Medicine

Concept Based Learning
Video Companion on Each Chapter
Next GeNeratioN
Comprehensive review series
“MEDICINE”
Active Recall Based
Integrated Edition
Published by Delhi Academy of Medical Sciences (P) Ltd.
HEAD OFFICE
Delhi Academy of Medical Sciences (P.) Ltd.
4-B, Grovers Chamber, Pusa Road,
Near Karol Bagh Metro Station,
New Delhi-110 005
Phone : 011-4009 4009
http://www.damsdelhi.com
Email: info@damsdelhi.com
ISBN : 978-93-89309-24-9
First Published 1999, Delhi Academy of Medical Sciences
© 2021 DAMS Publication

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any
means, electronic, mechanical, including photocopying, recording, or any information storage and
retrieval system without permission, in writing, from the author and the publishers.
This book contains information obtained from authentic and highly regarded sources. Reprinted
material is quoted with permission. Reasonable efforts have been made to publish reliable data and
information, but the authors and the publishers cannot assume responsibility for the validity of all
materials. Neither the authors nor the publishers, nor anyone else associated with this publication,
shall be liable for any loss, damage or liability directly or indirectly caused or alleged to be caused
by this book.
Neither this book nor any part may be reproduced or transmitted in any form or by any means,
electronic or mechanical, including photocopying, microfilming and recording, or by any
information storage or retrieval system, without permission in writing from Delhi Academy of
Medical Sciences. The consent of Delhi Academy of Medical Sciences does not extend to copying
for general distribution, for promotion, for creating new works, or for resale. Specific permission
must be obtained in writing from Delhi Academy of Medical Sciences for such copying.
Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are
used only for identification and explanation, without intent to infringe.
Typeset by Delhi Academy of Medical Sciences Pvt. Ltd., New Delhi (India).
Contents
Section 1 Central Nervous System 01 – 60
1. Cerebrovascular Accident and Dementia 5 – 14
2. Headache & Epilepsy 15 – 25
3. Multiple Sclerosis 26 – 28
4. Cranial Nerves 29 – 30
5. CNS Infections 31 – 35
6. Myelopathy 36 – 42
7. Motor Neuron Disease (MND) 43 – 44
8. Neuropathy, NMJ Disorders and Myopathy 45 – 53
9. Parkinson’s Disease and Gait Disorders 54 – 57
10. Miscellaneous 58 – 60
Section 2 Cardiovascular System 61 – 134

1. Clinical Examination 62 – 72
2. Ecg & Arrythmias 73 – 87
3. Rheumatic Fever and Infective Endocarditis 88 – 104
4. Cardiomyopathy 105 – 112
5. Hypertension & Coronary Artery Disease (CAD) 113 – 119
6. Heart Failure 120 – 132
7. Important One-Liners in Cardiology 133 – 134
Section 3 Respiratory Systems 135 – 176

1. Pulmonary Function Tests (PFT) & Respiratory Failure 137 – 142
2. ARDS and Pulmonary Vascular Disorders 143 – 146
3. Parenchymal and Pleural disorders 147 – 151
4. Airway Disorders 152 – 157
5. Interstitial Lung Diseases (ILD) 158 – 162
6. Miscellaneous 163 – 165
7. Acid Base-Balance (ABB) 166 – 176
Section 4 Gastrointestinal Tract and Liver 177 – 224

1. Esophagus 179 – 184
2. Stomach 185 – 189
3. Malabsorption Syndromes 190 – 196
4. Colon 197 – 200
5. Liver 201 – 219
6. Pancreatitis 220 – 224
Section 5 Endocrine System 225 – 272
1. Pituitary Gland 226 – 236
2. Thyroid Gland 236 – 245
3. Parathyroid Gland 246 – 248
4. DM 249 – 262
5. Adrenal Gland 263 – 272
Section 6 Nephrology 273 – 287

1. Acute Renal Failure (Acute Kidney Injury) 275 – 282
2. Chronic Renal Failure (Chronic Kidney Injury) 283 – 285
3. Renal Replacement Therapy (RRT) 286 – 287
Section 7 Rheumatology 288 – 316

1. Lupus Disorders 290 – 298
2. Arthritis Disorders 299 – 307
3. Vasculitis Syndrome 308 – 316
SECTION — 1
CENTRAL NERVOUS SYSTEM
Central nervous system is perhaps the most vital system of the human body. Loss of
Cerebral function (brain death) is equitable to a vegetative state.
The CNS comprises of billions of neurons performing a trillion activities. However, the
understanding of CNS remains limited due to human inability to replicate its function
artificially. The advancement in the field of Neuro-imaging; viz Functional MRI/SPECT
have definitely improved our knowledge and understanding of CNS in the recent past.
The CNS is very vast and performs a diverse range of functions. Hence medical graduates
have always found it difficult to learn the topic. Moreover the clinical examination is
exhaustive and needs to be understood to diagnose disorders.
Most textbooks use “pathology-based classification” to discuss CNS. They classify the
disorders into Vascular, Demyelinating, Infective, etc. However, this classification makes
integration of theory with clinical evaluation difficult. Hence, we prefer to discuss the
topic using “Neuro-axis” based classification.
sensorimotor area
frontal eye field

parietal lobe
frontal lobe
perfrontal
visual
area
Broca’s area
(in left hemisphere)
visual
temporal lobe asscciation
auditory auditory association

(including Wernicke’s area,
in left hemisphere)
Fig. 1.1
2 | Medicine
Approach to Central Nervous System Disorders:
Pyramidal Extra-pyramidal
Extends from Cortex → Muscle Consists of Basal Ganglia Complex
Dominant motor pathway Accessory motor pathway
Initiates and Executes all Motor movements Co-ordinates motor movement
Power Loss >>> Tone disorder Tone Disorder >>> Power loss
Spasticity / Flaccidity Rigidity / Hypotonia
Velocity dependent hypertonia Velocity independent
e.g Hemiplegia, Peripheral Neuropathy e.g. Parkinson’s Disease
UMN LMN
Extends from Cortex → Spinal cord Extends from Anterior Horn cell → Muscle
Hypertonia Hypotonia
Exaggerated DTR Diminished / Absent DTR
Extensor Plantar Flexor /Mute plantars
Muscle wasting is Rare Wasting Is a common feature
Fasciculation is Never seen Fasciculation common
Symptomatology of Cortex:
1. Cognition:
Spontaneous Response Verbal Response Painful Stimulus Brainstem Reflex
1. Awake   - -
2. Drowsy X  - -
3. Stuporous X X  -
4. Comatose X X X 
5. Brain-dead X X X X
Glasgow Coma Scale (GCS):

Prognostic scale in a patient of head injury.
No “O”
Min Score : 3, Max Score: 11.
E – Eye movement 

M – Motor Response  Components

V – Verbal Response 
• Applicable for the 1st 24hours of head injury.
• Worst score within 24hours is taken to ascertain prognosis.
• GCS < 7 or > 7 : < 85% Mortality or > 85% Survival correspondingly.
• Modern day usage: In ICU, as rough guideline to Neurological state.
Central Nervous System | 3
Eye Opening Verbal (nonintubated) Verbal (Intubated) Motor Activity

4–Spontaneous 5–Oriented and talks 5–Seems able to talk 6–Verbal command
3–Verbal stimuli 4–Disoriented and talks 3–Questionable ability 5–Localizes to pain
2–fainful stimuli 3–Inappropriate words to talk 4–Withdraws from pain
1–No response 2–Incomprehensible 1–Generally 3–Decorticate
sounds unresponsive 2–Decerebrate
1–No response 1–No response
2. Aphasia:
Repetition of Spoken
Comprehension Language N aming Fluency
Wernicke's Impaired Impaired Impaired Preserved or increased
Broca's Preserved (except Impaired Impaired Decreased
grammar) Impaired
Global Impaired Impaired Impaired Decreased
Conduction Preserved Impaired Impaired Preserved
3. Apraxia:
Definition: Inability to perform a task in the absence of motor weakness.
Site: Fronto – Parietal lesion.
Most common type of Apraxia – Ideo – motor Apraxia.
4. Seizure/epilepsy:
Seizure: A seizure is a paroxysmal event due to abnormal excessive or synchronous
neuronal activity in the brain.
Epilepsy: A syndrome characterized by 2 or more unprovoked seizures.
5. Cortical Sensation:
1. Tactile localization.
2. Two-point discrimination:
Most sensitive area : Lips + fingertips => 1-2mm can be differences.
Least sensitive area : Back => 5mm diff to differentiate.
3. Stereoagnosis: Ability to Identity a familiar object by its shape, Size, texture.
Astereoagnosis – Parietal Lobe sign.
4. Graph–asthesia: Ability to identity what is written on the body.
The cortical sensations are carried by the Dorsal column.
1 Cerebrovascular Accident
and Dementia
CONCEPTS
Â Concept 1.1 Types of Stroke
Â Concept 1.2 Cerebral Circulation
Â Concept 1.3 Manifestations of CVA
Â Concept 1.4 Brainstem syndromes
Â Concept 1.5 Thrombolysis in Stroke:
Â Concept 1.6 Hemorrhagic strokes
Â Concept 1.7 Dementia
Â Concept 1.8 Alzheimer’s Disease (AD) and

Other dementia syndromes
6 | Medicine
Concept 1.1 : Types of Stroke
Learning Objective: to understand the salient features and types of Stroke
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Presently CVA is classified on the basis of the pathology into:

1. Embolic stroke (Most common type of CVA).
2. Thrombotic:
a. Major artery thrombus.
b. Lacunar Infarct syndrome.
c. Cortical venous sinus thrombosis.
3. Hemorhagic:
a. IntracerbralHemorhage (MC among hemorrhagic CVA).
b. Sub-ArchnoidHemorrhage (SAH).
c. Subdural Hematoma & Extra-dural Hematoma (SDH&EDH).
Embolic Thrombotic Hemorrhagic
Definition Acute occlusion of the Chronic occlusion of the Bleeding from the vessel
vessel vessel
Epidemiology Bimodal > 65 yrs, M>>F 40-60 yrs, M>F
Risk Factors Young – Structural heart Hypercoagulable state Hypertension
disease
Elderly – Arrythmia
(MC – A.Fibrillation)
Onset Hyperacute Subacute Acute
FND Maximal at onset Progressive Headache -> FND
Risk of convulsions Maximum Minimum High
Risk of Raised ICT Low Low High
Recovery Early and complete Delayed and Partial Poor / No recovery
Diagnosis MRI and MR Angio MRI CT
Treatment
Immediate Self-limiting Thrombolysis Anti-edema drugs
Secondary prevention Anti-coagulation Anti-platelets, Statins, Control of risk factors
control risk factors,
Neuroprotective Rx
Prognosis Excellent Favorable Poor
Concept 1.2 : Cerebral Circulation
Learning Objective: to learn Cerebral circulation anatomy
Time needed
1 Reading
st
20 mins
2nd Reading 5 mins
Cerebral Circulation:
Fig. 1.2
Fig. 1.3
8 | Medicine
Concept 1.3 : Manifestations of CVA
Learning Objective: to understand the manifestations depending on area affected
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Artery affected Area involved FN D

Bilateral ACA Paracentral lobule Bilateral leg weakness - Paraplegia
Loss of Cortical sensation in both legs
Micturition centre Socially Un-inhibited Bladder
Prefrontal fibers Emotional Lability
Anti-social behavior
MCA
Deep perforating branch Internal Capsule Dense Hemiplegia
Lenticulostraite branch
a. Frontal Broca’s area Motor Aphasia
Misc Re-emergence of infantile reflexes :
Palmomental reflex
b. Parietal Angular gyrus Gerstmannsyndrome :
Acalculia
Agraphia
Right-Left confusion
Finger Agnosis (identification)
c. Temporal Anterograde amnesia
Learning disability
d. Occipital Cortical blindness (Anton-Babinski’s syn)
Prosapagnosia
(Defect in familiar face identification)
ICA
Opthalmic Artery End artery Amaroux Fugax (Mono-ocular blindness)
Concept 1.4 : Brainstem syndromes
Learning Objective: to learn Brainstem syndromes and its features
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
A. Midbrain Syndromes
Syndrome Site Cranial N . Other Features
Weber’s Cerebral Peduncle Ipsilateral 3rd Nerve Contralateral Hemiplegia
Benedicts Red Nucleus Ipsilateral 3rd Nerve Contralateral Tremor,
Chorea, Athetosis
Nothnagel’s Superior Cerebellar Ipsilateral 3rd Nerve Contralateral Cerebellar
Peduncle Ataxia
Claude’s Red Nculeus+Superior Ipsilateral 3rd Nerve Contralateral Tremor,
Cerebellar Peduncle Chorea Athetosis &
Cerebellar Ataxia
B. Pontine Syndromes
Syndrome Site Cranial N . Other Features
Foville’s Dorsal Pons Ipsilateral 6th, 7th Lateral Gaze Palsy, Contralateral Hemiparesis
Millard-Gubler Ventral Pons Ipsilateral 7th, 6th Only Abducens Palsy, Contralateral Hemiparesis
Only Fascicle
C. Medullary Syndromes
Syndrome Cranial N erve Other Features
Medial Medullary Syndrome Ipsilateral 12th Nerve Contralateral Incomplete Hemiparesis
And Contralateral Impairment of Tactile
And Proprioceptive Sense (Medial
Leminiscus)
Lateral Medullary Syndrome Ipsilateral 5th Nerve Cerebellar Peduncle: Ataxia of Limbs,
Ipsilateral Fibers of 9th & Falling to Side of Lesion:
10th Nerves Sympathetic Chain: Horner’s Syndrome
(Miosis, Ptosis, Decreased Sweating):
Loss of Taste: Nucleus And Tractus
Solitarius Numbness of Ipsilateral Arm,
Trunk, or Leg:
Spinothalamic Tract: Contralateral Loss of
Pain And Thermal Sense
10 | Medicine
Concept 1.5 : Thrombolysis in Stroke
Learning Objective: to learn the role of thrombolysis in Stroke
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Recombinant Tissue Plasminogen Activator (rtPA) is approved within Window period of

4.5 hours in Stroke. Total dose(Max)90mg iv (0.9 mg/kg).
Administration of Intravenous Recombinant Tissue Plasminogen Activator

(Rtpa) For Acute Ischemic Stroke (AIS):
Indication Contraindication
Clinical diagnosis of stroke. Sustained BP >185/110 mmHg despite treatment.

Onset of symptoms to time of drug administration Platelets <100,000; HCT <25%; glucose <50 or
<4.5 hb. >40° m9/dL.
CT scan showing no hemorrhage or edema of >1/3 Use of heparin within 48 h and prolonged PTT, or
of the MCA territory. elevated INR.
Age 18 > years Consent by patient or surrogate. Rapidly improving symptoms.
Prior stroke or head injury within 3 months; prior
intracranial hemorrhage.
Major surgery in preceding 14 days.
Minor stroke symptoms.
Gastrointestinal bleeding in preceding 21 days.
Recent myocardial infarction Coma or stupor.
Administration of rtPA
IV access with two peripheral IV lines (avoid arterial or central line placement). Review eligibility for rtPA.
Administer 0.9 mg/kg IV (maximum 90 mg) IV as 10% of total dose by bolus, followed by remainder of
total dose over 1 h.
Frequent cuff blood pressure monitoring.
No other antithrombotic treatment for 24 h.
Fa decline in neurologic status or uncontrolled blood pressure, stop infusion, give cryoprecipitate, and
reimage brain emergently.
Avoid urethral catheterization for ≥ 2 h.
Concept 1.6 : Hemorrhagic strokes
Learning Objective: to understand the difference between SDH and EDH
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Sub Dural Hemorrhage Extra-Dural Hemorrhage

Haematoma not adherent to suture lines Haematoma adherent to suture lines
Source : Cortical bridging veins Source : Extracranial arteries
Chronic subdural : Alcoholic & old age Head trauma
Acute subdural : Head trauma MC site – Temporo-parietal
C/F : Lucid Internals (Months) Lucid Interval (Short)
-> 1st episode of unconsciousness after injury due to
cerebral concussion
-> 2nd episode : due to Hematoma
CT scan : “CRESCENT SIGN” CT scan : “BICONVEX APPEARANCE”
Treatment is conservative Emergency Burr Hole evacuation
Poor prognosis Favourable Prognosis
Fig. 1.4
12 | Medicine
Concept 1.7 : Dementia
Learning Objective: to understand the classification and management of dementia
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Dementia:
Definition : Progressive irreversible loss of cognitive function (Higher Mental Function).
Amnesia : isolated defect of Memory. Causes are divided into:
Anterograde Retrograde
(Common) (Rare)
1. Head Trauma 1. Late stages of Alzeheimer’s
2. CNS infections 2. Benzodiazepines
3. Endocrine causes 3. Electroconvulsive therapy
4. Nutritional causes
5. Epilepsy (MTLE)
Dementia
PrimarySecondary (Reversible) Secondary
Alcohol abuse (Wernicke’s)

On Basis of MRI findings
CNS infections : TBM,
Neurosyphilis, Whipple’s
Trauma, Vascular
Misc : Normal Pressure
Generalized Localized
atrophy Hydrocephalus (NPH)
Alzheimer’s Fronto temporal dementia (FTD)
Diffuse Lewy body disease (DLB)

Concept 1.8 : Alzheimer’s Disease (AD) and Other dementia
syndromes
Learning Objective: to learn the genetics, Features and management of AD
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
AD is a primary dementia syndrome characterized by generalized atrophy, predominantly
of the Temporal and Parietal lobes. It affects Elderly Males (>50years) predominatly.
Due to defect in APP (Amyloid Precursor Protein) gene – on chromosome 21 , there
is production of dense abnormal amyloid in the (small) vessels leading to amyloid
angiopathy. This leads to neurodegeneration with formation of Senile and Neuritic
plaques. Also there is accumulation of TAU protein (Hence AD is part of Taupathy).
Genes: Presenilin -1 (PS1), Presenilin-2 (PS2), Apoε (Apo-Epsilon) predict penetrance-
Apo-ε 2 is the only protective allele.
Early stages of the disease mimics normal ageing and can delay diagnosis.
MMSE (mini-mental state examination) is the best screening test for Dementia.
MRI – reveals generalized atrophy. Genetic testing for APP gene confirms the disease.
Treatment: Donepezil approved but it only slows the progression (i.e. Palliative)
Prognosis: Unfavorable as the disease is relentless. No cure.
Disease First Symptom Mental Status N eurospsychiatry N eurology Imaging
AD Memory Loss Episodic Memory Irritability, Initially Normal Entorhinal Cortex
Loss Anxiety, And Hippocampal
Depression Atrophy
FTD Apathy: Poor Frontal/Executive Apathy, May Have Vertical Frontal, Insular,
Judgement/Insight, And/Or Language; Disinhibition, Gaze Palsy, Axial and/or Temporal
Speech/Language; Spares Drawing Overating, Rigidity, Dystonia, Atrophy; Usually
Hyperorality Compulsivity Alien Hand, or Spares Posterior
Mnd Parietal Lobe
DLB Visual Drawing and Visual Parkinsonism Posterior Parietal
Hallucinations, Frontal/Executive; Hallucinations, Atrophy;
Rem Sleep Spares Memory: Depression, Hippocampi
Behavior Disorder, Delirium-Prone Sleep Disorder, Larger Than in AD
Delirium, Capgras Delusions
Syndrome,
Parkinsonism
CJD Dementia, Variable, Frontal/ Depression, Myoclonus, Cortical Ribboning
Mood, Anxiety, Executive, Focal Anxiety, Psychosis Rigidity, And Basal Ganglia
Movement Cortical, Memory in Some Parkinsonism or Thalamus
Disorders Hyperintensity
on Diffusion/Flair
MRI
Vascular Often But Not Frontal/Executive, Apathy, Delusions, Usually Motor Cortical and/
Always Sudden; Cognitive Anxiety Slowing or Subcortical
Variable; Apthy; Slowing: Can Spasticity; can be Infarctions,
Falls Focal Spare Memory Normal Confluent White
Weakness Matter Disease
2 Headache and Epilepsy
CONCEPTS
Â Concept 2.1 Migraine And other Primary
Headache syndromes
Â Concept 2.2 Other Headache syndromes
Â Concept 2.3 Epilepsy
Â Concept 2.4 Status Epilepticus:
Â Concept 2.5 Important Epilepsy syndromes
Â Concept 2.6 Treatment of Epilepsy

Headache:
International Headache Society (IHS) Classification of Headaches
Primary: Secondary:
(Where Headache is the disease) (Is due to underlying pathology)
1. Head Trauma
Migraine type 2.Hemorrhage
Tension type 3. Infections – Sinusitis, Meningitis
Cluster type 4. Tumour
5. Dental Pain
6. Ophthalmic causes
Headache Symptoms that Suggest a Serious Underlying Disorder

Sudden-onset headache
First severe headache
“Worst” headache ever
Vomiting that precedes headache
Sub acute worsening over days or weeks
Pain induced by bending, lifting, cough
Pain that disturbs sleep or presents immediately upon awakening
Known systemic illness
Onset after age 55
Fever or unexplained systemic signs
Abnormal neurologic examination
Pain associated with local tenderness, e.g., region of temporal artery
16 | Medicine
Concept 2.1 : Migraine And other Primary Headache syndromes
Learning Objective: to learn the manifestations and management of Primary Headache
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Fig. 1.5
Tension Type Headache:

TTH occurs most commonly in a Middle aged Females > Males.
C/F:
a. Bilateral, Dull aching “Band like sensation”.
b. Scalp tenderness often associated with paraesthesia.
Rx : Acute : NSAIDS + Muscle relaxants. Chronic prophylaxis : SSRI /TCA.
Migraine Type Headache:

Predominantly affects Female aged 20-40 years.
Clinical Subtypes of Migraine:

CLASSICAL (20% cases) ATYPICAL (80% cases)
Site Hemicranial / Unilateral Bilateral
Character Throbbing Throbbing
Preceding symptoms Aura & Nausea - common Aura & Nausea - rare
Termination of attack Aborts with vomiting No vomiting
Duration 2-3 days 5-7 days
Simplified Diagnostic Criteria for Migraine

Repeated Attacks of Headache Lasting 4-72 h in Patients with a N ormal Physical Examination, no
other Reasonable Cause for the Headache, and:
At least 2 of the following features: Plus at least 1 of the following features:
Unilateral pain Nausea/vomiting
Throbbing pain Photophobia and phonophobia
Aggravation by movement
Moderate or severe intensity
Rx : Acute Management: (Put Acute and Chronic Side by Side Table**)
a. Triptans :Sumatriptan, Rizaritriptan => Preferred cause of faster onset.
b. Ergot alkaloids – ergotamine.
c. NSAIDS – Indomethacin.
Chronic Prophylaxis:
a. B-Blocker :Proponolol.
b. C-CCB : Verapamil, Flunarizine : is a Cerebro selective CCB.
c. AED : Valproate, Topiramate.
d. SSRI /TCA.
Prognosis : Favourable. No mortality. But Adversely affects Quality of life significantly.
18 | Medicine
Concept 2.2 : Other Headache syndromes
Learning Objective: to review the important Headache syndromes
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Cluster Headache Paroxysmal Sunct/suna

Hemicrania
Gender M>F F=M F~M
Pain
Type Stabbing. Boring Throbbing, boring, Burning, stabbing, sharp
Severity Excrusiating stabbing Severe to excruciating
Site Orbit, temple Excruciating Periorbital
Orbit, temple
Attack frequency 1/alternate day-8/d 1-20/d (<5/d for more 3-200/d
than half the time)
Duration of attack 15-180 min 2-30 min 5-240 s
Autonomic features Yes Yes Yes (prominent
conjunctival injection
and lacrimation)a
Migrainous featuresb Yes Yes Yes
Alcohol trigger Yes No No
Cutaneous trigges No No Yes
Indomethacin effect - Yes -
Abortive treatment Sumatriptan injection or No effective treatment Lidocaine (IV)
nasal spray
Oxygen
nVNSc
Prophyfactic treatment Verapamil Indomethacind Lamotrigine
Topiramate Topiramate
Melatoinin
Lithium Gabapentin
a
If conjunctival injection and tearing are not present, consider SUNA. bNausea, photophobia, or phonophobia; photophobia
and phonophobia the side of the pain. cNOn-invasive vagus nerve stimulation is FDA approved in episodic cluster headache
d
Indicates complete reponse to indomethacin.
Abbreviations: SUNA, short lasting unilaterral neuralgiform headache attacks with cranial autonomic features; SUNCT,
short-lasting unilateral neuralgiform headache...
Concept 2.3 : Epilepsy:
Learning Objective: to review the types and important epilepsy syndromes
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
• Epilepsy is a syndrome characterized by 2 or more Unprovoked seizures.
• Most Epilepsy have childhood onset. 10% have adult onset.
Fig. 1.6
Classification of Epilepsy
Classification of Seizures*
1. Focal Onset
(Can be further described as having intact or impaired awareness, motor or nonmotor onset, or evolve
from focal to bilateral tonic clonic)
2. Generalized Onset
Motor
Tonic-clonic
Other motor (e.g., atonic myoclonic)
Nonmotor (absence)
3. Unknown Onset
(Can be further described as motor or non-motor, or unclassified)
*Based on the new 2017 International League Against Epilepsy classification of seizure types (RS Fisher et al: Epilepsia 58:
522, 2017)
20 | Medicine
Grand Mal Petit Mal Myoclonic

MC – Elderly, Encephalopathy, MC - Children Myoclonus – only involuntary
Trauma movement in sleep.
Phases : 3-9 years. “Blank Stare”. 90% is due to Muscle fatigue.
Prodrome – Safety value Diagnosed by School teacher. 10% constitute Epilepsy.
Tonic - Apnea Each episode < 30 secs. D/D : SSPE.
Clonic - Aspiration 200-600 episodes/day. Juvenile Myoclonic epilepsy .
Post-ictal - Headache Minor motor activity may occur. Progressive Myoclonic epil.
Incontinence Precipitated by hyperventilation. Prion disease.
Myalgia Hypoxic Encephalopathy.
Concept 2.4 : Status Epilepticus:
Learning Objective: to learn the management of Status Epileticus
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Pharmacologic treatment of generalized tonic-clonic status

epilepticus (SE) in adults.
Fig. 1.7
CLZ, clonazepam; ECT, electroconvulsive therapy; LCM, lacosamide; LEV, levetiracetam;

LZP, lorazepam; MDZ, midazolam; PGB, pregabalin; PHT, phenytoin or fos-phenytoin;
PRO,propofol; PTB, pentobarbital; rTMS, repetitive transcranial magnetic stimulation;
THP, thiopental; TPM, topiramate; VNS, vagus nerve stimulation; VPA, valproic acid.
22 | Medicine
Concept 2.5 : Important Epilepsy syndromes
Learning Objective: to learn features and management of epilepsy syndromes
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
1. Juvenile Myoclonic Epilepsy (JME):

• Starts at adolescence.
• Characterized by myoclonic jerks which most commonly occur in the morning.
• 50% cases may also have GTC and 30%
• may have absence seizures.
• Convulsions are precipitated by sleep deprivation/ Alcohol.
• There is often a family history and EEG is diagnostic.
• Sodium valproate and Lamotrigine are approved for MOnotherapy
• Initial response to Anti-convulsants is favourable.
• But long-term remissions are uncommon making the prognosis poor
2. Lennox-GastautSyndrome :
• Most common Onset is in Childhood.
• Characterized by:
a. Multiple seizure types.
b. Multiple EEG abnormalities.
c. Progressive cognitive decline (Dementia).
• Refractory to medical therapy.
• Rufinamide is the new drug approved for the treatment and shows promise.
• However the prognosis remains Poor.
Mesial Temporal Lobe Epilepsy (MTLE) :

Characteristics of the Mesial Temporal Lobe Epilepsy Syndrome
History
Hostory of febrile seizures Rare generalized seizures
Family history of epilepsy Seizures may remit and reappear
Early onset Seizures often intractable
Clinical Observations
Aura common Postictal disorientation
Behavioral arrest/stare Memory loss
Complex automatisms Dysphasia (with focus in donimanat hemisphere)
Unilateral posturing
Laboratory Studies
Unilateral or bilateral anterior temporal spikes on EEG
Hypometabolism on interictal PET
Hypoperfusion on interictal SPECT
Material specific memory deficits on intracranial amobarbital (Wada) test
MRI Findings
Small hippocampus with increased signal on T2-weighted sequences
Small temporal lobe
Enlarged temporal horn
Pathologic Findings
Highly selective loss of specific cell populations within hippocampus in most cases
Abbreviations: EEG, electroencephalogram; MRI, magnetic resonance imaging; PET, positron emission tomography;
SPECT, single-photon emission computed tomography.
24 | Medicine
Concept 2.6 : Treatment of Epilepsy
Learning Objective: to learn to select Anti-epileptic treatment
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Generalized-Onset Focal Typical Absence Atypical Absence,

Tonic-Clonic Myoclonic, Atonic
First-Line
Lamotrigine Lamotrigine Valproic acid Valproic acid
Valproic acid Carbamazepine Ethosuximide Lamotrigine
Oxcarbazepine Lamotrigine Topiramate
Phenytoin
Levetiracetam
Alternatives
Zonisamide Topiramate Lamotrigine Clonazepam
Phenytoin Zonisamide Clonazepam Felbamate
Carbamazepine Valproic acid Clobazam
Oxcarbazepine Tiagabine Rufinamide
Topiramate Gabapentin
Phenobarbrtal Lacosamide
Primidone Exogabine
Lelbamate Phenobarbital
Primidone
Felbamate
When to Discontinue Therapy:

The following patient profile yields the greatest chance of remaining seizure free after
drug withdrawal: ( 1 ) complete medical control of seizures for 1 -5 years; (2) single
seizure type either focal or general ized; (3) normal neurologic examination including
intelligence; and(4) normal EEG. It seems reasonable to attempt withdrawal of therapy
after 2 years in a patient who meets all of the above criteria.
Management of Epilepsy in Pregnancy : Special condition:

1. No clear statistics whether pregnancy worsens or improves epilepsy.
2. Protocol of Rx during pregnancy:
a. Do not change the AED the mother is controlled on
b. Attempt for Monotherapy.
c. Optimise dosage by use of effective drug level monitoring.
d. Universal Folic acid supplementation to prevent neural tube defects.
3 Multiple Sclerosis
CONCEPTS
Â Chapter 3.1 Multiple Sclerosis
26 | Medicine
Chapter 3.1 : Multiple Sclerosis
Learning Objective: to learn to features, types and treatment of MS
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Multiple Sclerosis (MS) is a demyelinating disorder of CNS characterized by discreet

affection of multiple anatomical areas of CNS affecting young females.
Site C/F
1. Optic nerve (Most common) (65%) Diminision of vision (Optic neuritis)
2. MLF (Medical longitudinal fasciculus) Diplopia (IntranuclearOphthalmoplegia-INO)
3. Spinothalamic Tract Parasthesia (Tingling & Numbness)
4. Pyramidal Tract Hemiplagia / Paraplegia
5. Spinocerebellar Tract Cerebellar Ataxia
6. Dorsal column Sensory Ataxia (Romberg’s Sign +ve)
The McDonald criteria are used to diagnose MS. According to updates made in 2017, MS
can be diagnosed based on these findings:
two attacks or symptom flare-ups (lasting at least 24 hours with 30 days between
attacks), plus two lesions
two attacks, one lesion, and evidence of dissemination in space (or a different attack in
a different part of the nervous system)
one attack, two lesions, and evidence of dissemination in time (or finding a new lesion
— in the same location — since the previous scan, or presence of immunoglobulin, called
oligoclonal bands in the spinal fluid)
one attack, one lesion, and evidence of dissemination in space and time
worsening of symptoms or lesions and dissemination in space found in two of the
following: MRI of the brain, MRI of the spine, and spinal fluid
Approve Treatment options include Interferon Beta, Glatiramer acetate,
Natalizumab, Alemtuzumab, Fingolimod, Teriflunomide, Mitoxantrone.
Clinical Subtypes of M.S.:

RRMS – Relapsing Remitting M.S. (Commonest 80%).
SRMS – Secondary Relapsing M.S. SPMS – Secondary progressive M.S.
PPMS – Primary Progressive M.S. (Rarest+ Most severe).
KURTZKE’S Early Disability Scoring System (EDSS):
0 = no diability. No dependence.
10 = complete disability. Complete dependence.
Prognosis : Poor. Because the disease is unpredictable & relentless.
RRMS – Dependent by age of 55yrs. Bed ridden by age 65years.
PPMS – Dependant by age of 35yrs. Bed ridden by age 45 years.
4 Cranial Nerves
CONCEPTS
Â Chapter 4.1 Cranial Nerves
Chapter 4.1: Cranial Nerves
Learning Objective: to learn to major function and assessment of Cranial nerves
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Cranial N erve Major Function Reflex and Response Assessment

I Olfactory Sense of smell -
II Optic Afferent pathway for vision and light Menace response, papillary light
reflex, swinging light test
III Oculomotor Pupillary constriction Pupillary light reflex
Extraocular muscles (Other) Medial movement of globe
IV Trochlear Extraocular muscles (dorsal oblique) Ventrolateral rotation of globe
V Trigeminal Sensory to side of head and face Ear, eyelid and lip (facial) reflexes,
Motor to muscles of mastication pain perception from head septum
Chewing, jaw tone, muscle mass
(temporalis, masseter, pterygoid)
VI Abducens Extraocular muscle (retractor oculi) Eyeball retraction (corneal reflex)
Extraocular muscle (lateral rectus) Lateral movement of globe
VII Facial Motor to muscles of facial expression Ear, eyelid and lip (facial) tone reflexes
and movement, facial symmetry
VIII Vestibulocochlear Affterent branch of vestibular system Head posture, induced eyeball
Sense of hearing movement, normal vestibular
nystagmus, normal gait, blindfold test
Response to noise
IX Glossopharyngeal Sensory and motor to pharynx and Swallowing (palpation), gag reflex
X Vagus larynx (nasal tube), endoscopy, slap test
XI Accessory (vagal and recurrent laryngeal nerves)
XII Hypoglossal Motor to tongue Tongue size and symmetry

5 CNS Infections
CONCEPTS
Â Concept 5.1 TBM and CSF findings in Meningitis
Â Concept 5.2 Other Infections
Â Concept 5.3 Prion disease

Concept 5.1 : TBM and CSF findings in Meningitis
Learning Objective: to understand TBM and diagnostic role of CSF in meningitis.
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Tubercular Meningitis:
MC cause of Bacterial Meningitis in India/ Worldwide.
All age groups and Gender maybe affected by TBM.
BCG vaccination has been identified as a Protective factor, especially in Endemic areas.
The clinical features can vary widely. Ranging from Benign symptom like Headache to a
more ominous symptoms like Convulsions, Encephalopathy and Dementia.
Diagnosis : C.S.F analysis confirms the disease. (See Below Table).
Pathophysiology :
TBM is cause of Basal Meningitis.
↓
Hard Exudates at the Base of the skull on neuroimaging
↓
These Exudates block the Subarachnoid villi interfering with CSF reabsorption
↓
Non- obstructive / Communicating Hydrocephalus
Rx : Anti-Tubercular Therapy (ATT) + Steroids –Duration of 12-18 Months.
Prognosis : Favourable with early treatment.
C.S.F Pyogenic T.B.M Viral/Aseptic

Physical property Turbid Cob-web/Coagulam Clear
Biochemistry :
Proteins +++ ++ Normal / +
Sugar Very Low Normal / Mild Low Normal
Microbiology :
Total Cell count >1000 >200-600 N
Differential count Neutrophil +++ Lymphocytes +++ N
Special test Gram stain, Culture ZN stain, ADA PCR for HSV
CSF Manometry : Normal / Mild elevation Always elevated Normal
32 | Medicine
Concept 5.2 : Other Infections
Learning Objective: to review important CNS infections
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
1. Viral meningo-encephalitis:
MC cause of Sporadic viral encephalitis in the world is HSV (Herpes Simplex Virus 1)
C/f : Headache, Convulsion, FND – Mimics Stroke
Diagnosis : MRI – is Most specific, but lacks sensitivity.
It shows Bitemporal horn Hyperintensities on T2 weighted images
Frontal lobe hemorrhages may be seen in some cases.
Treatment : IV Acyclovir 500mg 8 hourly for 10-14 days.
Prognosis : Favourable. Long term complication – Scar epilepsy.
2. Cryptococcal meningitis:
Caused by encapsulated fungi – Cryptococcal neoformans.
In a HIV +ve patient, it is a AIDS defining complex (CD4 <200).
Pathophysiology: Less inflammation (due to immunocompromised status).
Subarachnoid villi are mechanically obstructed by fungal gelatinous sheet.
Interfering with CSF reabsorption and thus causing raised ICT.
C/F : Headache, symptoms of raised ICT – Papilloedema, Projectile vomiting. Absence
of neck stiffness is characteristic
In C.S.F = India Ink preparation can detect encapsulated fungi.
Gold standard is Cryptococcal antigen detection in CSF by ELISA.
Treatment : Amphotericin B followed bylifelong Fluconazole prophylaxis.
Prognosis : Unfavourable.
3. Neurocysticercosis (NCC):
Caused by infection by TaeniaSolium (Pork Tapeworm).
Larval stage is most infective stage of the parasite.
The most common source of infection is uncooked green leafy vegetables.
Young to middle aged adults are most commonly affected and present with focal
convulsion
MRI – reveals Ring-Enhancing lesion with “SCOLEX” inside – (Gold standard)
Treatment is with Albendazole and steroids for 21 days.
Long term complication is Scar epilepsy.
4. Subacute Sclerosing Pan- Encephalitis (SSPE):
SSPE is post-infective sequalae of Measles infection occurring 8-10 years after the
infection.
Average age of preesnetationos 10-18 years with symptoms of Neuro-regression,
Myoclonic jerks and gradual deterioration to death.
Diagnosis : EEG - Rademecker’s complex (periodic 3 Hz complexes).
Rx : Palliation in early stages in form of Ebonosin & Interferon therapy.
There is no Cure and the disease is terminal. Hence the best way to prevent is to ensure
universal vaccination against Measles.
34 | Medicine
Concept 5.3 : Prion disease
Learning Objective: to learn about Prion disease
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Prion is the only non-nucleated pathogen causing human disease.
Prion have neither DNA nor RNA. Present in both living (infectious particle) & non living
(crystalline) form. Hence limited data available.
History: 1st Prion disease discovered was the Mad cow disease (Bovine transmissible
spongiform encephalopathy). It was linked to the infamous Bone meal programme
practiced in UK slaughter houses. The cows were feed powdered bones of slaughtered
cows as a rich source of calcium and effectively achieving – “forced cannibalism”. After
few months, the cows developed a triad of Personality changes, Myoclonic jerks and
Death. Post-mortem revealed that the Brain of the cow had become like a kitchen
sponge. There was no cure. The only measure being prevention of the disease.
Based on the theory that the disese spreads by act of cannibalism – we discovered the
1st human prion disease in an African cannibal tribe – Kuru. However the evidence was
retrospective as the tribe had discontinued cannibalism.
The most common human prion disease is the Crueksfeld-Jacob disease (CJd). Also
called Human transmissable Spongiform encephalopathy for the similarity shared
with madcow disease. The main subset discovered were recipients of cadaveric organ
transplant. Corneal transplant can theoretically transmit the disease but risk is minimal
as cornea is avascular structure.
Mean age of presentation is 35 years, M>F.
The patients present with the classical triad of Personality changes, Myoclonic
epilepsy and Dementia followed by Death.
The only diagnosis is a Post-mortem brain biopsy with no cure at present except
prevention.
Fatal Familial Insomnia (FFI). Discovered in an African tribe.
Patients present with Insomnia, Dementia, Myoclonus followed by Death.
6 Myelopathy
CONCEPTS
Â Concept 6.1 Localisation of Myelopathy
Â Concept 6.2 Important Myelopathy Syndromes

36 | Medicine
Spinal Cord Anatomy
Fig. 1.8
38 | Medicine
Concept 6.1 : Localisation of Myelopathy
Learning Objective: to learn about identifying site of lesion in myelopathy
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
The differences between intramedullary and extra medullary compression:

Intramedullary Extramedullary
Symptoms –
Root pain – Uncommon Common
Vertebral pain – Uncommon Common
Funicular pain – Common Absent
Weakness – Late Early
Pattern- Descending loss Ascending loss
Sacral sparing- Present Absent
Signs –
Parasthesia – Descending Ascending
Brown seq. – Uncommon Common
Dissociative sensory loss Present Absent
UMN features – Late Early
LMN features – Prominent Unusual
Bladder/ bowel dys – Early Late
Horner’s syn – Absent Present (C8. T1)
Investigation –
Spinal subarachnoid block - Early &marked Late& less marked.
Localisation of spinal cord disorder:

Site Clinical features
Foramen magnum Cerebellar signs, horner’ssyndeome, down beat
nystagmus, lower cranial nerve palsy,
C2 Segment Suboccipital pain or sensory loss, Pain / temperature lost over face.
C3 – C5 Segment Weakness of respiratory muscles (phrenic C3 – C5)
Loss of Bicep jerk (C5)
Invert Supinator (C5)
Sensory loss over detoild (C5)
Quadriplegia
C4 – C5 Segment Quadriplegia but with preserved resp function.

C6 Segment Supinator jerk lost
Increase finger flexion
C7 Segment paresis of fingers, wrist extensors
Biceps /Supinator preserved
Triceps lost/ Inverted Triceps
C8/T1 Segment Parasis of finger/ wrist flexors
Finger flexor reflex lost
Horner’s syndrome
T3 Segment Sensory impairement in axilla
T4 Segment Sensory loss at nipples
T10 Segment Beevor’s sign
Loss of lower superficial abdominal reflex
T12 Segment Abdominal reflex preserved
L1 Segment Absent cremasteric reflex
Brisk knee/ Ankle jerk
L2 – L4 Segment Knee jerk lost
Paresis of flexor / adductors of thigh
Knee extensors
L5 – S1 Paresis of knee flexors
Paresis of Extensors of thing
Weakness of foot/ ankle movements
Ankle jerk is lost.
• In general cervical cord diseases are best localised by pattern of weakness, sensory
loss has less localising value.
• Thoracic cord disorders are best localised by sensory level, pattern of weakness has
less localising value.
• Lumbar cord disorders are localised by loss of reflexes and pattern of weakness.
40 | Medicine
Concept 6.2 : Important myelopathy syndromes
Learning Objective: to learn important myelopathy syndromes
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Brown Sequard syndrome/Hemi-section of the Cord:

Uncommon in Clinical Practice but a model to study the Physiological concepts of the
cord.
Hemisection : Ipsilateral loss of Dorsal column sensations
Contralateral loss of spinothalamic sensations (1/2 segments below the lesion)
Ipsilateral motor weakness (cortico-spinal tract)
Syringomyelia:
Definition : Abnormal & progressive dilatation of the central canal of the spinal cord.
It is commonly congenital & associated with Chiari - 1 malformation in 50% cases.
The MC is upper cervical cord. It is called Syringo-bulbia when it extends into medulla.
Inspite of being congenital it presents in the 2nd decade of life. This occurs because the
growth of the syrinx is proportional to growth of the spinal cord. Once cord achieves
adult dimensions, the further dilatation causes intradural compression.
C/F:
Sensory symptoms Motor symptoms Autonomic symptoms
Dissociate anaesthesia Upper-limb > Lower limb Bladder function affected
Spinothalamic sensation lost Asymmetrical
Dorsal column spared
“Suspended cape” distribution Distal > Proximal
Finger flexors first
Small muscle wasting
(chronic denervation)
Diagnosis : MRI confirms the disease.
Rx : Palliative : Acetazolamide.
Specific : Syringodural shunt – Decompression of the syrinx.
Prognosis : Unfavourable – since the Neurodeficit is irreversible. Surgery is high risk.
Neurofibromatosis (NF):
N F-1 (Peripheral N F) N F-2 (Central N F)
Von-RecklingHausen disease
Autosomal Dominant Autosomal Dominant
Neuro-Cutaneous syndrome > 85% present with Bilateral Schwanoma

1. Café-au-lait spots (Acoustic Neuroma)
2. Axillary freckling Sensori-neural deafness
3. Lisch nodules (Hamartomas on Iris)
4. Peripheral NF itself
< 10% present with Unilateral Schwanoma Multilevel Myelopathy
No Myelopathy No Cutaneous Markers
Diagnosis is clinical Diagnosed by MRI scan
Treatment is Cosmesis Recurrent spine surgery
Favourable prognosis – Normal Lifespan Poor Prognosis
Neurocutaneous Markers:
Markers Disease
1. Adenoma Sabaceum
[Hypertrophy of sweat glands over the face]
2. Ash-Leaf Macules Tuberous Sclerosis
[greyish macules extensor surface of elbow]
3. Shagreen’s patch [Hyperpigmentad patch over
sacrum – Best seen under Woods lamp]
Hamartoma’s over the mucous membrane & other Von Hipple – Landau’s disease
organs [Brain, lung, liver]
Tuff of hair at the site of meningocele Spina bifida.
Non-Compressive Myelopathy:
Transverse Myelitis N euro Myelitis Optica (DEVIC’s)
Introduction Functional transection of cord Autoimmune disease of cord
Epidemiology 20-30 years, Males > Females 20-30 years, Females > Males
Etiology Post-infective phenomenon Auto-immune disease
Site Mid-Thorasic cord Thorasic cord + Optic nerve
Clinical features Paraplegia Paraplegia
Distinct Sensory level Sensory Level
Prominent Bladder involvement Prominent Bladder
Clonus / Flexor spasms
Optic neurits –
Diminision of vision
Diagnosis MRI – Single level hyperintensity Long Segment disease – MRI
Antibody – Aquaporin 4 protein
42 | Medicine
Treatment
Acute stage IV Methyl Prednisolone Pulse Rx IV MP Pulse therapy
IVIG / Plasma Exchange
Chronic NIL – no recurrence Immunosupression
Prognosis Complete recovery in 6-8 weeks Incomplete recovery.
Relapses common
Excellent Prognosis Poor Prognosis
Non-Compressive Myelopathy (Ctd..):

Tabes Dorsalis Subacute Degeneration of cord
Introduction Degeneration of Dorsal column Degeneration of Dorsal column
(Predominantly) and Cortico-spinal tracts
Epidemiology 30-50 years, Males > Females 30-50 years, Males > Females
Etiology Neuro-syphilis (Tertiary syphilis) B12 deficiency
Clinical features Sensory ataxia Sensory ataxia
Rombergs sign +ve Rombergs sign +ve
Associations Dementia – General Paresis of Insane Glossitis
(GPI) Anaemia
Argyll-Robertson Pupil (ARP) Peripheral Neuropathy
MRI scan Dorsal column hyperintensity Dorsal column hyperintensity
Serology VDRL +ve Serum B 12 levels - Low
Treatment No Cure. Only Prevention Injection B12
Prognosis Poor – No recovery Excellent recovery
Conus Medullaris Cauda Equina Syndrome

The terminal part of the cord is affected Affects the lower Lumbar roots
(Horse Tail appearance)
Bilateral lesion. Asymmetrical lesion. LMN lesion.
Sacral and Coccygeal roots are affected Lower Lumbar roots affected.
Early & Prominent Bladder involvement Prominent Radicular Pain
Saddle-shaped anaesthesia Variable leg weakness
Loss of Anal tone & Variable areflexia in legs
Loss of Bulbocavernous reflex No Bladder involvement
Neurosurgical Emergency Medical management
Delay causes Permanent Bladdder control Prognosis unfavourable
7 Motor Neuron Disease (MND)
CONCEPTS
Â Concept 7.1 Motor Neuron Disease
44 | Medicine
Concept 7.1 : Motor Neuron Disease (MND)
Learning Objective: to learn understand the types, diagnosis of MND
Time needed
1st Reading 30 mins
2nd Reading 10 mins
MND is Characterized by the presence of UMN and LMN signs in the same patient.
Depending on which signs are predominant it is further subdivided into :
1. Classical - ALS – Amyotrophic Lateral Sclerosis
2. Predominant UMN - PLS – Primary Lateral Sclerosis
3. Predominant LMN - SMA – Spinomuscular atrophy
Etiopathogenesis: Idiopathic. In Familial cases – SOD gene mutation identified.
Degenerative disease affecting Corticospinal tract and Anterior Horn cell.
Clinical Features:
UMN LMN
Degeneration of Corticospinal Tract Degeneration of Anterior Horn cell
Predominantly in Lower limbs Predominantly in Upper limbs
Spasticity Hypotonia
Exagerrated DTRS Small muscle wasting
Extensor Plantars Fasciculation
Diagnosis : Is of exclusion. D/D of Motor Neuron Disease :
High Cervical myeloradiculopathy. Craniovertebral anomaly.
MRI Brain + Spine excludes above differential and suggest MND.
Treatment : Riluzole – Only palliative.
Prognosis : Terminal. Most common terminal event is Respiratory Complications.
8 Neuropathy,
NMJ Disorders and Myopathy
CONCEPTS
Â Concept 8.1 Classification of Neuropathy
Â Concept 8.2 Guillian Barre Syndrome (GBS)
Â Concept 8.3 Inherited Neuropathy
Â Concept 8.4 Neuro-Muscular Junction Disorders

(NMJ)
Â Concept 8.5 Myopathy

46 | Medicine
Concept 8.1 : Classification of Neuropathy
Learning Objective: to learn understand the types of peripheral neuropathy
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Classification of Peripheral Neuropathy:

A. Based on site of Pathology:
Axonal & Demyelinating Neuropathy
Axonal Demyelination
NCS : Amplitude : Severely affected Near Normal
Velocity : Near Normal Severely depressed
e.g. Trauma, Vascular, Toxin e.g. AIDP, CIDP
The recovery is often delayed & Partial Recovery is early & complete
Treatment of underlying cause DOC is Immunosupressive therapy
Poorer Prognosis Excellent Prognosis
B. Based on Modality affected:

Predominantly sensory → Nutritional (B1, B6, B12), Diabetes Mellitus, Heavy metal-
Arsenic, Cadmium, Drugs – Oxaliplatin.
Predominantly Motor → GBS, Lead poisoning, Diphtheria, Porphyria, Dapsone toxicity,
Recurrent hypoglycemia.
Autonomic neuropathy → Old Age, Diabetes Mellitus.
C. Based on Number affected:
Mononeuropathy → Trauma, Entrapment
Medical conditions associated with Entrapment :
a. Pregnancy
b. Hypothyroidism
c. Acromegaly
Polyneuropathy → Gullian Barre Syndrome (GBS)
Mononeuritis multiplex → In India – Leprosy. Worldwide – Polyarteritis Nodosa.
D. Based on Etiology:
Congenital & Acquired.
Congential Neuropathy is divided into Primary and Secondary.
Group of Primary congenital Neuropathy is called CHARCOT MARIE TOOTH disorders.
Concept 8.2 : Guillian Barre Syndrome (GBS)
Learning Objective: to learn understand the features and managemet of GBS
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
GBS is a polyneuropathy syndrome. GBS has following clinical subtypes :

1. AIDP – Acute Inflammatory demye linating polyneuropathy - 85% of cases.
2. Miller – Fischer variant
3. AMAN – Acute Motor Axonal Neuro pathy
4. ASMAN – Acute Sensori-Motor Axonal Neuropathy
Epidemiology of AIDP : 1-2nd decade of life.
Etiopathology: Post-infective phenomenon. MC organism associated – Campylobacter
jejuni.
Clinical features : Acute, Ascending, Flaccid, Symmetrical Quadriparesis Areflexia –
Absence of DTR’s.
Cranial Neuropathy is rare. If affected – 7th CN MC involved.
No Bladder Involvement.
No distinct Sensory Level. No sensory involvement.
Diagnosis : Typical clinical presentation.
C.S.F analysis – Albuminocytologic dissociation
Electro physiological studies reveals demyelinating polyneuropathy.
Principal Antiglycolipid Antibodies Implicated In Immune Neuropathies:

Clinical Presentation Antibody Target Usual Isotype
Acute Immune N europathies (Guillain-Barre Syndrome)
Acute inflammatory No clear patterns IgG (polyclonal)

demyelinating polyneuropathy GM1 most common
(AIDP) IgG (polyclonal) IgG (polyclonal)
Acute motor axonal neuropathy GDla, GM1, GMIb, GalNAc- IgG (polyclonal)
(AMAN) GD1a (<50% for any)
Miller Fisher syndrome (MFS) GQIb (>90%) IgG (polyclonal)
Acute pharyngeal cervicobrachial GTla (? most)
neuropathy (APCBN)
48 | Medicine
Chronic Immune N europathies
Chronic inflammatory P0, myelin P2 protein, PMP22, No clear pattern

demyelinating polyneuropathy neurofascin
(CIDP) (75%)
CIDP-M (MGUS associated) Neural binding sites IgG, IgA (monoclonal)
(25%)
Chronic sensory > motor SPGPf SGLPG (on MAG) (50%)
neuropathy IgM (monoclonal)
Uncertain (50%) IgM (monoclonal)

Multifocal motor neuropathy GM1,GalN Ac-GDI a, others IgM (polyclonal monoclonal)
(MMN) (25-50%)
Chronic sensory ataxic GDIb, GQ1 b, and other b-series IgM (monoclonal)
neuropathy gangliosides
Rx : Specific : IVIg / Plasmapheresis. With Supportive Physiotherapy and Rehabilatation.

Steriods are contraindicated as they produce paradoxical worsening of Neurodeficit.
Prognosis : Excellent with full recovery of Neurodeficit.
Complication : Respiratory paralysis – Needs Elective Mechanical Ventilation.
Concept 8.3 : Inherited Neuropathy
Learning Objective: to learn the Primary and Secondary inherited neuropathy
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Charcot-Marie-Tooth disorders (CMT):

a. CMTD -1
MC Type. Autosomal Recessive. Demyelinating in Pathology.
Presents in adolescents as foot drop/wrist drop.
Inverted “Champage bottle appearance” of the leg (Due to Selective wasting of
anterior group of muscles below knee).
Diagnosis – Clinical. Confirmed by Nerve Conduction Studies.
Rx: Prosthesis + Rehabilitation. Refractory to medical therapy.
Favourable prognosis.
b. CMTD -2
Autosomal dominant. Axonal in pathology. Benign (compared to CMTD-1).
Presentation is in Middle & old age with Foot/ Wrist drop as above.
Diagnosed clinically with Nerve conduction studies.
Favourable Prognosis.
c. CMTD -3 ->Dejerrinesoutas disease. Demyelinating in Pathology.
Presents in infancy with generalized hypotonis (Floppy baby)
Associated with poor feeding, respiratory distress & high fatality.
Worst prognosis. No cure.
Secondary Congenital Neuropathy:

N ame Defect Main affection Treatment
Fabry’s disease Alpha-galactosidase Premature atherosclerosis. Enzyme supplementation
deficicency Cardiomyopathy. available
Renovascular HTN
Refsum’s disease Defect in phytanic acid Thickened nerves Restrict phytanic acid in
metabolism Retinitis pigmentosa diet (all Veg oils)
Tangiers disease HDL transport defect Orange tonsils Low fat diet
Atherosclerosis
Porphyria Heme metabolism defect Abdominal pain Heme infusion during
Photosensitivity acute attack
50 | Medicine
Concept 8.4 : Neuro-Muscular Junction Disorders (NMJ)
Learning Objective: to learn understand the features and management of NMJ
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Neuro – Muscular Junction (NMJ) disorders:

Myasthenia Gravis Lambert-Eaton syndrome
Introduction Post-synaptic NMJ defect Pre-synaptic NMJ defect
Epidemiology 2nd decade, Female preponderant 5th decade, Males > Females
Etiology Auto-immune : Para-neoplastic :
AChR antibodies Anti-P/Q/Type Calcium channel

Antibodies.
Association Thymic Hyperplasia (65%) Small cell carcinoma of Lung
Thymoma (5-10%) Gastro-intestinal malignancy
Pathophysiology 1. Reduction in Number of AcHR Impaired AcH release from the pre-
2. Reduction in Efficacy of existing synaptic membrane.
AcHR
3. Complement mediated injury to Post-
synaptic membrane
Clinical features Ocular symptoms (Restricted to CN) Presents a Fluctuating proximal muscle
MC – 3rdCN - Ptosis weakness.
4th, 6th CN - Diplopia
5th CN - Difficulty in Mastication There is a transient improvement in
9,10th CN – Difficulty in Swallowing power on initial exertion.
12th CN – Difficulty in Bolus of food.
Ocular symptoms are very rare.
Within 3 years of onset, 85% progress to
Generalised MG. 15% escape forever
Constitutional symptoms of Malignancy
Generalised MG – Fluctuating Proximal – cachexia, Anorexia, Weight loss
muscle weakness.
Myasthenic crisis – Respiratory paralysis
requiring ventilator support
Diagnosis :
a. Serology Anti-AcHR antibodies (Gold standard) Anti-P/Q type Calcium channel
(SPECIFIC TESTS) Anti-MusK – Muscle-specific kinase antibodies
b. RNS (Sensitive) Decremental response

Repititive Nerve Incremental response
Stimulation SFEMG (Single Fiber Electro-
myography) Most sensitive test. But
technically demanding, Painful.
c. Clinical testing Edrophonium / Tensilon test
---
Treatment :
Palliative Pyridostigmine Pyridostigmine
Specific Immunosupressive therapy Chemotherapy
Additional tests HRCT-Thorax – Thymus abnormality HRCT –Thorax - SCCL
Prognosis Excellent Poor
52 | Medicine
Concept 8.5 : Myopathy
Learning Objective: to learn the features and management of myopathy
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Muscular Dystrophy (MD):

Disease Epidemiology Clinical features Diagnosis Treatment &
&Inheritance Prognosis
Duchenne’s 1st Decade Recurrent Falls Screening – CPK No cure.

(DMD) Male Dominant GOWER’S sign
Pseudo- Confirmatory – Steriods are
X-Recessive hypertrophy calf Western Blot palliative before 5
analysis of years of age
Cardiomyopathy Dystrophin gene Physiotherapy &
Dystrophin gene concentration Rehabilitation
Grave Prognosis
Terminal event-
Respiratory
complications
Becker’s (BMD) 2st Decade Proximal Muscle Same as above No cure.

X-recessive Male Dominant weakness
Dystrophin-Gene Cardiomyopathy Terminal event-
Cardiac failure
Facio- scapula- 3rd Decade Selective wasting Screening – CPK No cure.

Humeral (FSH) M=F of Facial and
Autosomal Shoulder girdle Physiotherapy &
(Both AR/AD) muscles Rehabilitation
Limb Girdle 4th Decade Selective wasting No cure.

Autosomal (Both M=F of Shoulder &
AR & AD forms) Pelvic muscles Physiotherapy &
Rehabilitation
Oculopharyngeal 5th decade Bilateral ptosis No cure.

Dystrophy M=F Dysphagia Physiotherapy &
Autosomal Rehabilitation
dominant only
Myositis Syndromes:
Polymyositis Dermatomyositis Inclusion Body
Myositis
Defination Inflammatory IP with skin manifestations Focal Myositis
Polymyopathy (IP) syndrome
Epidemiology 1-2nd decade 1-2nd decade 5th decade & beyond
Females >> Males Females >> Males Females >> Males
Associations Auto-immune diseases Internal Malignancy – GIT or None
Viz. SLE, Sjogren’s, Hematological
Scleroderma, MCTD
Clinical features Painful Proximal muscle Same as Poly + Skin changes : Distal more than
weakness. GOTTRON’S rash Proximal muscle
(Hyperpigmentation of weakness (ONLY
(NEVER affects Extra- knuckles) MYOPATHY with
ocular muscles EOM) this distribution of
V-sign – Necklace area weakness)
hyperpigment.
Can cause Dyphagia Shawl sign – Over the back
Tender nodules
Diagnosis Creatinine kinase levels Creatinine kinase
levels
a. Screening Creatinine kinase levels
b. Confirmatory Muscle Biopsy Muscle Biopsy Muscle Biopsy
Treatment
a. Palliative Steroids & NSAIDS Steroids & NSAIDS No treatment
b. Specific Longterm immune- Management of Malignancy
supression if any
Prognosis Favourable Favourable (if benign Poor
Poor (if associated Malignancy)
9 Parkinson’s Disease
and Gait Disorders
CONCEPTS
Â Concept 9.1 Movement disorders
Â Concept 9.2 Parkinson’s disease (PD)

Concept 9.1 : Movement disorders
Learning Objective: to learn the features and site of various movement disorders
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Disorder Description Site of Pathology Causes

1. Tremors :
a. Intentional/Kinetic Tremor is Present on Cerebellum Senile Degeneration
reaching to touch a Alcoholics
target Cerebellar Stroke
Drugs : e.g.
b. Resting Present only at Rest. Substantia Nigra Carbamazepine
Abolishes on activity. Parkinsonism
c. Essential Tremors Tremors present Anxiety Type A Personality

[Benign Familial provoked by emotion or Familial tremors.
Tremors] stress.
[Younger population] Abolishes on Alcohol
Consumption Metabolic
Cortex Encephalopathies
d. Asterexis Inability to Sustain a Hepatic
[Flapping tremors] Muscle contraction Uremic
Pseudo-tremor while performing a Carbon dioxide Narcosis
Complex motor activity
[>3 joint are involved]
Disorder Description Site of Pathology Causes

1. Chorea Rapid, jerky & Caudate a. Rheumatic chorea
Quasi – purpose Nucleus (Syndenham’s Chorea
[Semi-purposive} / Saint Vitus Dance)
b. Chorea gravidarum
c. Drug induced : Anti –
psychotics
d. Huntington’s disease
2. Hemi ballismus Violent flinging Sub thalamic Nucleus Vascular infarct

movement of the Degeneration
Proximal joints
3. Athetosis Slow writhing movement Putamen Wilson’s Disease

involving distal joints Vascular events
Degenerative
4. Fasciculations Twitching of Muscle Anterior Horn cell a. Motor Neuron

Degeneration Diseases
b. Syringomyelia
c. Thyrotoxic &
d. Carcinomatous
Myopathies
56 | Medicine
Concept 9.2: Parkinson’s disease (PD)
Learning Objective: to learn the features and management of PD
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
• Parkinson’s disease is an idiopathic parkinsonism syndrome affecting elderly males.
Clinical presentation is divided into 2 groups:

Motor Symptoms N on Motor
1. Resting Tremors : It starts as Asymmetric but 1. Depresstion [85% of patients]:

becomes symmetric by end of 2 years. Cause is Multifuctional :
Slow frequency ( 4 – 6 Hz) i. Endogenous - part of disease
Pin-Rolling tremors ii. Dopaminergic drugs.
iii. Social stigma
2. Bradykinesia : Slowing of the movement. They 2. Insomnia – DOC - Zolpidem
can have episodes of freezing (Akinesia), especially
while negotiating narrow passages and sharp turns.
[KinesiaParadoxica] : In emergency there is
remarkable agility in PD.
3. Rigidity : Cog –wheel Rigidity 3. Restless leg Syndrome – DOC
-Rigidity interrupted by Tremors. Dopamine agonists.
Festinantgait – components : Stooping posture 4. Erectile dysfunction – Sildenafel.

Broad Based gait
Short steppage 5. Detrusor sphincter dys-synergia :
Reduced arm swing. DOC :Teroludine
6. Postural hypotenstion : Rehabilitation
7. Sialorrhea : occurs due to Dysphagia –

More with Liquids compared to solids.
DOC – Anti cholinergics.
Diagnosis of PD is Clinical:
Treatment is by Dopaminergic agents, anticholinergics and Neuroprotective
agents.
1. Role of Deep Brain Stimulation (DBS): The best site of electrode placement:
a. In Tremor-dominant PD – Subthalamic nucleus.
b. In Dopamine-induced dyskinesia–Globus Pallidus.
Prognosis : of PD is favourable.
Respiratory complications are the most common cause of mortality.
Parkinson plus Syndromes : are predominantly patients diagnosed as PD having
additional features.
1. PD + Dysautonomia = Shy Drager Syndrome.
(Multi-system atrophy MSA(a).
2. PD + Early Dementia = Diffuse Lewy body disease.
3. PD + gaze palsy [Inferior first]/Recurrent falls =Progressive Supranuclear. Palsy
(PSP).
4. PD + Pyramidal = Multi system atrophy MSA(p).
5. PD + Cerebellar signs = Multi system atrophy MSA(c).
The diagnosis of PD plus syndrome is important for the following reasons :
a. Response to Syndopa therapy is poorer.
b. Progression of disease is faster.
c. Poorer Prognosis.
10 Miscellaneous
CONCEPTS
Â Concept 10.1 Bladder Disorders
Â Concept 10.2 Ataxia

Concept 10.1 : Bladder disorders
Learning Objective: to learn the different types of Bladder
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Pathology of bladder:
Bladder:
Total capacity : 400 – 800 cc
Supplied by : Sympathetic plexus : T12 to L1
Parasympathetic plexus: S2, S3, S4
Somatosensory → Pudendal Nerve → S2, 3, 4.
Social Inhibition performed by paracentral
lobule in the Frontal lobe.
Physiology of Micturation:
150 ml of Bladder filling : 1st stimulus passed – to void. Non–Painful.
Commonly Suppressed by Aware Adults. 450 – 600 ml : 2nd stimulus => unpleasant.
Frontal Lobe Bladder UMN (Spastic bladder) LMN (Hypotonic bladder)
Socially Un-inhibited Automatic bladder Spinal cord Over-distended bladder
Myelopathy
Frontal Lobe dysfunction Sensations : Usually Automatic Pelvic disorders affecting roots
Affection of Micturation centre evacuation
Sensations : Lost
Sensations preserved Motor Frequency, Precipitancy Complete Over distended with overflow
control intact evacuation
incontinence occurs. Dribbling of
urine Incomplete voiding
But Patient urinates at Odd
places due to lack of Social
awareness.
60 | Medicine
Concept 10.2 : Ataxia
Learning Objective: to learn the causes of Ataxia
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Ataxia:
Symmetrical Asymmetrical
Acute (Hours to Days) Intoxication : Alcohol, Lithium, Cerebellar Infarction.

Barbiturates Subdural hematoma. Cerebellar
Infections : Viral cerebellitis abscess.
Sub-acute (days to Weeks) Intoxication : Mercury, Gasoline, Cerebellar Glioma Metastatic

Chemotherapy & Alcohol tumours.
Nutritional : B12 deficiency Multiple sclerosis.
Chronic (months to years) Paraneoplastic syndrome Tabes Chiari Malformation.

Dorsalis Dandy-Walker malformation. Stable
Phenytoin toxicity Gliosis – Vascular.
SECTION — 2
CARDIOVASCULAR SYSTEM
1 Clinical Examination
CONCEPTS
Â Concept 1.1 Arterial Pulse
Â Concept 1.2 JVP examination : Best done in IJV

(valveless vein)
Â Concept 1.3 Pulsus Paradoxus
Â Concept 1.4 Heart Sounds
Â Concept 1.5 Heart Murmurs

Cardiovascular System
Concept 1.1 : Arterial Pulse
Best done by the method of Tri-section (3-finger method)
Pulse is a transmitted waveform of Left Ventricular contraction.
It can be examined in both Peripheral sites and Central(Carotid pulse) :
Fig. 2.1
Peripheral Pulse Assessment N ormal Findings

1. Rate
2. Rhythm
3. Volume
4. Condition of Vessel wall
5. Apex-Pulse deficit
6. Symmetry
Medicine
7. Radio-Femoral Delay
8. Distal Pulsations
Arterial Pulse Waveforms : Best Assessed in Carotid Pulse :

Waveforms nterpretation Significance
b. Pulsus Parvus
c. Pulsus tardus
d. Pulsus Bisferiens
Pulsus alternans
Medicine
Concept 1.2 : JVP examination : Best done in IJV (valveless vein)
Fig. 2.2
JVP waveforms Corresponding Cardiac e ent

a-wave
c-wave
x-descent
V wave
descent
Abnormal JVP waveforms Interpretation

Giant /Prominent a-waves
Cannon a-waves
Absent a waves
Severe TR
Cardiac Tamponade
Constrictive Pericarditis
Medicine
Concept 1.3 : Pulsus Paradoxus
Fig. 2.3
Physiology of Inspiration
Mec anism of ulsus aradoxus Cause
1. Hyperinflation of Lungs
2. Equalisation of Ventricular Pressures
. Impairedventricular Compliance
. Misc ( nknown)
Concept 1.4: Heart sounds
Heart Sounds: Relation to Cardiac Cycle (0.8s)
Rapid
Ejection
EC
Delayed ejection
Isovolunic
relaxation
S1 Sys S2 Isovolumic
(0.3) contraction
(A)-Atrial
systole
(O/S)
DIAS
S4 OS
(0.5s)
S3 PK
TP
Diastasis
(E)
Fig. 2.4
EC-Ejection Click – Due to Aortic valve opening (High pitched)

– May be Physiological/Sign of As
OS-Opening Snap – due to Mitral valve opening (High pckbed)
– Maybe Physiological/Sign of MS.
PK-Pericardial Knode – Constrich ve Pericarditis
TP-Tumour Plop – Occurs in LA mxyoma (Penduculated)
– Floats in LA cavity. Plops over MV when blood flows from LA→LV
– lso cause M.V area narrowing
LA
(mimic MS-Mild diastolic murmur)
MV
Medicine
S1 - Due to closure to A-V valves (Mitral/Tricuspid)

- High pitched sound-marks onset of SYSTOLE
LOUD S1 SOFT/MUFFLED S1
• Hyperdynamic states • Hypovolumic states
• Mitral Stenosis • Mitral Regurgitation
• Thin, lean chest wall • Obeste/Pericardial effusion
MS → Soft/Absent S1 – Associated MR
– Calcified M.V
– Atrial fibrulation
S1 - Due to closure of semilunar valves (Aortic/Pulm)

- High pitched-marks onset of Diastole
During Quiet Breath PYSIOLOGICAL WIDENED SPLIT PARODOXICAL SPLIT

(A2-P2) (A2-P2)
No Split Audible AUDIBLE SPLIT →
Deep inspiration Audible Split More Prominent Split Dissapears
A2-Early split
P2-Late (Except: ASD)
Fixed, Wide split
CAUSES
A2 → P2 P2 → A2
Defect is always in delayed component
RBBB LBBB
RVOT obs (PS)
n
LVOT obsn (AS)
Pulm HTN Systemic HTN
L → R Shunts: Single
pacemaker
chamber
ASD
Lead is placed in RV
(Easy)
S3 (Low-pitched) S4
Due to Rapid flow into Partially filled ventricles
During Ventricular relaxation During Atrial systole
(E) (A)
Always Pathological
Maybe Physiological
↓
In Symptomatic/Elderly patient→ SIGN OF HF
Concept 1.5 : Heart murmurs
Produced due to turbulence of blood flow.
Levine and Freeman’s grading of murmurs:
I — Very soft.
II — Soft.
III — Moderate.
IV — Loud with thrill. V — Very loud.
VI — Heard even when stethoscope slightly away from the chest wall.
Investigate murmur when:
1. Diastolic.
2. Continuous.
3. Grade III or more.
4. Early or late systolic.
5. Symptomatic patient.
TIMING (Relation of murmur to Cardiac CYCOE)

Systolic Phase Diastolic Continuous Murmors
AC TE MR* Early AR, PR A. Systemic: Pulmonary shunt
• Patent ductus Arteriosus
• Aorto-Pulmonary window
• Ruptured sinus of valsalva
LVOT obsn Mid MS,TS B. Artery: Venous shunt
RVOT obsn LA M OMAS • FIST LA (in Hemodialysis)
• Vascular tumours e.g.
Hemagniomas/Hepatoma
MVP* Late Carey-Coombs C. Venous engorgement of Breast
(Rheumatic during Preg/lactation
valvulitis)
PAN-S STOLIC M RM R
CHR. MR V.S.D MAMMAR SCO FFLE
Axilla/I.S.A TO APE
RADIATION RELATION OF RESPIRATION
R SIDED L SIDED
LVOT obstruction
(Mid systolic/E ection Inspiration Expiration

systolic)
HOCM (Sub-valvular Valvular AS Supravalvular: Coardation
No Radiation To carotid* To exact point in Back
Medicine
Miscellaneous murmurs
1. Austin flint murmur : In AR (like MS)
2. Graham steel murmur: PR
3. Seagull murmur : AR
4. Carey coomb’s murmur: MDM (RF)
5. Gibson’s murmur : PDA
6. Means’ murmur: Thyrotoxicosis (harsh pulmonary systolic murmur)
7. Maladie de Roger : VSD (small)
8. Click murmur syndrome : MVP
2 ECG & Arrythmias
CONCEPTS
Â Concept 2.1 Basics of ECG
Â Concept 2.2 AV Block/Heart Block
Â Concept 2.3 Supraventricular Tachyarrythmia
Â Concept 2.4 Digitalis toxicity
Â Concept 2.5 Ventricular Tachycardia

Medicine
Concept 2.1 : Basics of ECG
Q. Name the ECG lead?
Ans.:

Ans.:

Ans.:

Ans.:

Ans.:

Ans.:
Medicine
Q. 55 year old, chronic smoker presented Ans.:

with chronic dyspnea and swelling feet.
O/E- S3 present increasing on inspiration
on left lower parasternal area.
What is the qrs axis
hat is P wave abnormality
. 25 year old female, presented with Ans.:

chronic dyspnea and swelling of feet.
O/E- Mid diastolic murmur at apex noted
hat is the sign in V1 known as
hat is the sign in lead II known as
. 65 year old male with history of Ans.:

uncontrolled hypertension
O/E – BP- 160/100
LV S4 at apex is auscultated
hat are ecg findings in terms of
-qrs axis
-LVH or RVH
. 35 year old female with idiopathic Ans.:

pulmonary hypertension presented with
progressive dyspnea for 1 year
O/E- JVP is raised
S4 heard in left lower para sternum which
increases on inspiration
hat are ecg findings in terms of
-qrs axis
-LVH or RVH
Medicine
Q. Asymptomatic 30 year old male patient Ans.:

comes for routine health check up
O/E -wide split of S2 noted
hat is the main rs morphology
abnormality
. 55 year old male with past h/o Ans.:

anterolateral wall MI
O/E- Reverse split of S2 noted
hat is the rs morphology abnormality
Q. Determine QRS axis

Ans.:

Ans.:

Ans.:

Ans.:
Medicine
Concept 2.2 : AV Block/Heart Block
1. First-degree AV block: is classically characterized by a PR interval > 0.20 s. Since
the PR interval is determined by atrial, AV nodal, and His-Purkinje activation, delay in
any one or more of these structures can contribute to a prolonged PR interval.
Causes: include Athletes,Drugs- beta blockers, CCB,Hyperkalemia, Hypokalemia,
Infiltrative cardiomyopathy.
Usually asymptomatic. Early diagnosis and treatment prevents complications.
2. Second-degree heart block: Is present when some atrial impulses fail to conduct
to the ventricles.
Mobitz type I second-degree AV block (AV Wenckebach block) is characterized by
progressive PR interval prolongation prior to block of an atrial impulse.
• The pause that follows is less than fully compensatory (i.e., is less than two normal
sinus intervals), and the PR interval of the first conducted impulse is shorter than the
last conducted atrial impulse prior to the blocked P wave.
• difference between the longest and shortest PR intervals exceeds 100 ms.
In Mobitz type II second-degree AV block: Conduction fails suddenly and
unexpectedly without a preceding change in PR intervals.
• Causes include Ishemic heart disease, degenerative Heart disease
Treatment: Regardless of the site of origin of the escape rhythm, if it is slow and the
patient is symptomatic, a cardiac pacemaker is mandatory.
3. Third-degree AV block (Complete Heart block) : Is present when no atrial
impulse propagates to the ventricles. It is characterised by AV DISSOCIATION.
Causes : Degenerative, Infiltrative disorders,Metabolic –hyperkalemia,Inferior wall MI.
Treatment : Permanent pacemaker implantation irrespective of symptoms.
Q. Identify the arrythmia Ans.:

Q. Identify the arrythmia Ans.:
Q. Identify the arrythmia

Ans.:
Medicine
Concept 2.3 : Supraventricular Tachyarrythmia:
1. PSVT (Paroxysmal Supraventricular tachycardia) - affects 30-50yrs age, F>M
Re-entry(AVNRT) is responsible for the vast majority of cases of PSVT.
MC presenting symptom is episodic palpitation followed by diuresis(ANP release).
Treatment:
• In patients without hypotension, vagal maneuvers, particularly carotid sinus massage,
can terminate the arrhythmia in 80% of cases.
• If these maneuvers are unsuccessful, adenosine (12 mg intravenously) is the agent
of choice.
• Beta blockers may also be used to slow or terminate the tachycardia but are agents
of second choice.
• Digitalis glycosides have a slower onset of action and should not be used for acute
therapy.
• Class 1 and Class 3 anti-arrythmic drugs can be used in emergency
• In presence of shock, the treatment is Cardioversion.
2. Atrial Fibrillation : affectes elderly males females
MC cause is degenerative heart disease. Hyperthyroidism, Alcohol binge, Structural
heart disease (e.g. Mitral stenosis) can also cause A.fibrillation.
Majority present with palpitation. Shock is uncommon
Treatment:
• In unstable patients-electrical cardioversion is the treatment of choice.
• In stable patients - slowing of the ventricular rate becomes the initial therapeutic
goal. This may be most rapidly accomplished with beta- blockers and/ or calcium
channel antagonists.
Prior to cardioversion, precautions must be taken to reduce the risk of systemic
embolization. Patients should be anticoagulated to an INR of at least 1.8 for the prior
> 48 h who are not anticoagulated, a transesophageal echocardiogram can exclude the
presence of left atrial thrombus and allow safe cardioversion.
Oral Anticoagulation is indicated if CHA2DS2Vasc Score is >=2
Digoxin can be used in HF with A.fibrillation.
Ans.:

Ans.:

Ans.:

Ans.:

Ans.:
Medicine
Concept 2.4 : Digitalis toxicity
Cardiac
1. Sinus bradycardia
2. Ventricular premature beats
3. Bigeminy
4. PAT (paroxysmal atrial tachycardia)
5. Ventricular tachycardia
6. Ventricular fibrillation
xtracardiac
1. Nausea, vomiting
2 Diarrhoea
3. ynaecomastia
Management
1. Stop digoxin and measure electrolytes, blood urea, serum creatinine and digoxin levels
2. Correct potassium and dehydration
3. ive IV atropine in ections (0. mg) or do temporary pacing if severe bradycardia
4. For PAT, use b-blockers and for ventricular tachycardia, use lignocaine
5. For ventricular fibrillation, use DC defibrillator

Ans.:

Ans.:

Ans.:

Ans.:

Ans.:
Medicine
Concept 2.5 : Ventricular Tachycardia:
• Sustained ventricular tachycardia is defined as VT that persists for > 30 s or requires
termination because of hemodynamic collapse.
• Non sustained VT (three beats to 30 sec)
• The ECG diagnosis of VT is suggested by a wide-complex QRS tachycardia at a rate
exceeding 100 beats/min.
• The QRS configuration during any episode of VT may be uniform (monomorphic) or it
may vary from beat to beat (polymorphic).
Treatment:
• In patients with VT and organic heart disease, if marked hemodynamic compromise
is present or if there is evidence of ischemia, CHF, or central nervous system
hypoperfusion, the rhythm should be promptly terminated by (DC) cardioversion.
• If the patient with organic heart disease tolerates the VT well-amiodarone.
ECG C F V T
1. AV dissociation
2. QRS width: > 0.14 s with RBBB configuration
>0.16 s with LBBB configuration
3. QRS axis: Left axis deviation with RBBB morphology
Extreme left axis deviation (northwest axis) with LBBB morphology
4. Concordance of QRS in precordial leads
5. Morphologic patterns of the QRS complex
RBBB: Mono-or biphasic complex in V1
RS (only with left axis deviation) or QS in V6
LBBB: Broad R wave in V1 or V2 0.04 d

Onset of QRS to nadir of S wave in V1 or V2 of 0.07 s
Notched downslope of S wave in V1 or V2
Q wave in V6
Fig. 2.1

Ans.:

Ans.:

Ans.:

Ans.:

Ans.:
3 Rheumatic Fever
and Infective Endocarditis
CONCEPTS
Â Concept 3.1 Acute Rheumatic fever
Â Concept 3.2 Mitral Stenosis
Â Concept 3.3 Mitral Regurgitation
Â Concept 3.4 Aortic Stenosis
Â Concept 3.5 Aortic Regurgitation
Â Concept 3.6 Infective Endocarditis

Concept 3.1 : Acute Rheumatic fever
• Acute, recurrent inflammatory disease.
• Etiology agent is Group A hemolytic streptococcus. (serotypes of hemolytic
streptococcus are M types- 1, 3, 5, 6, 14, 18, 24, 27, 29).
• 3% of individual with untreated group A Streptococcus pharyngitis will develop
rheumatic fever.
• Peak incidence is between 5-15 yrs but may occur as late as 4th decade.
• Recurrence of rheumatic fever in previous rheumatic fever is 50%.
• Rheumatic fever has an average course of 6-12 wks.
• CRP tends to normalize earlier than ESR.
• Infection of pharynx and tonsils (not of the skin).
• Antigenic mimicry.
a. Group specific carbohydrate of group A Streptococcus and the glycoprotein of
heart valves.
b. Streptococcus cell membrane, streptococcal M protein sarcolemma and other
moieties of human myocardial cell.
Criteria for the Diagnosis of Rheumatic Fever

(Revised Jones Criteria 2015):
A. or all patient populations it e idence or preceding GAS infection
Diagnosis: Initial ARF 2 Ma or manifestations or 1 ma or plus 2 minor
manifestations
Diagnosis: recurrent ARF 2 Ma or or 1 ma or and 2 minor or minor
B. Ma or criteria
Low-risk populations Moderate and high-risk populations
Carditis Carditis
• Clinical and/or subclinical • Clinical and/or subclinical
Arthrits Arthritis
• Polyarthritis only • Monoarthritis or polyarthritis
• Polyarthraigia
Chorea Chorea
Erythema marginatum Erythema marginatum
Subcutaneous nodules Subcutaneous nodules
C. Minor criteria
Low-risk populations Moderate- and high-risk populations
Polyarthraigia Monoarthralgia
Fewer (≥ 8.5 C) Fever (≥ 8.5 C)
ESR ≥ 0 mm in the first hour and/or CRP ≥ .0 ESR ≥ 0mm/h anchor CRP ≥ .0 mg/dL Prolonged
mg.dL Prolonged PR interval, after accounting for PR interval, alter accounting for age (unless carditis
age variability less carditis is a ma or is a ma or criterion) variability (uncriterion)
Medicine
Treatment:
Primary prophylaxis:
1. Anti streptococcal antibiotics therapy
a. Oral pencillin V 500 mg BD for 10 d, or
b. Tab erythromycin 250 mg QID for 10 d, or
c. Inj Benzathine penicillin 1.2 MU deep I/M single dose ATD.
2. Clinical manifestations of disease therapy.
a. Arthritis – Aspirin 75-100 mg/kg/d for 4-6 wks.
b. Severe carditis (c CHF)- Predniso- lone 30 mg QID then tapered.
Secondary prophylaxis:
• Benzathine penicillin 1.2 MV deep 1/M every 3 wks or
• Oral penicillin V 250 mg BD or
• T. Sulfadiazine 1 gm/d or
• T. Erythromycin 250 mg / BD.
Category of patient Duration of rop ylaxis
Rheumatic fever without carditis For 5 year after the last attack of 21 year of age
(whichever is longer )
Rheumatic fever with carditis but no residual For 10 year after the last attack or 21 year age
valvular disease (whichever is longer )
Rheumatic fever with persistent valvular disease, For 10 year after the last attack, or 0 year of age
evident clinically or on echocardiography (whichever is longer) sometimes lifelong prophylaxis
Concept 3.2 : Mitral Stenosis
• (N) mitral valve (MV) size is 4-6 cm2.
• More common in females.
C :
a. Rheumatic heart disease (RHD)
b. Carcinoid, SLE, RA, Fabry’s disease
c. Congenital
d. Methylsergide, Amyloidosis
e. Lutembacher syndrome (congenital ASD+ acquired MS)
Mitral valve area Symptoms

2.5 cm 2
None
1.5-2.5 cm 2
Dyspnea on exertion
1-1.5 cm 2
PND
1 cm
2
Orthopnea
Severity of MS:
1. Duration of murmur : longer – more severe.
2. A2 – OS gap – It varies inversely with severity.
1. Stenotic gradient:
a. Mild < 5 mm Hg.
b. Moderate 5-15 mm Hg.
c. Severe > 15 mm Hg.
S1 in MS – Loud
Soft in mild MS, calcified valve,
associated MR, AR, AF, CHF
Lab Investigation:
ECG- P mitrale, AF, RAD, RVH.
CXR- Straightening of left heart border, double atrial shadow prominence of main
pulmonary artery, features of CHF.
Echo- TTE/TEE to look for gradient, size, severity, leaflet thickness, mobility, calcification,
suitability for BMV.
Treatment:
Medical:
1. Management of CHF (diet, diuretics, vasodilators, digitalis).
2. Management of AF.
3. Rheumatic fever prophylaxis.
4. Infective endocarditis prophylaxis.
Medicine
Surgical: 1. Balloon Mitral Valvotomy (BMV) is the preferred treatment in patients with
isolate MS with significant symptoms but free of LA thrombus
2. Mitral valve replacement (MVR) in cases with:
a. Associated MR.
b. Valve is deformed by previous operative manipulations.
c. Symptomatic –III, IV.
Concept 3.3 : Mitral Regurgitation
• More common in males.
Acute MR C ronic MR
IE Rheumatic
Acute MI Congenital
Trauma IHD, MVP
Acute RF Degenerative
Myocardial abscess CMP
LA myxoma Amyloidosis
CTD- Marfan, SLE, RA
Clinical Features:
Symptoms: Dyspnea on exertion, orthopnea, PND in acute MR, fatigue, exhaustion,
exertional dyspnea in chronic MR.
Signs: include hyperdynamic apex beat, Soft S1, Pan systolic murmur
Damage to anterior leaflet- murmur radiates posteriorly.
Damage to posterior leaflet- murmur radiates anteriorly.
LAB Investigations:
ECG – P mitrale, LVH, AF.
CXR- Cardiomegaly (LV type), CHF.
Echo- Doppler shows regurgitation, LA size.
Complications:
1. AF: More common in MS than in MR.
2. IE: More common in MR than in MS.
Surgical Treatment: MVR in symptomatic cases refractory to medical treatment and
in cases of Acute MR
Medicine
Concept 3.4 : Aortic Stenosis
• (N) aortic valve area in 3-4 cm2.
• More common in males.
CAUSES: can be Congenital, Rheumatic or degenerative (most common )
Symptoms: Syncope, Angina, Dyspnea

Signs: Pulsus parvus et tardus. Heaving apex beat, Paradoxical S2 split, Ejection systolic
murmur- in 2nd RICS, transmitted to carotid artery and or apex.
Silent AS in:
a. CCF.
b. MS / AS.
LAB Investigation:
• ECG- LVH, LBBB.
CXR- Post stenotic dilation of ascending aorta in valvular AS calcification of AV.
Complications:
LVF, CHB, arrhythmia, IE.
Treatment:
Medical - Mx of CHF, RF, IE, angina.
Surgical – Aortic valve replacement in symptomatic cases.
Concept 3.5 : Aortic Regurgitation:
Pure AR – males, associated with MV – females.
Causes:
Aortic al e disease Aortic root disease
Rheumatic Degenerative
I.E. Cystic medial necrosis
Trauma Marfan
Congenitally- bicuspid Aortic dissection
Large VSD Osteogenesis imperfecta
Associated c RA, AS Syphilitic aortitis
whipple, crohn s disease Takayasu s disease
Clinical Features:
1. Palpitations- earliest symptoms.
2. Exertional dyspnea- Next symptom – 1st symptom of diminished cardiac reserve.
3. PND, Orthopnea.
4. Angina – nocturnal, reduction in diastolic pressure at night accumulation.
Signs:
Signs of wide pulse pressure:
Lighthouse sign: Alternate flushing and blanching of forehead
andolfi s sign Change in papillary size c cardiac cycle
Bec er s sign Retinal artery pulsations (fundus)
Muller s sign Pulsations of uvula
De musset s sign Head pulsation
Corrigans s sign Dancing carotids
uinc e s sign Capillary pulsations on nail bed/lips
ocomotor brac ii Muscle knock
Collapsing pulse: Water hammer pulse
Bisferiens pulse:
Traube sign: Pistol shot heard in femoral A
Medicine
Duroziez sign: Systolic murmur heard over femoral A. when it is compressed proximally
and diastolic murmur when compressed distally.
Duroziez murmur: Diastolic murmur of femoral A
Hill sign: Difference of SBP b/w L/LL
Mild AR 20- 0 mm Hg
Moderate AR 0- 0 mmHg
Severe AR 0 mmHg
Rosent al sign Pulsation of liver
Ger ardt s sign Pulsation of enlarged spleen.
• Early diastolic murmur – high pitched blowing, 3rd ICS along left sternal border,
best heard in forward bending position.
Austin flint murmur is soft, low pitched, mid diastolic murmur heard at apex.
Produced by the displacement of anterior leaflet of mitral valve by AR stream.
Severity
1. Duration of diastolic murmur
2. Bisferiens pulse
3. Hill sign ( 0 mm)
. Apical impulse displacement
5. Marked peripheral signs
6. S1 soft, S2 single, S3
LAB Investigations:
ECG- LVH.
CXR- Cardiomegaly (LV type) – Cor bovium.
Treatment:
Medical – Mx of CHF, AF, RF, IE.
Surgical – AVR in refractory cases
Concept 3.6 : Infective Endocarditis:
Definition:
Infective Endocarditis is a microbial infection of the endothelial surface of the heart. The
characteristic lesion, vegetation, is a variably sized amorphous mass of platelets and
fibrin in which abundant micro organisms and scant inflammatory cells are enmeshed.
Sites of Infective Endocarditis:

1. Heart valves (MC).
2. Septal defect.
3. On chordae tendinae.
4. Mural endocardium.
5. Intracardiac devices.
Endarteritis:
Infection of arteriovenous shunts, arterio-arterial shunts (Patent ductus arteriosus)or
coarctation of aorta is known as endarteritis.
Types:
Acute:
a. Patient more toxic, febrile.
b. Involving (N) valve.
c. Rapidly damages cardiac structures.
d. Hematogenous spread to extra cardiac sites more common –metastatic infection.
e. Caused by virulent organisms – Staphylococcus aureus.
Subacute:
a. Indolent course.
b. Involves already damaged valve.
c. Metastatic infection – uncommon.
d. Caused by less virulent organism– Viridans, Streptococci, enterococci, coagulase –ve
staphylococcus.
Etiology:
Organisms Causing Major Clinical Forms of Endocarditis:
ercentage of Cases
ati e al e ndocarditis rost etic al e ndocarditis at ndicated ndocarditis in n ection Drug
Time of Onset (Months) after Valve Surgery Users
Community- Health Care- Rig t- Left- Total
Medicine
Ac uired Associated Sided Sided

Organism (n = 1718) (n = 1110) <2 (n = 144) 2-12 (n = 31) > 12 (n = 194) (n = 346) (n = 204) (n = 675)
Streptococci 0 13 1 9 31 5 15 12
Pneumococci 2 – – – – – – –
Enterococc 9 16 8 12 11 2 24 9
Staphylococcus 28 52d 22 12 18 77 23 57
aureus
Coagulase- 5 11 33 32 11 – – –
negative
staphylococci
Fastidious 3 – – – 6 – – –
gram-negative
coccobacilli
(HACEKgroup)
ram-negative 1 1 13 3 6 5 13 7
bacilli
Candida spp. <1 1 8 12 1 – 12 4
Polymicrobial/ 3 3 3 6 5 8 10 7
miscellaneous
Diphtheroids – <1 6 – 3 – –0.1
Culture-negative 9 3 5 6 8 3 3 3
The total number of cases s larger than the sum of right- and left-sided cases because the location of infection was not specified h some cases. Includes viridans
streptococci Streptococcus gallolyticus other non-group A, groupable streptococci and Abiotrophia and ranulicatella spp. (nutritionally variant, pyridoxal-
requiring streptococci). Primarily. E faecalis or nonspeciated isolates occasionally E. faecium or other, less likely species. Methicillin resistance is common among
these 5. aureus strains. Includes Haemophilus spp., Aggregatibacter aphrophilus. Aggregatibacter actinomycetemcomitans, Cardiobocterium hominis, Eikenella spp,
and Kingella spp.
Note: Data are compiled from multiple studies
HACEK organism (Haemophilus, Actino- bacillus, Cardiobacterium, Eikenella and
kingella) also caused SABE with large vegetations.
Endocarditis in intravenous drug abusers: Right side (MC)site:
1. Staph aureus(MC).
2. Pseudomonas.
3. Candida.
4. Polymicrobial infection.
Clinical features:
Culture – ve endocarditis:
1. Prior antibiotic use.
2. Pyridoxal required streptococci (Abiotro- phia).
3. HACEK group of organisms.
4. Bartonella.
5. Tropheryma whippeli (Whipple’s disease).
6. Libmann sack Endocarditis.
7. Marantic Endocarditis.
Symptoms Signs
Fever 50-85 Fever 80-90
Chills 2-75 Murmur 80-85
Sweats 25 Changing/new murmur 10- 5
Anorexia 25-55 Neurological abnormality 0- 0
Weight loss 25- 5 Embolic event 20- 0
Malaise 25- 0 Splenomegaly 15-50
Dyspnea 20- 0 Clubbing 10-20
Cough 20 Osler nodes 7-10
Stroke 1 -20 Splinter hemorrhage 5-15
Headache 15- 0 Petechiae 10- 0
Nausea/ vomiting 15-205 Janeway lesions -10
Chest pain 8- 5 Roth spots -10
Confusion 10-20
PERIPHERAL SIGNS in Infective Endocarditis.

Osler nodes: Small tender nodules over finger, toe pads, soles.
Janeway lesions: 1-4 mm non tender erythematous macules over palms, soles.
Petechiae: Over conjunctivae, palate,
buccal mucosa and upper extremities.
Clubbing: Seen in long standing cases. Roth spots: Oval retinal haemorrhage with
pale center. Also seen in CTD, anaemia
Splinter haemorrhage: Subungual, linear, dark streaks that may appear in endocarditis.
Medicine
Criteria for diagnosis of Infective Endocarditis:
Major Criteria:
Persistently positive blood culture, defined as recovery of a microorganism consistent
with infective endocarditis from:
• Blood cultures (22) drawn more than 12 hours apart, or
All of three or a majority of four or more separate blood cultures, with first and last
drawn at least 1 hr apart.
Single positive blood culture for Coxiella burnetti or anti-phase I lgG antibody titer>
1:800.
Evidence of endocardial involvement.
Positive echocardiogram (TEE advised for PVE or complicated infective endocarditis)
Oscillating intracardiac mass, on valve or supporting structures, or in the path of
regurgitant jets, or on implanted material, in the absence of an alternative anatomic
explanation, or abscess, or New partial dehiscence of prosthetic valve, or New valvular
regurgitation (increase or change in preexisting murmur not sufficient).
Minor Criteria:
Predisposition: predisposing heart condition or intravenous drug use Fever 38.0oC
(100.4oF).
Vascular phenomena: Major arterial emboli, septic pulmonary infarcts, mycotic aneu-
rysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions.
Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid fac-
tor.
Microbiologic evidence: positive blood culture but not meeting major criterion as noted
previously’ or serologic evidence of active infection with organism consistent with infec-
tive endocarditis.
Definite Infective Endocarditis:
Two major criteria, or
1 major + 3 minor criteria or
five minor criteria.
Treatment:
Antibiotic treatment for Infective Endocarditis caused by common
organisms:
Organism Drug, Dose, Duration Comments
Streptococci Penicillin 2- million units IV Avoid penicillin plus gentamicin if
Penicillin –susceptible q h for weeks. risk of aminoglycoside toxicity are
streptococci, S. bovis Penicillin 2- million units IV increased or case is complicated.
q th plus gentamycin 1mg/kg IM Can use ceftriaxone in patients
or IV q8h, both for 2 weeks. with non-immediate penicillin
Ceftriaxone 2 g/d IV as single allergy.
dose for weeks. se vancomycin in patients with
Vancomycin 15mg/kg IV q 12 h severe or immediate lactam
for weeks. allergy.
Relatively penicillin-resistant Penicillin million units IV Preferred for treatment of

streptococci q th for - wks plus gentamicin prosthetic valve endocarditis
1mg/kg IV q8th for 2 wks caused by penicillin-susceptible
streptococci continue penicillin
for wks in this setting
Penicillin- resistant/streptococci Penicillin - million units IV Can use streptomycin 7.5 mg/
pyridoxal – requiring q h plus gentamicin one mg/kg IV kg q12h in lieu of gentamicin
streptococci (Abiotrophia spp) q8h, both for - weeks. is not high - level resistance to
Enterococci streptomycin
Penicillin - million units IV Do not use cephalosporin or

q th plus gentamicin one mg/kg carbapenems for treatment of
IV q8h, both for - weeks. enterococcal endocarditis
Ampicillin 2g IV q h plus se vancomycin plus gentamicin
gentamicin 1 mg/kg IV q8th both for penicillin allergic patients or
for - weeks desensitize to penicillin
Vancomycin 15mg/kg IV q12th
plus gentamicin 1 mg/kg IV q8h
both for - weeks
Staphylococci Nafcillin or oxacillin 2 g q h May use 3-4 million units q 6h
Methicillin – susceptible for - weeks plus (optional) if isolate is penicillin susceptible
infecting native valves (no gentamicin 1 mg /kg IM or IV q8h (does not produce b- lactamase)
foreign device) for 3-5 days
Cefazolin 2 g IV q 8h for - Can use cefazolin regimen for
weeks plus gentamicin 1 mg/kg patients with non-immediate
IM or IV q 8h for 3-5 days penicillin allergy
Vancomycin 15 mg /kg IV q 12 h se vancomycin for patient with

for - weeks immediate (urticarial) or severe
penicillin allergy
Methicillin- resistant infecting Vancomycin 15 mg / kg IV q 12 No role for routine use of rifampin
native valves(no foreign device) for 4-6 days
Methicillin- susceptible, Nafcillin or oxacillin 2 g IV q h se gentamicin initial 2 weeks
infecting prosthetic valves for -8 weeks plus gentamicin 1 determine susceptibility to
mg /kg or IV q8h for 2weeks plus gentamicin before initiating
rifampin 00 mg po q8h for -8 rifampin if patient is highly
weeks allergic to penicillin ,use
regimen for methicillin –resident
staphylococci if b- lactam allergy
is of the minor, non-immediate
type ., can substitute cefazolin for
oxacillin /Nafcillin
Methicillin resistant , infecting Vancomycin 15 mg/ kg IV q 12 h se gentamicin during initial
prosthetic valves -8 weeks plus gentamicin 1 mg/ 2 weeks determine gentamicin
kg IM or IV q 8h for 2 weeks plus susceptibility before initiating
rifampin 00 mg PO q8h for -8 rifampin
weeks
Medicine
Indications of Surgery:
ndications or Cardiac Surgical nter ention n atients it ndocarditis
Surgery Re uired for Optimal Outcome
Moderate to severe congestive heart failure due to valve dysfunction
Partially dehisced unstable prosthetic valve
Persistent bacteremia despite optimal antimicrobial therapy
Lack of effective microbicidal therapy (e.g., fungal or Brucella endocarditis
S. aureus prosthetic valve endocarditis with and intracarditic compilation
Relapse of prosthetic valve endocarditic after optional antimicrobial therapy
Surgery to Be Strongly Considered for improved Outcome.
Perivalvular extension of infection.
Poorly responsive S. aureus endocarditis involving the aortic or mitral valve.
Large ( 10 mm in diameter) hyper mobile vegetations with increased risk of embolism, particularly with
prior embolic event or with significant valve dysfunction.
Persistent unexplained fever ( 10 days) in culture-negative native valve endocarditis.
Poorly responsive or relapsed endocarditic due to highly antibiotic-resistant enterococci or gram-negative
bacilli.
a
Surgery must be carefully considered; findings are often combined with other indications
to prompt surgery.
Prophylaxis:
ig -Ris Cardiac esions or ic ndocarditis rop ylaxis s Ad ised Before Dental
rocedures
Prosthetic heart valves.

Prior endocarditis.
nrepaired cyanotic congenital heart disease, including palliative shunts or conduits.
Completely repaired congenital heart defects during the months after repair.
Incompletely repaired congenital heart disease with residual defects ad acent to prosthetic material.
Valvulopathy developing after cardiac transplantationa.
Not a target population for prophylaxis according to recommendation of the European Society for Cardiology.
Source: Table created using the guidelines published by the American Heart Association and the European
Society of Cardiology (W Wilson at Circulation 11 :17 , 2007: and Habibe et al: Eur heart
0:2 9.2009).
Cardiac Conditions When Infective Endocarditis Prophylaxis Not

Recommended :
1. ASD.
2. CABG.
3. MVP without MR.
4. Cardiac pacemakers, implanted defibrillators.
Q. A 25 year old male patient

presented with fever of 3 weeks
duration with palpitations and
dyspnea.History of recurrent joint
pains 10 years back with some
injections every 3 weekly but non
compliance with medications.
These are the findings.Likely
diagnosis
Ans.:
. Integrate this findings to

complete the diagnosis
Ans.:
Medicine
. Integrate these findings to make

diagnosis
Ans.:
. These clinical findings will be

suggestive of
Ans.:
4 Cardiomyopathy
CONCEPTS
Â Concept 4.1 Cardiomyopathy
Â Concept 4.2 Dilated Cardiomyopathy:
Â Concept 4.3 Hypertrophic Cardiomyopathy:
Â Concept 4.4 Restrictive CMP
Â Concept 4.5 Comparision of Cmp:
Â Concept 4.6 Pericardial disorders

Medicine
Concept 4.1 : Cardiomyopathy
Dilated cardiomyopathy Dilation and impaired contraction of the left ventricle or both ventricles
Caused by familial-genetic, viral immune alcoholic-toxic, or unknown
factors or is associated with recognized cardiovascular disease
Hypertrophic cardio myopathy Left and/or right ventricular hypertrophy. Often asymmetric which
usually involves the interventricular septum
Mutations in sarcoplasmic proteins cause the disease in many patients
Restrictive cardiomyopathy Restricted filling and reduced diastolic size of either ventricle or both
ventricles with normal or near-normal systolic function.
Idiopathic or associated with other disease (e.g. Amyloidosis, end
myocardial disease)
Concept 4.2 : Dilated Cardiomyopathy:
Cardiac enlargement and impaired systolic function of ventricles.
• Reversible causes of DCM:
a. Hypophosphatemia.
b. Hypocalcemia.
c. Uremia.
d. Hypothyroidism.
e. Hyperthyroidism.
f. Hemochromatosis.
g. Alcohol.
h. Arrythmogenic.
i. HIV.
j. Pregnancy.
Holiday heart syndrome:

Atrial Fibrillation seen in patients (chronic alcoholic after a binge) present as
palpitations, syncope, chest discomfort Hypokalemia may play a role.
Clinical features: presents as Heart failure
Diagnosis : echocardiography/Cardiac MRI
Treatment : Anti-heart failure therapy is only palliative.
Cardiac Transplant is the only potential cure.
Medicine
Concept 4.3 : Hypertrophic Cardiomyopathy:
In appropriate hypertrophy that occurred in the absence of an obvious cause of
hypertrophy (AS/ HTN)
Diastolic dysfunction → LVEDP →
Pulmonary congestion & dyspnea.
Dynamic outflow obstruction:
a. SAM: Systolic anterior motion of MV.
b. ASH: Asymmetric septal hypertrophy.
• Clinical features:
a. Dyspnea.
b. Angina.
c. Syncope.
d. Sudden death.
Causes of Angina in HOCM.
Despite (N) epicardial coronary artery.
1. muscle mass.
2. inadequate capillary density.
3. diastolic filling pressure.
4. Ab (N) intramural coronary A.
5. Impaired vasodilatory reserve.
6. Systolic compression.
7. demand of Co2.
HCM is harsh, crescendo decrescendo

HCM AS
Carotid pulse Brisk upstroke Pulsus parvus et tardus
Murmur with Valsalva Opposite effect
↓with Squatting
Thrill ICS – L side 2 ICS – R side
Murmur radiation to carotids – +
Echo: ig ris group

1. Septum 1.3-1.5 X posterior wall in Sudden death, sustained VT
diastole.
Age 0 yrs
2. Narrowing of LV outflow tract.
Massive LVH
Management: Treatment done generally
of high risk group. Adverse genotype
Multiple familial SD
Presence of NSVT (non sustained VT)
Treatment:
Fig. 2.5
Medicine
Concept 4.4 : Restrictive CMP
Causes of Restricti e Cardiomyopat ies
nfiltrati e Bet een Myocytes
Amyloidosis
Primary (light chain amyloid)
Familial (abnormal transthyretin)
Senile (normal transthyretin or atrial peptides)
Inherited metabolic defects
Storage it in Myocytes
Hemochromatosis (iron)
Inherited metabolic defects
Fabry s disease
lycogen storage disease.
ibrotic
Radiation
Scleroderma
ndomyocardial
Possibly related fibrotic diseases:
Tropical endomyocardial fibrosis
Hypereosinophilic syndrome (Lo er s endocarditis)
Carcinoid syndrome
Radiation
Drugs: e.g., serotonin, ergotamine
Overlap with Other Cardiomyopathies
Hypertrophic cardiomyopathy/ pseudohypertrophic .
Minimally dilated cardiomyopathy.
Early-stage dilated cardiomyopathy.
Partial recovery from dilated cardiomyopathy.
Sarcoidosis.
ldiopat ic.
Can be familial.
Concept 4.5 : Comparision of CMP:
DILATED R S RC R RO C
1. Symptoms CHF – left sided Fatigue Dyspnea, fatigue CHF- Dyspnea, angina, Fatigue,
and weakness systemic/ Rig t S/S of systemic syncope, palpitations
pulmonary emboli disease Amyloidosis, iron
storage
2. C/E Moderate-severe Mild- moderate Mild cardiomegaly apical
cardiomegaly s /s Av cardiomegaly s /s systolic thrill and heave,
(Mitral) regurgitation Kussmaul (inspiratory brisk carotid upstroke s
in VP) common systolic M on
Valsalva
.C R Cardiomegaly-Left Mild Mild
PVH PVH LAE
4. ECG Sinus tachycardia Low voltage LVH
A/v arrhythmia Intraventricular condition ST/T ab(N)
ST/T ab(N) defects Ab(N) q waves
Av conduction defects
5. Echo LV dilatation dyspnea LV thickness small LV Asymmetrical septal
Ab(N) diastolic MV cavity (N) sys fn. Diastolic hypertrophy (ASH)
motion systolic dyspnea dysfunction. Narrow ASH left vent.
Outflow tract
Systolic ant. Motion
(SAM) of mitral valve
. Cardiac LV enlargement/ ↓ LV compliance Square ↓ LV compliance
catheterization M/T regurgitation root sign MR
Lt/Rt sided filling (N) sys. Fn Vigorous systolic function
pressure Lf/Rt pressure Dynamic LV outflow
↓ C.O Gradient
Medicine
Concept 4.6 : Pericardial disorders
1. Pericardial Effusion Tamponade :
Accumalation of fluid in the pericardium, resulting in impaired filling of the cardiac
chambers.
Causes:
Acute pericarditis, trauma, aortic dissection, cardiac surgery, CCF, hypothyroid, Koch’s
disease and Malignancy.
Signs/symptoms:
Tachycardia, hypotension and breathlessness.
Pulsus Paradoxus.
JVP- absent y,deep x,large a.
Decreased heart sounds.
Diagnosis:
CXR : Enlarged heart shadow. ECG : Low voltage.
2DECHO is diagnostic.
Treatment:
Therapeutic pericardiocentesis.
Prognosis:
Tamponade requires as little as 50cc collection if rapid enough.
Tamponade not relieved by pericardio-centesis is often lethal.
2. Constrictive Pericarditis:
Constrictive pericarditis is most often idiopathic.
It maybe due to post-acute pericarditis, radiation induced, or infectious (TB).
It presents as breathlessness, Kussmaul’s sign, pericardial knock and right heart failure.
Diagnosed by thickened pericardium on 2DECHO.
Treated by pericardectomy
5 Hypertension & Coronary
Artery Disease (CAD)
CONCEPTS
Â Concept 5.1 Hypertension
Â Concept 5.2 Resistant Hypertension and

Hypertensive emergency
Â Concept 5.3 Definition of Myocardial Infarction
Â Concept 5.4 Clinical Features of MI
Â Concept 5.5 Classification of MI
Â Concept 5.6 Management

Medicine
Concept 5.1: Hypertension
Learning Objective: To learn the diagnosis and management of Hypertension
Time needed
1st Reading 0 mins
2 Reading
nd
10 mins
Important Aspects of Blood Pressure Measurement:

Key Steps for Proper BP Specific nstructions
Measurements
Step 1: Properly prepare the 1. Have the patient relax, sitting in a chair (feet on floor, back supported)
patlert for >5 min.
2. The patient should avoid caffeine, exercise, and smoking for at least 0
min before measurement.
3. Ensure patient has emptied his/her bladder.
. Neither the patient nor the observer should talk during the rest period
or during the measurement.
5. Remove all clothing covering the location of cuff placement.
. Measurements made while the patient Is sitting or lying on an
examining table do not fulfill these criteria.
Step 2: se proper technique 1. se a BP measurement device that has been validated, and ensure that
for BP measurements the device is calibrated periodically.
2. Support the patient s arm (e.g., resting on a desk).
. Position the middle of the cuff on the patient s upper arm at the level of
the right atrium (the midpoint of the sternum).
. se the correct cuff size, such that the bladder enclrdes 80 of the arm,
and note If a larger- or smaller-than-normal cuff size is used.
5. Either the stethoscope diaphragm or bell may be used for auscultatory
readinas.
Step : Take the proper 1. At the first visit, record BP in both arms. use the arm that gives the
measurements needed higher reading for subsequent readings.
for diagnosis and 2. Separate repeated measurements by 1–2 min.
treatment of elevated . For auscultatory determinations, use a palpated estimate of radial pulse
BP/hypertension obliteration pressure to estimate SBP. Inflate the cuff 20– 0 mm Hg
above this level for an auscultatory determination of the BP level.
. For auscultatory readings, deflate the cuff pressure 2 mm Hg per
second, and listen for Korotkoff sounds.
Step : Properly document 1. Record SBP and DBP. If using the auscultatory technique, record SBP
accurate BP readings and OBP as onset of the first Korotkoff sound and disappearance of all
Korotkoff sounds, respectively, using the nearest even number.
2. Note the time of most recent BP medication taken before measurements.
Step 5: Average the readings se an average of 2 readings obtained on 2 occasions to estimate the
individual s level of BP.
BP Definition:
BP Measurement Definition
SBP First Korotkoff sound
DBP Fifth Korotkoff sound
Pulse pressure SBP minus DBP
Mean arterial pressure DBP plus one third pulse pressuret
Mid-BP Sum of SBP and DBP, divided by 2
BP Category:
BP Category SBP DBP
Normal 120 mm Hg and 80 mm Hg
Elevated 120–129 mm Hg and 80 mm Hg
Hypertension
Stage 1 1 0–1 9 mm Hg or 80– 19 mm Hg
Stage 2 ≥1 0 mm Hg or 290 mmHg
BP Patterns Based on ce and ut-of- ce Measurements:

O ce Clinic ealt care Setting ome on ealt care AB M Setting
Normotensive No hypertension No hypertension
Sustained hypertension Hypertension Hypertension
Masked hypertension No hypertension Hypertenson
White coat hypertension Hypertension No hypertension
The white coat effect (usually considered clinically significant when o ce SBP/
DBPs are 20/10 mm Hg higher than home or ABPM SBP/DBPs
Conditions suggesting secondary hypertension:
Conditions
• Drug-resistant/induced hypertension.
• Abrupt onset of hypertension.
• Onset of hypertension at <30 y.
• Exacerbation of previously controlled hypertension.
• Disproportionate TDD for degree of hypertension.
• Acceerated/malignant hypertension.
• Onset of diasto ic hypertension in older aduts (age 65 y).
• Unprovoked or excessive hypokalemia.
Medicine
Oinical ndications ysical Screening Additional/

xamination Tests Confirmatory
Tests
Common causes
Renal rinaiy tract infections Abdominal Renal Tests to
parenchymal obstruction, hematuria urinary mass (polycystic ultrasound evaluate cause
disease frequency and nocturia kidney disease) of renal disease
analgesic abuse family history skin pallor
of polycystic kidney disease
elevated serum creatinine
abnormal urinalysis
Renovascular Resistant hypertersion Abdominal Renal Duplex Bilateral
disease hypertension of abrupt systolic Deppler selective renal
onset or worsening or -diastolic bruit ultrasound intra-arterial
increasingly difficult to bruits over other MRA angiography
cortrol flash pulmonary arteries (carotid abdominal CT
edema (atherosclerotic) early- – atherosclerotic
onset hypertension, especially or fibro muscular
in women (fibromuscular) dysplasia),
hyperplasia) femoral
Primary Resistant hypertension Antiythmias Plasma Oral sodium
aldosteronism hypertension with hypokalemia (with hypo aldosterne/ loading test
(spontaneous or diuretic kalemia) enin ratio under (with 2 -h urine
induced) hypertension and especially atrial standardized aldosterone)
muscle cramps or weakness fibrillation conditions or IV saline
hypertension and incidentally (correction of infusion test
discovered adrenal mass hypokalemia with plasma
hypertension and obstructive and withdrawl aldosterone at
sleep apnea hypertension and of antagonists 4 h of infusion
family history of early-onset for –5 wk) Adrenal CT
hypertension or stroke scan, adrenal
vein sampling.
Obstructive sleep Resistant hypertension Obesity, Berlin Potysomnog-
apnea snoring fitful sleep breathing Mallampati dass Questionnaire raphy
pauses during sleep daytime IIHV loss of (8) Epworth
sleepiness normal nocturnal Sleepiness
BP fall Score (9)
overnight
oximetry
Drug or alcohol Sodium-containing antacids Fine tremor, rinary drug Response to

induced caffeine nicotine (smoking) tachycardia, screen (illicit withdrawal of
alcohol NSAIDs oral sweating drugs) suspected agent
contraceptives cydosporine or (cocaine,
tacrolimus sympathomimetics ephedrine, MAO
(decongestants, anorectics) inhibitors) acute
cocaine, amphetamines abdominal pain
and other illicit drugs (cocaine)
neuropsychiatric agents
erythropoiesis-stimulating
Pheochro- Resistant hypertension Skin stigmata of 24-h urinary CT or MRI scan
mocvtoma/oa paroxysmal hypertension neurofibroma- fractionated of abdomen/
raganglioma or crisis superimposed on tosis (cafe- metanephrine pelvis
sustained hypertension au-lait spots s or plasma
spells, BP lability, headache, neurofibromas) metanephrine s
sweating, palpitations, Orthostatic under standard
pallor positivefamily history hypotension conditions
of pheochromocytoma/ (supine position
paraganglioma adrenal with indwelling
incidentaloma IV cannula)
Cushing s Rapid weight gain, especialry Central obesity, Overnight 1 mg 24-h urinary
syndrome with central distribution moon face, dexamethasone free cortisol
proximal muscle weakness dorsal and suppression test excretion
depression hyperglycemia supraclavicular (preferably
fat pads, wide (1 multiple)
cm) violaceous midnight
striae, hirsutism salivary cortisol
Hypothyroidism Dry skin cold intolerance Delayed ankle Thyroid- None
constipation hoarseness reflex periooital stimulating
weight gain puffiness coarse hormone free
skin cold skin thyroxine
s.ow movement
goiter
Hyperthyroidism Warm, moist skin heat Lid lag fine Thyroid- Radioactive
intolerance nervousness tremor of the stimulating iodine uptake
tremulousness insomnia outstretched hormone free and scan
weight loss diarrhea proximal hands. warm, thyroxine
muscle weakness moist skin
Aortic oung patient with BP higher in Echocardio- Thoracic and
coarctation hypertension ( 0 y of age) upper extremities gram abdominal CT
(undiagnosed or than in lower angiogram or
repaired) extremities MRA
absent femoral
pulses.
Medicine
Nonpharma cological Interventions for Prevention
and Treatment of Hypertension:
onp armaco ogica Dose
Intervention
Weight loss Weight/body fat Best goal is ideal body weight, but aim for at least
a 1-kg reduction in body weight for most adults
who are overweight. Expect about 1 mm Hg for
every 1-kg reduction in body weight.
Healthy diet DASH dietary pattern Consume a diet rich in fruits, vegetables, whole
grains, and low-fat dairy products, with reduced
content of saturated and total fat.
Reduced intake of dietary Dietary Sodium Optimal goal is 1500 mg/d, but aim for at least a
sodium 1000-mg/d reduction in most adults.
Enhanced intake of dietary Dietary Potassium Aim for 500-5000 mg/d, preferably by
potassium consumption of a diet rich in potassium.
Physical activity Aerobic • 90 – 150 min/wk

• 5 – 75 heart rate reserve
Dynamic resistance • 90 – 150 min/wk

• 50 – 80 1 rep maxmium
• exercises, sets/exercise, 10 repetitions/set
Isometric distance • 2 min (hand grip), 1 min rest between

exercises, maximum voluntary contraction,
sessions/wk
• 8–10 wk
Moderation in alcohol Alcohol consumption • It individuaks who drink alcohol, reduce

intake alcohol to:
• Men: 2 drinks daily
Concept 5.2 : Resistant Hypertension and Hypertensive emergency:
Learning Objective: To learn the diagnosis and management of Refractory Hypertension
Time needed
1st Reading 20 mins
2 Reading
nd
10 mins
The diagnosis of resistant hypertension is made when a patient takes 3 antihypertensive
medications with complementary mechanisms of action (a diuretic should be
1 component) but does not achieve control or when BP control is achieved but requires
4 medications.
Refractory hypertension:
Failure to control BP despite use of at least 5 antihypertensive agents of different
classes, including a long acting thiazide-type diuretic, such as chlorthalidone, and a
mineralocorticoid receptor antagonist, such as spironolactone.
Hypertensive emergency:
Hypertensive emergencies are defined as severe elevations in BP (>180/120 mm Hg)
associated with evidence of new or worsening target organ damage (hypertensive
encephalopathy, ICH, acute ischemic stroke, acute MI, acute LV failure with pulmonary
edema, unstable angina pectoris, dissecting aortic aneurysm, acute renal failure, and
eclampsia).
Medicine
Fig. 2.6
Hypertensive Urgency:
Severe BP elevation in otherwise stable patients without acute or impending change in
target organ damage or dysfunction.
Fig. 2.7
Medicine
Intravenous Antihypertensive Drugs for Treatment of Hypertensive
Emergencies in patients with Selected Comorbidities:
Comorbidity Preferred Drug(s)* Commerts
Acute aortic dissection Esmolol, labetalol Requires rapid lowering of SBP to 120 mm
Hg.
Beta blockade should precede vasodilator
(e.g., nicardipine or nitroprusside)
administration, if needed for BP control or
to prevent reflex tachycardia or inotropic
effect SBP l20 mm Hg should be achieved
within 20 min.
Acute pulmonary edema Clevidipine, Beta blockers contraindicated.
nitroglycerin,
nitroprusside
Acute cororary syndromes Esmololt labetalol Nitrates given in the presence of PDE-5
nicardipine inhibitors may induce profound hypotension.
nitroglycerin Contraindications to beta blockers include
moderate-to-severe LV failure with
pulmonary edema, bradycardia ( 0 bpm),
hypotension (SBP 100 mm Hg), poor
peripheral perfusion, second- or third-degree
heart block and reactive airways disease.
Acute renal failure Clevidipine N/A
fenoldopam nicardipine
Eclampsia or preeclampsia Hydralazine labetalol Recures rapid BP owering. ACE inhibitors,
nicardipine ARBs, renin inhibitors, and nitroprusside
contraindicated.
Perioperative hypertension (BP Clevidipine, lntraoperative hypertension is most
≥1 0/90 rim Hg or SBP elevation esmolol, nicardipine, frequently seen during anaesthesia induction
≥20 of the preoperative value nitroglycerin and airway manipulation.
that persists for 15 mill)
Acute sympathetic discharge or Clevidipine, Recures rapid lowering of BP.
catecholamine excels states (e.g., nicardipine,
pheochronrocytoma, post-carotid phentolamine
endarterectomy status)
Concept 5. : Definition of Myocardial Infarction
Definition of Myocardial nfarction
Criteria for Acute Myocardial nfarction
The term acute myocardial infarction (Ml) should be used when there is evidence of myocardial necrosis in a
clinical setting consistent with acute myocardial ischemia. nder these conditions, any one of the following
criteria meets the diagnosis for Ml:
• Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin cTn ) with at least
one value above the 99th percentile upper reference limit ( RL) and with at least one of the following:
• Symptoms of ischemia
• New or presumed new significant ST-segmentT-wave (ST–T) changes or new ieft bundle branch block
(LBBB)
• Development of pathologic waves in the electrocardiogram (EC )
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
• Identification of an intracoronary thrombus by angiography or autopsy
Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic EC changes
of new LBBB, but death occurred before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased.
Percutaneous coronary intervention (PCI)–related Ml is arbitrarily defined by elevation of cTn values ( 5 x
99th percentile RL) in patients with normal baseline values ( 99th percentile RL) or a rise ofcTn values
20 if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive
of myocardial ischemia, or (ii) new ischemic EC changes, or (iii) angiographic findings consistent with
a procedural complication, or (iv) imaging demonstration ofnewlossof viable myocardium or new regional
wall motion abnormality are required
Stent thrombosis associated with Ml when detected by coronary angiography or autopsy in the setting of
myocardial ischemia and with a rise and/ or fall of cardiac biomarker values with at least one value above
the 99th percentile RL.
Coronary artery bypass grafting (CAB )-related Ml is arbitrarily defined by elevation of cardiac biomarker
values ( 10 x99th percentile RL) in patients with normal baseline cTn values ( 99th percentile RL). In
addition, either (i) new pathologic waves or new LBBB, or (ii) angiographic documented new graft or
new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality.
Medicine
Concept 5.4 : Clinical Features of MI:
• Chest pain: Levine sign- patient depicts retrosternal chest pain by making a fist.
• Sudden onset breathlessness/ loss of consciousness/Confusion/Profound weakness
Cardiac Biomarkers in MI:

Rise r ea (N )
H FABP 1.5 5-10 hr 24
Myoglobin 1-4 6-7 hr 24
Myosin light chain 6-12 2-4 d 6-12 d
Tn I 3-12 24h 5-10 d
Troponin T 3-12 12h-2d 5-14 d
MB –ck 3-12 24h 48-72 h
Enolase -10 24 h 48 h
LDH 10 24-48 h 10-1 d
Myosin heavy chain 48 5-6 d 14 d
ECG: leads helpful in diagnosing MI

Anterior : V1-v6
Anterolateral : V5-6, I, aVL
Anteroseptal : V3-4
Inferior : II, III, aVF
Posterior : V7-V9
R.V. extension : RV4 (most specific), V1, RV2
Concept 5.5 : Classification of MI:
Classification of Myocardial nfarction
ype Spontaneous Myocardial infarction
Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, ero-
sion, or dissection with resulting intraluminal thrombus in one more of the coronary arteries leading to
decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may
have underlying severe coronary artery disease (CAD) but on occasion nonobstructive or no CAD.
ype 2 Myocardial infarction Secondary to an sc emic mbalance
In instances of myocardial in ury with necrosis where a condition other than CAD contributes to imbal-
ance between myocardial oxygen supply and/or demand, e.g., coronary endothelial dysfunction, coronary
artery spasm, coronary embolism, tachy-brady-arrhythmias, anemia, respiratory failure, hypotension, and
hypertension with or without left ventricular hypertrophy.
ype Myocardial infarction Resulting in Deat en Biomar er alues are na ailable
Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic electro-
cardiogram (EC ) changes or new left bundle branch block (LBBB), but death occurring before blood
samples could be obtained or before cardiac biomarker could rise, or in rare cases, cardiac biomarkers were
not collected.
ype a Myocardial infarction Related to ercutaneous Coronary nter ention C
Myocardial infarction associated with PCI is arbitrarily defined by elevation of cardiac troponin (cTn) values
5 99th percentile upper reference limit ( RL) in patients with normal baseline values ( 99th percentile
RL) or a rise of cTn values 20 if the baseline values are elevated and are stable or falling. In addition,
either (i) symptoms suggestive of myocardial ischemia, or (ii) new ischemic EC changes or new LBBB,
or
(iii) angiographic loss of patency of a ma or coronary artery or a side branch or persistent slow or no flow
or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall
motion abnormality is required .
ype b Myocardial infarction Related to Stent rombosis
Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in
the setting of myocardial ischemia and with a rise and/or fall of cardiac biomarker values with at least one
value above the 99th percentile RL.
ype Myocardial nfarction Related to Coronary Artery Bypass Grafting CABG
Myocardial infarction associated with CAB is arbitrarily defined by elevation of cardiac biomarker values
10 99th percentile RL in patients with normal baseline cTn values ( 99th percentile RL). In ad-
dition, either (i) new pathologic waves or new LBBB, or (ii) angiographic documented new graft or
new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality.
Medicine
Concept 5.6 : Management:
STEMI:
Aspirin, blockade, Antithrombin therapy
a. 12 hrs.
Eligible for thrombolytic therapy.
• Thrombolysis.
a. Primary PCI- Gp II b/III a.
• Correct metabolic and electrolyte disorders, ACE I., nitrates.
a. 12 hrs.
Persistent symptoms.
Consider reperfusion therapy.
i.e., Aspirin, Sorbitrate, O2, Morphine, STK, Metoprolol, NTG, Heparin, Sedative,
laxative, Antihypertensive.
Dose of fibrinolytic:
STK : 1.5 MU/60 min.
Tpa : 100 mg/ 90 min.
15 mg stat → 50 mg in 30 min & then 35 mg in next 60 min.
rPA (reteplase) 2 *10 MU bolus, 30 min apart.
TNK – Tenecteplase 0.5 mg/kg.
SAK- 20 -30 mg/ 30 min.
C :
1. With in 4 hrs – Tenecteplase/ reteplase
2. 4-12 hrs (elderly) – STK
3. > 12 hrs in < 65 yrs – Thrombolysis
4. > 12 hrs in > 65 yrs- Primary PTCA
5. any time with shock – Primary PTCA
STEMI patient who is a

candidate for reperfusion
Intially seen at a
Intially seen at a non-
PCI-capable hospital* PCI-capable
hospital
Send to cath lab for

primary PCI
FMC-device time 90
min (Class I, LOE:A)
Transfer for angiography Administer fibrinolytic
and revascularization agent within 30
within 3-23 h for other min of arrival when
patients as part of an anticipated FMC-
invasive strategy device 120 min
(Class IIa, LOE:B) (Class I, LOE:B)
Diagnostic angiogram
Urgent transfer for Transfer for

PCI for patients primary PCI FMC
Medical with evidence of device time as
PCI CABG failed reperfusion or
therapy only soon as possible
reocculsion (Class and 120 min
IIa, LOE:B) (Class I, LOE:B)
Fig. 2.8
6 Heart Failure
CONCEPTS
Â Concept 6.1 Definition and causes of Heart Failure
Â Concept 6.2 Differential diagnosis
Â Concept 6.3 Treatment

Concept .1 : Definition and causes of eart Failure
Clinical syndrome that results from structural or functional impairment of ventricular
filling or ejection of blood leading to symptoms of dyspnea and fatigue and signs of
edema and rales.
Etiologies of Heart Failure:

Depressed n ection raction
Coronary artery disease: Nonischemic dilated cardiomyopathy:
Myocardial infarctiona Familial/genetic disorders
Myocardial ischemiaa Infilatrative disordersa
Chronic pressure overload: Toxic/drug-induced damage:
Hypertensiona Metabolic diosrdera
Obstructive valvular diseasea Viral
Chronic volume overload: Chagas disease
Regurgitant valvular disease Disorders of rate and rhythm:
Intracardiac (left-to-right) shunting Chronic bradyarrhythmias
Extracardiac shunting Chronic tachyarrhythmias
Chronic lung disease:
Cor pulmonale
Pulmonary vascular disorders
reser ed ection raction -
Pathologic hypertrophy: Restrictive cardiomyopahty:
Primary (Hypertrophic cardiomy-opathies Infiltrative disorders (amyloidosis, sarcoidosis)
Secondary (hypertension) Storage diseases (hemochromatosis)
Aging Fibrosis
Endomyocardial disorders
High-Output States
Metabolic disorders Excessive blood flow requirements:
Thyrotoxicosis Systemic arteriovenous shunting
Nutritional disorders (beriberi) Chronic anemia
a
Indicates conditions that can also lead to heart failure with preserved e ection fraction.
Medicine
Concept .2 : Differential diagnosis
Cardiogenic ulmonary edema on cardiogenic pulmonary edema
Acute coronary event + -
Cardiac output state Low flow High flow
S gallop + -
JVP (N)
Crackles Wet Dry
nderlying non-cardiac disease - +
ECG Ischemia (N)
Cardiac enzymes (N)
Pulmonary capillary pressure > 18 mm <18 mm
Intrapulmonary shunt Small Large
Edema fluid/serum protein 0.5 0.7
-RA Findings:
PCWP Findings
10-15 mm Hg Early division (dilatation of upper lobe veins)
15-20 mm Hg Diversion (basal pulmonary veins narrowed and vein diameter mm in 1st
intercostal space
20-25 mm Hg Diversion and interstitial edema ( erley B and A lines)
25- 5 mm Hg Intra alveolar edema ( Bat Wing appearance)
Concept 6.3 : Treatment:
1. General therapeutic measures:
a. Restrict salt intake to < 3 gm/d.
b. Recommend regular, moderate exercise.
c. Avoid antiarrhythmic agents for asymptomatic arrhythmias.
d. Avoid NSAIDS as they are generally sodium salts.
e. Provide influenza and pneumococcal immunization.
2. Diuretics:
a. Administration diuretics to all patients with heart failure and fluid accumulation.
b. Weight daily to select / adjust dose.
c. Treat diuretic resistance by:
i. I/V administration.
ii. Use diuretics in combination (furosemide + metolazone).
d. Administer short term dopamine to enhance renal blood flow.
3. ACE inhibitors:
a. To be given to all pts c LV systolic failure and LV dysfunction without heart failure:
b. contra-indications of ACE inhibitors are:
i. High output angioedema.
ii. Pregnancy.
iii. Hypotension.
iv. S creatinine > 3 mg/dl.
v. S. Potassium > 5.5 mmol/l.
vi. B/L renal artery stenosis.
4. adrenergic blockers:
a. Administration to all NYHA class II or III Patients with systolic HF, often together
with ACE I and diuretics.
b. Contra- indications:
i. Bronchospastic disease.
ii. Symptomatic bradycardia or advanced heart block.
iii. Mental Instability.
5. Digoxin:
Use in patients with LV systolic HF along with diuretics, ACEI, blockers, especially
useful in with AF and fast ventricular rate.
Medicine
6. Other measures:
a. Spironolactone in patients with class IV symptoms.
b. ARB in patients who don’t tolerate ACEI.
c. Hydralazine.
d. Avoid CCB for treatment of HF.
Drugs to Decrease Preload: Nitrates, Diuretics

Drugs to Increase Pumping: Digoxin
Drugs to Decrease Afterload: Ace Inhibitors
7 Important One-Liners
in Cardiology
Most Common:
• MC congenital heart disease (CHD)-VSD.
• MC cyanotic CHD - TOF.
• MC CHD c central cyanosis in neonates- TGA.
• MC CHD without manifestations - Bicuspid Aortic valve.
• MC CHD surviving in adulthood - ASD
MC cause of R.F - group A hemolytic streptococci.
• MC cardiac lesion in RF - Rheumatic carditis.
• MC lesion in RF – Migratory arthritis.
• MC cause of Angina - Atherosclerosis.
• MC valvular lesion post MI - MR.
• MC cause of RVF - LVF.
• MC aortic aneurysm - Abdominal.
• MC heart tumor - Benign.
• MC benign heart tumor - Myxoma.
• MC site of myxoma - Left atrium.
• MC site of origin of LA myxoma- Interatrial septum in vicinity of fossa ovalis.
• MC tumor in children - Rhabdomyoma, Fibromas.
• MC site of tumor in children- Ventricles.
MC cause of calcification of tumor- Fibroma.
• MC primary cardiac malignancy - Sarcoma.
• MC metastatic tumor (in no.) - Ca lung.
• MC metastatic tumor ( in incidence) - Malignant melanoma.
• MC cause of hypertension : Essential HT.
• MC cause of 2 hypertension : Renoparenchymal HT.
Medicine
Nicoladoni Braham Sign:
Seen in AV fistula. On pressing AV fistula, heart rate decreases.
Signs:
1. Homan sign : DVT
2. Carvallo sign : TR
3. Freidrich sign : RCMP, CP
4. Kussmaul sign : RCMP, CP
5. Pardees sign in ECG – MI
Cardiovascular Involvement In Various Syndromes:

Syndrome Cardio ascular n ol ement
Holt- dram ASD
Kartagener Dextrocardia
N oonan PV dysplasia, HOCM
Weber Osler rendu AV fistula
Williams As (supravalvular)
ervell Lange Nielsen Long t Syndrome
Romano ard Long T syndrome
Friedrich ataxia HOCM
Cystic fibrosis Cor pulmonale
Ehler danlos Arterial dilatation
Marfan AR, MR
Down Endocardial cushion defect, ASD, TOF
Turner Coarctation of aorta
Teratogenic disorders:
1. Rubella- PDA, Pulmonary A Stenosis.
2. Alcohol - VSD.
3. Phenytoin- PS.
4. Thalidomide- Phocomelia.
5. Lithium - Ebstein anomaly.
SECTION — 3
RESPIRATORY SYSTEM
INTRODUCTION: Respiration, or the uptake of O2 and removal of CO2 from the

body as a whole, is the primary goal of the lung. The respiratory system includes
not only the lungs but also the Respiratory Center in the Brainstem, the chest wall,
the respiratory muscles and pulmonary circulation.
Physiology of Gas Exchange: Alveolus is the functional unit of the lung. The
process of Gas exchange involves 3 steps:
1. Ventilation: Is the air inhaled into the lungs. Ventilation is not constant.
Through the lung. It is minimum at Apex and Maximum at the base.
2. Perfusion: The entire cardiac output of the right heart is delivered to the
lungs. The respiratory Muscles receive 4-6% of Cardiac output during normal
breathing. The blood supply to the muscles may increase to 15-40% during
periods of respiratory distress. The perfusion is maximum at the base of the
lungs and minimum at the apex.
3. Diffusion: Is a passive process and occurs across the Alveolar Basement
membrane.
The Cardinal symptoms of RS disorders include cough (Most common),
Breathlessness (Most dreaded) and Hemoptysis (Most common site is Bronchial
artery)
Approach to RS disorders: RS system disorders are common in practice and
should be suspected when the patient has any 1/more of the cardinal symptoms.
The patient must undergo detailed clinical evaluation along-with radiological tests
viz. Chest X-ray, HRCT, Gallium scan, CT-Pulmonary Angiography (CTPA) to help
identify the structural defects in the lung.
Functional status of the disease can be evaluated by Pulmonary Function Tests
(PFT) which includes Spirometry and DLCO (Diffusion Capacity of lung to Carbon
monoxide)
In Emergency cases, Arterial Blood Gas (ABG) analysis can provide vital clue to
identify the types of respiratory failure and the probable cause along-with the
severity of the defect in gas exchange.
Classification of RS Disorders:
1. Airway disorders: e.g. Asthma, Bronchiectasis,COPD.
2. Parenchymal and Pleural disorders: e.g. Pneumonia, ARDS, Pleural effusion
3. Interstitial lung diseases (ILD’s): e.g. Hypersensitivity pneumonitis,
Sarcoidosis, Silicosis, Idiopathic ILD’s
4. Pulmonary Vascular diseases: e.g. Pulmonary hypertension, PTE
5. Miscellaneous: e.g. OSAH syn, Lung Cancers, Tuberculosis
1 Pulmonary Function Tests (PFT)
& Respiratory Failure
CONCEPTS
Â Concept 1.1 Spirometry
Â Concept 1.2 DLCO
Â Concept 1.3 Types of Respiratory Failure

138 | Medicine
Concept 1.1: Spirometry
Learning Objective: To understand the Basic physiology and Interpretation of
Spirometry in the evaluation of RS disorders.
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
• PFT is an important test for the functional assessment of Lung function.

• PFT includes both Spirometry and DLCO.
• Spirometry is both Sensitive (Early) and Specific for the diagnosis of both Obstructive
and Restrictive lung diseases.
SPIR METR Measures the Functional i.e the Dynamic Lung

Volumes.
PFT records following parameters, using the 2 loops of the Spirometry; viz
a. Flow-Volume loop and.
b. Volume Time loop.
a. FVC(Forced vital capacity)
b. FEV1 (Forced expired volume in first second)
c. MEFR-Mid expiratory Flow rate:
Considering a Huge variability of normal individual volumes amongst population, the
ratio i.e FEV1 /FVC(as percentage)- (TIFFANEAU-PIRELLI INDEX) is considered
the most accurate and most important parameter of the Spirometry.
Conventional spirometry cannot measure non dynamic values, viz. TLC, RV and ERC.
Fig .1
es iratory System | 139
Normal Lung Volumes:
Lung volumes Male Female
TLC 6.4 L 4.9 L
FRC 2.2 L 2.6 L
RV 1.5 L 1.2 L
IV 4.8 L 3.7 L
VC 1.7 L 1.4 L
ERV 3.2 L 2.3L
SPIROMETRY
FEV1 3.8 L 2.8 L
FEV1 % (FEV1/FEC) 76% 77%
FE F25-75% 4.8 L/S 3.6 L/S
FVC 4.8 L 3.3 L
Interpretation of Spirometry:
FVC
Or Pulmonary
Vascular Diseases
Fig. .2
Causes of Different Pattern:

Obstructive Restrictive - Parenchymal Restrictive -Extraparencymal
Asthma Sarcoidosis Neuromuscular Causes
Copd Idiopathic Pulm Fibrosis GBS, Myasthenia, Mnd
Bronchiectasis Pneumoconiosis Diaphragmatic Palsy
Cystic Fibrosis Drugs Chest Wall Causes
Bronchiolitis Radiation Obesity, Kyphosis, Etc
Broncho-reversibility (BR): is defined as increase in the FEV1 after 15 minutes post-
Salbutamol inhalation.
Bronchoreversibility >= 12% is considered Excellent and is diagnostic of Bronchial
Asthma
Bronchoreversibility < 11% is considered Partial and is specific for diagnosis of COPD.
140 | Medicine
RESPIRATORY MEDICIN E IMAGES DISCUSSION

Q. A heavy smoker with following chest.
Diagnosis?
Ans.:
Q. Following CXR is suggestive of which

disease?
Ans.:
Q. This patient has chronic cough and

productive sputum. Diagnosis?
Ans.:
Concept 1.2 : DLC
(Diffusion capacity of Lung to Carbon mono-oxide)
Learning Objective: To know the practical procedure of the test and interpret the
results.
Time needed
1 Reading
st
15 mins
2 Reading
nd
5 mins
DLCO Complements Spirometry in diagnosis of lung diseases.

DLCO assesses diffusion of gases from the Alveolus into the bloodstream.
Procedure: The patient inhales a mixture of helium (10%), carbon monoxide
(0.3%), oxygen (21%) and nitrogen (68.7%), hold their breath for ten seconds
and then exhale fully. The levels of exhaled helium and carbon monoxide are used to
calculate DLCO.The results may need to be corrected for the patient’s haemoglobin.
Interpretation:
Decreased DLCO Increased DLCO
Emphysema Acute Asthma
Interstitial Lung diseases (ILD) Alveolar Hemorrhage e.g. Good Pastures syndrome ,
Wegener’s granulomatosis
Pulmonary Hypertension Chronic, congestive heart failure
Acute LVF / Shock Polycythemia
Anaemia
142 | Medicine
Concept 1. : Respiratory failure
Learning Objective: To understand the various mechanisms of Gas exchange defects
along-with their diagnosis and common causes.
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Type Mechanism PaO2 PaCO2 Causes A-a Gradient

I Alveolar flooding Decreased Decreased Pulmonary edema, ARDS,
/ Normal Acute Asthma Increased
II Hypoventilation Decreased Increased COPD, Central, NM
causes, Mechanical Normal
III Alveolar atelectasis Decreased Increased Post-operative
NA
IV Respiratory muscle Decreased Increased Shock
Hypoperfusion NA
• Most common mechanism of Hypoxemia is V:Q mismatch.
• Only Type 1 and Type 2 Respiratory failure that occur due to pulmonary causes i.e.
Increased Alvelolar-arterial(A-a) gradients are considered True Respiratory failure.
2 ARDS and Pulmonary
Vascular Disorders
CONCEPTS
Â Concept 2.1 ARDS
Â Concept 2.2 Pulmonary Hypertension
Â Concept 2.3 Pulmonary Thromboembolism

144 | Medicine
Concept 2.1: ARDS
Learning Objective: To understand the causes. Pathophysiology and management of
ARDS
Time needed
1 Reading
st
20 mins
2 Reading
nd
5 mins
Acute Respiratory Distress syndrome is the most severe form of lung injury characterize
by atelectasis/collapse of >2/3rd of the alveoli.
Etiopatho :-
Known Risk Factors
Direct Lung Injury Indirect
• Pneumonia Profound systemic inflammation
MC
• Aspiration
• Inhalation Diffuse alveder edema
• SEPSIS*
• Near drawning Altelectasis • Blood transfusion
• Blunt hrauma
• Perelrahing trauma Shunt formation Type 1
(Hypoxemia)
• Presents with acute onset of breathlessness
• Mimics cardiogenic pulmonary edema and also called “Shock LUNG”
• Diagnosis is made by Berlin’s guidelines
• Most important diagnostic and prognostic parameter is Carico’s index
Most imp Parameter VALUES MIN IMUM PEEP. (support) SEVERITY GRADE
CARICO’s index* 200-300 ≥ 5 cms of H2O MILD
PaO2 100-200 ≥ 5 cms of H2O MOD
FiO2
<100 ≥ 10 cms of H2O SEVERE
Mainstay of treatment is Early and Effective use of Mechanical Ventilation. The special
recommendations for Ventilation in ARDS are:
a. Low Tidal Volume (6ml/kg) : To prevent “Volutrauma”
b. High PEEP ventilation : To prevent atelectasis
ECM (Extra-corporeal membrane oxygenation) can be considered
Maintaining sub-normal CVP(4- cms) is recommended.
Prognosis remains poor due to high acute mortality.
Concept 2.2: Pulmonary ypertension
Learning Objective: To identify the causes, Manifestations and management
of Pulmonary hypertension (Especially Pulmonary arterial
Hypertension – PAH)
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
• Pulmonary hypertension is defined as increase in the Mean PAP of >20mm of Hg

at rest during a right heart catheterization. Assessment of the pulmonary artery
wedge pressure further classifies the causes into pre-capillary (Pulmonary Arterial
Hypertension <=15mm of Hg) and Post-capillary (Pulmonary venous Hypertension
>15mm of Hg)
• Isolated PAH is most commonly Idiopathic. It can be secondary to HIV infection,
Autoimmune disease, Drug and Toxins in minority of cases
• In early stages, the presentation is vague and delays diagnosis
• In late stages, the patient presents with features of Right Heart failure
• PAH can be treated with oral endothelin receptor antagonists (Bosentan, Ambrisentan
– convenient oral route but modest efficacy only) as first line when disease is
uncomplicated and mild. In PAH with Heart failure, the first line treatment consists
of parenteral prostacyclin derivatives which are more potent. Lung transplant is the
only potential cure.
Drugs Approved IN PA
Oral Endothelin receptor antagonist (ERA) Bosentan, Ambrisentan
Prostacyclin derivative Epoprostanol, Iloprost, Treprostinil
PDE5 inhibitors Sildenafil, Tadalafil
Soluble guanyl cyclase stimulator Riociguat
Selective Prostaglandin I2 receptor agonist Selixipag
146 | Medicine
Concept 2. : Pulmonary Thromboembolism
Learning Objective: To identify the causes, Manifestations and management of PAH
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
• PTE is defined as embolization of a clot into pulmonary vasculature

• Most common source is Lower Limb Deep Vein Thrombosis (DVT)
• Most common symptom is acute onset of breathlessness
• On examination there is Paucity of Lung signs inspite of hypoxemia
• Most common ECG finding is Sinus Tachycardia
• S1q3T3 pattern on ECG is Rare but specific for diagnosis
• CTPA (CT-Pulmonary Angiography) is the diagnostic test
Rx - SEVERITY - P.T.E* - Echocardio
Based on RV function
Preserved RV Hypokinesia / Hypotension

(Mild PTE) (Mod / Severe P.T.E)
Parenteral Anticoagul • I.V. Thrombolysis (rtPA)
W.P
- 7 - 14 days
c/I
If - Sx embolectomy
Chornic prophy: Oral Antico agulation.
Rivaroxaban ( ral Factor a inhibitor) is preferred due to safety
nly in presence of Treatment failure R Intolerance to oral anticoagulation IVC filter
placement is considered.
Prognosis with prompt treatment is Favourable.
3 Parenchymal and
Pleural disorders
CONCEPTS
Â Concept 3.1 Pneumonia
Â Concept 3.2 Pleural Effusion

148 | Medicine
Concept .1: Pneumonia
Learning Objective: To learn about the Causes, Presentation and management of
Pneumonia
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
• PNE MONIA is defined as Suppurative infection of the lung parenchyma

characterized by consolidation (solidification) of lung tissue.
• Most common route of entry is Aspiration > Inhalation.
Specific Pathogens:
< 6 months RSV
Young adults S. pneumoniae.
Elderly H. influenzae, M. catarrhalis, Mycobacterium tuberculosis
Chronic lung disease Streptococcus pneumoniae, H. influenzae, M. catarrhalis.
Severe hypogammaglobinemia Streptococcus pneumoniae, H. influenzae.
Severe neutropenia Pseudomonas aeruginosa.
CD 4 + count
< 500/ul M. tuberculosis.
< 200/ul P. carinii, H. capsulatum, Cryptococcus.
< 50/ul MAI, CMV.
Long term glucocorticoids M. tuberculosis, Nocardia.
Specific Types of Pneumonia:

Pneumococcal Rusty sputum, Icterus, Lobar pneumonia
Staphylococcal Pneumatocoeles, Pneumothorax
Klebsiella Red currant jelly sputum, UZ involvement
Legionella Atypical pneumonia –Subacute presentation, Exposure to Moist environment,
Diarrhea, Hyponatremia, Increase LDH and CK
Mycoplasma Hemolytic anaemia (Cold Agglutinin)
Erythema multiforme, Encephalitis, Transverse myelitis, Raynaud’s, GBS
Chlamydia LZ involvement, VDRL +ve, Hepatosplenopmegaly
Q-fever Thrombocytopenia, B/L Lower lobe, Endocarditis, Hepatitis with granuloma
CMV Commonest Viral Pneumonia in IC Host Lymphadenopathy, Hepatosplenomegaly
Anthrax Hemorrhagic Mediastinitis
Pneumocystis Interstitial Pneumonia
• Complication of Community Acquired Pneumonia(CAP)
Septicemia:
Para pneumonic effusion.
Respiratory failure.
Lung abscess.
• ARDS
Treatment:
Rx-CAP – SEVERITY GRADING B.T.S
C - Confusion
U- Urea >7.1 mmol. “1 point”-
R- R.R > 30.min presence of
each parameter
B- B.P < 90/60 mm
• max-‘5’
65 – Age > 65 years
score
MILD MOD SEVERE
0-1 2-3 4-5
Opd WARD ICU
Single drug Double durg Triple drug
• DOXY (FQ) (FQ) +
+
( (
OR (Imipenanam OR piperacillin) +
3rd gen. cephalo (Aminoglycosides)
• AZITH
OR
OR
Almox+calv
• FQ
(Levo / Moxi)
• Macrolides must be included in treatment if atypical infection is suspected

• Metronidazole (anaerobic cover) is aspiration is probable cause
• Vancomycin if MRSA is suspected
• In Renal failure/Critically ill cases of MRSA – Linezolid is preferred.
Prognosis of Classical Pneumonia is Favourable due to low mortality and low complication
rates.
150 | Medicine
Concept .2: Pleural Effusion:
Learning Objective: To identify Causes based on various characteristics of the effusion.
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
• Pleural effusion is defined as Accumulation of fluid in pleural space.
Causes:
Transudative:- Increased venous pressure or hypoproteinemia.
Exudative:- Increased leakage of pleural capillaries secondary to infection,
inflammation or malignancy.
• Transudative • Exudative
• CHF • Neoplastic disease
• Cirrhosis • Infectious disease
• Ne p hrot i c syndrome • Pulmonary embolus
• Sarcoidosis • Hemothorax
• Hypoal- buminemia • Chylothorax
• Clinical Features include pleuritic pain and breathlessness in severe cases.

• Examination reveals Decreased Air entry, Decreased TVF and TVR on affected side
with Stony dull note on percussion.
• Radiology is diagnostic of effusion.
• Diagnostic pleural tapping is mandatory for identification of cause.
Exudative pleural effusion has at least one of the following criteria (Light’s
criteria):
• Pleural fluid protein / serum protein > 0.5.
• Pleural fluid LDH / serum LDH > 0.6.
• Pleural fluid LDH > 2/3 of upper limit of normal for serum LDH.
Glucose - < 60mg/dl seen in Other rare causes
• Parapneumonic effusion • Paragonimiasis

• Malignant disease • Hemothorax
• Rheumatoid disease • ChurgStrauss
• Lupus pleuritis
Amylase Increase levels seen in:
• Pancreatitis.
• Malignant tumor.
• Esophageal rupture.
Cases of Right Sided Effusions:

• Fluid retaining states – CHF, CRF, Cirrhosis.
• Amoebic liver abscess, sub phrenic abscess.
• Meig’s syndrome.
• Thoracic duct involvement below D5 level.
Causes of Left Sided Effusions:

• Pancreatitis.
• Pericardial inflammation.
• Esophageal rupture.
• Left sided sub diaphragmatic abscess.
• Thoracic duct above D5 level.
4 Airway Disorders
CONCEPTS
Â Concept 4.1 Asthma
Â Concept 4.2 Bronchiectasis
Â Concept 4.3 COLD (Chronic Obstructive

Lung Disease)
Concept 4.1: Asthma
Learning Objective: To learn Clinical Presentation and management of Asthma.
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Bronchial Asthma is defined as

Hyper-responsiveness of the airways to a multitude of stimuli, which is marked by
episodic bronchoconstriction; inflammation of the entire airway predominantly affecting
the large airways.
• It affects Children (M>F) most commonly, though Can occur at any age.
Types:
Extrinsic/ Allergic/ Exogenous Intrinsic/ nonallergic/ Endogenous
Pathophysiology Induction of vagal reflex via release of Sensitized receptors in mucosa

histamine from mast cells
History– Onset. Childhood and young adult Infancy and adult
Family h/o allergic disorder Uncommon
Salicylate sensitivity absent Present
Clinical course – Paroxysmal asthma Chronic asthma
Status asthmaticus- infrequent Frequent
Sinus infection / nasal polyp. Infrequent Common
Favorable course Unfavorable course
Pathology– IgE increase Normal
Skin test positive Negative
Treatment– Mast cell inhibitors Little effect
Clinical Features:
• Triad of paroxysmal dyspnea, cough and wheezing.
• Life threatening features include (same as Indications for Mechanical Ventilation):
1. Orthopnea,
2. Inability to speak complete sentences
3. Inability to recline.
4. Pulse 110/min,
5. R 30/min,
154 | Medicine
6. Pulsus paradoxus,
7. Presence of Central Cyanosis
8. Silent chest on auscultation
9. impending respiratory muscle fatigue and
10. altered neurological status.
Variants:
A. NOCTURNAL ASTHMA : Overnight fall of 20% in FEV1 or PEFR.
Responds to Inhaled Corticosteroids (ICS)
B. EXERCISE INDUCED ASTHMA : typically occurs 30 mins after exercise.
Prevented by working out in climate controlled environment. ICS with Sal- meterol
used for prophylaxis. Longterm LABA has no role in treatment.
Obstructive pattern with Exellent bronchoreversibility is diagnostic.
ABG -In Acute attack : Hypoxia (Type 1 respiratory failure), Hypocapnia, resp.
alkalosis.
DOC for Acute attack is Salbutamol (Nebulisation is best route)
Management of Chronic Asthma:

Mildintermittent Mild Persistent Moderate Severe persistent
Persistent
Symptoms 1 –2 /week 1 –2 /week Daily Persistent
Nocturnal 2 / month 2 /month 1/week Frequent

Symptoms
Spirometry Normal Ab normal Ab normal Ab normal
FEV1/PFER 80% 80% 60 – 80% 60%
PFER variability < 20% 20 – 30% >30% 30%
Treatment SABA - SOS ICS + SABA SOS ICS + LABA High dose ICS +
If needed > once a + SABA SOS LABA + SABA
day move to step II SOS
DRU S APPR VED IN Asthma

Mast cell stabiliser Sodium chromoglycate
Leucotriene antagonist Montelukast
Mab against IgE Omalizumab
Mab against IL-5 Reslizumab, Mepolizumab
Mab against IL-4 Dupilumab
• Acute mortality is low making prognosis favourable.
Concept 4.2: Bronchiectasis
Learning Objective: Pathophysiology, Presentation and management of Bronchiectasis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Bronchiectasis is defined as permanent and irreversible dilatation of

medium si ed airways.
Most common risk factor is Tuberculosis infection
Typically affects middle aged (30-50) Females> Males
Cylindrical bronchiectasis is most common type.
Presents with recurrent LRTI, copious expectoration
Early and Severe clubbing along with coarse inspiratory crepitations with post-tussive
change are characteristic signs
HRCT is the gold standard and shows signet-ring appearance, tram-track appearance.
Palliative Medical therapy includes Antibiotics, Mucolytics
Chest Physiotherapy with postural drainage of secretions has best success in
preventing progression of the disease
Lung transplant offers potential cure
Prognosis is poor due to multiple complications which include:

• Hemoptysis.
• Recurrent pneumonia.
• Lung abscess.
• Pneumothorax.
• Cor pulmonale.
• Secondary Amyloidosis.
Ma or Etiologies of Bronchiectasis and Proposed orkup:

Pattern of Lung Involvement Etiology by Category Workup
(Examples)
Focal Obstruction (aspirated foreign Chest imaging (chest x-ray and/
body, tumor mass) or chest computed tomography);
bronchoscopy
Diffuse Infection (bacterial, nontu- Sputum Gram’s stain/culture;
berculous mycobacterial) stains/ cultures for acid-fast
bacilli and fungi. If no pathogen is
identified, consider bronchoscopy
with bron-choalveolar lavage.
156 | Medicine
Immunodeficiency (hypogamma- Complete blood count with

globulinemia, HIV infection, differential immunoglobulin
bronchiolitis obliterans after lung measurement; HIV testing
transplantation)
enetic causes (cystic fibrosis, Measurement of chloride levels
Kartagener’s syndrome, a1 in sweat (for cystic fibrosis),
antitrypsin deficiency) a1 antitrypsin levels; nasal or
respiratory tract brush/biopsy
(for dyskinetic/ immotile cilia
syndrome); genetic testing
Autoimmune or rheu- Clinical examination with careful
matologic causes (rheumatoid joint exam, serologic testing
arthritis, Sjogren’s syndrome, (e.g., for rheumatoid factor).
inflammatory bowel disease) Consider workup for allergic
immune- mediated disease bronchopulmonary aspergillosis,
(allergic bronchopulmonary especially in patients with
aspergillosis) refractory asthma.a
Recurrent aspiration Test of swallowing function and
general neuromuscular strength
Miscellaneous (yellow nail Guided by clinical condition
syndrome, traction bronchiectasis
from postradia- tion fibrosis or
idiopathic pulmonary fibrosis)
Idiopathic Exclusion of other causes
aSkin testing for Aspergillus
reactivity; measurement of serum
precipitins for Aspergillus, serum
IgE levels, serum eosinophils, etc
Fig. .
Concept 4. : C LD (Chronic bstrctive Lung disease)
Learning Objective: To learn Clinical Presentation and Management of COLD.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Chronic bstructive Pulmonary Disease (C PD) is defined as

chronic small airway obstruction with partial bronchoreversibility.
Typically affects Elderly (>50) Males > Females
Most important risk factor is Smoking
Presents with Chronic cough (> 8weeks) with intermittent exacerbations.
H. influenzae is the most common bacterial cause of acute exacerbation of COPD
Steroids (For shortest time possible) are indicated for Acute exacerbation only. No
role of steroids in chronic prophylaxis.
Spirometry is the Gold standard test for diagnosis
Management: Depends on Severity of the C LD
Fig. .4
GOLD class 1 & Category A: ONLY need Smoking cessation. No medication

GOLD Class 1 & Category B: Start Chronic Prophylaxis with LABA
GOLD Class 2: Add LAMA (Long-Acting Anti-Muscaranic agent – Tiotropium)
GOLD Class 3&4 (Severe and Most Severe) – Add Oral Roflumilast
Lung Transplant is the only potential cure.
Longterm Home Oxygen therapy is the only treatment which prolongs
survival once Cor-Pulmonale occurs.
5 Interstitial Lung Diseases
(ILD)
CONCEPTS
Â Concept 5.1 Hypersensitivity Pneumonitis (HP)
Â Concept 5.2 Sarcoidosis
Â Concept 5.3 Idiopathic ILD’s

Concept 5.1: ypersensitivity Pneumonitis ( P)
Learning Objective: To learn causes, Clinical Presentation and Management of HP.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
HP is also known as Extrinsic allergic alveolitis and due to exposure to organic dust.
H.P syndromes Antigen involved
MC Farmer’s lung MC Thermophilic Achnomyces

Bagossis ___”_____
MC Urban area: Avian dropping (Pigeon)
Bird-Fanciers
Cigerrate factory A. fumigates
Tobacco mill (rolten tobacco)
Compost worker ___”_____
Familiar H.P Bacillus subtilis (molds-wooden furnil, walls)
Hot tub lung* (Hot springs/geysers) Alypical mycobacter (MAC)
Majority present with Chronic cough with intermittent exacerbation.
Diagnostic Value of Bronchoalveolar Lavage in Interstitial Lung Disease

Condition Bronchoalveolar Lavage Finding
Sarcoidosis Lymphocytosis CD :CD8 ratio .5 most specific
of diagnosis
Hypersensitivity pneumonitis Marked lymphocytosis (>50%)
Organizing pneumonia Foamy macrophages; mixed pattern of increased
cells characteristic; decreased CD4:CD8 ratio
Eosinophilic lung disease Eosinophils >25%
Diffuse alveolar bleeding Hemosiderin-laden macrophages, red blood cells
Diffuse alveolar damage, drug toxicity Atypical hyperplastic type I pneumocytes
Opportunistic infections Pneumocystis carinii, fungi, cytomegalovirus-
transformed cells
Lymphangitic carcinomatosis, alveolar cell Malignant cells
carcinoma, pulmonary lymphoma
160 | Medicine
Alveolar proteinosis Milky e uent, foamy macrophages and

lipoproteinaceous intraalveolar material (periodic
acid Schiff stain-positive)
Lipoid pneumonia Fat globules in macrophages
Pulmonary Langerhans cell histiocytosis Increased CD1+ Langerhans cells, electron
microscopy demonstrating Birbeck granule in
lavaged macrophage (expensive and difficult to
perform)
Asbestos-related pulmonary disease Dust particles, ferruginous bodies
Berylliosis Positive lymphocyte transformation test to beryllium
Silicosis Dust particles by polarized light microscopy
Lipoidosis Accumulation of specific lipopigment in alveolar
macrophages
HP responds to immunosuppression and has favourable prognosis
Concept 5.2 : Sarcoidosis
Learning Objective: To identify Clinical Presentation and Management of Sarcoidosis.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Sarcoidosis - Multisystem A.I.D:

a ‘T’-Cell hyperactivity
b Non-caseating granulator
Epidemio- -5 yrs F M
C/f: ACUTE R CHRON IC MC manifestations
UVEO-PAROTID fever I – LUNG –occurs 4 stages:
• Uveatis II – Only Hilar LN
• Parotihs III – Hilar LN Pulm infiltrates
• Fever IV – Only Pulm infiltrates
• Cranial mono-neuropathy V – Interstitial fibrosis
(MC-LMN 7th CN palsy)
Most dreaded Skin:- “LUPUS PERNIO”
Only organ involvement mortality} Distribution-Eyebrows, cheeks
3. HEART - Infiltrahve CMP
Predisposed Tachyarm-V-TACH
Sudden cardiac death
Asis:-
Screening tests
GS
Specific
i) Radiological: CXR, HRCT Gallium scan BAL*:
ii) S.ACE levels: > 70% cases Good senschivity CD4: CD8 .5 confirms.
Rx: Longterm immunosuppression.

• Favourable prognosis
162 | Medicine
Concept 5. : Idiopathic ILD’s
Learning Objective: To learn types and Management of COLD.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Idiopathic ILDs are classified based on HRCT findings and Lung Biopsy changes.
Idiopathic I.L.D’s
N AME & PATHOLOGY HRCT BIOPSY RX
EPIDEMIO
U.I.P* Unknown agent WORST features “HETERO- NINTEDANI
(USUAL ↓ in ILD: GENOUS” areas Tyro-kinase
Interstitial Selective destructn “B/L Honey-comb of Fibroblashing inhibitor
Pneumonia) appear” proliferaten ONLY falliahre
Type 1
M>>F 30-50 yrs Trachion G.S* Lung Tx
↓
Bronchiect
Idiopathic pneumocyle
Pulmonary Proliferation of
Fibrosis type 2
↓
pneumocyte
VEGF*
• Angiogenesis
• Fibrosis
N.S.I.P + MC Sub-pleural “HOMO- Steroid respons
(Non-Specific) Type ILD calcificn GENOUS” areas Favour prog.
30-50 years Associated c + of fibroblast
C.T.D –vi3 Areas “Honey- prolifern
F<<M
SLE, Sclero comb”
M<F
MCTD & R.A
3. Desquamative Interstitial Pneumonia (DIP) – Only ILD which exclusively
occurs in smokers. Steroid responsive, favourable prognosis
4. Acute Interstitial Pneumonia (AIP) – mimics ARDS and has high mortality.
Unresponsive to steroids. Poor prognosis
5. Cryptogenic organizing Pneumonia (COP) – can mimic infective
bronchopneumonia. It is a diagnosis of exclusion. Responsive to steroids,
Favourable prognosis.
6 Miscellaneous
CONCEPTS
Â Concept 6.1 OSAH syndrome
Â Concept 6.2 Lung cancers

164 | Medicine
Concept .1: SA syndrome
Learning Objective: To learn about Sleep Apnea, its complications and its Management.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Obstructive Sleep Apnea-Hypopnea syndrome is defined as recuurent episodes
of Apnea (no air flow for 10 seconds) and/ or hypopnea (A 30% reduction in
airflow for at least 10 sec during sleep that is accompanied by either a 3% desaturation
or an arousal) during sleep due to Functional collapse of the airways
• Risk factors for Obstructive sleep apnea/hypopnea syndrome include obesity,
craniofacial factors such as micrognathia, family history of OSAHS and male sex.
• Hypothyroid and acromegaly are systemic diseases associated with OSAHS.
• Key symptoms of OSAHS include daytime somnolence and nocturnal breathing dis-
turbances (loud snoring, snorting, gasping, or breathing pauses)
• Polysomnography with Anea-Hypopnea Index (AHI) >= 5 episodes/hour is diagnostic
Conse uences of SA :
Fig. .5: Flow chart of the proposed pathophysiologic mechanisms and consequences of obstructive sleep
apnea. CV, cardiovascular; QOL, quality oflife; Htn, hypertension; CHF, congestive heart failure; CVA,
cerebrovascular accident; Pulm htn, pulmonary hypertension; DM, diabetes mellitus
• The primary therapy for OSAHS is continuous positive airway pressure (CPAP),
delivered through a nasal or nasal-oral mask.
Concept .2: Lung cancers
Learning Objective: To learn salient features and differences between the common
types of lung cancers.
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
N SCCL (70%) LUN G CAN CERS SCC

ADENOCARCINOMA OAT Cell Ca.
SQUAMOUS TB
MC Asia/India MC Common among smokers
World wide-(F),
Male smokers
Nonsmokers
Affects Affects L Multicentric
MC Cough Late symp-Cough MC cough

• EARLY METASTASIS
Frank hemophy EARLY METASTASIS
• Inoperable
Constitutional B/L Hilar LN
Early cavitation Intermediale prog PARANEOPLASTIC:

PANCOAST syn* BIOLOGICAL: Eaton Lambert
BEVACIZUMAB* Ectopic ACTH
HyperCa++ IMMUNOLOGICALS: • SVC obstruction

MC -PTHrP Anti-EGFR agents • Tumor embolism
HRCT + Biopsy GEFTINIB / ERLOTINIB CHEMOSENSITIVE

Anit-ALK agents PROPHYLACTIC
CRANICAL RADIATn
Late metastatis (Anaplastic lymphones) WORST prognosis
Amenable-Sx Kinases-CRIZO TINIB High relapses*
BEST prognosis ALECTINIB
CERITINIB
7 Acid Base-Balance (ABB)
CONCEPTS
Â Concept 7.1 Physiology of ABB
Â Concept 7.2 ABG interpretation
Â Concept 7.3 Metabolic Acidosis
Â Concept 7.4 Metabolic Alkalosis
Â Concept 7.5 Respiratory Acidosis
Â Concept 7.6 Respiratory Alkalosis

Concept .1: Physiology of ABB
Learning Objective: To learn various physiological mechanisms regulating pH.
Time needed
1st Reading 15 mins
2 Reading
nd
5 mins
RENAL TUBULES-Most Potent Role in ABB

• Human Body is in a “Pro-acidic” state.
• N pH -7.40 (Slightly Basic)
• Regulators of pH/Mechanisms of ABB-Potent
Buffering Resp. Mech. Renal mech*

Most imp* (Minor role) by excreting (MOST POTENT)
HCO3-- Acid in form of CO2 ↓
Back up: ACIDIFICATION OF URINE
PO4 — (Bones) ↓
P SI L -ABB : PR -ACIDIC State

MECHANISMS –ABB
1) BUFFERING 2. R.S. (MINOR) 3. RENAL (POTENT)

(At tissue level) Exc. Acid
[H+] + [HCO3--] [CO2]
↓
PCT DCT
M. imp. Extracellular
HCO3 H+
Reabsorbn Secretion
↓
ACID-BASE DISORDERS PRIMARY MECHAN ISM COMPEN SATE RESPON SE

MET. ACIDOSIS ↓ ↓ ↓ ↓ HCO3— ↓ CO2 RESP ALKAL
(SAME)
MET. ALKALOSIS HCO — CO2
(SAME)
RESP. ACIDOSI (OPP) CO2 (HYPOVENTILAT) HCO3—MET.ALKAL
↓↓
RESP. ALKALOSIS ↓ ↓ CO2 (HYPERVENTILY) ↓HCO3--
(OPP)
168 | Medicine
• Combinations of above (2 or 3) – common
• N pH maybe True N OR or compensated resp. Cannot exclude presence AB defects
• Which 2 cannot co-exist together?
BOTH RESPIRATORY DEFECTS*
• In 10 Metabolic disease, Resp compensation
occurs within (mins/hours) Always present
• In 10 Respiratory disease, metabolic (Renal)
Compensation occurs over (weeks/months)
If compensation, Absent
Presents indicates
ACUTE nature
CHRONIC Nature
• Compensatory response CAN

NEVER over-correct the pH
Concept .2: Identification of ABB disorders
Learning Objective: To diagnose ABB disorders based on ABG (Arterial Blood gas
analysis)
Time needed
1 Reading
st
15 mins
2 Reading
nd
5 mins
STEPWISE –AB disease –ABG

TRUE NORMAL
1) pH < 7.35-7.45 >
ACIDOSIS ALKALOSIS
Compensated
< >
7.40
2) Direction of e.g. ACIDOSIS (↓↓)

movement
Either CO2/HCO3—
In relation
to direction
Same direct Opp direct
of pH
movement 1 METABOLIC
O
1O RESP
3) Presence of
compensatory
response Always
present Presence
(Full / Parhal) CHRONIC
170 | Medicine
Concept . : Metabolic Acidosis
Learning Objective: To identify causes and management of Metabolic Acidosis.
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
METABOLIC ACIDOSIS ↓↓PLASMA HCO3—
Calculate: ANION-GAP (AG) – 10-12 mEq
AG=
Unmeans-anions Unmeas. Cation
(HAGMA) • Albumin K+
1/
• Ketones Ca++ more
1/ Mg++
• Lactates more ↓↓
• Urates
RARE
• PO4—
• SO4— MC
AG=
meas. Cations meas. Anions
(NAGMA) Na
+
C1- + hco3—
↓↓
HAGMA * (<12) NAGMA (10-12)
1/more of HYPER CHLOREMIC ACIDOSI

unmeasured anions
HAGMA N AGMA
1. Ketones: DKA, Starvation A. GI causes: (Loss-HCO3 -- in stools)
• Small bowel diarrhea
• Pancreatic diar/fistula
2. Lactates: biguanides sepsis, shock • Laxahve abuse
3. Urates: A.K.I, B Renal causes:
• Advanced-C.K.I (GFR < 25 ml/min)
(Defect in Acidification of urine) - R.T.A
4. PO4 — Advanced CKI, Rhabdomyolysis
Expected Vc1-Low
5. SO4 -- (Drugs/Toxins)
Salicylate, methanol, Polyethylene glycol - UAG* = VNA++UK+ UCI-
Paraldehyde
D/D-GI vs RENAL
LOW / HIGH /
NEGATIVE POSITIVE
Rx: Palliative Specific – Cause
HCO3—Supplementation – pH < 7.20
Total HCO3-- deficit

× x wt (kgs)
dose = 0.3 24 –pt’s
value
Prog - Favourable AG
Calculation (HAGMA)
* HCO3--
(Pts AG-12)
Identify
(24 –Pt’s HCO3--) mixed ABD
<0.8 0.8-2. <2.
HAGMA Isolated
HAGMA HAGMA
+NAGMA
+
ACEI + (DKA)
+ met. Alkallosis
(Loop divrehes)
Compensation in case of Metabolic acidosis i.e. expected change in CO2 due to acidosis
is calculated using Winter’s formula: (1.5*Pts HCO3 value) + 8 +/- 2.
In the given question, the ph is 7.20 indicating acidosis. (Hence NOT Option D)
HCO3 is less than normal indicating Primary Metabolic acidosis.
According to Winter’s formula: Expected PaCO2 in this patient should be 30+/-2 mm.
Since the PaCO2 in the report is as expected, there is no additional respiratory defect
and the change in PaCO2 (i.e. Respirator Alkalosis) is compensatory to the primary
defect.
172 | Medicine
In a case of High Anion gap Metabolic acidosis, it is important to identify the presence
of Mixed Metabolic defects.
Hence, we calculate Ratio = AG / HCO3 i.e. (Pts Anion Gap – 12) /(24 – Pts HCO3).
Based on the value, the following interpretation:

Value – 0.8-2 : Isolated HAGMA
<0.8 : HAGMA + NAGMA
>2 : HAGMA + Metabolic alkalosis
METABOLIC ACIDOSIS
Calculate AG
HAGMA NAGMA
CALCULATE Calculate
/ Ratio UAG – High
(Renal)
Concept .4: Metabolic Alkalosis
Learning Objective: To identify causes and management of Metabolic Alkalosis.
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
METABOLIC ALKALOSIS- Plasma HCO3--
CAUSES: Based on
Low (Cl- responsive) HIGH (Cl- - refractory)

GI causes Renal causes
(Loss of H+CI- feom (Excess H+ secretion into urine)
stomach
(Hypochloremic alk) Inherited channelopaty Chronic drug use
• Pyloric stenosis BARRTER’S Loop diuretes
• Ca stomach GITELMAN’s Thiazides
(Gastric outlet obs)
LIDDLE’S (Pseudo- Exagenous steroids
• Ialrogenic: Hyper Aldo)
Continous RT drain
• Antacid abuse
174 | Medicine
Concept .5: Respiratory Acidosis
Learning Objective: To identify causes and management of Respiratory Acidosis.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
• HYPOVENTIALTION Syndromes: PaCO2 > 45mm
CEN TRAL NM Mechanical
Defect in Resp. drive Resp. apparatus weakness Over-burden on Resp. apparatus
• Brainstem disorders • Cx myelopathy • Obesity
• GBS, Myasthe • Kyphoscoliosis
• SLE (Shrinking lung syn) Misc: COLO exacerbn
Apnea-Hypaap
Direct Drowsiness,
c/f: PaCO2 Irritability
Neuronal box
Resp centre Disturbs sleep

Daytime somnolence
arousal
Cerebral Morning headache
vasodilation
↓PaCO2 — PaO2 - & its manifestations
Asis: Suspician ABG* Rx: Vent. Support

Underlying cause
Concept . : Respiratory Alkalosis
Learning Objective: To identify causes and management of Respiratory Alkalosis.
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Hyperventilation - Paco2 < 35mm of Hg
MC Psychogenic Physio Compensatory response to

Hypoxemia
PaO2 Normal
Panic, Fear 3rd trimester Pregnancy PaO2↓↓

Anxiely
All causes except Hypoventn
c/f: ↓PaCO2 Direct Asymptomatic
Resp. Alkalosis ppts Hypoca++
Earliest (Sensory) Motor Cardiac

• Penoral T/N Taetany conduction
defect
• Paraesthesia
sis - ABG
Rx:- Paper bag ventilation Underlying
+
(Closed arcuit ventilation) cause
176 | Medicine
SECTION — 4
GASTROINTESTINAL TRACT AND LIVER
Introduction
The gastrointestinal (GI) tract extends from the mouth to the anus and comprises
several organs with distinct functions.
Gut compartmentalization: The organs are separated by specialized & independently
controlled thickened sphincters that aid in gut compartmentalization.
Functionally the gut wall is organized into:
a. The mucosa serves as a barrier to luminal contents and as a site for transfer of
fluids or nutrients.
b. Gut smooth muscle mediates propulsion from one region to the next.
c. Serosal layer provides a supportive foundation and permits external input.
Interactions with other organ systems :
a. Pancreaticobiliary conduits deliver bile and enzymes into the duodenum.
b. A rich vascular supply is modulated by GI tract activity.
c. Lymphatic channels assist in gut immune activities.
d. Intrinsic gut wall nerves provide the basic controls for propulsion and fluid
regulation.
e. Extrinsic neural input provides volitional or involuntary control to degrees that are
specific for each gut region.
The GI tract serves two main functions :
a. assimilation of nutrients and
b. elimination of waste.
Average Gastrointestinal Secretion in normal individual :
a. Total Salivary secretion : 750-1500ml/day
b. Total gastric secretion : 1000-1200ml/day
c. Total pancreatico-biliary secretion : 1500-2500ml bicarbonate + 2000ml/day
d. Total GI secretion per day : 6000-7500ml. Total excreted : 200-400ml/day.
1 Esophagus
CONCEPTS
Â Concept 1.1 Basics of Esophagus
Â Concept 1.2 Classification of Esophageal disorders
Â Concept 1.3 Motility disorders
Â Concept 1.4 Barretts esophagus

180 | Medicine
Concept 1.1: Basics of Esophagus
Learning Objective: To understand the Basic physiology and Anatomy of Esophagus
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Anatomy : Length of esophagus is 25-45 cms.

The esophageal mucosa has a protective squamous histology that does not permit
significant diffusion or absorption. However it is less acid resistant.
Esophagus has 2 sphincters:
1. Upper esophageal sphincter (UES) : consists of the cricopharyngeus and inferior
pharyngeal constrictor muscles. Both are striated muscles innervated by excitatory
somatic lower motor neurons and exhibit no myogenic tone and receive no inhibitory
innervation. The UES remains closed owing to the elastic properties of its wall and
to neurogenic tonic contraction of the sphincter muscles. Inhibition in the central
nervous system opens the sphincter muscles in concert with forward displacement of
the larynx by the suprahyoid muscles.
2. Lower esophageal sphincter (LES) : composed of smooth muscle and is innervated
by parallel sets of parasympathetic excitatory and inhibitory pathways.
It remains closed because of its intrinsic myogenic tone, which is modulated by the
excitatory and inhibitory nerves. It opens in response to the activity of the inhibitory
nerves.
The neurotransmitters of the excitatory nerves are acetylcholine and substance P,
Inhibitory transmitters are vasoactive intestinal peptide (VIP) and nitric oxide.
The function of the LES is supplemented by the striated muscle of the diaphragmatic
crura, which surrounds the LES and acts as an external LES.
Physiology of swallowing : Swallowing has 3 phases.viz. oral, pharyngeal and
esophageal.
Oesophageal peristaltic waves are of 3 types. Viz. Primary, Secondary and tertiary.
Transit time : in order of seconds to minutes
astrointestinal ract and iver | 181
Concept 1.2: Classification of Esophageal disorders
Learning Objective: To understand the classification of Esophageal disorders
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Oesophageal disorders :
1. Motility disorders Achalasia Cardia
Diffuse Oesophageal spasm (DES)
Scleroderma Oesiophagus
2. Inflammatory Oesophagitis
Viral –HSV, Varicella oster, CMV, HIV
Fungal – Candidiasis
Drug induced
Corrosive poisoning
Iatrogenic - sclerotherapy
3. Bleeding related Oesophageal varices

Mallory Weiss tear
Boerheeve’s syndrome
. Reflux disorder ERD

Barretts oesophagus
Hiatus hernia
5. Neoplastic Malignancy
. Miscellaneous Plummer-Vinson syndrome

Oesophageal webs/strictures
Diverticuli
Schatzki ring
182 | Medicine
Concept 1.3: Motility disorders
Learning Objective: To learn the motility disorders of Esophagus
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Achalasia Cardia : is a motor disorder of the esophageal smooth muscle in which the
LES does not relax normally with swallowing, and the esophageal body undergoes non-
peristaltic contractions.
Typically affects 2nd-4th decade. No gender preponderance.
Primary idiopathic achalasia accounts for most of the patients.
Secondary achalasia may be caused by gastric carcinoma that infiltrates the esophagus,
lymphoma,Chagas’ disease, certain viral infections, eosinophilic gastroenteritis, and
neurodegenerative disorders.
Clinical Features
Dysphagia, chest pain, and regurgitation are the main symptoms. Dysphagia appears
early, occurs with both liquids and solids, and is worsened by emotional stress and
hurried eating.
Diagnosis
A chest x-ray shows absence of the gastric air bubble and an air-fluid level in the
mediastinum in the upright position represents retained food in the esophagus.
Barium swallow shows proximal esophageal dilation, “Birds Beak” Sign.
Cholecystokinin (CCK), which normally causes a fall in the sphincter pressure,
paradoxically causes contraction of the LES (the CCK test).
Endoscopy is helpful in excluding the secondary causes of achalasia.
Treatment
Medical line unsatisfactory.
Endoscopic intrasphincteric injection of botulinum toxin
Balloon dilatation reduces the basal LES pressure by tearing muscle fibers.
Heller’s extramucosal myotomy of the LES, is equally effective.
Laparoscopic myotomy is the procedure of choice.
Reflux esophagitis and peptic stricture may follow successful treatment.
Diffuse Esophageal Spasm : Diffuse esophageal spasm is characterized by
nonperistaltic contractions, usually of large amplitude and long duration. An esophageal
motility pattern showing hypertensive but peristaltic contractions has been called
“nutcracker esophagus.”
Pathophysiology Nonperistaltic contractions are due to dysfunction of inhibitory
nerves. Patchy neural degeneration localized to nerve processes, rather than nerve cells.
Diffuse esophageal spasm may progress to achalasia.
Clinical Features
chest pain, dysphagia, or both.
Diagnosis
Barium swallow shows the “corkscrew” esophagus.
The barium swallow is frequently normal in diffuse esophageal spasm.
DES is a manometric diagnoses. However the abnormalities may be episodic.
Treatment
Reassurance and tranquilizers are helpful in allaying apprehension.
184 | Medicine
Concept 1.4: Barretts esophagus
Learning Objective: To learn the manifestation and treatment of Barrett’s Esophagus
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Barrett’s oesophagus
Replacement of Squamous epithelium to Columnar epithelium in the lower 1/3rd of the
oesophagus constitutes Barrett’s oesophagus. (more acid/pepsin-resistant)
Barrett’s esophagus is more common in men, particularly white men.
Barrett’s esophagus is arbitrarily divided into :
long-segment (_2–3 cm) or short-segment (_2–3 cm) disease;
Longsegment disease is present in 0.5% of population and short-segment disease in
15%.
Barrett’s epithelium progresses through a dysplastic stage before developing into
adenocarcinoma. The rate of cancer development is 0.5% per year; those with long-
segment disease have a risk of developing esophageal cancer that is 30 to 125 times
the risk of the general population.
Barrett’s esophagus can also lead to chronic peptic ulcer of the esophagus with high
(midesophageal) and long strictures.
Established metaplasia does not regress with treatment; thus, acid suppression and
fundoplication are indicated only when active esophagitis is also present.
The need and frequency of surveillance endoscopies in patients is debated.
The risk of developing esophageal adenocarcinoma is related to the length involved.
Once high-grade dysplasia is detected, treatment of choice is esophagectomy of the
Barrett’s segment.
Photodynamic laser or thermocoagulative mucosal ablation and endoscopic mucosal
resection are being evaluated as alternatives.
2 Stomach
CONCEPTS
Â Concept 2.1 Basics of Stomach
Â Concept 2.2 Peptic Ulcer disease
Â Concept 2.3 Gastritis

186 | Medicine
Concept 2.1: Basics of Stomach
Learning Objective: To understand the Basic physiology and Anatomy of Stomach
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Stomach : Consists of Antrum, body and pylorus.

Lined by columnar epithelium.
Consists of 2 Cells : Chief and Parietal cell.
Protective barriers in stomach.
Gastric motor activities exhibit regional variability:
(1) the proximal stomach serves a storage function by relaxing
(2) the distal stomach exhibits phasic contractions that propel solid food residue against
the pylorus, where it is repeatedly propelled proximally for further mixing before it
is emptied into the duodenum;
Transit time in hours – 2-5 hours
Gastric protective mechanisms : Physiology
Pre-Epithelial : Mucous layer, Bicarbonate layer
Epithelial : Prostaglandins, Restitution, Immune cells
Post-epithelial : Vascularity, immune cells.
Concept 2.2: Peptic Ulcer disease
Learning Objective: To learn manifestations and management of Peptic ulcer disease
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Peptic Ulcer disease (PUD)

Burning epigastric pain exacerbated by fasting and improved with meals is a symptom
complex associated with peptic ulcer disease (PUD).
Pathophysiology :
PUD encompasses both gastric and duodenal ulcers.
Ulcers are defined as a break in the mucosal surface 5 mm in size, with depth to the
submucosa.
Duodenal ulcers (DUs) and gastric ulcers (GUs); share many common features in terms
of pathogenesis, diagnosis, and treatment, but several factors distinguish them.
Etiology
H-Pylori related PUD :
Flagellate, micro-aerophilic bacilli. Resistant Cocci form.
Epidemiology : Usually > 80% population infected before 20 years of age.
Poor socio-economic factors and poor sanitation are main factors.
Gastric infection with the bacterium H. pylori plays important role in majority of PUD.
Clinical features : Presnts with PUD symptoms. Usually not responding to PPI regimen.
Also patients may get frequent relapses unless H.Pylori is diagnosed and treated.
Complications : This organism also plays a role in the development of gastric mucosal-
associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma.
Diagnosis :
Non-Invasive : Urease Breath test.
Invasive : Rapid Urease test , Staining, Culture.
Treatment :
Triple Drug therapy :
Category 1 : Azithromycin/Clarithromycin.
Category 2 : Amoxacillin/ Metronidazole.
Category 3 : Proton pump inhibitor – Omeprazole.
188 | Medicine
NSAID induced PUD : Prostaglandin Physiology.
NSAID – non dose-dependant. No class effect.
Incidence is high due to OTC sale of NSAID and wide its therapeutic usage.
Classical history is usually diagnostic.
Pathophysiology is direct (ION trapping) and indirect (inhibition of PG synthesis.)
Treatment is symptomatic.
Concept 2.3: Gastritis
Learning Objective: To understand the types and features of GAstritis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Types A Gastritis : Antral, Autoimmune.

Common in females
Presentation with PUD symptoms and symptoms of autoimmune disease viz.
Anaemia – Pernicious anaemia. Hashimotos thyroiditis.
Anti parietal cell antibody vs anti-Intrinsic factor antibody > 80%.
Increased risk of MALTomas.Treatment supportive.
Prognosis good.
Type B gastritis. : Body, NSAID and H.Pylori related.

Common in males.
Refractory. High recurrence. Risk of adenocarcinoma.
Prognosis worse.
Medical treatment : Diet , Posture
H2 blockers
Proton pump inhibitors
Antacids
Cytoprotective agents.
H-Pylori treatment
Surgical measures :
Billroth Type 1 & 2.
Vagotomy.
3 Malabsorption Syndromes
CONCEPTS
Â Concept 3.1 Basics of Malabsorption syndromes
Â Concept 3.2 Tests for Malabsorption
Â Concept 3.3 Fat Malabsorption syndromes
Â Concept 3.4 Biopsy findings in Malabsorption

syndromes
Concept 3.1: Basics of Malabsorption syndromes
Learning Objective: To learn relevant physiology of Malabsorption syndromes
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Malabsorption Syndrome : constitutes a broad spectrum of conditions due to

malabsorption of 1 or more nutrients with multiple etiologies and varied clinical
manifestations.
Almost all of these clinical problems are associated with diminished intestinal absorption
of one or more dietary nutrients. E.g. B12, Iron, Lactase deficiency.
The only clinical situations in which absorption is increased are hemochromatosis and
Wilson’s disease, in which there is increased absorption of iron and copper, respectively.
Steatorrhea is increase in stool fat excretion of > 6% of dietary fat intake.
Majority of malabsorptive disorders are associated with Steatorrhea except
the following:
a. Primary lactase deficiency : is associated with lactose “malabsorption,”
b. Pernicious anemia : is associated with a marked decrease in intestinal absorption
of Cobalamin (vitamin B12) due to an absence of gastric parietal cell intrinsic factor
required for cobalamin absorption.
Also abdominal discomfort and diarrhea occur.
192 | Medicine
Concept 3.2 : Tests for Malabsorption
Learning Objective: To learn tests and approach to Malabsorption syndromes
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Malabsorbed nutrient aboratory finding

(1) Fat uantitative -72 hr stool fat on a defined diet ( of fat intake) ualitative
– Sudan III stain
(2) Carbohydrate a) D- ylose test -25 gram D-xylose given orally, and urine is collected for 5
hrs. It is abnormal when there is .5 gm excretion.
False ve Delayed gastric emptying, poor renal Function.
b) Lactose tolerance test- Oral lactose is given which is followed by a little rise
in blood glucose level. Also abdominal discomfort and diarrhea occur.
( ) Protein a) Decreased serum albumin
b) Focal nitrogen –False–ve due to bacteria
c) Measuring focal radioactivity after giving radioactive protein.
d) 1 antitrypsin clearance-Increased fecal loss of 1- antitrypsin.(As it is
resistant to proteolysis ). 1 antitrypsin clearance (Clearance 1 ml/d is
abnormal)
2 hr volume of stool stool conc. of 1antitrypsin Serum 1 antitrypsin
conc.
( ) Vitamin B12 a) Macrocytosis
b) Decreased serum vitamin B12 level.
c) Schilling test-
(i) 58 Co-labeled cobalamin is given by month followed by I.m. in ection
of non-radioactive vit B12.2 hr urine is collected. Abnormal test is
10 excretion of radioactive cobalamin.
(ii) 58 Co-labeled Cobalamin is bound to intrinsic factor. If excretion
improved,-pernicious anemia. If still 10 Excretion proceed to stage
III.
(iii) 58 Co-labeled cobalamin bound with pancreatic enzymes. If excretion
improved chronic pancreatitis.If excretion still low proceed to stage
IV.
(iv) 5 days of antibiotics – If excretion improve-bacterial overgrowth. If
still low Ideal disease.
TESTS in Various etiologies of Malabsorption:
Results of Diagnostic Studies in Steatorr ea of arious tioiogies
d-Xylose Test Sc illing est Duodenal Mucosal
Biopsy
Chronic pancreatitis Normal 50 abnormal, if Normal
abnormal, normal with
pancreatic enzyme
treatment
Bacterial overgrowth Normal or only Often abnormal if sually normal
syndromes modestly abnormal abnormal, normal after
antibiotic treatment
Ileal disease Normal Abnormal Normal
Celiac disease Decreased Normal Abnormal: probably
flat
Intestinal Normal Normal Abnormal: dilated
lymphangiectasiaia lymphatics
194 | Medicine
Concept 3.3 : Fat Malabsorption syndromes
Learning Objective: To learn the different fat malabsorption syndromes
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
A. Coeliac disease :
(nontropical sprue, celiac disease, glutensensitive enteropathy.)
Appears in Infants or second decade of life.
The symptoms can range from significant malabsorption to aymptomatic cases.
Anti-endomysial Ab, Anti-Gliadin and Anti-Tissue transglutaminase Ab, Anti-Reticulin
IgA assist in diagnosis.
Treatment is Avoidance of Gluten
Failure to Respond to Gluten Restriction : The most common cause of persistent
symptoms is continued intake of gluten since Gluten is ubiquitous.
The remainder constitute a heterogeneous group (whose condition is often called
refractory sprue) that includes some patients who (1) respond to restriction of other
dietary protein, e.g., soy; (2) respond to glucocorticoids; (3) are “temporary,” i.e., the
clinical and morphologic findings disappear after several months or years; or (4) fail
to respond to all measures and have a fatal outcome, with or without documented
complications of celiac sprue, such as development of intestinal T cell lymphoma.
Patients with more severe involvement with celiac sprue may obtain temporary
improvement with dietary lactose and fat restriction while awaiting the full effects of
total gluten restriction, which is primary therapy.
Associated Diseases Celiac sprue is associated with dermatitis herpetiformis (DH).
B. Tropical Sprue :
Chronic diarrhea in a tropical environment is most often caused by infectious agents
including G. lamblia, Yersinia enterocolitica, C. difficile, Cryptosporidium parvum, and
Cyclospora cayetanensis, among other organisms.
Broad-spectrum antibiotics and folic acid are most often curative.
Folic acid alone will induce a hematologic remission as well as improvement in appetite,
weight gain, and some morphologic changes in small intestinal biopsy.
C. Whipple’s disease :
Organism : T.Whippllei
Clinical features:
a) Most frequently occur in middle aged male.
b) Gastrointestinal symptoms are common. They include diarrhoea steatorrhoea,
abdominal pain, weight loss, protein losing enteropathy with hypoalbuminemia, and
edema. (75%).
c) Migratory large joint oligo/polyarthritis. (80%).
d) Respiratory involvement with pleurisy, pulmonary infiltrates.
e) Cardiac involvement – Coronary arteritis, pericarditis, conduction defects,
endocarditis, valvular involvement.
f) CNS involvement (10%)- Depression, seizures, myoclonus, meningitis, dementia,
hypothalamic syndrome (In- somnia, hyperplasia, polydipsia).
The diagnosis is established by histo- pathological examination of duodenum which
demonstrate infiltration of the lamina propria with PAS-positive macrophages that
contain gram positive bacilli.
Septran (Co-Triamoxazole) for 1 year is drug of choice.
196 | Medicine
Concept .4 : Biopsy findings in Malabsorption syndromes
Learning Objective: To learn Biopsy findingsin Malabsorption syndromes
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Diseases that can be Diagnosed on Small Intestinal Mucosal Biopsies:

Lesions at ologic indings
Diffuse, Specific
Whipple s disease Lamina propria includes macrophages containing material
positive on periodic acid-Schiff staining
Agammaglobulinemia No plasma cells either normal or absent villi ( flat mucosa )
Abetalipoproteinemia Normal villi epithelial cells vacuolated with fat postprandially
Patchy, Specific
Intestinal lymphoma Malignant cells in lamina propria and submucosa
Intestinal lymphangiectasia Dilated lymphatics clubbed villi
Eosinophilic gastroenteritis Eosinophil infiltration of lamina propria and mucosa
Arnyloidosis Amyloid deposits
Crohn’s disease Noncaseating granulomas
Infection by one or more microorganisms Specific organisms
Mastocytosis Mast cell infiltration of lamina propria
Diffuse, Nonspecific
Celiac disease Short or absent villi mononuclear infiltrate epithelial cell
damage hypertrophy of crypts
Tropical sprue Similar to celiac disease
Bacterial overgrowth Patchy damage to villi lymphocyte infiltration
Folate deficiency Short villi decreased mitosis in crypts megalocytosis
Vitamin B12 deficiency Similar to folate deficiency
Radiation enteritis Similar to folate deficiency
ollinger-Ellison syndrome Mucosa ulceration and erosion from acid
Protein-calorie malnutrition Villous atrophy secondary bacterial overgrowth
Drug-induced enteritis Variable histology
4 Colon
CONCEPTS
Â Concept 4.1 Basics of Colon
Â Concept 4.2 Inflammatory Bowel Disease
Â Concept 4.3 Treatment of IBD

198 | Medicine
Concept 4.1 : Basics of Colon
Learning Objective: To learn relevant physiology and anatomy of Colon
Time needed
1st Reading 10 mins
2 Reading
nd
5 mins
Colon :
Consists of ascending colon, transverse colon and descending colon.
Length is 80cms.
Mucosa has Haustrations.
The colonic mucosa dehydrates the stool, decreasing daily fecal volumes from the 1000
to 1500 mL delivered from the ileum to the 100 to 200 mL expelled from the rectum.
The colonic lumen possesses a dense bacterial colonization that ferments undigested
carbohydrates and short-chain fatty acids.
Colonic motor patterns exhibit a to and- fro character that facilitates slow fecal
desiccation. The proximal colon serves to mix and absorb fluid, the distal colon exhibits
peristaltic contractions and mass actions that function to expel the stool.
The colon terminates in the anus, a structure with volitional and involuntary controls
to permit retention of the fecal bolus until it can be released in a socially convenient
setting.
Transit time in hours to days – 18-30 hours.
Concept 4.2 : In ammatory Bowel Disease:
Learning Objective: To learn manifestations and management of IBD
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Differences between Ulcerative Colitis and Crohn’s Disease:

eatures lcerati e colitis Cro n s disease
Incidence 11/100000 7/100000
Sex ratio Equal ratio Males more common
Monozygotic twins -18 concordance 8-58 concordance
Smoking may prevent disease May cause the disease
Oral contraceptive No increased risk Relative risk
Appendectomy Not protective Protective
ross blood in stools Present Rare
Mucus Present Rare
Systemic symptoms Rare Present
Pain Rare Present
Abdominal mass Rare Present
Perineal disease Absent Present
Fistula Absent Present
Small intestinal obstruction Absent present
Colonic obstruction Rare Present
Response to antibiotic Absent Present
Recurrence after surgery Absent Present
ANCA positivity 0-70 5-10
Rectal sparing Rare Present
Continuous disease Present Rare
Cobblestone appearance Absent Present
ranuloma Absent Present
Abnormal small int. Absent Present
Abnormal terminal ileum Rare Present
Segmental colitis Absent Present
Asymmetrical colitis Absent Present
Stricture Rare Present
200 | Medicine
Concept 4.3 : Treatment of IBD:
Fig. 4.1: edical anage ent of infla atory o el disease. A A, a inosalicylic acid;
C , Crohn s disease; C, ulcerative colitis.
Indications for Surgery:

lcerati e Colitis Cro n s Disease
Intractable disease Fulminant disease Toxic Small Intestine:
megacolon Colonic perforation Massive colonic Stricture and obstruction unresponsive to medical
hemorrhage Extracolonic disease Colonic therapy Massive hemorrhage Refractory fistula
obstruction Colon cancer prophylaxis Colon Abscess
dysplasia or cancer Colon and rectum:
Intractable disease Fulminant disease Perianal
disease unresponsive to medical therapy
Refractory fistula Colonic obstruction Cancer
prophylaxis Colon dysplasia or cancer
5 Liver
CONCEPTS
Â Concept 5.1 Liver Function Tests
Â Concept 5.2 Acute Viral Hepatitis
Â Concept 5.3 Approach to Chronic Hepatitis
Â Concept 5.4 Chronic Hepatitis B
Â Concept 5.5 Chronic Hepatitis C
Â Concept 5.6 Autoimmune Hepatitis:
Â Concept 5.7 Cirrhosis:
Â Concept 5.8 Portal Hypertension

202 | Medicine
Concept 5.1 : Liver Function Tests
Learning Objective: To learn interpretation and role of LFT in diagnosis
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Liver is a complex organ executing multiple functions
Hence, one test is insu cient to assess Liver function
We prefer a battery of tests as follows:
a. Tests Based on Detoxification Functions: S.Bilurubin
b. Tests assessing inflammation: SGPT, SGOT,GGTP
c. Tests assessing Synthesis function: Albumin, Prothrombin Time
Fig. 4.2
Summary of pattern of LFT in various disorders:
Type of Disorder Bilirubin Aminotransferases Alkaline Albumin rot rombin ime
osp atase
Hemolysis/ ilbert s Normal to 8 mol/l Normal Normal Normal Normal
syndrome (5 mg/dL)
85 due to indirect
fractions
No bilirubinuria
Acute hepatocellular Both fractions may Elevated, often 500 Normal to x Normal sually normal. If
necrosis (viral and be elevated I , ALT AST normal elevation 5x above control
drug hepatitis, Peak usually follows and not corrected by
hepatotoxins, acute aminotransferases parenteral vitamin
heart failure) Bilirubinuria K, suggests poor
prognosis
Chronic Both fractions may Elevated, but usually Normal to x Often decreased Often prolonged
hepatocellular be elevated 00 I normal elevation Fails to correct with
disorders Bilirubinuria parenteral vitamin K
Alcoholic hepatitis, Both fractions may AST:AIT 2 Normal to x Often decreased Often prolonged
cirrhosis be elevated suggests alcoholic normal elevation Fails to correct with
Bilirubinuria hepatitis or cirrhosis parenteral vitamin K
Alcoholic hepatitis, Both fractions maybe Normal to moderate Elevated, often x Normal, unless Normal
cirrhosis elevated elevation normal elevation chronic
Obstructive aundice Bilirubinuria Rarely 500 I Elevated, often x Normal If prolonged,
normal elevation will correct with
parenteral vitamin K
Infiltrative sually normal Normal to slight Fractionate, or Normal Normal
diseases (tumor, elevation confirm liver origin
granulomata) partial with 5 nucleotidase
bile duct obstruction or glutamyl
transpeptidase
astrointestinal ract and iver |
203
204 | Medicine
Concept 5.2 : Acute Viral Hepatitis
Learning Objective: To learn manifestations and management of viral hepatitis
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
ETIOLOGY – The etiological agents for acute viral hepatitis are:
1. Hepatitis A virus – RNA virus, picorna family.
2. Hepatitis B virus – DNA virus, hepadna family.
3. Hepatitis C virus – RNA virus, Flavi family.
4. Hepatitis D virus – RNA virus, viroid family.
5. Hepatitis E virus – RNA virus, Alpha family.
6. Hepatitis G virus – RNA virus, Flavi family.
7. TT virus.
Pathology:
The typical morphologic lesion of all types of viral hepatitis are similar and consist of pan
lobular infiltration with mononuclear cells, hepatic cell necrosis, hyperplasia of Kupffer
cells and variable degrees of cholestasis.
• Hepatic cell regeneration is present evident by mitotic figures, multi nucleated cells
and rosette and pseudo acinar formation.
• Mononuclear infiltration consists of lymphocytes, plasma cells and eosinophils.
• Liver cell damage consists of necrosis, cell drop out ballooning of cells, aci- dophilic
degeneration of hepatocytes (councilman bodies). Bridging necrosis indicates more
severe lesion.
In hepatitis C, there is relative paucity of inflammation.
The antigens localized to cytoplasm are – HAV, HBS Ag, HCV and HEV
The antigens localized to nucleus are – HbcAg, HDV
Clinical and Epidemiological Features of Viral Hepatitis:
eature A B C D
Incubation (days) 15- 5, mean 0 0-180, mean 0-90 15-1 0, mean 50 0-180, mean 0-90 1 - 0, mean 0
Onset Acute Insidious or acute Insidious Insidious or acute Acute
Age preference Children, young oung adults (sexual Any age, but more Any age (similar to Epidemic cases: young adults
adults and percutaneous), common in adults HBV) (20– 0 years): sporadic cases:
babies, toddlers older adults ( 0)
Transmission
Fecal-oral +++ +++
Percutaneous nusual +++ +++ +++
Perinatal +++ +° +
Sexual ± ++ +° ++
Clinical
Severity Mild Occasionally severe Moderate Occasionally severe Mild
Fulminant 0.1 0.1–1 0.1 5-20 1-2
Progression to None Occasional (1–10 ) Common (85 ) Common None
chronlclty (90 of neonates)
Carrier None 0.1– 0 15– .2 Variable None
Cancer None (neonatal infection) + ± None
Prognosis Excellent Worse with age, Moderate Acute, good Chronic, Good
debility poor
Prophylaxis lg. Inactivated HBI , recombinant None HBV vaccine (none Vaccine
vaccine vaccine for HBV carriers)
Therapy None lnterferon Pegylated interferon Pegytated Interferon None
Lamivudine Adefovir plus ribavirin, ±
Pegylated interferon telaprevir, boceprevir
Entecavir
Telbivudine
205
Tenofovir
206 | Medicine
Diagnosis Approach in Patients Presenting with Acute epatitis:
Serologic ests of atient s Serum
BsAg lgM Anti- lgM Anti- Anti- Diagnostic nterpretation
A Bc C
+ + Acute hepatitis B
+ Chronic hepatitis B
+ + Acute hepatitis A superim-posed on chronic hepatitis B
+ + + Acute hepatitis A and B
+ Acute hepatitis A
+ + Acute hepatitis A and B (HBsAg below detection threshold)
+ Acute hepatitis B (HBsAg below detection threshold)
+ Acute hepatitis C
Complications:
• Relapsing hepatitis – seen in hepatitis A.
• Cholestatic hepatitis – seen in hepatitis A, E.
• Serum sickness hepatitis B. like syndrome –
• Essential mixed hepatitis C, B. cryoglobulinemia –
• Fulminant hepatitis – mainly seen in hepatitis B, C, E (Pregnancy).
• Chronic hepatitis – Hepatitis B, C. Hepatitis D coinfection does not affect the chronicity
of acute hepatitis B infection. Superinfection and hepatitis D increases the severity of
chronic hepatitis B.
• Hepato cellular carcinoma – hepatitis B, C.
• Pancreatitis, myocarditis, atypical pneumonia, aplastic anemia, transverse myelitis
and peripheral neuropathy.
• Giannotti – crosti syndrome – In children, hepatitis B presents with anicteric hepatitis,
a non-pruritic popular rash of face, buttocks and limbs and lymphadenopathy.
Prognosis:
The poor prognostic markers of acute hepatitis are:
1. Advance age.
2. Ascites.
3. Hepatic encephalopathy.
4. Peripheral edema.
5. Prolonged PT.
6. Low serum albumin level.
7. Hypoglycemia.
8. High serum bilirubin level.
Treatment:
• Bed rest, high carbohydrate diet.
• Specific treatment is indicated for acute hepatitis C infection. Antiviral therapy with
interferon alpha 3 million units s/c three times a week is given.
208 | Medicine
Concept 5.3 : Approach to Chronic Hepatitis
Learning Objective: To learn approach to Chronic hepatitis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Liver disorders in which hepatic inflammation and necrosis continue for at least 6 months.
Approach to Chronic active hepatitis

tiology Age Gender Association Diagnostic tests
1. He B&D All / Males Orient, African countries HBsAg
Drug users, Homosexuals, HBV-DNA
Immunosupressed.
2. Hep C All / Equal Blood transfusion Drug Anti-HCV Ab
users, Hemodialiysis HCV RNA by PCR
. Autoimmune 14-25 yrs Females Multisystem involvement ANA, ASMA,
Anti-LKM, LsAg
. Drug induced 3rd – 5th dec Female Drug history Anti-Histone
Drug level
5. Wilsons 10- 0yrs Equal Family history, Hemlysis K-F ring, Biopsy
Neurological symptoms Cu, Cerupl. level
Concept 5.4 : Chronic Hepatitis B
Learning Objective: To learn features and management of Chronic Hepatitis B
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
• After acute hepatitis B, chances of chronicity depends on the age. Infection at birth is
associated with a clinically silent acute infection but 90% chances of chronic infection.
While the infection in young adulthood is associated with clinically apparent acute
hepatitis with a risk of 1% of chronicity.
• The clinical features range from asymptomatic infection to fatal hepatic failure.
Fatigue is the most common symptom, along with intermittent deepening of jaundice,
malaise and anorexia.
• Complications of cirrhosis occur in end stage chronic hepatitis and include ascites,
edema, bleeding gastroesophageal varices, hepatic encephalopathy, coagulopathy
and hypersplenism. Extrahe- patic complications of chronic hepatitis B include
arthritis, purpuric cutaneous lesions (leukocytoclastic vasculitis), immune complex
glomerulonephritis and polyarteritis nodosa.
• Acute hepatitis like clinical feature can occur in pt of chronic hepatitis B due to-
1. Superinfection with other viral hepatitis.
2. Emergence of pre core mutant.
3. Conversion from replicative to non- replicative phase.
4. Conversion from non-replicative to replicative phase.
5. Withdrawal of immunosuppressed drugs.
Laboratory Features:
• ALT tends to be more elevated than AST, but once cirrhosis is established,AST tends
to exceed ALT.
• ALP are normal.
• Serum bilirubin levels are moderately increased.
• Hypoalbuminemia occur.
• PT is prolonged in severe or end stage disease.
Prognosis – The poor prognostic factors are:
• Chronic active hepatitis.
• Patient in replicative phase.
Treatment – Indications for treatment of chronic hepatitis are:
1. Detectable markers of HBV replication.
2. Elevated ALT levels.
3. Chronic hepatitis on liver biopsy.
Drugs Used Are:
eature B ami udine Adefo ir nteca ir elbi udine enofo ir 210
|
Route of Subcutaneous Oral Oral Oral Oral Oral
administration in ection
Duration of 8-52 weeks ≥52 weeks ≥ 8 weeks ≥ 8 weeks ≥52 weeks ≥ 8 weeks
therapy
Medicine
Tolerability Poorly tolerated Well tolerated Well tolerated Well tolerated Well tolerated Well tolerated
creatinine creatinine
monitoring monitoring
recommended recommended
Hbe ag Seroconversion
1 year Rx 18-20 1 -21 12 21 22 21
1 year Rx NA p to 50 yrsd 1 2yrs 0 2yrs 0 5yrs
5yrs
Log10 HBV DNA
Reduction (mean copies/ml)
HBeAg-reactive 4.5 5.5 Median 3.5-5 .9 6.4 6.2
HBeAg-negative 4.1 . - .7 Median .5- .9 5.0 5.2 4.6
HBV DNA PCR Negative ( 00- 00 copies/mL
1000 copies/mL for adefovir) at end of yr 1
HBeAg-reactive 10-25 - 1 -21 7 (91 0 7
4yrs
HBeAg-negative 0-7 8-77 90 88 9
ALT Normalization at end of yr 1
HBeAg-reactive 9 1-75 8- 1 8 77 8
HBeAg-negative - 8 2-79 8-77 78 7 7
HBsAg loss yr 1 - 1 0 2 1
1 year 12 5yr after 1yr No data 5 at yr 5 at yr No data 8 at yr 5
of Rx
Histologic Im-
provement (≥2
point reduction in
HAI)
HBeAg-reactive 8 months 9- 2 5 - 8 72 5 7
after
HBeAg-negative 8 months after 1- 70 7 72
Viral resistance None 15- 0 1yr None 1yr 1 1yre p to 5 yr1 0 yr1
70 5yrs 29 5yrs 1.2 yrse p to 22 0 through yr5
yr2
Pregnancy C C C C B B
category
Cost ( ) for 18,000 52,500 5 ,500 58,700 5 ,500
1yr
enerally, these comparisons are based on data on each drug tested individually versus placebo in registration clinical trials because, with rare exceptions, these
comparison are not based on head-to-head testing of these drugs, relative advantages and disadvantages should be interpreted cautiously. Although standard interferon
a administered daily or three times a week is approved as therapy for chronic hepatitis B, it has been supplanted by PE IFN, which is administered once a week
and is more effective. Standard interferon has no advantages over PE IFN. Duration of therapy in clinical efficacy trials use in clinical practice may vary. Because
of a computer- generated randomization error that resulted in misallocation of drug versus placebo during the second year of clinical trial treatment, the frequency
of HBeAg seroconversion beyond the first year is an estimate (Kaplan-Meier analysis) based on the small subset in whom adefovir was administered correctly. 7
during a year of therapy ( at year ) in lamivudine-resistant patients. Despite its Class C designation, lamivudine has an extensive pregnancy safety record in
women with HIV/AIDS. Approximately 17, 00 for lamivudine-refractory patients.
Abbreviations: ALT, alanine aminotransferase HAI, histologic activity index HBeAg, hepatitis B e antigen HBsAg, hepatitis B surface antigen HBV, hepatitis B
virus NA, not applicable PE IFN. pegylated interferon PCR, polymerase chain reaction Rx, therapy yr, year.
211
212 | Medicine
Concept 5.5 : Chronic Hepatitis C
Learning Objective: To learn features and management of Chronic Hepatitis C
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
The risk of developing chronic hepatitis C infection after acute hepatitis C is 85-90%.
Chronic hepatitis C tends to be very slowly and insidiously progressive. Progression is
more likely in patients with:
• Old age.
• Longer duration of infection.
• Advanced histologic stage and grade.
• Type 1b genotype.
• Increased hepatic iron.
• More complex quasispecies diversity.
Clinical Features:
• Fatigue is the most common symptom.
• Jaundice is rare.
• Immune complex mediated extrahepatic complications are less common in chronic
hepatitis B, with the exception of essential mixed cryoglobulinemia.
• Other extrahepatic complications unre- lated to immune complex are Sjogren’s
syndrome planus, and porphyria cuta- nea tarda.
• Characteristic episodic fluctuation of amino transferase is seen.
• Anti LKM 1 antibodies are seen (also seen in auto immune hepatitis type II).
Treatment:
Genotype a reatment- ai e atients it out Cirr osis
RECOMMENDED D RATION
Daily fixed-dose combination of elbasvir (50mg)/grazoprevir (100mg) for patients in 12 weeks
whom no baseline NS5A RASs§ elbasvir are detected
Daily fixed-dose combination of ledipasvir (90mg)/sofosbuvir ( 00 mg) 12 weeks
Daily fixed-dose combination of ledipasvir (90 mg)/sofosbuvir ( 00mg) for patients 8 weeks
who are non-black, HIV-uninfected, and whose HCV RNA level is
Daily fixed-dose combination of paritaprevir (150mg)/ritonavir (100mg)/ombitasvir 12 weeks
(25mg) with dasabuvir ( 00 mg) as part of an extended-release regimen or plus twice-
daily dosed dasabuvir (250 mg), with weight-based ribavirin
Daily simeprevir (150mg) plus sofosbuvir ( 00mg) 12 weeks

Daily fixed-dose combination of sofosbuvir ( 00mg)/velpatasvir (100mg) 12 weeks
Daily daclatasvir ( 0mg*) plus sofosbuvir ( 00mg) 12 weeks
Genotype a reatment- ai e atients it Compensated Cirr osis

Daily fixed-dose combination of elbasvir (50mg)/grazoprevir (100mg) for patients in 12 weeks
whom no baseline NS5A RASs§ elbasvir are detected
Daily fixed-dose combination of sofosbuvir (90 mg)/velpatasvir ( 00mg) 12 weeks
Genotype b reatment- ai e atients it out Cirr osis

Daily fixed-dose combination of elbasvir (50mg)/grazoprevir (100mg) 12 weeks
Daily fixed-dose combination of ledipasvir (90 mg)/sofosbuvir ( 00mg) for patients 8 weeks
who are non-black, HIV-uninfected and whose HCV RNA level is
Daily simeprevir (150mg) plus sofosbuvir ( 00mg) 12 weeks
Daily daclatasvir ( 0mg) plus sofosbuvir ( 00mg) 12 weeks
Genotype b reatment- ai e atients it Compensated Cirr osis

Daily fixed-dose combination of sofosbuvir ( 00 mg)/velpatasvir (100mg) 12 weeks
Genotype 2 reatment- ai e atients it out Cirr osis

Alternative D RATION
Daily daclatasvir ( 0 mg) plus sofosbuvir ( 00mg) 12 weeks
214 | Medicine
Genotype 2 reatment- ai e atients it Compensated Cirr osis

ALTERNATIVE D RATION
Daily daclatasvir ( 0 mg) plus sofosbuvir ( 00mg) 1 weeks to 2
weeks
Genotype reatment- ai e atients it out Cirr osis

Daily daclatasvir ( 0 mg) plus sofosbuvir ( 00mg) 12 weeks
Genotype reatment- ai e atients it Compensated Cirr osis

Daily daclatasvir ( 0 mg) plus sofosbuvir ( 00mg) with or without weight-based 2 weeks
ribavirin
Genotype reatment- ai e atients it out Cirr osis

(25mg) and weight-based ribavirin
Daily fixed-dose combination of ledipasvir (90mg)/ sofosbuvir ( 00mg) 12 weeks
Genotype reatment- ai e atients it Compensated Cirr osis

(25mg) and weight-based ribavirin
Genotype or reatment- ai e atients it it out Cirr osis

For decompensated cirrhosis- Liver transplant is the best treatment option
Concept 5.6 : Autoimmune Hepatitis:
Learning Objective: To learn features and management of Autoimmune hepatitis
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Clinical Features:
• The onset may be insidious or abrupt.
• There is history of recurrent episodes of jaundice.
• Patients are usually young female.
• Fatigue, anorexia, amenorrhea, acne are common.
• In some patients arthritis, cutaneous vasculitis, erythema nodosum, colitis, sicca
syndrome, pericarditis, pleurisy, anemia and azotemia occur.
• ALT and AST elevation.
• Serum bilirubin level is moderately elevated.
• Hypergammaglobulinemia is common.
• Anti LKM 2 is seen in drug induced hepatitis.
• Anti LKM 3 is seen in chronic hepatitis D.
a b ype
Age/sex oung women oung women Older man oung women
Antibody ANA Anti LKM 1 Low anti LKM 1 Liver Soluble Ag
Treatment lucocorticoids lucocorticoids Interferon lucocorticoids
Treatment:
The mainstay is glucocorticoids (80% response rate).
216 | Medicine
Concept 5.7 : Cirrhosis:
Learning Objective: To learn features, complications and management of cirrhosis
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Definition: Cirrhosis is defined as an irreversible chronic injury of the hepatic parenchyma
and include extensive fibrosis in association with the formation of regeneration nodule.
Nodules may vary from <3mm (micronodules) to several cm in size.
Classification – It is classified into:

1. Alcoholic cirrhosis
2. Post necrotic cirrhosis
3. Biliary cirrhosis
4. Cardiac cirrhosis
5. Metabolic cirrhosis
6. Drug related cirrhosis
7. Cryptogenic cirrhosis
Complications of Cirrhosis:
1. Portal hypertension.
2. Ascites.
3. Hepatic encephalopathy.
4. Spontaneous bacterial peritonitis.
5. Hepato renal syndrome.
6. Coagulopathy.
7. Hepato cellular carcinoma.
Child Pugh Classfication of Cirrhosis:

actor 2
1. S.Bilirubin (mg ) 2.0 2.0-3.0 .0
2. S.Albumin (g ) .5 3.0-3.5 .0
3. Ascites None Easily controlled Poorly controlled
. Neurological disorder None Minimal Advanced coma
5. PT/INR 0- , 1.7 - , 1.7 – 2. , 2.
Stages are:
A. Score of 5-6 (compensated).
B. Score of 7-9 (decompensated).
C. Score of>10 (decompensated).
Concept 5.8 : Portal Hypertension
Learning Objective: To learn features and management of Portal hypertension
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Classification:
Classification of ortal ypertension
Prehepatic:
Portal vein thrombosis.
Splenic vein thrombosis.
Massive splenomegaly (Banti s syndrome).
Hepatic:
Presinusoidal:
Schistosomiasis.
Congenital hepatic fibrosis.
Sinusoidal:
Cirrhosis-many causes.
Alcoholic hepatitis.
Postsinusoidal:
Hepatic sinusoidal obstruction (venoocclusive syndrome).
Post hepatic:
Budd-Chiari syndrome.
Inferior vena caval webs.
Cardiac causes:
Restrictive cardiomyopathy.
Constrictive pericarditis.
Severe congestive heart failure.
Clinical Features:
The clinical manifestation of portal hypertension include:
1. Hemorrhage from gastroesophageal varices.
2. Splenomegaly with hypersplenism.
3. Ascites.
4. Acute and chronic hepatic encephalopathy.
218 | Medicine
The major sites of collateral involve:

1. Esophagogastric varices – Left gastric vein and short gastric vein join with
esophageal vein of caval system.
2. Haemorrhoids – superior haemorrhoidal vein of portal system to middle and
inferior haemorrhoidal vein of the caval system.
3. Caput medusae – remnants of the umbilical circulation of fetus present in the
falciform ligament.
4. Retroperitoneal vein.
5. Bare area of liver
Treatment:
1. Beta–adrenergic blockers with propranolol or nadolol reduces portal pressure
through vasodilatory effects on both the splanchnic arterial bed and the portal venous
system in combination with reduced cardiac output. They are helpful in preventing
first variceal bleed and subsequent episodes after an initial bleed. The goal of therapy
is to reduce the pulse by 25%.
2. Treatment of specific cause.
3. Decompression through portal systemic shunts – Transjugular Intrahepatic Porto
systemic shunt (TIPS).
Management of Recurrent Variceal Haemorrhage:
Fig. 4.3: anage ent of recurrent variceal hae orrhage. his algorith descri es an approach to
anage ent of patients ho have recurrent leeding fro esophageal varices. nitial therapy is generally ith
endoscopic therapy often supple ented y phar acologic therapy. ith control of leeding, a decision needs
to e ade as to hether patients should go on to a surgical shunt or if they are Child s class A and e
considered for transplant, or if they should have and e considered for transplant if they are Child s class
or C . , trans ugular intra hepatic portosyste ic shunt.
6 Pancreatitis
CONCEPTS
Â Concept 6.1 Classification and causes
Â Concept 6.2 Acute pancreatitis
Â Concept 6.3 Complications of Acute Pancreatis

Concept .1 : Classification and causes
Learning Objective: To learn causes and classification of pancreatitis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Pancreatitis is of two types depending on the duration viz.

a. Acute pancreatitis < 2 weeks
b. Chronic pancreatitis > 6 weeks more often months
Etiology : remember the following acronym:
“A” – Alcohol
Anatomic – pancreatic division, Annular pancreas
Auto-immune – Sjogrens syndrome
“B” – Bile stones / Gallstones
Biliary duct strictures
“C” – Carcinoma
Cholestrol - Hypertriglyceridemia
Connective tissue disorder - TTP
“D” – Drugs – Anti-HIV , Valproate, Sulfonamides
“E” – ERCP
Others - Post surgery
Trauma
Renal failure
Infections – Coxsackie, Mumps
222 | Medicine
Concept 6.2 : Acute pancreatitis
Learning Objective: To learn features, stages and management of pancreatitis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Clinical features :
1. Pancreatic colic : Epigastric radiating to back, scalding in nature and worsens on
food, nocturnal and lying down.
2. Associated symptoms : nausea, vomiting, fever
3. Related to malabsorption : Steatorrhea, B12 deficiency
Pathophyiology :
Stage 1 : Auto-digestion
Stage 2 : enzyme activation and neutrophilic infiltrate
Stage 3 : necrosis
Stage 4 : inflammatory cascade activation with SIRS (ARDS)
Diagnosis : Clinical suspicion is vital to early detection
Biochemistry : Tests for pancreatitis per se : Serum Amylase, Lipase, Trypsinogen.
Tests for Etiology : lipid profile, CRP, ANA, Creatinine
X-ray abdomen : shows calcification in chronic cases only
USG – poor tool as pancreas is a retroperitoneal structure
CT scan – is the gold standard for acute pancreatitis.
Endoscopic ultrasound
ERCP vs MRCP.
Treatment is conservative:
Prognosis : In acute cases it is poor with mortality of 30-50%. Based on CT score.
Severity Index in Acute Pancreatitis

Points
Grade of acute pancreatitis
Normal pancreas 0
Pancreatic enlargement alone 1
Inflammation compared with pancreas and peri pancreatic fat 2
One peripancreatic fluid collection 3
Two or more fluid collections 4

Degree of pancreatic necrosis
No necrosis 0
Necrosis of one-third of pancreas 2
Necrosis of one-half of pancreas 4
Necrosis of more than one-half of pancreas 6
C se erity index C S C grade necrosis score -

224 | Medicine
Concept 6.3: Complications of Acute Pancreatis
Learning Objective: To learn complications of Acute pancreatitis
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Complications of Acute Pancreatis

LOCAL
Necrosis Pancreatic ascites
Sterile Disruption of main pancreatic duct
Infected Leaking pseudocyst
Pancreatic fluid collections Involvement of contiguous organs by necrotizing
Pancreatic abscess pancreatitis
Pancreatic pseudocyst Massive intraperitoneal hemorrhage
Pain Thrombosis of blood vessels
Rupture (splenic vein, portal vein)
Hemorrhage Bowel infarction
Infection Obstructive aundice
Obstruction of gastrointestinal tract (stomach,
duodenum, colon)
S S MC
Pulmonary Renal
Pleural effusion Oliguria
Atelectasis Azotemia
Mediastinal abscess Renal artery and/or renal vein thrombosis
Pneumonitis Acute tubtilar necrosis
Adult respiratory distress syndrome Metabolic
Cardiovascular Hyperglycemia
Hypotension Hypertriglyceridemia
Hypovolemia Hypocalcemia
Sudden death Encephalopathy
Nonspecific ST-T changes in electrocardiogram Sudden blindness (Purtscher s retinopathy)
simulating myocardial infarction Central nervous system
Pericardial effusion Psychosis
Hematologic Fat emboli
Disseminated intravascular coagulation Fat necrosis
Gastrointestinal hemorrhage" Subcutaneous tissues (erythematous nodules)
Peptic ulcer disease Bone
Erosive gastritis Miscellaneous (mediastinum. pleura, nervous
Hemorrhagic pancreatic necrosis with erosion into system)
ma or blood vessels
Portal vein thrombosis, variceal hemorrhage
SECTION — 5
ENDOCRINE SYSTEM
1 Pituitary Gland
CONCEPTS
Â Concept 1.1 Hyper-Prolactinemia (Hyper-PRL)
Â Concept 1.2 Acromegaly
Â Concept 1.3 Hypopituitarism
Â Concept 1.4 Diabetes Insipidus (DI)
Â Concept 1.5 SIADH

ndocrine System
Concept 1.1 : Hyper-Prolactinemia (Hyper-PRL)
Learning Objective: To understand the causes, features and management of Hyper-
PRL
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Hyperprolactinemia is the most common pituitary hormone hypersecretion syndrome.
Causes:
I. Physiological:
II. Drugs:
III. Pituitary Hypersecretion:
• Prolactinoma.
IV. Hypothalamic-Pituitary Stalk Damage:
V. Systemic Causes:
• Hypothyroidism.
• Chronic renal failure.
• Cirrhosis.
• Epilepsy.
Clinical Features:
1. The cardinal feature of hyperprolactinaemia are galactorrhoea and hypogonadism.
2. In women this causes secondary amenorrhoea, oligomenorrhoea or menorrhagia and
anovulation with infertility.
3. In men there is decreased libido, erectile impotence or visual loss (due to optic nerve
compression. Galactorrhea is uncommon in males.
Investigations:
1. The levels of serum prolactin will be increased.
2. TRH stimulation test.
Treatment – Identify and treat underlying cause.

Medicine
Concept 1.2 : Acromegaly
Learning Objective: To understand the causes, features and management of
Acromegaly
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Growth Hormone excess: Acromegaly: Causes:

Causes of Acromegaly
Excess Growth Hormone Secretion Prevalence, %
Pituitary 98
Densely or sparsely granulated GH cell adenoma 60
Mixed GH cell and PRL cell adenoma 25
Mammosomatotrope cell adenoma 10
Plurihormonal adenoma
GH cell carcinoma or metastases
Multiple endocrine neoplasia 1 (GH cell adenoma)
McCune-Albright syndrome
Ectopic sphenoid or parapharyngeal sinus pituitary adenoma
Extrapituitary tumor <1
Pancreatic islet cell tumor
Lymphoma
Excess Growth Hormone-Releasing Hormone Secretion
Central <1
Hypothalamic hamartoma, choristoma, ganglioneuroma <1
Peripheral <1
Bronchial carcinoid, pancreatic islet cell tumor, small cell lung cancer,
adrenal adenoma, medullary thyroid carcinoma, pheochromocytoma
Clinical features:
If growth hormone hypersecretion occur before epiphysis have fused gigantism will
result. And if it occurs in adult life after epiphyseal closure acromegaly will occur.
Investigations:
1. Screening is done by IGF-1 levels which are raised.
2. The diagnosis is confirmed by failure of growth hormone suppression to<1ug/L within
1-2 hours of oral glucose load (75 gm)(Confirmatory test).
3. Prolactin levels are increased(in 25%).
4. Growth hormone rise after TRH administration(in 60%).
ndocrine System
Treatment:
Fig 5.1: Management of acromegaly. GH, growth hormone; CNS,

Central Nervous System; IGF, insulin-like growth factor.
Fig 5.2
Medicine
Concept 1.3 : Hypopituitarism
Learning Objective: To understand the causes and features of Hypopituitarism
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Causes:
I. Hypothalamus.
Congenital:
1. Kallmann syndrome.
2. Prader-Willi syndrome.
3. Laurence-Moon-Biedl syndrome.
4. Frohlich syndrome.
5. Septo-optic dysplasia.
Acquired:
1. Tumours-Craniopharyngioma.
2. Head injury(stalk section).
3. Surgery.
4. Radiotherapy-radiation usually cause hypothalamic damage.
5. Granuloma-sarcoidosis, tuberculosis.
II. Pituitary:
1. Developmental-pituitary dysplasia/aplasia, primary empty sella
2. Neoplasms-pituitary adenoma, parasellar mass (meningioma, germinoma,
ependymoma, glioma), craniopharyngioma, Rathke’s cyst, pituitary metastasis.
3. Vascular.
4. Pituitary apoplexy.
5. Infections-tuberculosis, histoplasmosis, toxoplasmosis, Pneumocystis carinii.
6. Traumatic-surgery, radiation, head injury.
7. Infilterative-hemochromatosis, s arcoidosis, histiocytosis X.
Clinical Features:
1. Earliest hormone to be lost is growth hormone secretion.
2. Next luteinising hormone secretion is impaired causing loss of libido in males and
amenorrhoea in females. In both sexes axillary and pubic hairs decreases.
3. The next hormone to be lost is TSH.
4. The last hormone to be lost is ACTH.
ndocrine System
Investigations:
Hormone Tests Interpretation
Growth hormone Insulin tolerance test Normal response is
GHRH test GH>3ug/L
L-arginine test
L-dopa test
Prolactin TRH test Increase of >200% of Baseline
ACTH Insulin tolerance test Cortisol>20ug/dL
CRH test ACTH increase 2-4fold
And cortisol>20ug/dL
Metyrapone test 11-deoxycortisol>7.5ug/dl
Or ACTH>75pg/ml
Cosyntropin test Cortisol>21ug/dl, Aldosterone>4ng/dlabove baseline
TSH T3,T4,TSH
LH,FSH LH,FSH levels
GnRH test LH increase by>10 IU/L,FSH by 2IU/L.
Treatment:
Hypopituitarism is usually treated by measurement of end organ hormones-thyroxine,
cortisone, testosterone, estrogen.
ormone deficit Hormone replacement
ACTH Hydrocortisone, cortisone, prednisone
TSH Thyroxine
FSH/LH Males-testosterone enanthate,testosterone skin patch
Females-conjugated estrogen, progesterone, estradiol skin patch
GH Somatotropin
Medicine
Concept 1.4: Diabetes Insipidus (DI)
Learning Objective: To understand the causes, features and management of DI
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Diabetes Insipidus:
The diagnostic criteria are:
• Polyuria –24 hr urine volume >50ml/kg body wt.
• Urine osmolality <300mmol/kg
• Urine specific gravity <1.006.
Causes:
1. Central DI
A. Acquired: Head trauma, Neoplams, Infection, Granuloma
B. Congenital Malformations:
C. Genetic:
2. Nephrogenic DI (Tubules refractory to ADH action)
A. Acquired
B. Drugs
C. Metabolic-hypercalcemia, hypercalciuria, hypokalemia.
D. Obstruction-ureter, urethra.
E. Vascular-sickle cell disease, acute tubular necrosis.
F. Granuloma-sarcoidosis.
G. Infiltration-amyloidosis.
H. Neoplasm-sarcoma.
I. Pregnancy.
J. Idiopathic.
K. Genetic-x-linked recessive, autosomal recessive,autosomal dominant.
Treatment:
Cranial DI: Desmopressin an analogue of ADH is given.
Nephrogenic DI:
Thiazide-By inducing a state of sustained electrolyte depletion so that glomerular filtrate
is more completely reabsorbed isoosmotically in proximal tubule. Also thiazides reduces
gfr and thus the fluid load on the tubules.
Indomethacin-by inhibiting PG.
ndocrine System
Concept 1.5 : SIADH
Learning Objective: To understand the causes, features and management of SIADH
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
It is characterised by hyponatremia caused by a sustained release of ADH in the absence
of osmotic and non-osmotic stimuli.The diagnostic criteria are:
1. Hyponatremia.
2. Decreased plasma osmolality (<280mosm/kg).
3. In appropriately increased urine osmolality (>150 mosm/kg).
4. Urine sodium >20meq/L.(Na excretion due to increase in ECF occur because
sympathetic nervous system,renin-angiotensin and atrial natriuretic factor release
are preserved).
5. Normal thyroid and adrenal functions.
Common Etiologies of the Syndrome of

Inappropriate Antidiuretic Hormone Secretion (SIADH)
Tumors
Pulmonary /mediastinal (bronchogenic carcinoma, mesothelioma, thymoma),duodenal carcinoma, pancreatic

carcinoma. Ureteral/prostate carcinoma. Uterine carcinoma, nasopharyngeal carcinoma, leukemia )
Central N ervous System Disorders
Mass lesion (tumors brain abscesses, subdural hematoma )

Inflammatory disease (encephalitis, meningitis, systemic lupus erythematosus).
Erythematosus, acute intermittent porphyria, multiple sclerosis )
Degenerative / demyelinative disease ( Guillane- Barre syndrome, spinal cord lesions )
Miscellaneous (subarachnoid hemorrhage, head trauma acute psychosis delirium tremens pituitary stalk
secretion trans sphenoidal adenomectomy, hydrocephalus
Drug – Related
Stimulated release of AVP ( nicotine, phenothiazine, tricycles

Direct renal effects and/or potentiation of AVP antidiuretic effects (dDAVP, oxytocin prostaglandin synthesis
inhibitors )
Mixed or uncertain actions (ACE inhibitors )
Mixed or uncertain action (ACE inhibitors, carbamazepine and oxcarbazepine Chlorpropamide, Clofibrate,
dozapine,
Cyclophosphamide, 3,4- methylenedioxymethamphetamine Omeprazole; serotonin reuptake inhibitors,
vincristine)
Medicine
Pulmonary
Infection (tuberculosis acute bacterial and viral pneumonia aspergillosis empyema Mechanical / ventilator
causes (acute respiratory failure, COPD,
Positive – pressure ventilation
Other causes
Acquired immunodeficiency syndrome (AIDS) and AIDS – related complex prolonged – strenuous exercise
(marathon triathlon, ultramarathon, hot-weather hiking) Senile atrophy
Idiopathic
Clinical Features:
The symptoms are those of hyponatremia including-nausea vomiting, headache,
somnolence, seizures, and coma.
Lab Diagnosis
• Hyponatremia with low plasma osmolality.
• Urine osmolality low but higher than that of plasma.
• Plasma levels of ADH elevated in relation to plasma osmolality.
• Low BUN and low serum uric acid levels.(because of dilution and increased clearance
in response to volume expanded state.)
Differential diagnosis-The other Causes of yponatremia:

Differential Diagnosis of yponatremia Based on Clinical Assessment of
Extracellular Fluid Volume (Ecfv):
Clinical Findings Type I, Type II, Type III Siadh and Siad
Hypervolemic Hypovolemic Euvolemic Euvolemic
History:
CHF, cirrhosis, or nephrosis Yes No No No
Salt and water loss No Yes No No
ACTH-cortisol deficiency and/ No No Yes No
or nausea and vomiting
Physical examination:
Generalized edema, ascites Yes No No No
Postural hypotension Maybe Maybe mabyea No
ndocrine System
Laboratory:
BUN, creatinine High-normal High-normal Low-normal Low-normal
Uric acid High-normal High-normal Low-normal Low-normal
Serum potassium Low-normal Low-normal Normal Normal
Serum urate High High Low Low
Serum albumin Low-normal High-normal Normal Normal
Serum cortisol Normal-high Normal-high lowe Normal
Plasma renin activity High High low Low
Urinary sodium (meq per unit of Low lowh high high
time) G
a
Postural Hypotension may occur in secondary (ACTH-dependent) adrenal insufficiency even
though extracellular fluid volume and aldosterone are usually normal. bSerum potassium maybe
high if hypovolemia is due to aldosterone deficiency. cSerum potassium maybe low if vomiting
causes alkalosis, dSerum cortisol is low if hypovolemia is due to primary adrenal insufficiency
(Addison’s disease). eSerum cortisol will be normal or high if the cause is nausea and vomiting
rather than secondary (ACTH-dependent) adrenal insufficiency. fPlasma renin activity may be high
if the cause is secondary (ACTH) adrenal insufficiency. gUrinary sodium should be expressed as the
rate of excretion reather than the concentration. In a hyponatremic adult, an excretion are >25
meq/d (or 25 eq/mg of creatine) could be considered high. hThe rate of urinary sodium excretion
may be high if the hypovolemia is due to diuretic abuse, primary adrenal adrenal insufficiency, or
other causes of renal sodium wasting. iThe rete of urinary sodium excretion may be low if intake is
curtailed by symptoms or treatment.
Abbreviations: ACth, adrenocorticotropic hormone; BUN, blood urea nitrogen; CHF, congestive
heart failure; SIAD, syndrome of inappropriate antidiuresis.
Treatment:
In acute SIADH:
• For mild symptoms-Fluid restriction.
• For severe symptoms-infusion of hypertonic saline. If the correction is rapid it
produces central pontine myelinosis characterised by quadriparesis,ataxia and
abnormal extraocular movements. Therefore the sodium should be raised by no more
than 12meq/L/24 hr.
In chronic SIADH:
• Fludrocortisone(by causing retention of sodium).
• Newer drug is CONIVAPTAN which is approved for its treatment (DOC).
In type I hyponatremia(Hypervolumic)-fluid restriction,solute diuresis,cardiotonics,albumin to

correct the effective hypovolemia. Hypertonic saline is contraindicated as it worsen the sodium
retention and oedema and may precipitate cardiovascular decompensation.
In type II hyponatremia (hypovolumic)-correcting the loss of sodium and water,

replacing the deficit. Fluid restriction and ADH antagonist is contraindicated as they
cause more water depletion.
2 Thyroid Gland
CONCEPTS
Â Concept 2.1 Hypothyroidism
Â Concept 2.2 Hyperthyroidism

ndocrine System
Concept 2.1: Hypothyroidism
Learning Objective: To learn the causes, features and management of Hypothyroidism
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Hypothyroidism:
• Iodine deficiency is the most common cause of hypothyroidism.
• In areas of iodine sufficiency autoimmune (Hashimoto’s thyroiditis) and iatrogenic
causes are most common causes of hypothyroidism.
Cause of hypothyroidism
Primary Hypothyroidism
Acquired:
Hashimoto’s thyroiditis
Iodine deficiency (endemic goiter)
Drug blocking synthesis or release of T4 (e.g., lithium, Ethionamide, sulfonamides, iodide)
oitrogen in foodstuffs or as endemic substances or pollutants Cytogens in foodstuffs or as endemic
substance or pollutants cytokines (infiltration (amyloidosis, hemochromatosis, sarcoidosis, Riedel s Struma,
Cystinosis, Scleroderma)
Post ablative thyroiditis due to 131I surgery or therapeutic irradiation for nonthyroidal malignancy
Congenital:
Iodide transport or utilization defect (NIS or pendrin mutation)
Iodotyrosine dehalogenase deficiency
Organification disorder (TPO deficiency or dysfunction)
Defect in thyroglobulin synthesis or processing thyroid agenesis or dysplasia
TSH receptor defects
Thyroidal agenesis or dysplasia
THS receptor defect
Thyroidal G1 protein abnormalities (pseudo hypoparathyroidism protein type Ia)
Idiopathic TSH unresponsiveness
Transient (Post-Thyroiditis) Hypothyroidism:
Following subacute, painless, postpartum thyroiditis
Consumptive hypothyroidism:
Rapid destruction of thyroid hormone due to D3 expression in large hemangiomas or hemangioendotheliomas
Defect of Thyroxine –to Triiodothyronine conversion:
Selenocysteine insertion sequence binding protein 2 (SBP2) defect
Medicine
Drug induced thyroid destruction:

Tyrosine kinase inhibitor (e.g. sunitinib)
Central hypothyroidism:
Acquired
Pituitary origin (secondary)
Hypothalamic disorders (tertiary )
Bexarotene (retinoid X receptor agonist)
Dopamine and/or severe illness
Congenital
TSH deficiency or structural abnormality
TSH receptor defect
Resistance to Thyroid Hormone:
Generalized
“Pituitary” dominant
Symptoms:
• Tiredness, weakness (most common symptom).
• Dry skin.
• Cold intolerance.
• Hair loss.
• Difficulty in concentration & poor memory.
• Constipation.
• Weight gain with poor appetite.
• Dyspnea.
• Hoarse voice.
• Menorrhagia followed by oligomenorrhoea and amenorrhea.
• Paresthesia.
• Impaired hearing.
Signs:
• Dry coarse skin, cool extremities (most common).
• Puffy face, hands, feet (myxedema).
• Diffuse alopecia.
• Brady cardia.
• Peripheral edema.
• Delayed tendon reflex relaxation.
• Carpal tunnel syndrome.
• Serous cavity effusion.
ndocrine System
Laboratory Evaluation of patients with suspected HypothyRoidism or Thyroid Enlargement

Free T4 Value TPO- Ab Diagnosis
TSH > 10 mUIL
Low + Primary hypothyroidism due to autoimmune thyroid disease
Low normal + Primary “subclinical hypothyroidism (autoimmune)
Low or low normal - Recovery from systemic illness
External Irradiation drug induced congenital hypothyroidism
iodine deficiency
Seronegative autoimmune thyroid disease
Rare thyroid disorder (e.g., amyloidosis, sarcoidosis)
Recovery from subacute granulomatous thyroiditis
Normal ± Consider TSH or T4 assay artifacts
elevated - Thyroid hormone resistance
TSH 5-10 mU/L
Low low – normal + Early primary autoimmune hypothyroidism
Low low normal - Milder forms of non- autoimmune hypothyroidism (see above)
Central hypothyroidism with impaired TSH bioactivity

Elevated - Consider thyroid hormone resistance
T4 to T3 conversion blockade (e.g. amiodarone)
TSH 0.5-5 Mu/l
Low normal - Central hypothyroidism
Salicylate or phenytoin therapy
Desiccated thyroid or T3 replacement
TSH <0.5 µ U/L
Low normal - “ Post hyperthyroid “ hypothyroidism (131) or surgery)
Central hypothyroidism
T3 or desiccated thyroid excess
Post excess levothyroxine withdrawal
* initial tests: serum TSH, serum free T4 TPO- Ab.
T4 triiodothyronine T4 thyroxine – thyroglobulin antibody, TPO – Ab, thyroid peroxidase autoantibody,
TSH, thyroid stimulating hormone +, present – not present
Medicine
Concept 2.2: Hyperthyroidism
Learning Objective: To learn the causes, features and management of Hyperthyroidism
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Hyperthyroidism:
Thyrotoxicosis – State of thyroid hormone excess.
Hyperthyroidism – Result of excessive thyroid function.
Causes:
I. Primary hyperthyroidism – (decrease TSH):
1. Grave’s disease (75%).
2. Toxic multinodular goiter (15%).
3. Toxic adenoma (10%).
4. Functioning thyroid carcinoma metastases.
5. Activating mutation of the TSH receptor.
6. Struma ovarii.
7. Iodine excess – Jod – basedow phenomena.
II. Thyrotoxicosis without hyperthyroidism:
1. Subacute thyroiditis.
2. Silent thyroiditis.
3. Amiodarone, radiation.
4. Thyrotoxicosis factitia (Ingestion of excess thyroid hormone).
III. Secondary hyperthyroidism – ( increase TSH)
1. TSH secreting pituitary adenoma.
2. Thyroid hormone resistance syndrome.
3. Chorionic gonadotropin – secreting tumors.
4. Gestational thyrotoxicosis.
ndocrine System
Cause of Thyrotoxicosis
Sustained Hormone Overproduction (Hyperthyroidism)
Low TSH,High RAIU
Graves disease
Toxic multinodular goiter
Toxic adenoma
Chorionic gonadotropin-induced
Gestational hyperthyroidism
Physiologic hyperthyroidism of pregnancy
Familial gestational hyperthyroidism dueto TSH receptor mutations
Trophoblastic tumors
Inherited nonimmune hyperthyroidism associated with TSH receptor or G protein mutations
Low TSH, Low RAIU
Iodide-induced hyperthyroidism ( od-Basedow effect)
Amiodarone-associated hyperthyroidism due to iodide release
Struma Ovarii
Metastatic functioning thyroid carcinoma
Normal or Elevated TSH
TSH-secreting pituitary tumors
Thyroid hormone resistance with pituitary predominance
Transient Hormone Excess (Thyrotoxicosis)
Low TSH, Low RAIU
Thyroiditis
Autoimmune
Lymphocytic thyroiditis (silent thyroiditis, painless thyroiditis, postpartum thyroiditis)
Acute exacerbation of Hashimoto’s disease
Viral or post viral
Subacute (granulomatous, painful, postviral) thyroiditis
Drug-induced or associated thyroiditis
Amiodarone
Lithium, interferon- , interleukin-2, M-CSF
Infectious thyroiditis
Exogenous Thyroid Hormone
Iatrogenic overreplacement
Thyrotoxicosis factitia
“Hamburger” thyrotoxicosis
Natural foodstuffs
Thyromimetic compound (e.g. tiratricol PLB)
Occupational exposure to thyroid hormone (e.g. pill manufacturing, veterinary occupations)
Medicine
Grave’s Disease:
Prevalence – Age is usually between 20 – 50 years.More in females (10 times more
common).High iodine intake is associated with increase prevalence.
Clinical Features:
Symptoms:
• Hyperactivity, irritability and nervousness leading to a sense of easy fatigability are
the most common symptoms.
• Heat intolerance and sweating.
• Palpitations – due to sinus tachycardia or supraventricular tachycardia.
• Weight loss despite an increased appetite and is due to increased metabolic rate.
• Diarrhea.
Signs:
• Tachycardia is the most common sign.
• Fine tremors of outstretched hands.
• Presence of goitre. Thyroid bruit
• Skin is warm, moist due to vasodilatation.
• Palmar erythema is present.
• Plummer’s nail – retraction of nail from its bed (Onycholysis).
• Pruritus, urticaria and diffuse hyperpigmentation.
• Diffuse alopecia is seen in upto 40% patients.
Grave’s / Thyroid Associated Ophthalmopathy:
• Earliest manifestations are sensation of grittiness, eye discomfort and excess tearing.
• Lid retraction (Dalrymple’s sign) causing a staring look with exposure of upper sclera
can occur in any form of thyrotoxicosis and is the result of sympathetic over activity .
Signs:
Lid lag – Von Graefe’s sign.
Absence of wrinkling of forehead on looking up – Joffroy’s sign.
Decreased frequency of blinking – Stellwag’s sign.
Absence of convergence – Mobius sign.
Ophthalmoplegia – Weakness of ocular muscles due to edema and cellular infiltration
of muscles. Most frequent muscles involved are lateral rectus and inferior oblique.
The most serious manifestation is compression of the optic nerve at the apex of the
orbit, leading to papilledema, peripheral field defects and permanent loss of vision.
Ophthalmopathy worsen over initial 3 –6 month → plateau over l year- Spontaneous
improvement
ndocrine System
Many scoring systems have been used to gauge the extent and activity of the orbital changes in Graves’
disease. The “NO SPECS” scheme is an acronym derived from the following eye changes:
0 = No signs or symptoms.
1 = Only signs (lid retraction or lag), no symptoms .
2 = Soft-tissue involvement (periorbital edema).
3 = Proptosis (>22 mm).
4 = Extraocular-muscle involvement (diplopia).
5 = Corneal involvement.
6 = Sight loss.
Thyroid Dermopathy:
• It occur in <5% of pts. with Grave’s disease.
• It almost always occur in the presence of moderate to severe ophthalmopathy.
• Most common site is anterior and lateral aspects of the lower leg → pretibial myxedema.
• Thyroid acropachy is a form of clubbing found in patients with Grave’s disease.
• Thyroid dermopathy usually appears 1 to 2 years after the development of Grave’s
hyperthyroidism.
• It may improve spontaneously.
Lab. Investigations:
• Microcytic anemia and thrombocytopenia.
• Elevated serum bilirubin and liver enzymes.
• Serum free T3 and T4 levels are elevated.
• Serum TSH levels are very low.
• Presence of antibodies:
Fig. 5.3
Medicine
1. Thyroid stimulating immunoglobulin is a marker for Grave’s disease.
2. TSH – receptor antibody is seen in 75% pt.
3. Antimicrosomal / antiperoxidase antibody is also present
Thyroid scan with radioactive iodine is useful in patients with nodular goiter and
hyperthyroidism to determine:
1. Whether there is an autonomous hyperfunctioning nodule.
2. Whether multiple nodules are hyperfunctioning
3. Whether nodules are cold or hot.
Treatment:
Options Indications
1. Antithyroid drugs First episode in patients < 40years
2. Subtotal thyroidectomy • Recurrent hyperthyroidism after course of antithyroid drugs in

patients <40years.
• Initial treatment in, males with large goiter and in those with severe
hyperthyroidism.
• Poor drug compliance.
3. Radioiodine • Patients > 40 years.

• Recurrence following surgery irrespective of age.
• Other serious illness irrespective of age.
Immediate control of symptoms should be treated with propranolol.

1. Antithyroid drugs:
Carbimazole
Methimazole
Propylthiouracil.
Treatment is monitored on the basis of free T4 levels measured after 4 weeks.
2. Subtotal thyroidectomy:
Control of thyrotoxicosis with antithyroid drugs followed by potassium iodine is
needed prior to surgery to avoid thyrotoxicosis crisis and to reduce the vascularity
of the gland.
Major complications of surgery – bleeding, laryngeal edema, hypoparathyroidism
and damage to recurrent laryngeal nerve.
3. Radioiodine:
Pretreatment with antithyroid drugs for at least a month to prevent the risk of
thyrotoxicosis crisis.
Antithyroid drugs must be stopped 3 to 5 days before radioiodine administration
to achieve optimum iodine uptake.
Dose 5mci to 15mci.
Absolute contraindication to radioiodine treatment are pregnancy and breast
feeding.
ndocrine System
When given to female patients conception must be postponed for one year.
For ophthalmopathy:
• High dose steroids
• Orbital decompression
• External beam radiotherapy of orbit.
For dermopathy:
• Topical glucocorticoid ointment.
• Usually self – limiting.
3 Parathyroid Gland
CONCEPTS
Â Concept 3.1 Hypercalcemia
ndocrine System
Concept 3.1: Hypercalcemia
Learning Objective: To learn the causes, features and management of Hypercalcemia
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Causes:
A. Parathyroid – related.
1. Primary hyperparathyroidism:
Solitary adenoma (80%).
Multiple endocrine neoplasia.
2. Lithium therapy (In 10% of treated pt., by predisposing to adenoma).
3. Familial hypocalciuric hypercalcemia (ab normal sensing of blood Ca by PTH)
II. Malignancy:
1. Solid tumor with metastases – breast Ca.
2. Solid tumor with release of PTH related peptide – Ca lung, kidney.
3. Hematological malignancies – Multiple myeloma, lymphoma, leukemia .(Direct bone
marrow invasion & increase vit D in B cell lymphoma).
III. Vitamin D related:
1. Vitamin D intoxication.
2. Sarcoidosis, granulomatous disease. (increase vit D synthesis in macrophages).
3. Idiopathic hypercalcemia of infancy (William’s syndrome – Ab normal sensitivity to vit
D).
IV. High bone turnover
1. Hyperthyroidism (bone resorption exceeding bone formation).
2. Immobilization.
3. Thiazides (Na depletion → increase Na & Ca resorption → hypercalcemia).
4. Vit A intoxication (increase bone resorption).
V. Associated with renal failure:
1. Severe secondary hyperparathyroidism.
2. Aluminum intoxication (Ca incorporation into bone is impaired).
3. Milk – alkali syndrome (Due to excessive intake of calcium leading to hypercalcemia,
alkalosis and renal failure = Burnett’s disease).
Hyperthyroidism and cancer account for 90% cases of hypercalcemia.

In malignancy associated hypercalcemia–the detection of hypercalcemia and death is <6 months.
10% sq. cell Ca pt. develop hypercalcemia though skeletal metastases are more common with small cell and
adeno carcinoma but they rarely produce hypercalcemia.
Medicine
Clinical features:
Ca level 11.5 – 12.0mg/dl – Fatigue, depression, mental confusion .Anorexia, nausea,
vomiting, constipation. Polyuria. short QT interval.
Ca level 13.0 – 15mg/dl – Calcification in kidney, skin, vessels, lung, heart & stomach.
Renal failure.
Ca level 15 – 18mg /dl – Coma.
Cardiac arrest.
Treatment:
1. Hydration with mild forced diuresis.
2. Bisphosphonates.
They are powerful inhibitors of bone resorption, by inhibiting osteoclast action.
First generation – Etidronate.
Second generation – Pamidronate.
Third generation – Zoledronate.
3. Calcitonin – It block bone resorption and increase urinary Ca excretion.
4. Glucocorticoids – They are useful in hypercalcemia due to
Multiple myeloma.
Leukemia.
Hodgkin’s disease.
Ca Breast.
Vit D intoxication.
Sarcoidosis.
5. Dialysis – Treatment of choice for patients with renal failure.
6. I.V. phosphate – Only in severely hypercalcemic patients with cardiac or renal failure.
7. Other drug:
Plicamycin – by inhibiting bone resorption.
Gallium nitrate – By inhibiting bone resorption & altering bone crystal structure.
Fig. 5.4
4 DM
CONCEPTS
Â Concept 4.1 Introduction
Â Concept 4.2 Classification of DM
Â Concept 4.3 Type 1 DM
Â Concept 4.4 Type 2 DM
Â Concept 4.5 Glucose lowering agents:
Â Concept 4.6 Acute Complications of DM
Â Concept 4.7 Chronic Complications

Medicine
Concept 4.1 : Introduction
Learning Objective: To understand the physiology, History and Definition of DM
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Physiology:
Insulin is secreted by islet cells of Langerhans in the pancreas.
Main actions of insulin are:
1. Increased transport of glucose,amino acids and potassium into the insulin sensitive
cells. The cells which do not require insulin for glucose uptake are-brain kidney
tubules, intestinal mucosa and red blood cells.
2. Activation of glycogen synthase and glycolytic enzymes.
3. Stimulation of protein synthesis and inhibition of protein degradation.
4. Fatty acid synthesis.
Historical aspects:
Year Insulin discoveries.
1921 Banting and Best demonstrate blood sugar lowering effects of pancreatic extract.
1922 Insulin was first used in human.
1925 First international insulin unit defined.
1955 Structure of insulin delineated.
1982 Recombinant DNA insulin becomes available.
Definition:
DM includes a group of metabolic disorder that share the phenotype of.
Hyperglycemia. DM defined by any one of the following criteria:
1. Symptoms of DM (polyuria, polydipsia, weight loss) plus random blood glucose
200mg/dl.
OR
2. Fasting plasma glucose 126mg/dl. (Fasting is defined as no calorie intake for at
least 8hr).
OR
3. Plasma glucose 200mg/dl 2hrs after an oral glucose tolerance test with 75gm of
glucose.
OR
4. Hb A1C >6.5%.(Updated new criteria in Harrison 19th ed.)
ndocrine System
Criteria for the Diagnosis of Diabetes*

Increased Risk*
Test N ormoglycemia Impaired Impaired High Risk Diabetes†
Fasting Glucose
Glucose Tolerance
PG, fasting (mg/dl) <100 100-125 ≥ 12
PG, 2-hour (mg/dl) <140 140-199 ≥ 200
Hemoglobin AIC (%) 5.7-6.4 ≥ .5
PG, casual (mg/dl) ≥ 200 mg/dl
plus symptoms
of diabetes
*Risk for diabetes is continuous, extending below the lower limit and becoming disproportionately greater at the higher
end of the ranges shown.
In the absence of unequivocal hyperglycemia, a diagnostic result should be confirmed by repeat testing.
Medicine
Concept 4.2 : Classification of DM
Learning Objective: To understand the types of DM
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Classification:
I. Type 1 diabetes – There is – cell destruction leading to absolute Insulin deficiency.
It is further divided into 2 types:
A. Immune mediated.
B. Idiopathic.
II. Type 2 diabetes – It is characterized by variable degrees of insulin resistance,
impaired insulin secretion and increased glucose production.
III. Other specific types of diabetes:
A. Genetic defects of – cell function.
These occur before the age of 25 years and are characterised by impaired insulin
secretion with no defect in insulin action. They are inherited in an autosomal
dominant pattern. Responsive to OHA.
1. MODY 1. chromosome 20.(Hepatocyte nuclear transcription factor 4 ).
2. MODY 2. chromosome 7.(Glucokinase).
3. MODY 3. Most common type. Chromosome 12. (HNF 1 ).
4. MODY 4. chromosome 13.(Insulin promoter factor 1).
5. MODY 5. chromosome 17.(HNF 1 ).
6. MODY 6. chromosome 2.(Neuro D1).
B. Genetic defect in insulin action:
1. Type A insulin resistance(Absent/dysfunctional insulin receptor).
2. Leprechaunism.
3. Rabson – Mendenhall Syndrome.
4. Defect in post receptor signal transduction.
C. Diseases of exocrine pancreas– (when pancreatic islets are destroyed by
more than 80%):
1. Pancreatitis.
2. Pancreatectomy.
3. Neoplasia.
4. Cystic fibrosis.
5. Hemochromatosis.
6. Fibro calculous pancreatopthy/ Tropical calcific pancreatitis/Malnutrition
related DM.
D. Endocrinal disorders:
1. Acromegaly.
2. Cushing’s syndrome.
ndocrine System
3. Glucagonoma.
4. Pheochromocytoma.
5. Hyperthyroidism.
6. Somatostatinoma.
7. Aldosterone induced hypokalemia.
E. Drug / Chemicals:
1. Pentamidine.
2. Nicotinic acid.
3. Glucocorticoids.
4. Thyroid hormone.
5. Diazoxide.
6. – agonist.
7. Thiazides.
8. Phenytoin.
9. - Interferons.
10. Protease inhibitors.
11. Clozapine.
12. – blockers.
13. Vacor.
F. Infections:
1. Congenital rubella.
2. Cytomegalovirus.
3. Coxsackie.
4. Adenovirus.
5. Mumps.
G. Immune – mediated syndromes:
1. Stiff – man syndrome.
2. Anti – insulin receptor antibodies.
H. Genetic syndromes:
1. Down’s syndrome.
2. Klinefelter’s syndrome.
3. Turner’s syndrome.
4. Wolfram’s syndrome.
5. Friedreich’s ataxia.
6. Huntington’s chorea.
7. Laurence – moon – Biedl syndrome.
8. Myotonic dystrophy.
9. Porphyria.
10. Prader – Willi syndrome.
Medicine
IV. Gestational diabetes mellitus:
It is defined as
1. Plasma glucose >140 mg% after 75gm of glucose. (WHO criteria).
or
2. After 100gm glucose-(Carpenter/Coustan diagnostic criteria)-ADA criteria.
1hr later plasma glucose 180mg/dl.or
2hr later plasma glucose 155mg/dl. or
3hr later plasma glucose 140mg/dl.
ndocrine System
Concept 4. : Type 1 DM
Learning Objective: To understand the salient features of Type 1 DM
Time needed
1st Reading 20 mins
2 Reading
nd
5 mins
Type 1 DM
Type 1 DM develops as a result of synergistic effect of genetic, environmental and
immunological factors that ultimately destroy the pancreatic beta cells.
Genetic factors – HLA DR3, HLA DR4.
Environmental factors – Coxsackie, rubella, bovine milk proteins, Nitrosourea.
Immunological factors – Islet cell autoantibodies, CD8+ T cell cytotoxicity.
Differential Diagnosis of ype A Diabetes
Diabetes type Anti-Islet Genetic Comments

Auto antibodies
Type 1A Positive >90% HLA 30-50% DR3 and 90% non-Hispanic white children
DR4 50% black
HLA 90% DR3 or Children
DR4 50% Latin
HLA<3% American
DQBI+0602 Children
Type 1B Negative Unknown Rare in whites
Type 2 Negative Unknown If AB+, likely LADA, and

HLA is similar
To type IA
Other Negative MODY mutation Other

syndromes
Ab, antibody; HLA, human leukocyte antigen; LADA, Latent Autoimmune Diabetes Adult; MODY,
Maturity-onset Diabetes of the Young.
• Insulin is the treatment of choice

• No role of OHA
• Higher risk of Diabetic Ketoacidosis as compared to T2DM
Medicine
Concept 4.4 : Type 2 DM
Learning Objective: To understand the salient features of Type 2 DM
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Type 2 DM:
It is characterised by three pathophysiological abnormalities.
1. Insulin resistance – This is caused by the decreased ability of Insulin to act
effectively on peripheral target tissues – muscles, liver. The post receptor signaling
defects which causes reduced translocation of GLUT 4 to the plasma membrane is
the main causes of insulin resistance. This insulin resistance is responsible for post
prandial hyperglycemia.
2. Impaired insulin secretion – Initially insulin secretion increases in response to
insulin resistance, later it decreases due to-Glucose toxicity – chronic hyperglycemia
impairs islet function.
Lipo toxicity – Due to elevation of free fatty acid levels, which worsens -cells
function.
3. Increased hepatic glucose production – Due to increase gluconeogenesis and it
leads to fasting hyperglycemia.
Risk Factor for type 2 Diabetes Mellitus:

Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Obesity (6MI >25 kg/m’ or ethnically
relevant definition fa overweight) Physical inactivity.
Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander).
Previously identified with IF , I T, a an hemoglobin Alc of 5.7- . History of DM or delivery of baby
>4 kg (9 lb) Hypertension (blood pressure >140/90 mmHg).
HDL cholesterol level <35 mg/dL (0.90 mrmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L).
Polycystic ovary syndrome or acanthosis nigricans
History of cardiovascular disease.
Abbreviations: BMI, body mass index; GDM, gestational diabetes mellitus; HDL, high-density lipoprotein; IFG, impaired
fasting glucose; IGT, impaired glucose tolerance.
Complications of Insulin Therapy:

1. Hypoglycemia.
2. Insulin resistance.
3 Insulin lipoatrophy and lipohypertrophy.
4. Insulin allergy, edema.
ndocrine System
Treatment Goals for Adults with Diabetes

Index Goal
Glycaemic control
A1C <7.0%
Pre-prandial capillary plasma glucose 70–130 mg/dL
Peak postprandial capillary plasma glucose <180 mg/Dl
Blood pressure <130/80
Lipids
Low-density lipoprotein 100 mg/dL
High-density lipoprotein 40 mg/dL in men >, 50 mg/dL in women
Triglycerides 150 mg/dL
Fasting hyperglycemia syndromes:

1. Somogyi phenomenon(rebound effect)- This is hypoglycemia induced hyperglycemia due to increased
secretion of counter regulatory hormones. Reduction of insulin dose is needed.
2. Dawn phenomenon-Early morning hyperglycemia, may be due to increased hepatic glucose production or
decreased peripheral utilization or both. Increased dose of insulin is needed.
Concept 4.5 : Glucose lowering agents:
Agents used for Treatment of Type 1 or Type 2 Diabetes
Mechanism Examplesa Hbabc Agent-Specific Agent-Specific Contraindications
Of Action Reduction Advantages Disadvantages
(%)B
ORAL
Medicine
Biguanides Hepatic Metformin 1-2 Weight neutral, Diarrhea, Serum creatinine >1.5 mg/
glucose do not cause nausea, lactic dl (men) >1.4 mg/dl (women)
production hypoglycemia, acidosis (see text), CHF, radiographic
inexpensive, contrast studies, hospitalized
extensive patients, acidosis
experience,
CV events
-Glucosidase Gl glucose Acarbose, 0.5-0.8 Reduce l flatulence, Renal/liver disease
inhibitors absorption miglitol, postprandial liver function
voglibose glycemia tests
Dipeptidyl Prolong Alogliptin, 0.5-0.8 Well tolerated, Hypoglycemia, Reduced dose with renal
peptidase IV endogenous anagliptin, do not cause weight gain disease; one associated with
inhibitors GLP-1 action gemigliptin, hypoglycemia increase heart fail-ure risk;
linagliptin, possible association with ACE
teneligliptin, inhibitor-induced angioedema
vildagliptin
Insulin Insulin Glibornuride, 1-2 Short onset of Hypoglycemia Renal/liver disease
secretagogues secretion gliciazide, action, lower
glimepiride, postprandial
glipizide, glucose,
gliquidone, inexpensive
glyburide,
glyclopyramide
Insulin Insulin Nateglinide, 0.5-1.0 Short onset of Hypoglycemia Renal/liver disease
secretagogues: secretion repaglinide, action, lower
nonsulfonylureas mitiglinide postprandial
glucose
Sodium-glucose Urinary Canagliflozin, 0.5-1.0 Insulin Urinary Limited clinical experience;
cotransporter 2 glucose dapagliflozin, secretion and vaginal moderate renal insufficiency
inhibitors excretion empagliflozin and action infections,
independent dehydration,
exacerbate
tendency to
hyperkalemia
Thiazolidinediones Insulin Rosiglitazone, 0.5-1.4 Lower insulin Peripheral CHF, liver disease
resistance, pioglitazone requirements edema, CHF,
glucose weight gain,
utilization fractures,
macular edema
Parenteral
Amylin agonists Slow gastric Pramlintide 0.25-0.5 Reduce Injection, Agents that also slow GI
emptying, postprandial nausea, risk of motility
glucagon glycaemia, hypoglycemia
weight loss with insulin
GLP-1 receptor Insulin, Exenatide, 0.5-1.0 Weight loss, Injection, Renal disease, agents that also
glucagon, liraglutide, do not cause nausea, risk of slow GI motility; medullary
slow gastric dulaglutide hypoglycemia hypoglycemia carcinoma of thyroid
emptying, with insulin
satiety secretagogues
insulin Glucose Not limited Known safety Injection,
utilization, profile weight gain,
hepatic hypoglycemia
glucose
production, and
other anabolic
actions
Medical Insulin Low- calorie, 1-3 Other health Compliance
ndocrine System
nutrition therapy resistance, low-fat diet, benefits difficult, long-

and physical Insulin exercise term success
activity secretion low
Medicine
Concept 4. : Acute Complications of DM
Learning Objective: To understand the acute complications of DM
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
1. Diabetic Ketoacidosis:
Essentials of diagnosis:
1. Blood sugar >250mg%.
2. Serum ketones positive.
3. pH < 7.3.
4. HCO-3< 15meq/L.
Management of Diabetic Ketoacidosis

1. Confirm diagnosis ( plasma glucose, positive serum ketones, metabolic acidosis).
2. Admit to hospital; intensive care setting may be necessary for frequent monitoring of if pH <7.00 or
unconscious.
3. Assess:
Serum electrolytes (K+, Na+, Mg2+, CI-, bicarbonate, phosphate)
Acid-base status-pH, HCO3 -, PCO2 , -hydroxybutyrate
Renal function (creatinine, urine output)
. Replace fluids: 2- L of 0.9 saline over first 1- h (10-20mL/kg per hour) subsequently, 0. 5 saline
at 250-500mL/h; change to 5% glucose and 0.45% saline at 150-250mL/h when plasma glucose reaches
250mg/dL (13.9 mmol/L).
5. Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg per hour by continuous IV infusion;
increase two-to threefold if no response by 2-4h. if the initial serum potassium is <3.3 mmoI/L (3.3
meq/L), do not administer insulin until potassium is corrected.
6. Assess patient: What precipitated the episode (noncompliance, infection, trauma, pregnancy, infarction,
cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).
7. Measure capillary glucose every 1-2 h; measure electrolytes (especially K+, bicarbonate, phosphate) and
anion gap every h for first 2 h.
8. Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1- h.
9. Replace K , 10 meg/h when plasma K 5.0-5.2 meq/l (or 20- 0 meq/L of infusion fluid), EC normal,
urine flow and normal creatinine documented administer 0-80 meq/h when plasma K .5 meq/L or if
bicarbonate is given. If initial serum potassium is >5.2 mmol/L.
10. See text about bicarbonate or phosphate supplementation.
11. Continue above until patient is stable, glucose goal, is 8.3-13.9 mmol/L (150-250 mg/dL), and acidosis
is resolved. Insulin infusion may be decreased to 0.05-0.1 units/kg per hour.
12. Administer long-acting insulin as soon as patient is eating. Allow for a 2-4 hour overlap in insulin
infusion and SC insulin injection.
ndocrine System
2 Non Ketotic Hyperosmolar Coma:
Essentials of diagnosis:
• Blood sugar > 600mg/dl.
• Serum osmolality > 310 mosm/kg.
• pH > 7.3.
• HCO-3 > 15meq/L.
• Normal anion gap.
Laboratory Values in Diabetic Ketoacidosis (DKA) and Hyperglycemic

Hyperosmolar State (HHS) (Representative Ranges at Presentation):
DKA HHS
Glucose , mmol/L (mg/dL)
a
13.9-33.3 (250-600) 33.3-66.6 (600-1200)
Sodium, meq/l 125-135 135-145
Potassiuma,b Normal to Normal
Magnesium a
Normal Normal
Chloridea
Normal Normal
Phosphatea b
Normal Normal
Creatinine Slightly Moderately
Osmolality (mOsm/mL) 300-320 330-380
Plasma ketones a
++++ +/-
Serum bicarbonatea, meq/l <15 Normal to slightly
Arterial pH 6.8-7.3 >7.3
Arterial P 2
a
, mmHg 20-30 Normal
Anion gapa (Na- [CI + HCO3]) Normal to slightly
a
Large changes occur during treatment of DKA, bAlthough plasma levels may be normal or high at presentation, total-body
stores are usually depleted.
Treatment:
Fluid deficit is 9 to 10L, hence it is has higher mortality than DKA.
Fluid → Total fluid deficit (9 – 10L) should be reversed over 1 –2 day:
• Initially 1 – 3L 0.9% normal saline over first 2 –3hr.
• Later 0.45% saline at 200 –300ml/hr.
Insulin → Bolus of 5 –10 units, then:
• Infusion at rate of 3 –7U/hr.
• Infusion should be continued until the patient start eating.
Medicine
Concept 4.7 : Chronic Complications
Learning Objective: To understand the chronic complications of DM
Time needed
1st Reading 30 mins
2 Reading
nd
10 mins
Chronic Complications:
Diabetes-Related Complications
Microvascular
Eye disease:
Retinopathy (non-proliferative/proliferative)
Macular edema
Neuropathy:
Sensory and motor( mono- and polyneuropathy)
Autonomic
Nephropathy (albuminuria and declining renal function)
Macrovascular:
Coronary heart disease
Peripheral arterial disease
Cerebrovascular disease
Other:
Gastrointestinal (gastroparesis, diarrhea)
Genitourinary (uropathy/sexual dysfunction)
Dermatologic
Infectious
Cataracts
Glaucoma
cheiroarthropathya
Periodontal disease
Hearing loss
Other comorbid conditions associated with diabetes (relationship to hyperglycemia is uncertain): depression,
obstructive sleep apnea, fatty liver disease, hip fracture, osteoporosis (in type 1 diabetes), cognitive
impairment or dementia, low testosterone in men
Thickened skin and reduced joint mobility.
a
5 Adrenal Gland
CONCEPTS
Â Concept 5.1 Hyperaldosteronism
Â Concept 5.2 Cushing’s syndrome
Â Concept 5.3 Adrenal insu ciency

Medicine
Concept 5.1: Hyperaldosteronism
Learning Objective: To learn the causes, features and management of
Hyperaldosteronism
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Primary Aldosteronism:
Excess aldosterone independent of RA system.
Causes:
1. Aldosterone producing adrenal adenoma (Conn’s syndrome).
2. Hyperplasia of adrenal glands.
3. B/L cortical nodular hyperplasia/ idiopathic hyperaldosteronism (MCC).
4. Aldosterone producing carcinoma – 1%.
Clinical Features:
• Patient presents with diastolic hypertension.
• Features of hypokalemia – muscles weakness, fatigue, cramps.
• Polyuria – results from impairment of urinary concentrating ability.
• Edema is characteristically absent. (escape phenomena from Na retaining effect of
aldosterone).
Investigations:
• Hypokalemia.
• Hypernatremia.
• Metabolic alkalosis.
• S. aldosterone/ Plasma renin activity (>30).
• Renal venogram for localization of tumor.
Diagnostic Criteria:
1. Diastolic hypertension without edema.
2. Hyposecretion of renin that fails to increase appropriately during volume depletion –
Upright posture, Na depletion.
3. Hypersecretion of aldosterone that does not suppress appropriately in response to
volume expansion.
Management:
• Na+ restriction.
• Aldosterone antagonist – Spironolactone.
• Conn’s syndrome – Surgery is the definitive treatment.
ndocrine System
Secondary Aldosteronism:
Increased production of aldosterone in response to activation of the renin – angiotensin
system.
Causes:
1. Pregnancy
2. Malignant hypertension
3. Accelerated hypertension
4. Renal artery stenosis
5. Diuretics
6. Hepatic failure
7. Renin producing tumors – Primary reninism.
8. Bartter’s syndrome
9. Gitelmann’s syndrome
Treatment:
• Correction of hypokalemia.
• Correction of underlying cause.
Medicine
Concept 5.2: Cushing’s syndrome
Learning Objective: To learn the causes, features and management of Cushing’s
syndrome
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Cushing Syndrome:
Causes:
A. Exogenous – The most common cause of Cushing’s syndrome is exogenous steroids.
B. Endogenous – It is of 3 types:
1. Pituitary Cushing’s syndrome (Cushing’s disease).(MC endogenous cause)
2. Adrenal Cushing’s syndrome.
3. Ectopic Cushing’s syndrome.
Signs and Symptoms of Cushing’s Syndrome

BodyCompartment/ System Signs and Symptoms
Body fat Weight gain, central obesity, rounded face, fat pad on back of neck
( buffalo hump )
Skin Facial plethora, thin and brittle skin, easy bruising, broad and purple
stretch marks, acne, hirsutism
Bone Osteopenia, osteoporosis (vertebral fractures), decreased linear growth in

children
Muscle Weakness, prox’mal myopathy (prominent atrophy of gluteal and upper

leg muscles with difficulty climbing stairs a getting up from a chair)
Cardiovascular system Hypertension, hypokalemia, edema, atherosclerosis
Metabolism Glucose intolerance/diabetes, dyslipidemia
Reproductive system Decreased libido, in women amenorrhea (due to cortisol-mediated

inhibition of gonadotropin release)
Central nervous system Irritability, emotional lability, depression, sometimes cognitive defects; in
severe cases, paranoid psychosis
Blood and immune system Increased susceptibility to infections, increased white blood cell count,
eosinopenia, hypercoagulation with increased risk of deep vein thrombosis
and pulmonary embolism
ndocrine System
Fig. 5.5
Medicine
Treatment: Anti-adrenal agents (Metyrapone) and correct the cause
ndocrine System
Concept 5. : Adrenal insu ciency
Learning Objective: To learn the causes, features and management of Addison’s
syndrome
Time needed
1 Reading
st
30 mins
2 Reading
nd
10 mins
Adrenal Insu ciency:

Causes:
1. Primary adrenocortical deficiency (Addison’s disease)
2. Secondary adrenocortical deficiency – due to destructive process at the hypothalamic
– pituitary level leading to CRH or ACTH deficiency
Long term suppression of hypothalamo – pituitary – adrenal axis by exogenous
glucocorticoids followed by inappropriate withdrawal.
Addison’s Disease:
Addison’s disease results from destruction of more than 90% of the gland.
Causes:
1. Idiopathic atrophy (autoimmune) (65%).
Sporadic
Type I Polyglandular autoimmune syndrome.
Type II Polyglandular autoimmune syndrome.
2. Surgical ablation
3. Infections –TB M.C.C in India.
4. Inflammation – Sarcoidosis
5. Hemorrhage – Anticoagulant therapy.
6. Invasion – Secondaries from breast, lung.
7. Metabolic
Congenital adrenal hyperplasia
Drugs – Enzyme inhibitors (Ketoconazole, metyropane).
Cytotoxic agent (mitotane).
8. Haemochromatosis.
Medicine
Signs and Symptoms Caused by Glucocorticoid Deficiency

TB>Fatigue, lack of energy
Weight loss, anorexia
Myalgia, joint pain
Fever
Normochromic anemia, lymphocytosis, eosinophilia
Slightly increased TSH (due to loss of feedback inhibition of TSH release) Hypoglycemia (more frequent
in children)
Low blood pressure, postural hypotension
Hyponatremia (due to loss of feedback inhibition of AVP release)
Signs and Symptoms Caused by Mineralocorticoid Deficiency rimary Adrenal nsu ciency Only
Abdominal pain, nausea, vomiting
Dizziness, postural hypotension
Salt craving
Low blood pressure, postural hypotension
Increased serum creatinine (due to volume depletion) Hyponatremia
Hyperkalemia
Signs and Symptoms Caused by Adrenal Androgen Deficiency
Lack of energy
Dry and itchy skin (in women)
Loss of libido (in women)
Loss of axillary and pubic hair (in women)
Other Signs and Symptoms
Hyperpigmentation (primary adrenal insufficiency only) (due to excess of proopiomelanocortin POMC -
derived peptides)
Alabaster-colored pale skin (secondary adrenal insufficiency only) (due to deficiency of POMC-derived
peptides)
Abbreviations: AVP, arginine vasopressin; TSH, thyroid-stimulating hormone.

ndocrine System
Diagnosis:
Fig. 5.6
Medicine
Treatment:
• Hydrocorticoids (cortisol) is the main stay of treatment (20 – 30mg).
• Mineralocorticoid supplementation is done with 0.05 – 0.1mg fludrocortisone with
sodium intake of 3 –4g/d.
• In female patients daily replacement with 25 – 50mg of DHEA (Dehydroepiandroste-
rone).
Clinical and Laboratory Features of an Adrenal Crisis
Dehydration, hypotension, or shock out of proportion to severity of current illness.
Nausea and vomiting with a history of weight loss and anorexia.
Abdominal pain, so-called acute abdomen.
Unexplained hypoglycemia.
Unexplained fever.
Hyponatremia, hyperkalemia, azotemia, hypercalcemia, or eosinophilia.
Hyperpigmentation or vitiligo.
Other autoimmune endocrine deficiencies, such as hypothyroidism or gonadal failure.
Fig. 5.7
SECTION — 6
NEPHROLOGY
Introduction to Nephrology:
Kidneys are highly complex organs performing diverse functions viz.
1. Excretory function : Urine formation.
2. Homeostatic function: Water and Acid-Base Balance (ABB)
3. Hormonal function: EPO synthesis and Vitamin D activation.
Renal Blood Flow(RBF): Kidneys are highly vascular organs receiving 25% of
cardiac output. Additionally, endowed with Auto-regulatory mechanisms which get
activated in presence of adverse conditions like dehydration, hypotension, renal
artery stenosis and help maintain adequate GFR by increasing the glomerular
capillary pressure.
Assessment in Renal disease includes:
1. Urinalysis: includes a. Hematuria b. RBC Casts c. Pyuria and d. Proteinuria.
2. Ultrasonography – KUB is both specific and sensitive for Obstructive uropathy
3. Functional assessment can be done by GFR estimation (Direct & Indirect method)
In a suspected case of Renal Dysfunction, the screening tests recommended
are:
A. Serum Creatinine: Creatinine is produced by the non enzymatic dehydration of
muscle creatine. It is freely filtered at the glomerulus and hence, its clearance
is a relatively reliable index of GFR. However, creatinine production changes
significantly according to the muscle mass of the body and dietary factors.
eGFR (estimated GFR) – Cockroft Gault Formulae:

eGFR = (140-Age)*Body Weight(kgs)/72*S. Cre- atinine (*0.85 for females).
B. Serum Cystatin C: as an alternative to Creatinine: Cystatin C is produced by

all nucleated cells of the body independent of renal conditions, increased protein
catabolism, or dietetic factors. Moreover, it does not change with age or muscle
mass like creatinine does.
Its biochemical characteristics allow free filtration in the renal glomerulus, and
subsequent metabolism and reabsorption by the proximal tubule. For these reasons,
serum cystatin C has been suggested to be an ideal endogenous marker of GFR.
Renal Biopsy is indicated in following specific circumstances:
1. Acute renal failure which is unresolving and for which a cause is not evident.
2. Nephrotic syndrome if one suspects a primary glomerular disease.
3. Proteinuria of 2 g/24h/1.73 m2 along with an abnormal urine sediment with or
without functional deterioration.
4. Hematuria associated with an abnormal urine sediment or proteinuria.
5. Systemic diseases associated with kidney dysfunction, such as systemic lupus
erythematosus, Good pasture’s syndrome and Wegener’s syndrome, to confirm
the extent of renal involvement and to guide management; and
6. Suspected transplant rejection, the differentiate it from other causes of acute
renal failure and to guide management.
Acute Renal Failure
1 (Acute Kidney Injury)
CONCEPTS
Â Concept 1.1 Diagnosis of AKI
Â Concept 1.2 Causes of AKI
Â Concept 1.3 Management of Acute Kidney Injury
Â Concept 1.4 Tubulo-interstitial disorders
Â Concept 1.5 Glomerular disorders

276 | Medicine
Concept 1.1: Diagnosis of AKI
INDEX: RENAL disorders
A.K.i Parameters C.K.I.

PRESERVED CMD-USG* LOST
N / Enlarged SIZE-USG N / SHRUNKEN
Fluctuates-Posm depends on Uosm Isothenuria* (Same as Posm)

cause
Hyaline CASTS BROAD/WAXY
Uncommon ANAEMIA COMMON
Absent CKi-MBD PRESENT
Diagnosis is confirmed by KDI Criteria

(Any 1 of the following Criteria):
1. urine output <=0.5ml/kg/hr >= 6 consecutive hours
2. Rise in S.Creatinine > 0.3mg/dl from baseline <= 48hours
3. Rise in S.Creatinine > 1.5*Baseline (OR 50% Rise)<= 7 days
Ne rolo y | 277
Concept 1.2: Causes of AKI
CAUSES - AKI
MC
Pre-Renal REN AL (Intrinsic) Post-Renal

60-85% cases 10-15% of cases 1-5% cases
1. Hypovolumia 95% 5% Obstructive uropathy
2. Hypotension
3. Drugs-disud
Autoregular
Tubulo-Interstitial GN
c/f OLIGURIC MC disorders
(V.O< 400 ml/d)
ANURIA
(V.O<100 ml/d)
Non-Oliguric presentation • Hematuria • Loin pain
( S. Create inspite N • Proteinuria • Dysuria
urine output) • Urgency
• Frequency
APPROACH-AKI
Collecting system on Post-renal Aki

the Usly
Only 1-5%
NORMAL
Parameters PRE-REN AL REN AL AKI

Pathology RAAS activation Na+ / H2O Loss-conc.ability Na+ is lost urine
reabsorption urate reabsorption dilute urine
BUN-Creat > 20:1 <12:1
UNa +
<20 mEq < 40 mEq
FENa+ <1% <2%
Uosm >500 masm/L <350 mosm/L
CASTS HYALINE Granular/cellular
Echotexture Usly NORMAL Increased
Single best parameter ABSENT DETECTABLE*
Novel Markers→ NGAL, Kim-1, IL-18
→
278 | Medicine
Concept 1. : Management of Acute Kidney In ury
PALLIATIVE (DIALYSIS)
1. UREA > 100
2. Creat > 7
3. Serious uremic features
4. Refractory Pulm edema
5. Refractory pH < 7.20
6. Refractory K+ > 6.5 mEq
Single most important indicn URGENT DIALYSIS
7. Ingestion of dialyzable boxin:
Eg: Salicylates
Methanol
Lithium
Polyethylene glycol
Ne rolo y | 279
Concept 1.4: Tubulo-interstitial disorders
AIN
MC
ATN * (Tubules- Site of Renal injury)
A A . rone- ascular insu cient 95% Drug-induced
NSAIDS, Sulfa-drugs Penicillin,
MC
1. Untreated Pre-renal Aki Cephalosporin
2. SEPSIS (Disrupt the micro-circulation of the tubules) Rifampicin, F.Q.
3. C.I.N. Contrast agents
PHYSIO-Site of concentration Remaining 5% cases:
4. Drugs: Aminology consides • Viral infection
5. Toxins: Heavy metal (Cd, Hg) • Auto immune disease
DIRECT-Luminal contents • Lymphoproliferative disorders
6. Cryoglobulins
7. Myoglobin
8. Hemoglobinuria
• ONLY Supportive RX • Stop offending drug
• Underlying cause • Supportive only
4-6 weeks Recovery 1-2 wks
1-5% Risk of long-term dialysis <1%
Good PROGNOSIS Excellent
280 | Medicine
Concept 1.5: lomerular disorders
lomerular Diseases:
Five Main Clinical Presentation of Primary Glomerulopathies are:
1. Acute nephritic syndrome.
2. Rapidly progressive glomerulonephritis (subacute glomerular inflammation).
3. Nephrotic syndrome.
4. Asymptomatic abnormalities of urinary sediment (hematuria, proteinuria).
5. Chronic glomerulonephritis.
GN A BASED ON CLINICAL PRESENTATION
• HEMATURIA • ANASARCA
• HYPERENSION • DYSLIPIDEMIA
• RELATIVELY RAPID • HYPERCOAG STATE
• ↓ ↓ GFR • PRESERVED GFR
• <3.5 G/D/1.73M2 • 3.5 G/D/1.73M2 PROEINUMRIA
• PROTEINURIA
NEPHRITIC SYN NEPHROTIC SYNDROME
↓ ↓
• IgA nephropathy Children MCD

• P.S.G.N
Adult FSGS
• Lupus nephritis
Elderly Membranous nephropathy
• Post infective
• Vasculins
B Based on Mesongial involvement of Renal Bx
+ PROLIFERATIVE GN - NON PROLIFERATIVE
• Mesangioproliferative GN • MCD FSGS

• Mesangiocapillary GN • Membranous
• Cresentric GN
Ne rolo y | 281
1. IgA Nephropathy (Berger’s Disease):
• This is the most common form of primary glomerular disease in the world.
• It progresses to end stage renal disease in 20 to 40% of patients affected over a
20 years period.
• Gross, intermittent hematuria, which is glomerular, is the presenting symptom.
• There is presence of abnormal protein-uria. Mesangial IgA is present.
• No therapeutic regimen has been shown to clearly affect outcome in IgA ne-
phropathy.
2. Acute Poststreptococcal Glomerulonephritis:
• It is most common cause of GN in India. Nephritis develops 1 –3 weeks after
pharyngeal or 4-6weeks after cutaneous infection with ‘nephrogenic’ strains of
group A beta – hemolytic streptococci.
• Diagnosis depends on a positive pharyngeal or skin culture, rising antibody
titers (Anti-DNAase, ASO, Anti-Hyal- uronidase) and hypocomplementemia (only
for 4-6 weeks of illness. Serum C3 levels normalizes later). Renal biopsy reveals
diffuse proliferative GN.
• Treatment consists of correction of fluid and electrolyte imbalance. Penicillin is
given to eradicate residual streptococcal infection. Long-term prophylaxis is not
recommended since the risk of relapse is low unlike Rheumatic Fever.
• In most cases the disease is self – limited, although the prognosis is less favorable
and urinary abnormalities are more likely to persist in adults.
3. Goodpasture’s Syndrome (Pulmonary-Renal Syndrome):
• This is characterized by lung haemorrhage, GN and circulating antibody to
basement membrane, usually in young men. Hemoptysis may precede nephritis.
• Rapidly progressive renal failure is typical
• Circulating anti – glomerular basement membrane (GBM) antibody and linear
immune – fluorescence on renal biopsy establishes the diagnosis.
• Plasma exchange may produce remission.
• High Acute mortality makes the prognosis unfavourable.
282 | Medicine
mmunofluorescence attern N otes

Chronic Renal Failure
2 (Chronic Kidney Injury)
CONCEPTS
Â Concept 2.1 Definition, causes and Stages
Â Concept 2.2 Clinical and laboratory manifesta-

tions of uremic syndrome
284 | Medicine
Concept 2.1: Definition causes and Stages
Definition:
CKI is defined as a gradual decline in GFR over a period of 3 months.
It most commonly presents with uremic symptoms. The symptoms usually manifest
once the GFR < 25ml/min which corresponds to more than 70% nephron loss.
Common Causes:
1. Diabetic nephropathy.
2. Hypertension.
3. Chronic glomerulonephritis.
4. Polycystic kidney disease.
5. Chronic pyelonephritis.
6. Interstitial nephritis.
7. Alport’s syndrome.
Fig. 6.1: Stages of Chronic Renal Failure

Ne rolo y | 285
Concept 2.2: Clinical and laboratory manifestations of uremic
syndrome:
System Clinical Manifestations
Skin Paleness and hyperpigmentation
Ecchymosis and hematomas
Pruritus
Skin necrosis (calciphylaxis)
Bullous lesions
Cardiovascular Volume overload and systemic hypertension
Accelerated atherosclerosis and ischemic heart disease
Left ventricular hypertrophy
Heart failure Rhythm disturbances Uremic pericarditiso/
Neurologic Cerebrovascular accidents
Encephalopathy Seizures
Peripheral and automatic neuropathy
Gastrointestinal Anorexia
Nausea and vomiting Malnutrition
Uremic fetor
Inflammatory and ulcerative lesions
Gastrointestinal bleeding
Hematologic Anemia
Leukocyte and immune system dysfunction (tendency to infections)
Platelet dysfunction (bleeding diathesis)
Bone Renal osteodystrophy
Growth retardation in children
Muscle weakness
Amyloid arthropathy secondary to 2
- microglobulin deposition
Endocrine Sexual dysfunction Infertility in woman
Glucose intolerance due to insulin
Resistance Hyperlipidemia
Laboratory Hyponatremia (if excessive water intake)
Hyperkalemia Hyperphosphatemia Hypercalcemia Hypermagnesemia
Hyperuricemia Metabolic acidosis
Renal Replacement Therapy
3 (RRT)
CONCEPT
Â Concept 3.1 Renal Replacement Therapy
Ne rolo y | 287
Concept .1: Renal Replacement Therapy
HEMODIALYSIS (HD) PERITON EAL (P.D)
• Vascular access • Intraperitoneal
(Cannula, AV-fistula) Catheter placement
(High complication rates) ( 1% risk-Peritonitis)
(Bleeding, sepsis, Thrombosis) Low complication rate
• Limited availability • NO Problem
• HIGH COST • Lower Cost
• Hug Hemodyn-shift • Los shift
MC – HYPOTENSION • Better tolerated
SCD - in CMP 15% EF • Safe I n CMP
• Safe in Post cardiac
HENCE CONTRAINDICATED
Sx Patients
• Infection transmission: • NO RISK
HCV, Hep B, HIV, CMV
• Risk-Hypoglycaemia Hyperglycemia/wt gain
(High glucose-P.D fluid)
Preferred form Poor F.R
Excellent F.R 15-25 ml/min
800-1200 ml/min ONLY a backup / restore
SECTION — 7
RHEUMATOLOGY
• Rheumatology is the study of systemic auto-immune diseases (AID).

• ANA is most sensitive Antibody and Best screening test for A.I.D.
Rheumatology
IMAGES N OTES
eumatolo y
1 Lupus Disorders
CONCEPTS
Â Concept 1.1 SLE
Â Concept 1.2 Systemic Sclerosis (SSc)
Â Concept 1.3 Sicca syndrome

eumatolo y
Concept 1.1 : SLE
Learning Objective: To understand the salient features and management of SLE
Time Needed
1st reading 30 mins
2 look
nd
10 mins
• SLE is a systemic auto-immune disease characterized by “Lupus rash” and is a disease

of unknown etiology. 90% of cases are women of child-bearing age.
IMAGES N OTES
Medicine
Jaccoud’s Arthropathy
eumatolo y
Anti-erythrocyte Antibody
(DIRECT COOMB’S TEST)
Medicine
Antibody Prevalence, Antigen Recognized Clinical Utility

%
Antinuclear antibodies 98 Multiple nuclear Best screening test; repeated
negative tests make SLE unlikely
Anti-dsDNA 70 DNA (double-stranded) High titers are SLE-specific and in
some patients correlate with disease
activity, nephritis, vasculitis
Anti-Sm 25 Protein complexed to 6 Specific for SLE no definite clinical
species of nuclear U1 correlations; most patients also have
RNA anti- RNP; more common in blacks
and Asians than whites
Anti-RNP 40 Protein complexed to U1 Not specifi for SLE high titers
RNA associated with syndromes that have
overlap features of several rheumatic
syndromes including SLE: more
common in blacks than whites
Anti-Ro(SS-A) 30 Protein complexed to hy Not specific for SLE associated
RNA, primarily 60 kDa with sicca syndrome, predisposes
and 52 KDa to subacute cutanecus lupus, and to
neonatal lupus with congenital heart
block; associated with decreased risk
for nephritis
Anti-La (SS-B) 10 47-kDa protein Usually associated with anti-Ro;
complexed to hY RNA associated with decreased risk for
nephritis
Antihistone 70 Histones associated with More frequent in drug-induced lupus
DNA(in nucleosome, than in SLE
chromatin)
Antiphospholipid 50 Phospholipids 2 Three tests available-ELISAs for
glycoprotein 1( -2 1) cardiolipin and 2 1, sensitive
cofactor, prothrombin prothrombin time(DRVVT);
predisposes to clotting, fetal loss,
thrombocytoperia
Antierythrocyte 60 Erythrocyte membrane measured as direct Coombs test;
a small proportion develops overt
hemolysis
Antiplatelet 30 Surface and altered associated with thrombocytopenia,
cytoplasmic antigens on but sensitivity and specricity are not
platelets good; this is not a useful dinical test
Antineuronal (includes 60 Neuronal and lymphocyte In some series, a positive test in CSF
antiglutamate receptor) surface antigens correlates with active CNS Lupus
Antiribosomal P 20 Protein in ribosomes In some series, a positive test in
serum correlates with depression or
psychosis due to CNS Lupus
eumatolo y
AUTOIMMUN E CRISIS MILD SLE FLARE

• IV Methyl Prednisolone I gm/day for 3-5 days • Oral Prednisolone for 6-8 weeks
(PULSE THERAPY) • Followed by tapering of steroids
• This is followed by oral prednisolone (dosage : • Add Steroid sparing agents from day I (min.
1-2 mg/kg/day) Time for Onset of action is 6 weeks)
Choice of Steroid sparing agents for long-term immunosuppression:

Hydroxychloroquine>Mycophenolate mofetil>Azathioprine>MTX
For Refractory case : Anti-B cell therapy are approved
MAb against CD-20 MAb against BAF/Blys
IV Rituximab IV Belimumab
Eradicates B-cells Prevents Activation
• Unpredictable course, ADR of long term immunosuppression,

• High Cost of therapy and High mortality makes the prognosis Poor.
Medicine
Concept 1.2: Systemic Sclerosis (SSc)
Learning Objective: To understand the salient features and management of SSc
Time Needed
1st reading 30 mins
2 look
nd
10 mins
• Systemic sclerosis affects Middle aged Females>Males

• Earliest manifestation is Raynaud’s phenomenon
• Skin manifestations occur in stages:
a. Early stages: Inflammation and edema over affected area
b. Late stages: Induration and Fibrosis of the skin.
TYPES: Limited SSc Diffuse Systemic SSc
Based on Extend of skin involved Restricted to face and distal to Proximal to the Elbow with Trunk
elbow involvement present. Organ
involvement is more common
Associated features present CREST* Syndrome 10% • Lungs: NSIP* (ILD)
associated with primary Billiary • Pulmonary hypertension
cirrhosis • Risk of RP N
• Mononeuritis multiplex
(MNM)*
Specific Antibody Anti-centromere Ab Anti-topoisomerase I antibody
(commercial name: SCL-70)
Manifestation reatment Options

Raynaud’s Phenomenon CCB/ILOPROST
Skin Fibrosis D-Penicillamine
Non-Specific Interstitial Pneumonia (NSIP) Steroids
Pulmonary Hypertension Iloprost
Risk of RP N Reduced by Early ACEI use
Mononeuritis Multiplex (Asymmetrical Neuropathy) Steroids
• Anti-fibrillin (U3RNP antibody) is prognostic as its presence is assocated with increased
risk of PAH and RPGN.
• Treatment is only palliative and depends on manifestations.
• Since there is no cure, prognosis is unfavourable.
eumatolo y
IMAGES N OTES
Medicine
Concept 1.3: Sicca syndrome
Learning Objective: To understand the salient features and management of Sicca
syndrome
Time Needed
1st reading 30 mins
2nd look 10 mins
• Sicca syndrome affects middle aged F>>M

• Secondary causes include SLE, SSc, RA, MCTD, Vasculitis, Primary Biliary cirrhosis
and Chronic Active hepatitis
• Glandular involvement (Exocrine-Lacrimal and Salivary gland) leads to dryness of
eyes and mouth respectively
• Extra-glandular manifestations include:
Arthritis : MC, Cirrhosis, NSIP, Mononeuritis multiplex,
Interstitial Nephritis,Distal Renal Tubular acidosis (RTA)
Lymphoma (DREADED)
TYPES: * Sicca syndrome 2* sicca syndrome
Extra-glandular* More Common Uncommon
Risk of Lymphoma High None
Specific Antibody High Titres Low Titres
Immuno-supression Majority need due to organ Palliative Only
involvement
Prognosis Poor Favourable
2 Arthritis Disorders
CONCEPTS
Â Concept 2.1 Rheumatoid Arthritis
Â Concept 2.2 Spondyloathropathies(SpA)
Â Concept 2.3 Crystal induced arthropathies

Medicine
Inflammatory Arthritis are divided into 2 broad groups based on the number
of joints affected:
1. Pauci-arthritis (<5 joints)
2. Poly-arthritis (>= 5 joints)
Fig. 7.1
eumatolo y
Concept 2.1: Rheumatoid Arthritis:
Learning Objective: To understand the salient features and management of RA.
Time Needed
1st reading 30 mins
2 look
nd
10 mins
• RA affects 20-40 yrs, F >> M

• Majority cases are Sporadic (No Family history)
• It is the MC cause of Inflammatory Polyarthritis
Diagnostic Criteria: EULAR/ACR Criteria For Rheumatoid Arthritis:

Score
Joint Involvement 1 large joint (shoulder, elbow, hip, knee, ankle) 0

2-10 large joints 1
1-3 small joints (MCP, PIP, thumb IP, MTP, wrists) 2
4-10 small joints 3
>10 joints (at least 1 small joint) 5
Serology Negative RF and negative ACPA 0

Low-positive RF or Low-positive anti-CCP antibodies ( times 2
ULN) 3
high-positive RF or High-positive anti-CCP antibodies (>3 times
ULN)
Acute-Phase Reactants Normal CRP and normal ESR 0

Abnormal CRP or abnormal ESR 1
Duration of Symptoms <6 weeks 0

≥ weeks 1
N ote: These criteria are aimed at classification of newly presenting patients who have at least one oint with definite clinical
synovitis that is not better explained by another disease. A score of ≥ fulfills requirements for definite RA.
Abbre iations ACPA, anti-citrullinated peptide antibodies; CCP, cyclic citrullinated peptides; CRP, C-reactive protein;
ESR, erythrocyte sedimentation rate; IP, interphalangeal joint; MCP, metacarpophalangeal joint; MTP, metatarsophalangeal
joint; PIP, proximal interphalangeal joint; RF, rheumatoid factor; ULN, upper limit of normal.
Medicine
Treatment is based on Disease Activity which is based on:
CDAI (Clinical disease activity Index).
< 2.5 = Remission
2.5-10 = Mild RA
10-22 = Mod RA
>22 = Severe RA
Specific/1st line therapy: DMARDS Only
Palliative therapy: NSAIDs/ Steroids.
Start DMARD as per Mild RA Moderate RA Severe RA
the CDAI score and Low Dose MTX Dual DMARD therapy Triple DMARD therapy
re-assess after 6 weeks
High Dose MTX
If RA goes in Remission Add 2nd DMARD (HCQ Add 3rd DMARD
OR Improvement in / SAA / Leflunomide)
CDAI > 6.5, continue Add 3rd DMARD
same treatment
CONSIDER NEWERA ENTS IN RA
• Newer agents for RA include following groups of drugs:
a. Biologicals : (Mab’s)
• Monoclonal antibodies derived from LIVE cell cultures.
b. Immunologicals : (-tinib’s)
• Tyrosine kinase inhibitors (Small Molecule agents)
Prognosis with Early treatment is Favourable.
POOR PROGNOSTIC FACTORS IN RA:
1. Female gender
2. Advanced age at onset (>40 years)
3. >=10 joints involvement at diagnosis
4. Extra-articular features
5. High RAF Titres
6. High ACPA Titres
7. Early Radiological evidence of erosions
8. High Acute phase reactants
9. Smoking
10. Poor socio-economic status/educational level
eumatolo y
IMAGES N OTES
Medicine
Concept 2.2: Spondyloathropathies(SpA)
Learning Objective: To understand the salient features and management of SpA
Time Needed
1st reading 30 mins
2 look
nd
10 mins
Spondyloarthropathies are a group of disorders having following common
features:
• Strong Family history of arthropathy (HLA-B27positive)
• Enthesitis is primary site of joint involvement
• Axial involvement is not uncommon
• RA Factor is negative
• Extra-articular features predominate
• Excellent response to NSAIDS
Axial-dominant (Spine affected) Appendicular-dominatn

(peripheral joints)
Symmetrical with
Ankylosing Spondylosis (AS) Predominant Small Joint
Male dominant arthropathy involvement
90% : HLA-B27 association
MC affects: Sacro-illiac joint Asymmetrical with Predominant
leading to low Back Pain Large Joint involvement
70%: arthritis is preceded by
Recurrent unilateral uveitis
eumatolo y
IMAGES N OTES
Medicine
Concept 2.3: Crystal induced arthropathies
Learning Objective: To understand the salient features and management of Crystal
induced arthropathies
Time Needed
1 reading
st
20 mins
2nd look 5 mins
CRYSTAL – Induced Arthropathy

arameters Gout seudogout
Crystal deposited in the affected Mono-Sodium Urate Calcium Pyro-Phosphate crystals
joint (MSU:Needle Shaped Crystals) (CPPD: Rhomboid)
Epidemiology 30-50Years <50 yrs
M>>F M>>F
Etiology:90% Renal tubular defect in urate Joint degeneration
excretion
10% cases High non-veg diet Hypercalcemia:
Drugs: PZA, Thiazide PTH adenoma
Drink: Beer>Wine Paraneoplastic syn
MC Clinical manifestation Inflammatory Mono-arthritis (1st Inflammatory Oligo-arthritis

MTP<Ankle jt) (Knee<Hip<shoulder jt)
Screening test S. Uric Acid levels S. Calcium levels
Diagnostic test Strong Negative Birefringence Mild positive birefringence
Acute attack (1st line agent) NSAIDS NSAIDS
Approved alternatives for Acute • Colchicine, -

attack • Canakinumab
(MAb against IL-I )
With renal failure Intraarticular steroids Intraarticular steroids
Chronic prophylaxis (Target) S. Uric Acid < 6 mg/dl Slow joint degeneration
Treatment Options • 1st: X.O. Inhibitors: • Encourge Mobility
Allopurionol/Febuxostat • Physiotherapy
• Pegloticase (For Refractory • Avoid un-necessary Calcium
cases) & D3 supplements
Prognosis Favourable (Joint is preserved/ Unfavourable (joint damage is
Surgery rarely indicated) irreversible and majority and
need joint replacement surgery)
eumatolo y
IMAGES N OTES
3 Vasculitis Syndrome
CONCEPTS
Â Concept 3.1 Large vessel vasculitis
Â Concept 3.2 Medium vessel vasculitis
Â Concept 3.3 Small vessel vasculitis
Â Concept 3.4 Behcet’s syndrome

eumatolo y
Vasculitis Syndrome
Vasculitis : Classification Based on Si e of Vessel Affected:
A. Large vessel : Giant Cell arteritis, Takayasu’s arteritis
B. Medium vessel : Polyarteritis Nodosa, Kawasaki’s disease
C. Small vessel : Further sub-classified based on ANCA.
1. ANCA positive : Wegener’s granulomatosis

Microscopic Polyangiitis (MPA) Churg Strauss
syndrome
2. ANCA Negative : Henoch-Schloein Purpura(HSP)
Bechet’s syndrome
Medicine
Concept 3.1: Large vessel vasculitis
Learning Objective: To understand the features and management of Large vessel
vasculitis
Time Needed
1st reading 30 mins
2nd look 10 mins
Giant Cell arteritis (Previously Temporal Arteritis)

• Classically affects Post-menopausal females (>50years)
GCA MANIFESTATIONS
Carotid A. in ol ement is common olymyalgia R eumatica*
xternal Carotid A. branc es nternal Carotid A. branc es n Cases
MC RAR
MC: Superficial Temporal A Irreversibel Blindenss* (Dreades) • Symptom complex
• Unilateral/Bilateral throbbing consisting of myalgia,
Headache* which worsens low grade fever,
on supine position with scalp anorexia and weight loss
tenderness >= 3 months duration
• Diploma Other Manifestations causing Death* • Can be seen in other
rheumatologic condition
• Jaw Claudication pain • Stroke-20% also
• MI-2%
• Paraesthesia over face
ESR is a screening test
Temporal artery Biopsy is the gold standard
USG shows non compressible “Halo-sign”
Steroids remain the Mainstay of treatment.
6-8 weeks course offers remission and discontinued in 6 months in majority
Empirical Steroids (Without confirmatory diagnosis) is ONLY indicated in cases
with OCULAR symptoms with impending Blindness.
Prognosis with Early diagnosis and treatment is Good.
eumatolo y
Takayasu’s arteritis (Aortic Arch syndrome/Pulseless disease)
• Takayasu’s arteritis affects 10-20 years, F>M
Artery Involved Manifestation

Subclavian Artery (MC) UL Caludication/Unequal Pulse
Carotid Artery/Vertebral Artery Recurrent TIA/Young Stroke
Coeliac Artery Chronic Mesentric Insufficiency
Renal Artery Renal Artery Stenosis (Young HTN)
Coronary Artery Young MI
Fig. 7.2
Steroids remain the Mainstay of treatment.

Majority require life-long immunosuppression
Also Palliative Stenting has to be done for the pre-existing stenosis
Young age is affected, Unpredictable course of the disease,
High cost of treatment and ADR of immunosuppression
POOR PROGNOSIS
Medicine
Concept 3.2: Medium vessel vasculitis
Learning Objective: To understand the features and management of Medium vessel
vasculitis
Time needed
1 reading
st
30 mins
2 look
nd
10 mins
Polyarteritis Nodosa:
Classic polyarteritis nodosa (PAN) is a multisystem, necrotizing vasculitis of small and
medium-sized muscular arteries in which involvement of the renal and visceral arteries is
characteristic. Classic PAN does not involve pulmonary arteries.
Mean age of onset of PAN is approximately 50 years of age, M > F
Organ System Percent Incidence Clinical Manifestations
Renal 60 Renal failure, hypertension.
Musculoskeletal 64 Arthritis, arthralgia, myalgia.
Peripheral nervous system 51 Peripheral neuropathy, mononeuritis multiplex.
astrointestinal tract 44 Abdominal pain, nausea and vomiting, bleeding, bowel

infarction and perforation, cholecystitis, hepatic infarc-
tion, pancreatic infarction.
Skin 43 Rash, purpura, nodules, cutaneous infarcts, livedo re-

ticularis, Raynaud’s phenomenon
Cardiac 36 Congestive heart failure, myocardial infarction,

pericarditis
enitourinary 25 Testicular, ovarian, or epididymal pain
Central nervous system 23 Cerebral vascular accident, altered mental status, seizure
Treatment:
Prednisolone, 1 mg/kg per day, and cyclophosphamide, 2 mg/kg per day is the main
treatment with excellent response. Death usually results from GIT complications like
bowel infarcts, perforation and CVS causes.
eumatolo y
Concept 3.3: Small vessel vasculitis
Learning Objective: To understand the features and management of Small vessel
vasculitis
Time Needed
1 reading
st
30 mins
2 look
nd
10 mins
Wegener’s Granulomatosis:
Granulomatous vasculitis of the upper and lower respiratory tracts together with
glomerulonephritis. M: F = 1:1. The disease can be seen at any age (mean age of onset
is approximately 40 years).
Lung involvement: Multiple, bilateral, nodular cavitary infiltrates (biopsy reveals typical
necrotizing granulomatous vasculitis).
Renal involvement is characterized by a focal and segmental glomerulitis that may
evolve into a rapidly progressive crescentic glomerulonephritis.
Clinical Features:
1. Severe paranasal sinus pain and drainage and purulent or bloody nasal discharge with
or without nasal mucosal ulceration. Nasal septal perforation may follow, leading to
saddle nose deformity.
2. Pulmonary involvement: Asymptomatic infiltrates or may be clinically expressed as
cough, hemoptysis, dyspnea and chest discomfort.
3. Eye involvement (52% of patients): Mild conjunctivitis to dacryocystitis, episcleritis,
scleritis, granulomatous sclerouveitis, ciliary vessel vasculitis, and retro orbital mass
lesions leading to proptosis.
4. Skin lesions (46% of patients): Papules, vesicles, palpable purpura, ulcers, or
subcutaneous nodules.
5. Cardiac involvement (8% of patients): Pericarditis, coronary vasculitis, or, rarely,
cardiomyopathy.
6. Nervous system manifestations (23% of patients): Cranial neuritis, Mononeuritis
multiplex etc.
7. Renal disease (77% of patients): Dominates the clinical picture and, if left
untreated, accounts directly or indirectly for most of the mortality in this disease.
8. Nonspecific symptoms and signs such as malaise, weakness, arthralgia, anorexia,
and weight loss, fever are present in majority.
Markedly elevated ESR, mild anemia and leukocytosis, mild Hypergammaglobulinemia
(particularly of the IgA class), and mildly elevated rheumatoid factor may be seen.
Approximately 90% of patients have a positive c-ANCA (anti proteinase 3
antibodies).
Medicine
Treatment:
1. Glucocorticoids should be administered together with cyclophosphamide.
2. Methotrexate together with glucocorticoids may be considered as an alternative
for initial therapy.
3. Azathioprine, in doses of 1 to 2 mg/kg per day, has proven effective in some patients.
Henoch-Schonlein Purpura:
• Henoch-Schonlein purpura (anaphy- lactoidpurpura) is a systemic vasculitis syndrome
characterized by palpable purpura, arthralgia, gastrointestinal signs and symptoms,
and glomerulonephritis. It is a small vessel vasculitis.
• Most patients range in age from 4 to 7 years.
• HSP is due to immune-complex deposition. Several triggering antigens have been
suggested including upper respiratory tract infections, various drugs, foods, insect
bites and immunizations.
• IgA is the antibody class most often seen in the immune complexes.
Clinical Features:
1. The typical palpable purpura (most commonly distributed over the buttocks and lower
extremities) is seen in virtually all patients.
2. Most patients develop polyarthralgia in the absence of frank arthritis.
3. Gastrointestinal involvement, is characterized by colicky abdominal pain usually
associated with nausea, vomiting, diarrhea, or constipation often accompanied by
the passage of blood and mucus per rectum.
4. The renal involvement is usually characterized by mild glomerulonephritis leading to
proteinuria and microscopic hematuria, with RBC casts in urine.
Mild leukocytosis, a normal platelet count, and occasionally eosinophilia are seen. Se-
rum complement components are normal, and IgA levels are elevated in about 50%
of patients.
Treatment:
Prednisone in doses of 1 mg/kg per day and tapered according to clinical response has
been shown to be useful. Many patients recover without therapy.
eumatolo y
Concept .4: Behcet’s syndrome
Learning Objective: To understand the features and management of Behcet’s syndrome
Time Needed
1st reading 30 mins
2 look
nd
10 mins
Behcet’s Syndrome:
Recurrent oral and genital ulcerations as well as ocular involvement.
It affects mainly young adults, with males having more severe disease than females.
Clinical Features:
1. The recurrent aphthous ulcerations. Genital ulcers resemble the oral ones.
2. Skin lesions: Folliculitis, erythema nodosum, an acne-like exanthema, and
infrequently vasculitis are seen.
3. Iritis, posterior uveitis, retinal vessel occlusions and optic neuritis can be seen.
4. Arthritis of Behcet’s syndrome is not de- forming and affects the knees and an- kles.
5. Superficial or deep peripheral vein thrombosis is seen in one-fourth of the patients.
Diagnostic Criteria for Behcet’s Disease:

Recurrent oral ulceration plus two of the following:
1.Recurrent genital ulceration.
2.Eye lesions.
3.Skin lesions.
4.Pathergy test.
Leukocytosis and elevated ESR and CRP are seen.
Antibodies to human oral mucosa are also found.
Treatment:
1. Mucous membrane ulcers may respond to topical glucocorticoids. In more serious
cases thalidomide (100 mg/d) is effective.
2.Thrombophlebitis is treated with aspirin, 325 mg/d.
3.Colchicine or interferon alpha can be beneficial for the arthritis of the syndrome.
4. Uveitis and CNS involvement require systemic glucocorticoid therapy (prednisone, 1
mg/kg per day) and azathioprine (2 to 3 mg/kg per day), or cyclo- sporine (5 to 10
mg/kg per day).
Medicine
IMAGES N OTES

Medicine

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Medicine

Uploaded by

Copyright:

Available Formats

Concept Based Learning

Video Companion on Each Chapter

Comprehensive review series

First Published 1999, Delhi Academy of Medical Sciences

© 2021 DAMS Publication

Section 2 Cardiovascular System 61 – 134

Section 3 Respiratory Systems 135 – 176

Section 4 Gastrointestinal Tract and Liver 177 – 224

Section 6 Nephrology 273 – 287

Section 7 Rheumatology 288 – 316

frontal eye field

auditory auditory association

Glasgow Coma Scale (GCS):

Eye Opening Verbal (nonintubated) Verbal (Intubated) Motor Activity

Â Concept 1.2 Cerebral Circulation

Â Concept 1.3 Manifestations of CVA

Â Concept 1.4 Brainstem syndromes

Â Concept 1.5 Thrombolysis in Stroke:

Â Concept 1.6 Hemorrhagic strokes

Â Concept 1.7 Dementia

Â Concept 1.8 Alzheimer’s Disease (AD) and

Presently CVA is classified on the basis of the pathology into:

Artery affected Area involved FN D

Recombinant Tissue Plasminogen Activator (rtPA) is approved within Window period of

Administration of Intravenous Recombinant Tissue Plasminogen Activator

Clinical diagnosis of stroke. Sustained BP >185/110 mmHg despite treatment.

Sub Dural Hemorrhage Extra-Dural Hemorrhage

PrimarySecondary (Reversible) Secondary

Alcohol abuse (Wernicke’s)

Alzheimer’s Fronto temporal dementia (FTD)

Diffuse Lewy body disease (DLB)

Â Concept 2.2 Other Headache syndromes

Â Concept 2.3 Epilepsy

Â Concept 2.4 Status Epilepticus:

Â Concept 2.5 Important Epilepsy syndromes

Â Concept 2.6 Treatment of Epilepsy

Headache Symptoms that Suggest a Serious Underlying Disorder

Tension Type Headache:

Migraine Type Headache:

Clinical Subtypes of Migraine:

Simplified Diagnostic Criteria for Migraine

Cluster Headache Paroxysmal Sunct/suna

Grand Mal Petit Mal Myoclonic

Pharmacologic treatment of generalized tonic-clonic status

CLZ, clonazepam; ECT, electroconvulsive therapy; LCM, lacosamide; LEV, levetiracetam;

1. Juvenile Myoclonic Epilepsy (JME):

Mesial Temporal Lobe Epilepsy (MTLE) :

Generalized-Onset Focal Typical Absence Atypical Absence,

When to Discontinue Therapy:

Management of Epilepsy in Pregnancy : Special condition:

Multiple Sclerosis (MS) is a demyelinating disorder of CNS characterized by discreet

1. Optic nerve (Most common) (65%) Diminision of vision (Optic neuritis)

2. MLF (Medical longitudinal fasciculus) Diplopia (IntranuclearOphthalmoplegia-INO)

3. Spinothalamic Tract Parasthesia (Tingling & Numbness)

4. Pyramidal Tract Hemiplagia / Paraplegia

5. Spinocerebellar Tract Cerebellar Ataxia

6. Dorsal column Sensory Ataxia (Romberg’s Sign +ve)

Clinical Subtypes of M.S.:

Cranial N erve Major Function Reflex and Response Assessment

XII Hypoglossal Motor to tongue Tongue size and symmetry

Â Concept 5.2 Other Infections

Â Concept 5.3 Prion disease

C.S.F Pyogenic T.B.M Viral/Aseptic

Â Concept 6.2 Important Myelopathy Syndromes