoxidase from Neutrophils elaborates Gastric hyperacidity occurs during:
monochloramines from these compounds 1. Zollinger Ellison syndrome
which causes gastric injury. 1. Ca++ associated i.e. renal failure, hyperparathyroidism
2. Elaborates enzyme phospholipase → damages
surface epithelium. Morphology: [06, 08]
Gross:
3. Proteases, phospholipase → Break glycoprotein -
- Round to oval, sharply punched out defect
lipid complex in mucus → No first line defense
with relatively straight walls.
mechanism.
- Margins are generally in level with surrounding
4. ↑ Acid and↓ HCO3– secretion.
mucosa or slightly elevated.

Pathology
- Depth may vary; superficial lesions extend till Features Benign Ulcer Malignant Ulcer
mucosa while deep excavated ulcers have base 1. Age Younger age Older age
in muscularis propria. 2. Sex Markedly Slightly common
- Base is smooth and clean owing to peptic common in in males
digestion of exudate. males
- Base of ulcer may have thrombosed or even 3. Duration of Weeks to years Weeks to
patent blood vessels. symptoms months
- Surrounding mucosa creates mucosal folds 4. Location Commonly lesser Commonly
radiating from crater in a spoke like fashion. curvature of greater curvature
pylorus and of pylorus &
Note: antrum antrum
- Peptic ulcers are solitary in more than 80% patient 5. Gross
- Lesions < 0. 3cm diameter tend to be shallow features
- Lesions > 0.6 cm are likely to be deep ulcers. a. Size Small Large
b. Shape Regular Irregular
c. Mucosal Radiating Interrupted
folds
d. Ulcer bed Haemorrhagic Necrotic
6. Barium Punched out Irregular filling
studies ulcer defect
7. Acidity Usually normal- May be normal-
to - low to-even
achlorhydria
V 8. Therapy Responds well to Usually does not
medical therapy respond to
medical therapy
Complications [05, 07, 08, 09]
1. Bleeding:
- Most common complication (MCQ 2013 KU)
- Occurs in 15-30% patients.
- Accounts for 25% of ulcer deaths.
Microscopy: - Life threatening
4 Distinct zones
- May be first indication of ulcer.
- Base and margin have a superficial thin layer of
2. Perforation:
necrotic fibrinoid debris.
- Occurs in 5% of patients.
- Beneath the necrotic layer lies zone of non
specific inflammatory infiltrate with neutrophils - Accounts for 2/3rd of ulcer death.
predominantly. - Rarely presents first indication of ulcer.
- In deeper layers, especially in the base of ulcer, 3. Obstruction due to edema or scarring:
there is active granulation tissue infiltrated - In 2% patients
with mononuclear leucocytes. - Most often due to pyloric ulcers, also with
- Granulation tissue rests on a more solid fibrous duodenal ulcer.
or collagenous scar. - Cause incapacitating, cramp like, abdominal pain.
GIT
CARCINOMA OF STOMACH 2. Environmental factors:

Past Questions: a. Diet:
1. Describe the aetiopathogenesis, gross and • Nitrites (Water, preserved food)
microscopic features of carcinoma stomach. • Smoked and salted foods, pickled
(4+2+4=10) [01 Dec] vegetables, chili
2. Discuss the aetiopathogenesis, classification, • Lack of fresh fruit and vegetables.
gross and microscopic features of carcinoma • Consumption of dietary carcinogens like
stomach. (3+3+2+2=10) [02 June] benzopyrene, N - nitrosocompounds.
3. Early gastric carcinoma [06 Dec] b. Low socioeconomic status.
c. Cigarette smoking
WHO Classification [02]
3. Host factors:
1. Epithelial tumors:
- Chronic gastritis (Hypochlorhydria, intestinal
- Intraepithelial neoplasia: Adenoma
metaplasia)
- Adenocarcinoma
- Partial gastrectomy (favours efflux of bile,
• Papillary alkaline food)
• Tubular - Gastric adenoma.
• Tubulopapillary - Barrett esophagus (tumor of gastroesophageal
• Mucinous junction)
• Signet ring 4. Genetic factors:
• Undifferentiated - Blood groups A are at high risk
• Adenosquamous - Family history increases likelihood.
- Small cell carcinoma
- Hereditary non-polyposis colon cancer syndrome.
- Carcinoid tumor.
- Familial gastric carcinoma syndrome (e-cadherin
2. Non epithelial tumors:
mutation) V
- Leiomyoma
- Schwannoma Types
- Granular cell tumor 1. On the basis of depth of invasion:
- Leiomyosarcoma a. Expanding (confined to mucosa and submucosa)
- GI stromal tumor b. Infiltrating (extends below submucosa)
- Kaposis sarcoma 2. Macroscopic subtypes:
- Others a. Early: Exophytic, flat/depressed, excavated.
3. Malignant Lymphoma b. Advanced: Ulcerative, fungating (polypoid)
Lauren classification scirrhous (linitis plastica), colloid (mucoid)
♦ Intestinal type, diffuse type 3. Histologic subtypes
Etiopathogenesis [01, 02] a. Intestinal type
- Tubular
Risk factors:
- Papillary
1. H-pylori infection:
- Tubulopapillary
- ↑ed risk 5-6 fold in intestinal type.
- Mucinous
- Inflammation → chronic gastritis → Atrophy →
- Adenosquamous
Intestinal metaplasia → Dysplasia → carcinoma.
- Undifferentiated.
- Long standing mucosal inflammation:
b. Diffuse type:
hypochlorhydria, ↓ pepsin secretion.
- Signet ring.

Pathology
Morphology [01, 02] TUBERCULOSIS OF INTESTINE

A. Location Pathogenesis
- Pylorus and antrum: 50-60% TB of intestine can occur in 3 forms:
- Cardia: 25% Hyperplastic
- Body and fundus: Rest Primary Secondary caecal
Note: Lesser curvature is involved more than greater tuberculosis
curvature. - Due to ingestion - Swallowing - Variant of
of contaminated of coughed occurring
B. Depth of invasion:
milk up infective secondary to
- Early gastric carcinoma: Confined to mucosa
material pulmonary - TB
and submucosa.
- Advanced gastric carcinoma: extends beyond
sub mucosa into muscular coat. Organisms are seed to mucosal lymphoid aggregates
of small and large bowel.
C. Macroscopic patterns:
a. Exophytic: Protrusion of tumor mass into ↓
lumen. Undergo granulomatous inflammation
b. Flat or depressed: No obvious tumor mass ↓
within the mucosa. Advanced cases with flat Lead to ulceration of overlying mucosa
surface → Linitis plastica or leather bottle
Morphology Gross Microscopy
appearance
c. Excavated: Shallow or deep erosive crater Primary - Affected - Initially there is
present in the wall. In advanced cases, craters Intestinal lymphnodes primary complex of
are indentified by their heaped up, beaded TB enlarged, Ghon's focus.
V margins and necrotic base with neoplastic matted and - Typical tubercular
tissue extending to surrounding mucosa and caseous. granulomatous
walls. - Healing by inflammatory
D. Histological patterns: fibrosis and reaction with
Intestinal type calcification casseous necrosis
- Malignant glands, abundant mucin in lumen. Secondary - Ulcers which - Initially there is
- Intestinal metaplasia Intestinal are transverse primary complex
- Desmoplasia TB to long axis of or ghons focus
- Neoplastic cells with apical mucin. the bowel - Typical tubercular
Diffuse type: - May be coated granulomatous
- Gastric type mucous cells but don't form glands with caseous inflammatory
- Mucin formation which expand the malignant material reaction with
cells and push the nucleus to periphery → i.e. - Serosa studded casseous necrosis.
signet ring like cells. with visible - Granulomatous
E. Metastasis: tubercles. inflammatory
- Supraclavicular sentinal node: Virchow node - Transverse reaction with
fibrous central caseation
- To periumbilical region forming subcutaneous
nodule called as sister Mary Joseph nodule. strictures and - Mucosa and
intestinal submucosa show
- Local invasion to duodenum, pancreas,
obstruction in ulceration
retroperitonueum.
advanced cases
- Bilateral metastasis to ovary: Krukenberg tumor.

GIT
TYPHOID OF INTESTINE APPENDICITIS

Pathogenesis Past Questions:
Typhoid bacillus ingested through contaminated food 1. Give pathogenesis of this lesion. [3][PBQs 2013]
or water.
Etiopathogenesis [PBQs 2013]
↓
Etiology:
During asymptomatic period of about 2 weeks, Bacilli
1. Obstructive causes (50 - 80%)
invade the lymphoid follicles and Peyer's patches of
- Fecolith
small intestine
- Gall stone
↓
- Tumor
Bacilli invade blood stream causing bacteremia
- Ball of worms (oxyuriasis vermicularis)
↓
- Foreign body.
Eventually bacilli are localized in the intestinal
lymphoid tissue, mesenteric lymph nodes, in the liver - Diffuse lymphoid hyperplasia (in children)
gall bladder and in the spleen. 2. Non - obstructive causes:
Note: - Hematogenous spread of generalized infection
- S. typhi are able to survive in gastric acid. - Vascular occlusion
- Once in small intestine, are taken up by and invade - Inappropriate diet lacking roughage.
m-cells. Pathogenesis:
- Organisms are then engulfed by mononuclear cells - Obstruction of lumen →↑ intraluminal
in underlying lymphoid tissue. pressure → stasis, ischemia → Bacterial
proliferation → inflammatory response → V
Morphology
Appendicitis
Gross:
Morphology:
- Site: Terminal ileum commonly
Gross:
- Oval typhoid ulcer with long axis along the
- Normal glistening serosa is converted into dull,
length of the bowel.
granular, red membrane (early acute
- Base of ulcer is black.
appendicitis)
- Margins of ulcer slightly raised.
- Later stage → Abscess formation within wall
- Never significant fibrosis along with ulceration and foci of suppurative
Microscopically: necrosis in mucosa (acute suppurative
- Submucosal peyers patches > 8 cm in diameter. appendicitis)
- Neutrophils accumulate within superficial - Further appendicial compromise leads to large
lamina propria and macrophages containing area of hemorrhagic green ulceration of
bacteria, RBCs and nuclear debris mixed with mucosa and green-black gangrenous necrosis
lymphocytes and Plasma cells in lamina through the wall extending to serosa (Acute
propria. gangrenous appendicitis)
Complications - This stage is followed by rupture and

suppurative peritonitis.
- Perforation of the ulcers and haemorrhage

Pathology
AMOEBIC COLITIS
Etiology
♦ Most common type of amoebic infection caused
by E. histolytica.
Cysts of entamoeba
↓
Ingested through contaminated food and water.
↓
Excystation occurs in small intestine
↓
Trophozoite in colon
↓
Dysentery develops when amoebae attach to
Microscopy: colonic epithelium
- Diagnosis of acute appendicitis requires ↓
neutrophilic infiltration of muscular propria. 1. Lytic action of trophozoites (by cysteine
- Neutrophils and ulceration also present within protease, lectin and amoeba pore)
mucosa. 2. Induce apoptosis, invade crypts and burrow
- Early stage: Congestion and edema of laterally up to lamina propria
appendix wall 3. Recruits neutrophils, causes tissue damage
- Later stage: mucosa sloughed off, wall ↓
necrotic, and blood vessels thrombosed. Creates flask shaped ulcer with a narrow neck
V - Impacted foreign body or fecolith may be seen and broad base.
in lumen. Gross features:
Complication: - Sites: Cecum, Ascending colon, sigmoid colon
- Peritonitis after appendicial perforation. rectum, Appendix.
- Appendicular abscess. - Early lesions appear as small areas of elevation
- Pyelophlebitis with thrombosis of partial on mucosal surface
venous drainage. - Advanced cases → typical flask shaped ulcers.
- Liver abscess. Microscopy:
- Bacteremia - Ulcerated area with chronic inflammatory cells
- Mucocele - Trophozoites of entamoeba in inflammatory
- Adhesion to greater omentum, small intestine exudates and are concentrated at advancing
or other abdominal structures. margin of lesion.
- Edema and vascular congestion in areas
Note: Diagnosis of acute appendicitis may be surrounding ulcers
confused with:
Complications:
1. Mesenteric lymphadenitis. 1. Amoebic liver abscess
2. Sacroilitis 2. Amoebic hepatitis
3. Mittelschmerz 3. Perforation
4. Ectopic pregnancy 4. Hemorrhage
5. Meckel diverticulitis 5. Formation of Amoeboma

GIT
NECROTISING ENTEROCOLITIS ULCERATIVE COLITIS & CROHN'S

♦ Most common in premature infants DISEASE
♦ Incidence of disease inversely proportional to Past Questions:
gestational age. 1. Write gross and microscopic finding in ulcerative
colitis. (1+1=2)[KU 2013]
Pathogenesis
2. Enumerate the important causes of ulceration in
♦ Uncertain large intestine. Describe the gross and
♦ Believed multifactorial in causation. microscopic features of lesions in ulcerative
colitis. (3+3+4=10) [01 June]
♦ In addition to prematurity, most case are
3. Discuss aetiopathogenesis of ulcerative colitis.
associated with enteral feeding. Describe the morphology and complications of
♦ This suggests that some postnatal insult (such as ulcerative colitis. (3+3+4=10) [10 July]
introduction of bacteria) sets in motion, the 4. What is ulcerative colitis? Describe the difference
cascade culminating in tissue destruction. between ulcerative colitis and crohns disease.
(10) [11 July]
♦ No single bacterial pathogen has been linked to
disease Etiology and pathogenesis [10]
♦ Most investigators believe that the two disease
♦ Large no. of inflammatory mediators like platelet
result from a combination of defects in host
activating factor (PAF) has been implicated. interaction with intestinal microbiota, intestinal
♦ These factors promote enterocyte apoptosis and epithelial dysfunction, and aberrant mucosal
compromise inter cellular tight junction immune response.
1. Genetics: NOD -2 Polymorphism
♦ Thus increasing mucosal permeability
2. Mucosal immune responses
♦ This permits transluminal migration of gut 3. Epithelial defects
bacteria leading to vicious cycle of inflammation, 4. Microbiota V
mucosal necrosis and further bacterial entry.
♦ Eventually terminate into sepsis and shock.
Morphology
Gross:
- Site of involvement: Terminal ileum, caecum,
right colon.
- Involved segment is distended, friable and
congested or may be frankly gangrenous.
- Intestinal perforation may be seen.
Microscopy:
- Mucosal or transmural coagulative necrosis
- Ulceration
- Bacterial colonization
- Submucosal gas bubbles.
- Reparative changes like: granulation, fibrosis
Note: Abdominal radiographs often demonstrate gas
within the intestinal wall (pneumatosis intestinalis)

Pathology
Comparing morphology
CROHNS disease Ulcerative colitis [01, 13]
Sites: Terminal ileum, ileocaecal valve, caecum Sites: Rectum, colon
Gross features Gross features
1 Skip lesions 1. Skip lesions are not seen
2. Strictures 2. Pancolitis, ulcerative proctitis, ulcerative
protosigmoiditis or backwash ileitis
3. Apthous ulcer, may progress and multiple lesions 3. Involved colon mucosa is slightly red and granular.
often coalesce into elongated serpentine ulcer along
axis of bowel
4. Cobble stone appearance 4. Broad based ulcers
5. Fissures develop between mucosal folds and may 5. No serpentine ulcers
extend deeply to become fistula tracts
6. Intestinal wall is thickened and rubbery because of 6. Pseudopolyps with mucosal bridges.
transmural edema, inflammation submucosal fibrosis
and hypertrophy or muscularis propria.
7. Creeping fat 7. Mucosal atrophy
8. Serosal surface is normal
9. Strictures do not occur
Microscopy Microscopy
1. Abundant neutrophils infiltration 1. Inflammatory infiltrate
2. Cluster of Neutrophils within a crypt called crypt 2. Crypt abscesses
V abscess
3. Distortion of mucosal architecture 3. Epithelial metaplasia
4. Epithelial metaplasia/pseudopyloric metaplasia 4. Inflammatory process is limited to the mucosa
5. Paneth cell metaplasia 5. Granulomas absent
6. Noncaesating granulomas

GIT
Complications: iv. Loss of SMAD's

v. Loss of p53
Crohns Disease Ulcerative colitis
vi. Activation of telomeres
1. Malabsorption due to 1. Toxic megacolon 2. Microsatellite instability pathway.
impaired fat, B12,
- Multiple mutations occur but of different
protein and electrolyte genes and unlike APC mutation, no
absorption morphologically identifiable changes are seen.
2. Fistula formation 2. Perianal fistula Steps:
i. Basic mutation
3. Stricture formation 3. Carcinoma ii. Loss of DNA repair gene example: TGF-B
4. Malignancy → receptor gene and BAX gene.
lymphoma more often iii. Repetitive DNA sequences (microsatellites)
than adenocarcinoma become unstable during replication cycle
iv. Right sided colon cancer tends to have more
CARCINOMA OF COLON microsatellite instability.
Past Questions: 3. Dietary factors:
1 Discuss the etiopathogenesis of carcinoma colon. Low fiber diet
2. Describe the gross and microscopic features of ↓Stool bulk

carcinoma colon. Add a note on staging of
↑Fecal transit time
carcinoma colon. (3 +2 +2 + 2 + 3 = 10) [04 June]
3. Discuss the etiopathogenesis of carcinoma colon. Stay longer in contact Increased toxic oxidative
Describe the gross and microscopic features of with mucosa byproducts of carbohydrate
carcinoma colon. Add a note on staging of digestion by bacteria V
carcinoma colon. (3 +2 +2 + 2 + 3 = 10) [04 June]
♦ Always comprises of adenocarcinoma Genetic Alteration
♦ Peak incidence 60-79 yrs

Refined diet Potential carcinogen
Risk Factors with low ↑by Normal flora
♦ Excess dietary calorie intake vitamin - A, C, E increased secretion of Bile acids
♦ Low content of unabsorbable vegetable fibers. ↑
♦ High content of refined carbohydrates. High cholesterol intake in red meat
♦ Intake of red meat. Adenoma-carcinoma sequence:
♦ Persistent adenomas Normal colon
Germline/somatic mutation Mutation at APC 5q21
♦ Pre-existing diseases like inflammatory bowel of cancer suppressor genes
disease and diverticular disease.
Mucosa at risk
Pathogenesis [04] Methylation abnormalities Mutation at APC β -catenin
inactiviation of normal alleles
1. APC/β - Catenin pathway.
Adenomas
i. Loss of APC gene (first hit) Homozygous loss of additional Mutation at K-RAS‚ p53
ii. Inactivation of normal alleles (second hit) cancer suppressor genes (Additional mutation)
iii. Point mutation of K-RAS gene Carcinoma

Pathology
Morphology [04] 2. Lymphatic spread

i. Location: 3. Hematogenous spread to liver, lung, brain,
- Ascending colon: 22% bones, ovary
- Transverse colon: 11% Staging

- Descending colon: 6% Based on American joint committee on cancer
- Rectosigmoid colon - 55% TNM classification of colorectal carcinoma
- Other - 6% Tumor
ii. Gross features: Tis : In sites dysplasia or intramucosal carcinoma
Right sided growth T1 : Tumor invades submucosa
- Large cauliflower like, soft, friable mass T2 : Tumor invades into, but not through,
projecting into lumen (fungating, polypoid muscularis propria
carcinoma) T3: Tumor invades through muscularis propria
- Obstruction is uncommon T3a : Invasion < 0.1cm beyond muscularis
- Later, the neoplasm may penetrate the bowel propria
wall and appear as subserosal and serosal T3b: Invasion 0.1cm to 0.5 cm beyond
white firm mass. muscularis propria
Left Sided growth T3c : Invasion > 0.5cm to 1.5cm beyond
- Annular, encircling lesions that produce so msucularis propria
called "Napkin ring" constrictions of the bowel T3d: Invasion > 1.5cm beyond muscularis
- Margins of Napkin ring are heaped up, beaded
V propria
and firm and the mid region is ulcerated. T4: Tumor invades adjacent organs or visceral
- Lumen is markedly narrowed. peritoneum
- Proximal bowel may be distended. T4a : Invasion into other organs or structures.
iii. Microscopy: Similar in both sides T4b : Invasion into visceral peritoneum
- 95% → Adenocarcinoma of varying grades out Regional lymphnodes
of which 10% are mucin secreting colloid Nx : Lymph nodes can't be assessed.
carcinoma.
N0: No regional lymph node metastasis.
- Range from tall columnar cells invading
N1: Metastasis in one to three regional lymph
submucosa, muscularis propria to
nodes.
undifferentiated, frankly anaplastic mass.
N2: Metastasis in four or more regional lymph
- Desmoplastic stromal response
nodes.
- Sometimes mucin with in the cell: Signet ring.
Distant metastasis
Spread
Mx : Distant metastasis can't be assessed
1. Direct spread: most common
M0 : No distant metastasis
- Circumferentially into bowel wall
M1: Distant metastasis or seeding of abdominal
• Directly into depth of bowel wall to serosa,
organs.
pericolic fat, peritoneal cavity

GIT
POLYPS OF LARGE INTESTINE c. Inflammatory polyp (pseudopolyp)

Classification d. Lymphoid polyp
1. Non-neoplastic polyp: 2. Neoplastic polyp:
a. Hyperplastic polyp a. Adenoma (Tubular, villous, tubulovillous)
b. Hamartomatous polyp b. Polypoid carcinoma
- Juvenile polyp: Cystically dilated c. Familial polyposis syndrome:
- Peutz - Jeghers polyp: Tree like branches of - Familial polyposis coli, Gardner's syndrome,
muscularis mucosa [MCQs 013 KU] Turcot's syndrome, Juvenile polyposis
syndrome
Comparison of tubular and villous adenoma
Tubular adenoma Villous adenoma
- Most common (75%) Neoplastic polyps - Less common than tubular
- Mean age of occurrence: 3rd decade - In 6th decade of life.
- Usually Asymptomatic - Usually symptomatic
- Site: most often in distal colon and rectum - Distal colon and rectum.
Grossly:
- Single or multiple - Round to oval exophytic masses
- Sessile or pedunculated - Usually sessile
- Size vary from < 1cm to large spherical masses with - Size vary from 1 - 10 cm diameter
an irregular surface
- Usually, the larger lesions have recognizable stalks
Microscopy: V
- Branching tubules embedded in lamina propria - Presence of many slender, finger like villi which
- Lining epithelial cells are of large intestinal type with appear to arise directly from area of muscularis
diminished mucus secreting capacity, large nuclei mucosa
and increased mitotic activity. - Each papilla has fibrovascular stromal core that is
covered by epithelial cells.
Malignant transformation: low risk - High risk

Pathology
Genetic:
ACUTE PANCREATITIS - Mutations in the cationic trypsinogen (PRSS1)
♦ It is reversible pancreatic parenchymal injury, and trypsin inhibitor (spink1) genes
associated with inflammation. Mechanical
♦ In acute pancreatitis, glands can return to normal - Gallstones
if underlying cause of pancreatitis is removed. - Trauma
♦ In contrast, chronic pancreatitis is defined by - Iatrogenic injury
irreversible loss of exocrine pancreatic
- Operative injury
parenchyma.
- Endoscopic procedures with dye injection
Etiopathogenesis Vascular
Etiologic factors - Shock
Metabolic: - Atheroembolism
- Alcoholism - Vasculitis
- Hyperlipoproteinemia Infections
- Hypercalcemia - Mumps
- Drugs (e.g. azathioprine)
Pathogenesis:

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GIT

FAST TRACK BASIC SCIENCE MBBS -5-

-6- FAST TRACK BASIC SCIENCE MBBS

GROSS ANATOMY Embryological importance:

FAST TRACK BASIC SCIENCE MBBS -7-

ORAL CAVITY - In man: Teeth replaced only once so called

1. Pulp: Contains vessels, nerve and ↓

Development: - Muscles from: 1st, 4thand 6th branchial arches.

FAST TRACK BASIC SCIENCE MBBS -9-

2. Muscular uvula - Near the median plane palatine - Pulls up uvula

3. Levator veli palatine - Superior surface of palatine - Elevates soft plates

5. Palatoglossus - Inferior surface of palatine - Pulls up root of

-10- FAST TRACK BASIC SCIENCE MBBS

2. Extrinsic muscles [05 June]

FAST TRACK BASIC SCIENCE MBBS -11-

Parts of the tongue

-12- FAST TRACK BASIC SCIENCE MBBS

Structure within parotid gland [08 Dec]

FAST TRACK BASIC SCIENCE MBBS -13-

-14- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -15-

Comparison between nosopharynx, oropharynx and laryngopharynx

-16- FAST TRACK BASIC SCIENCE MBBS

- It is loosely attached to the walls by extra-

FAST TRACK BASIC SCIENCE MBBS -17-

-18- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -19-

Lesser Sac or omental bursa Boundaries:

Applied Aspects: Recto uterine pouch of Douglas

-20- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -21-

Constrictions: 4 constrictions normally [08]

-22- FAST TRACK BASIC SCIENCE MBBS

STOMACH These structures are:

FAST TRACK BASIC SCIENCE MBBS -23-

Venous drainage: Nerve supply

-24- FAST TRACK BASIC SCIENCE MBBS

Congenital anomaly: d. Nerve supply is more abundant, with large

1. Mucosa: Simple columnar epithelium iii. Pyloric glands:

FAST TRACK BASIC SCIENCE MBBS -25-

SMALL INTESTINE ♦ 6m long

1. Mention the extent and relations of second part Duodenum:

-26- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -27-

- Venous drainage: Splenic, superior mesentric

-28- FAST TRACK BASIC SCIENCE MBBS

JEJUNUM AND ILEUM 2. Describe the differences between the jejunum

Differences between Jejunum and ileum [09 July, 03 Nov]

Features Jejunum IIeum

2. Walls Thicker and more vascular Thinner and less vascular

3. Lumen Wider and often empty Narrower and often loaded

4. Mesentery a. Window present a. No windows

8. Solitary lymphatic Fewer More numerous

- Villi are taller and - Villi are shorter and

FAST TRACK BASIC SCIENCE MBBS -29-

Blood supply: - This rotation is counter clockwise, Aprox. 270°

Parts 2. Fixed except Appendix, transverse colon and

Position [04 July] 3. Splenic 1. Upward to left

-32- FAST TRACK BASIC SCIENCE MBBS

Blood supply Ascending colon:

1. Lumen small, Irregular outline. RECTUM AND ANAL CANAL

8. Muscularis externa→ Thin d. Peritoneal relations

i. Amoebiasis c. Sources of development