GENERAL MEDICINE

PAPER - 2

SMAHRT NOTES
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1. Pyogenic Meningitis – Causes, Etiopathogenesis, C/F,
inv. Dx and Mx [22, 21, 19, 18, 14, 12, 11]
a. CSF in TB meningitis [21, 09, 05]
b. CSF in Pyogenic Meningitis [19]
c. Enumerate causes of meningitis [11]

Ans.
PYOGENIC meningitis is defined by the presence of.
polymorphonuclear leucocytes ('pus cells') in CSF.

Causes of Meningitis:
Causes of PYOGENIC meningitis: {Box 25.63}
In India, H. influenzae B & Strep. pneumoniae are the
MCC of bacterial meningitis in children.
Pathogenesis: Infection  immune response  pia–arachnoid membrane become infiltrated with
inflammatory cells  Pus then forms in layers, which may later organise to form adhesions 
obstruct the free flow of CSF  hydrocephalus or damage the cranial nerves at the base of brain.

Headache, drowsiness, fever & neck stiffness.

In severe bacterial meningitis the patient may be
comatose
Some specific feature of each:
- a/w Otitis media – in pneumococcal & Haemophilus
- Pneumococcal meningitis – a/w pneumonia
- Listeria monocytogenes – affects mostly
immunosuppressed or people with diabetes, alcoholics
and pregnant women
- Meningococcal meningitis – progress to sepsis rapidly with rash
{morbilliform, petechial or purpuric}

 Lumbar puncture is mandatory unless there are contraindications

where blood cultures will be taken.
 Lumbar puncture will help differentiate the causative
organism

 There is an untreated mortality rate of around 80%.

Treatment of PYOGENIC meningitis of

Treatment of PYOGENIC meningitis of

 Adjunctive glucocorticoid therapy is

useful in reducing hearing loss and
neurological sequelae
 In meningococcal disease, mortality is
doubled if the patient presents with features of sepsis rather than meningitis.
Close contacts of patients with meningococcal infection
should be given 2 days of oral rifampicin.
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2. Enumerate involuntary movements. Discuss etiopath, C/F & Mx of Parkinson's Disease [22, 21, 19,
18, 16, 12]
a. Choreoathetosis [21]
b. Huntington's chorea [21]
c. Tardive Dyskinesia [18]
d. Different causes of Parkinsonism [14]
e. Sydenham’s chorea [13]
f. Chorea [11]
g. Drug treatment of Parkinsonism [06]
Ans.
 Disorders of movement lead to either extra movement
(hyperkinetic disorders) or too little movement (hypokinetic
disorders).
 In either case, the lesion often localises to the basal ganglia &
rarely to cerebellar or brainstem.

Hyperkinetic Disorders
Tremor is caused by alternating agonist/antagonist muscle  Essential tremors
1) Tremor contractions and produces a rhythmical oscillation of the body  Parkinson’s Disease
part affected  Drug-induced PD
Chorea refers to jerky, brief, purposeless involuntary
2) horea ▪ Huntington’s disease
movements, appearing fidgety & affecting different areas.
 They suggest disease in the Caudate nucleus ▪ Complication of levodopa
treatment
Slower, writhing movement of the limbs are often combined with chorea and have similar
3) thetosis causes
• More dramatic form of chorea;
• Causes violent flinging movements of one limb
4) allism (monoballism) or one side of the body (hemiballism). Seen in Stroke
• They suggest disease in the contralateral subthalamic
nucleus
▪ Sustained muscle contraction causing abnormal postures ± ▪ Generalised dystonia –
tremor seen in children
5) ystonia ▪ Some dystonias occur only with specific tasks – Ex: writer’s ▪ Focal dystonias in adults
cramp (e.g., torticollis)
 Hypnic jerks –
physiological at the onset
6) Myoclonus Shock-like muscle jerks
of sleep
 Epilepsy
 Tourette’s syndrome
Tics are stereotyped repetitive movements, such as blinking,  Huntington’s & Wilson’s
7) Tics winking, head shaking or shoulder shrugging diseases
 Post-streptococcal
Hypokinetic Disorders
 Idiopathic Parkinson’s
Parkinsonism Akinesia, Rigidity, Tremor, Loss of postural reflexes etc. disease;
 Drug-induced
Usually psychiatric; if
Catatonia Mutism; Sustained posturing and waxy flexibility neurological, is most
commonly of vascular origin

Parkinsonism is a clinical syndrome characterised primarily by

bradykinesia, with associated tone (rigidity), tremor and loss
of postural reflexes. There are many causes but the most
common is Parkinson’s disease (PD).
:
 Average age of onset is about 60 years
 Genetic factors: Having a first-degree relative with PD
confers a 2–3 times  risk.
 In most patients the cause remains unknown.
 The hallmarks of PD are pigmented dopaminergic neurons
in the substantia nigra and the presence of α-synuclein and
other protein inclusions in nigral cells (Lewy bodies). Lewy
bodies increase with disease progression.
– The loss of dopaminergic neurotransmission is responsible for many of the clinical
features.
Motor symptoms –
Bradykinesia  increasingly small handwriting (‘micrographia’), difficulty tying shoelaces or buttoning
clothes, and difficulty rolling over in bed.
Tremor – It is typically a unilateral resting tremor affecting limbs, jaw and chin but not the head.
Rigidity causes stiffness and a flexed posture.
Loss of postural reflexes
 On neurological examination .
Cognition is spared in early disease; if impaired, consider an
alternative diagnosis, such as dementia with Lewy bodies.
Non-motor symptoms – in sense of smell
(hyposmia), anxiety/depression, constipation and
REM sleep behavioural disturbance (RBD), sexual
problems (erectile failure, loss of libido or
hypersexuality), drooling and weight loss.
– The diagnosis is clinical.
Structural imaging (CT or MRI) is usually normal for
age
Functional dopaminergic imaging (SPECT or PET) is
abnormal, even in the early stages, but does not
differentiate between the different forms of
degenerative parkinsonism and so is not specific
for PD.

PD is progressive and incurable, with a variable

prognosis.
Drug treatment for PD remains symptomatic rather
than curative
Drugs for PD should not be stopped abruptly, as
this can precipitate malignant hyperthermia.
LD is most effective for relieving akinesia and
rigidity – if these doesn’t relieve on LD (1000
mg/day), then consider alternate
diagnosis.
Dopamine receptor agonists

COMT inhibitors – Ex: entacapone and

tolcapone.
Surgery –
 Deep brain stimulation (DBS), reserved
for individuals with medically refractory tremor or motor fluctuations
 Intracranial delivery of fetal grafts or specific growth factors remains experimental.
Physiotherapy, occupational therapy and speech therapy.

HD is an autosomal dominant disorder of movements

Etiology:
 HD occurs due to expansion of a trinucleotide CAG repeat in the Huntingtin gene on chromosome 4.
 The disease frequently demonstrates the phenomenon of anticipation, in which there is a younger
age at onset as the disease is passed through generations, due to progressive expansion of the
repeat.
Clinical features:
 HD typically presents with a progressive behavioural disturbance, abnormal movements (usually
chorea), and cognitive impairment leading to dementia.
 Onset under 18 years is rare but patients may then present with parkinsonism rather than chorea
(the ‘Westphal variant’).
 There is always a family history.
Management
 The diagnosis is confirmed by genetic testing;
 Brain imaging may show caudate atrophy but is not specific to HD.
 Management is symptomatic – The chorea respond to neuroleptics {Ex: risperidone or sulpiride,
or tetrabenazine}. Depression and anxiety are common and may be helped by medication.
– aka St Vitus dance
:
 It is a late neurological manifestation that appears at least 3 months after the episode of acute
rheumatic fever, when all the other signs may have disappeared.
 It is more common in females. Speech may be explosive and halting. Spontaneous recovery
usually occurs within a few months. Approximately one-quarter of affected patients will go on to
develop chronic rheumatic valve disease.
: purposeless, involuntary, choreiform movements of the hands, feet or face
:
Investigations:
 measure ESR & CRP; Serology for ASO antibodies;
 Echocardiography typically shows mitral regurgitation; it may also demonstrate aortic
regurgitation and pericardial effusion.
The aims of management are to limit cardiac damage and relieve symptoms
Bed rest – as it lessens joint pain and reduces cardiac workload
Antibiotics – A single dose of benzathine benzylpenicillin (1.2 million U IM) or oral
phenoxymethylpenicillin (250 mg 4 times daily for 10 days) should be given on diagnosis to
eliminate any residual streptococcal infection.
Aspirin – to relive joint pain – should be continued until the ESR has fallen and then gradually
tailed off
Glucocorticoids: These produce more rapid symptomatic relief than aspirin and are indicated in
cases with carditis or severe arthritis.
Cardiac failure should be treated as necessary – Ex: valve replacement; pacemaker insertion etc.
For Long-term prophylaxis – benzathine benzylpenicillin (1.2 million U IM monthly) or Oral
phenoxymethylpenicillin (250 mg twice daily)
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3. Classify epilepsy. Discuss the Mx of status epilepticus [22, 21, 18, 11, 08]
a. Focal seizure disorder [11]
 b. Epilepsy – classify, C/F & treatment [05]
c. Clonus [05]
Ans.
is a chronic disorder, the hallmark of which is
recurrent, unprovoked seizures.
A seizure can be defined as the occurrence of signs and/or
symptoms due to abnormal, excessive or synchronous
neuronal activity in the brain.
:
:

Focal epilepsy Generalised epilepsies

Occurs when both the hemispheres
Caused by localised become involved – mostly genetic in
cortical activity with origin. It can be: -
or without Tonic–clonic seizures: an initial ‘aura’
awareness  patient becomes rigid (tonic) &
: unconscious  jerking (clonic)
movements emerge for 2 minutes at
 false most  flaccid state of deep coma.
recognition (déjà During the attack, urinary incontinence and
vu). tongue-biting occur
Absence seizures always start in
 visual changes childhood. They can occur so frequently (20–30 times a
(lights & blobs of day) that they are mistaken for daydreaming or poor
concentration in school
colour)
Myoclonic seizures: brief, jerking
movements, predominating in the arms

sensory Atonic seizures: brief loss of muscle
alteration tone  heavy falls
(burning, tingling) Tonic seizures – a/w generalised in
tone
 Clonic seizures: similar to tonic–clonic
jerking. seizures but there is no preceding tonic
phase
:
 Seizure activity is usually apparent on EEG as spike and
wave discharges.
 :
 : Status epilepticus is seizure activity not
resolving spontaneously, or recurrent seizure with no
recovery of consciousness in between.
:
 In patients with pre-existing epilepsy, the most likely
cause is a fall in antiepileptic drug levels.
 In de novo status epilepticus – r/o precipitants such
as infection (meningitis, encephalitis), neoplasia and
metabolic derangement (hypoglycaemia,
hyponatraemia or hypocalcaemia)
– it is usually clinical.
Complications: Cyanosis, pyrexia, acidosis, sweating,
aspiration, hypotension, cardiac arrhythmias and renal
or hepatic failure.
:

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4. Trigeminal neuralgia [22, 15, 12, 11]
a. Operative treatment of trigeminal neuralgia [09]
Ans.
is characterised by unilateral lancinating facial pain, most commonly involving
the 2nd and/or 3rd divisions of the trigeminal nerve territory, usually in patients over the age of 50 yrs.
Etiopathogenesis: Mostly idiopathic condition
 It may be due to an irritative lesion, an aberrant loop of artery or a benign lesion, involving the
trigeminal root zone.
 It is also seen in multiple sclerosis due to a plaque of demyelination in the brainstem.
Clinical features
The pain is repetitive, severe and very brief (seconds or less).
Pain is triggered by touch, a cold wind or eating.
Spasms make the patient wince and sit silently (tic douloureux).
Rarely, there may be combined features of trigeminal neuralgia & cluster headache (‘cluster–tic’).
Management
: Pain often responds to Carbamazepine
 Alternate drugs: Oxcarbazepine, gabapentin, pregabalin, amitriptyline or glucocorticoids
: only if medication is ineffective or poorly tolerated
Microvascular decompression – MC done
 Other surgical options: Balloon compression of the nerve root; Localised injection of alcohol or
phenol into a peripheral branch of the nerve; Radiofrequency thermocoagulation; Glycerol
rhizolysis & Stereotactic radiosurgery.
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5. Stroke – Definition, types, common causes, C/F & Mx [21, 11]
a. Ischemic Stroke [22]
b. Complications of stroke [17]
c. Risk factors for ischaemic Stroke [16]
d. Computerised tomography in stroke [08]
e. Etiology of stroke in young [08]
Ans.
Stroke {CVA} is defined as rapidly developing clinical signs of focal (or global) disturbance of
cerebral function with symptoms lasting ≥ 24h or leading to death with no apparent cause other
than of vascular origin. {WHO}
:
:

Computed tomography (CT) scanning

– to identify stroke & to exclude non-
stroke lesions.
 Most practical & most widely used
method for brain imaging in cases
of stroke
 Small cerebral infarcts may never
show up on CT scans
 Abnormal perfusion of brain tissue
can be imaged with CT after
injection of contrast media (i.e., CT
perfusion scanning).
 CT scans can’t distinguish
haemorrhagic from ischaemic
strokes
Magnetic resonance imaging (MRI) –
MRI diffusion weighted imaging (DWI)
can detect ischaemia earlier than CT
 MRI is more sensitive than CT in detecting strokes
affecting the brainstem and cerebellum, and, unlike
CT, can reliably distinguish haemorrhagic from
ischaemic strokes
Contraindications to MRI: cardiac pacemakers and
claustrophobia on entering the scanner.

Ischemic stroke occurs due to sudden occlusion of an

intracranial vessel, with reduction in blood flow to the
brain area supplied by that vessel
Etiopathogenesis: Occlusion happens either due to in situ thrombosis or embolus from a distant site
MCC – thromboembolic disease 2° to atherosclerosis in the major extracranial arteries (carotid
artery and aortic arch).
20% of infarctions are due to embolism from the heart, and a further 20% are due to
thrombosis in situ {within lenticulostriate arteries}  lacunar infarctions.
Uncommon causes: Hypercoagulable disorders, Drugs (cocaine, amphetamine), Moyamoya etc.
Ischemia  hypoxia  release of inflammatory mediators by microglia & astrocytes  cell
death.
If blood flow is restored
before significant
amount of cell death,
patient may experience
only transient
symptoms, i.e., a TIA
(transient ischemic
attack).
Clinical features
Both Ischemic stroke &
TIA are characterised
by a rapid-onset, focal
deficit of brain
function.
 The clinical presentation of stroke depends on which arterial territory is involved and the size of
the lesion – Examples:
If lesion is in cerebral hemisphere  U/L motor deficit, a higher cerebral function deficit such
as aphasia or neglect, or a visual field defect.
If lesion is in brainstem or cerebellum  Ataxia, diplopia, vertigo and/or B/L weakness
Severe headache + vomiting at the onset of the focal deficit  suggests intracerebral
haemorrhage.
Management of ischemic stroke – (refer above).
 Rapid Reperfusion (thrombolysis and thrombectomy) in ischaemic stroke can reduce the extent
of brain damage & disability
 Statins (atorvastatin 80 mg daily or rosuvastatin 20 mg daily)
 Aspirin - 300 mg daily – start immediately after an ischaemic stroke – to recurrence.
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6. Classify MND. Discuss the C/F, inv. & Mx of Amyotrophic Lateral Sclerosis [19, 15, 09, 08, 05, 03]
a. Motor Neuron Disease (MND) [17, 13, 11]
b. Draw a diagram of motor and plate. What are the types, their C/F of motor neuron disease? [06]
Ans.
is a neurodegenerative condition caused by loss of upper and
lower motor neurons in the spinal cord, cranial nerve nuclei and motor cortex.
:
 Most cases are sporadic but 10% of cases are familial – Abnormalities in the superoxide
dismutase (SOD1) gene account for about 20% of such cases.
 Classifications of
MND:
 MC form of MND is
Amyotrophic Lateral
Sclerosis (ALS), and
many use the terms
MND and ALS
interchangeably.
:
: to
exclude alternative diagnoses
Blood tests –  creatine kinase.
Sensory and motor nerve conduction studies – in
amplitude of motor action potentials due to axonal loss.
EMG confirms the typical features of widespread denervation
and re-innervation.
Genetic testing – to detect mutations found in SOD1, FUS,
TARDBP and C9orf72 that may help predict risk and
phenotype of disease in those with a family history of MND.
:
 Patients should be managed within a multidisciplinary service,
including physiotherapists, speech & occupational therapists,
dietitians, ventilatory and feeding support, and palliative care teams
 Riluzole, a glutamate release antagonist, is licensed for ALS but has only a modest effect,
prolonging median survival by about 2–3 months.
 Non-invasive ventilation & feeding by percutaneous gastrostomy prolongs
survival

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7. Tuberculous meningitis – C/F, Dx, Complications & Mx [17, 13, 02]
Ans.
Tuberculosis (TB) is caused by infection with Mycobacterium tuberculosis (MTB)
:
TB meningitis most commonly occurs shortly after a primary infection in childhood or as part of
miliary tuberculosis.
It is now uncommon in developed countries except in immunocompromised individuals
The usual local source of infection is a caseous
focus in the meninges or brain substance
adjacent to the CSF pathway.
: Onset is much slower than in
other bacterial meningitis over 2–8 weeks.

Lumbar puncture – ICP; CSF is straw colored

with cobweb-like appearance; lymphocytes,
proteins and glucose.
CSF smear & culture – to detect tubercle bacillus –
takes up to 6 weeks.
Brain imaging {CT, MRI} – show hydrocephalus,
brisk meningeal enhancement + intracranial
tuberculoma.

Start
chemotherapy
(incl. pyrazinamide).
The use of glucocorticoids in
addition to ATT has been
controversial.

Surgical ventricular
drainage – If
obstructive
hydrocephalus
develops.
Skilled nursing –
for adequate
hydration and
nutrition
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8. Subarachnoid hemorrhage – C/F, Lab inv. Dx & Mx [17, 15, 09]
a. Intracerebral haemorrhage – risk factors & CT scan features [07, 06]
Ans.
Subarachnoid haemorrhage (SAH), less common than ischaemic stroke, is defined as bleeding into
the subarachnoid space within the intracranial vault
Etiopathogenesis:
Age & sex – Women> men and the condition usually present before the age of 65
85% of SAH cases – occurs due to saccular or ‘berry’ aneurysms arising from the bifurcation of
cerebral arteries {in the region of the circle of Willis}
Sites: Anterior communicating artery > Posterior communicating artery > Middle cerebral artery.
There is risk in 1st-degree relatives of those with saccular aneurysms, PCKD & congenital
connective tissue defects such as Ehlers–Danlos syndrome
10% of SAH cases are non-aneurysmal haemorrhages (so-called peri-mesencephalic haemorrhages)
5% of SAH cases are due to AV malformations and vertebral artery dissection
Clinical features
There may be loss of consciousness at the onset, so suspect SAH if a patient is found comatose
SAH typically presents with a sudden, severe, ‘thunderclap’ headache (often occipital), which
lasts for hours or even days – accompanied by vomiting, BP & neck stiffness or pain.
It commonly occurs on physical exertion, straining and sexual excitement.
O/E: patient is usually distressed and irritable, with photophobia.
may reveal a subhyaloid haemorrhage (it represents blood tracking along the subarachnoid space
around the optic nerve).
, such as hemiparesis or aphasia, may be present at onset if there is an
associated intracerebral haematoma.
may be present due to local pressure from an aneurysm of the posterior
communicating artery, but this is rare.
Investigations – CT brain scanning and lumbar puncture are required.
A negative CT result does not exclude SAH, since small amounts of blood in the subarachnoid space cannot be
detected by CT.
Lumbar puncture after 12 hours of onset – detect xanthochromia.
A +ve CT or +ve LP  cerebral angiography – to determine the optimal approach to prevent
recurrent bleeding
Management
(30–60 mg IV for 5–14 days, followed by 360 mg orally for a further 7 days) – to
prevent delayed ischaemia in the acute phase.
Insertion of platinum coils into an aneurysm (via an endovascular procedure) or surgical clipping of
the aneurysm neck – to  risk of both early and late recurrence.
AV malformations can be managed either by surgical removal, by ligation of the blood vessels that
feed or drain the lesion, or by injection of material to occlude the fistula or draining veins.
Complications of SAH:
Obstructive hydrocephalus (that may require drainage via a shunt)
Delayed cerebral ischaemia due to vasospasm (which may be treated with vasodilators),
Hyponatraemia (best managed by fluid restriction)
Systemic complications associated with immobility, such as chest infection & DVT.
 Intracerebral Haemorrhage
:
Occurs due to rupture of a blood vessel within the brain
parenchyma
It can also occur in a patient with SAH if the artery
ruptures into the brain substance as well as the
subarachnoid space.
Risk factors:
Hemorrhage into the brain parenchyma  immediate
cessation of function in that area  haemorrhage may
expand over the first minutes or hours + cerebral
oedema progression of the neurological deficit  If big enough, there can be shift of the
intracranial contents,  transtentorial coning & sometimes rapid death.
If the patient survives, the haematoma is gradually absorbed, leaving a haemosiderin-lined slit
in the brain parenchyma.
– hyperdense collection of blood, often with surrounding hypodense edema n the
Brain.
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9. Migraine – etiology, C/F & Mx [15, 12, 09]
a. Four triggering factors of migraine [22]
b. Classic Migraine [21]
c. Mention four recent drugs used in migraine [14]
d. Treatment of Migraine [11]
e. Drug treatment of Migraine [05]
Ans.
Migraine is a familial disorder characterised by recurrent attacks of headache widely variable in
intensity, frequency & duration. Attacks are commonly U/L & are usually a/w anorexia, N & V.
:
▪ Pulsatile dilatation of certain large cranial vessels is the immediate cause of pain
▪ Second to tension-type as most common cause of headache
▪ Women > Men.
▪ Initial attack may occur at any age & Family history often positive.
▪ Migraine has a strong genetic component.
▪ Triggering factors of migraine attacks: glare, bright lights, sounds, hunger, stress, physical
exertion, hormonal fluctuations, lack of sleep, alcohol, or other chemical stimulation. Women
have sensitivity to attacks during menstrual cycle
:
 Classical Migraine triad: Premonitory visual (scotoma or scintillations), sensory, or motor
symptoms; U/L throbbing headache; N & V.
 Most pts do not have visual aura or other premonitory symptoms and are therefore referred to as
having “common migraine.”
 Photo- and phonophobia common. Vertigo may occur.
 An attack lasting 4–72 h is typical, as is relief after sleep.

- 3 approaches to migraine treatment:

 Non-pharmacologic – Ex: Avoid pt-specific triggers;
 Drug therapy:
 Prophylaxis –
 Tricyclic antidepressants are a good first choice for
young people with difficulty falling asleep;
 Verapamil is a first choice for prophylaxis in the elderly.

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10. Asterixis [15]
Ans.
Asterixis refers to a brief, arrhythmic interruptions of sustained voluntary muscle contraction,
usually observed as a brief lapse of posture of wrists in dorsiflexion with arms outstretched;
Aka “negative myoclonus” or “liver flap”
: seen in any
encephalopathy related to drug
intoxication, organ system failure,
or CNS infection.
: It occurs due to
abnormal function of diencephalic
motor centers that regulate the
agonist and antagonist tones.
:
 Extend the arms  dorsiflex the
wrists, and spread the fingers 
observe for the “flap” at the
wrist.
 To test asterixis at Hip Joint: keep the patient in a supine position with knees bent and feet flat on the table,
leaving the legs to fall to the sides  Negative myoclonus of the lower limbs at the hip joints repetitively occurs
and is appreciated by looking at the knees.
: correct the underlying disorder.
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11. Mention the differences in findings between UMN & LMN lesion [11]
a. Lower motor neuron lesion [12]

Ans.
 Lower motor neuron lesion
Lower motor neuron lesion is a lesion which affects nerve fibers traveling from the anterior horn of
the spinal cord to the relevant muscle(s).
The LMNs directly innervate skeletal muscle and have cell bodies in the anterior horn of the spinal
cord (ventral horn) and at cranial nerve nuclei.
LMNs receive information from UMNs & relay that information from the spinal cord to their target.
Poliomyelitis & spinal muscular atrophy are 2 classic examples of isolated LMN disease
Causes of LMN:
They can be hereditary, sporadic or immune-mediated.
MCCs – trauma to peripheral nerves that serve the axons & and Viruses that selectively attack
ventral horn cells {Ex: Polio}.
Hereditary causes – Ex: Spinal muscular atrophies (SMAs); ALS.
Sporadic causes – Ex: Clostridium botulinum, Cauda equina syndrome; Bell’s palsy
Immune-mediated neuropathies – Ex: Guillain–Barré syndrome
Clinical Features of LMN lesion:
Disuse atrophy of the muscle {shrinkage of muscle fiber finally replaced by fibrous tissue}
Flaccid paralysis (spastic paralysis in UMN).
Muscle paresis, fasciculations, hypotonia/atonia, hyporeflexia/areflexia.
Negative Babinski sign
Segmentation of symptoms – only muscles innervated by the damaged nerves will be
symptomatic.
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12. Write the technique of doing lumbar puncture. Write the normal & abnormal CSF finding [09, 06]
a. Xanthochromia in CSF [07]
Ans.
Lumbar puncture
Lumbar puncture (LP) is the technique used to obtain both a CSF sample and an indirect measure
of intracranial pressure
:
To investigate infections (meningitis or encephalitis), subarachnoid haemorrhage and
inflammatory conditions (multiple sclerosis, sarcoidosis and cerebral lupus).
In idiopathic intracranial hypertension the LP itself is therapeutic
:
ICP;
If there is a risk of local haemorrhage (thrombocytopenia, DIC or anticoagulant treatment) &
In patients with local site infection
:
After local anaesthetic injection, a needle is inserted between lumbar spinous processes (usually
between L3 & L4) through the dura and into the spinal canal.
ICP can be deduced (if patients are lying on their side) via connecting to manometer and CSF
removed for analysis.
After LP, postural headache is common (due to  CSF pressure) – this can be  by using smaller
or atraumatic needles
 Xanthochromia
The presence of bilirubin resulting in yellow discoloration of the CSF is known as xanthochromia.
The process of conversion from heme to bilirubin in the CSF takes 6 to 12 hours and can only
happen in vivo by the enzyme oxygenase. Therefore, xanthochromia is best identified 6 to 12 hours
after the onset of a bleed
:
Sub-arachnoid haemorrhage {MC}
Other causes: acute intracerebral hemorrhage, brain tumors, infection, protein & severe
systemic jaundice.
The reliable way to test for xanthochromia is the use of spectrophotometry
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13. How do you clinically localize the anatomical level of lesion in spinal cord diseases? What are the
C/F of intramedullary lesion at C4, C5 & C6 (cervical level 4,5,6)? [07]
Ans.

Atrophy of sternomastoid muscle

Downbeat nystagmus
C2 sensory loss and cerebellar signs
Horner’s syndrome
Lower cranial nerve palsy
Hemiplegia Cruciata – The paresis or paralysis of ipsilateral lower limb and contralateral
upper limb (due to arm fibres crossing before the leg fibres at the lower part of the
medulla)
▪ Suboccipital pain or sensory loss;
▪ Descending tract of V nerve (pain and temperature loss over the face)
▪ Exaggerated trapezius reflex.
Loss of trapezius reflex.
Complete paralysis below the neck; Impaired breathing
Inverted biceps jerk
Inverted brachioradialis jerk (supinator jerk)
Sensory loss over deltoid.
▪ Loss or diminished biceps and supinator reflexes
▪ Exaggerated finger flexor reflex
Paresis of muscles of the wrist and fingers
Preservation of biceps and supinator reflexes
Exaggerated finger flexor reflexes
Inverted triceps reflex.
  Weakness and wasting of the small muscles of the hand
 UMN signs in the lower limb
 Horner’s syndrome
▪ Girdle pain or paraesthesia
▪ Segmental LMN involvement (very difficult to make out clinically)
▪ Autonomic nervous system dysfunction
Sensory impairment in axilla
Sensory impairment below the level of nipple
The abdominal reflex is impaired or lost (in all quadrants).
Positive Beevor’s sign (intact upper abdominal reflexes and absent lower abdominal
reflexes with pull of umbilicus more than 3 cm on raising the head).
Abdominal reflex preserved
Sensory loss in the lower limbs starts from the level of groin.
Brisk ankle and knee jerks
Absence of cremasteric reflex.

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14. Peripheral neuropathy – etiology, C/F & inv. [05]
a. Two causes of Peripheral Neuropathy [21]
Ans.
Peripheral neuropathy is a general term and refers to any
disorder affecting peripheral nervous system.
Clinical Features
Motor nerve involvement produces features of a LMN lesion
Symptoms and signs of sensory nerve involvement depend
on the type of sensory nerve involved – small-fibre
neuropathies are often painful.
Autonomic involvement may cause postural hypotension,
disturbance of sweating, cardiac rhythm and
gastrointestinal, bladder and sexual functions;
Treatment
Identify & correct the underlying cause—proper control of
diabetes, reducing exposures to toxins, withdrawing the
causative drug, etc.
Treatment of symptoms –
Gabapentin, tricyclic antidepressants & carbamazepine can be used to control neuropathic
symptoms such as pricking pain and burning sensation
 Physiotherapy, use of ankle-foot orthoses, splints, and walking assistance devices can
significantly improve lifestyle in the face of significant disability
Prevention of complications— Ex: Proper foot and nail care to prevent ulcer formation.
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15. Acute onset paraplegia – etiology, Dx & Mx [04]
Ans.
Acute paraplegia (weakness or paralysis in the legs) is a particular emergency because acute
compressive lesions of the cord are reversible
Onset is within minutes to hours
Causes Of Acute Paraplegia – Trauma; Transverse myelitis; Anterior spinal artery syndrome
Diagnosis – History of trauma; Electrophysiology, LP; Radiological examinations with x-ray, CT, MRI
Management:
In traumatic paraplegia – Glucocorticoids to edema (dexamethasone, methylprednisolone)
Early surgery, either decompression by laminectomy or vertebral body resection, should be
considered.
Time is of the essence in treatment; fixed motor deficits (paraplegia or quadriplegia) once
established for >12 h do not usually improve, and beyond 48 h the prognosis for substantial motor
recovery is poor.
In transverse myelitis – treatment is with high-dose i.v. methylprednisolone.
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16. Cerebellar ataxia [04]
Ans.
Cerebellar ataxia is a syndrome of incoordination involving gait, limbs and speech which results
from disorder of cerebellum or its connections.

:
▪ Brain MRI or CT scan is the initial test of choice
▪ For symmetric ataxias – Toxicology screens; vitamin B1, B12, and E levels; thyroid function
tests; antibody tests for syphilis and Lyme infection; antigliadin and anti-GAD antibodies;
paraneoplastic antibodies; and CSF studies
▪ Genetic testing – to r/o inherited ataxias
: Treat the cause –
Glucocorticoids for Parainfectious ataxia
Ataxia with antigliadin antibodies and gluten enteropathy may improve with a gluten-free diet.
 Vitamins B1, B12, and E supplements to pts with deficient levels.
Avoid phenytoin and alcohol in pts with ataxia of any cause.
Cerebellar hemorrhage may require emergent surgical treatment to prevent fatal brainstem compression.
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1) Myasthenia gravis (incl. Dx & Tt) [22, 20, 18, 16, 13]
Ans.
Myasthenia gravis is an immunologically mediated disorder affecting neuromuscular transmission
Etiopathogenesis:
It is an autoimmune disorder  Autoantibodies directed against acetylcholine receptors (AChRs)
at NMJs  blockage of neuromuscular transmission and complement-mediated inflammatory
response.
Can be a/w a thymoma.
Clinical Features: It is characterized by fluctuating muscle weakness worsened by repetitive use &
improved by resting
Characteristic distribution:
 Cranial muscles (eyelids, extraocular muscles, facial weakness, “nasal” or slurred speech, dysphagia);
 Limb muscles (often proximal and asymmetric) become involved.
Myasthenic crisis is defined as an exacerbation of weakness, usually with respiratory failure,
sufficient to endanger life
Reflexes and sensation normal.
Complications: Aspiration pneumonia (weak bulbar muscles), respiratory failure (weak chest wall
muscles), exacerbation of myasthenia with NMJ blockers (quinolones, macrolides, aminoglycosides, procainamide,
propranolol, nondepolarizing muscle relaxants).
Diagnosis:
▪ AChR antibodies—positive antibodies are diagnostic.
▪ Tensilon (edrophonium) test: The edrophonium 2 mg is given initially IV and further 8 mg given a
minute later  improvement of the muscle power within 30 seconds & persists for 2 or 3 minutes.
▪ EMG—repetitive stimulation produces rapid decrement in amplitude of evoked motor responses.
▪ Chest CT/MRI—search for thymoma.
▪ Consider thyroid and other studies (e.g., ANA) for associated autoimmune disease.
▪ Ice test: Ptosis improves by more than 2 mm when ice is applied to the (shut) affected eye lid for
more than 2 minutes.
Treatment –
To maximise activity of Ach at remaining receptors in the NMJ – Give anticholinesterase drug –
pyridostigmine, initial dose of 30–60 mg 3–4 times daily.
Atropine/diphenoxylate or loperamide to block muscarinic side-effects like diarrhoea & colic.
To immunological attack:
 Plasmapheresis or IV immune globulin (IVIg; 400 mg/kg per day for 5 days)
 Glucocorticoids - begin prednisone at low dose (15–25 mg/d), increase by 5 mg/d every 2–3 days until marked clinical improvement or
dose of 50–60 mg/d is reached
 Other immunosuppressive drugs – mycophenolate mofetil, azathioprine, cyclosporine,
tacrolimus, cyclophosphamide etc.
Thymectomy
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2) Bell's palsy [21, 12, 10, 09]
Ans.
▪ Bell's palsy is defined as idiopathic, peripheral facial paralysis or paresis of acute onset
▪ It is the MC type of facial paralysis
Aetiology
1. Viral Infection – herpes simplex, herpes zoster or the EBV.
2. Vascular Ischaemia of the nerve – induced by cold or emotional stress.
3. Hereditary – The canal is narrow because of hereditary predisposition and this makes the nerve
susceptible to early compression with the slightest oedema. 10% cases of Bell palsy have a positive
family history.
4. Autoimmune Disorders
5. Risk of Bell palsy is more in diabetics (angiopathy) and pregnant women (retention of fluid).
Clinical Features – Onset is sudden; Paralysis may be complete or incomplete
Patient is unable to close his eye.
On attempting to close the eye, eyeball turns up and out (Bell phenomenon).
Saliva dribbles from the angle of mouth.
Face becomes asymmetrical.
Tears flow down from the eye (epiphora).
Pain in the ear may precede or accompany the nerve paralysis.
Noise intolerance (stapedial paralysis) or loss of taste (involvement of
chorda tympani)
Diagnosis is always by exclusion.
All other known causes of peripheral facial paralysis should be excluded by careful history,
complete otological and head and neck examination, X-ray studies, blood tests etc.
Nerve excitability tests are done and compared with the normal side to monitor nerve
degeneration.
Localizing the site of lesion
helps in establishing the Medical management Surgery
aetiology Steroids: Prednisolone is the drug of choice.
Treatment: » If patient reports within 1 week, the adult dose Nerve
of prednisolone is 1 mg/kg/day divided into decompression
General measures:
morning and evening doses for 5 days. Patient is relieves pressure
1. Reassurance. seen on the fifth day. on the nerve fibres
2. Analgesics –relieve ear pain. » If paralysis is incomplete or is recovering, dose is and thus improves
3. Care of the eye to protect tapered during the next 5 days. the
against exposure keratitis. » If paralysis remains complete, the same dose is microcirculation of
continued for another 10 days and thereafter the nerve
4. Physiotherapy of the facial
tapered in next 5 days (total of 20 days).
muscles
Prognosis: 85 to 90 % of the patients recover fully. 10 to 15 % recover incompletely.
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3) Encephalitis [20]
a. Viral encephalitis [12]
Ans.
Encephalitis refers to an acute, usually diffuse, inflammatory process affecting the brain.
Encephalitis can be viral {MC}, bacterial, fungal, protozoal, or helminthic in etiology.
Viral Encephalitis – An infection of the brain parenchyma commonly associated with meningitis
(“meningoencephalitis”).
– MCC – herpesviruses (HSV, VZV, EBV).
In herpes simplex encephalitis, the temporal lobes are usually primarily affected, whereas CMV can
involve the areas adjacent to the ventricles (ventriculitis).
Arboviruses {Ex: Japanese encephalitis virus} – cause Epidemics of encephalitis
Other viruses – Rabies, measles, poliovirus, Influenza A virus etc.
– Viruses invade the host at a site outside the CNS and replicate.
Most viruses reach the CNS via blood.
But, HSV, rabies, and herpes zoster virus travel to the CNS directly from nerve endings in a
retrograde manner.
Once in the brain, the virus and the host’s inflammatory response disrupt neural cell function.

Viral encephalitis presents with acute onset of headache, fever, focal neurological signs (aphasia
and/or hemiplegia, visual field defects) and seizures.
Disturbance of consciousness ranging from drowsiness to deep coma
: Neuroimaging {CT scan & MRI} and lumbar puncture (LP)
The CSF will show: Normal glucose; Moderately elevated proteins & Moderate lymphocytosis
Serology for arboviruses and HIV testing
Brain biopsy, body fluid specimen cultures and PCR – to know the cause.
:
For HSV encephalitis  IV acyclovir (10 mg/kg every 8 h) for 2-3 weeks
CMV encephalitis can be treated with ganciclovir, foscarnet, cidofovir etc.
No therapy currently available for enteroviral, mumps, or measles encephalitis.
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4) Complex partial seizure [17, 07]
Ans.
: Focal seizure with impairment of consciousness or awareness is termed as CPS.
Awareness may become impaired if spread occurs to the temporal lobes.
:
 Patients stop and stare blankly, often blinking repetitively, making smacking movements of
their lips or displaying other automatisms, such as picking at their clothes.
 After sometime consciousness returns
: The age of onset, preceding aura, longer duration and post-ictal symptoms usually make
these easy to differentiate from childhood absence seizures
(Refer 3rd LQ of epilepsy for treatment)
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5) Guillain Bare Syndrome [15, 03]
a. CSF in GB syndrome [21]
Ans.
GBS is an acute monophasic illness causing a rapidly progressive polyneuropathy with weakness or
paralysis.
:
 An autoimmune response triggered by the preceding infection (respiratory or GIT) causes
demyelination
 GBS is an ascending motor > sensory polyneuropathy accompanied by areflexia, motor paralysis,
and elevated CSF total protein without pleocytosis
 Many GBS variants – Ex: Miller Fisher syndrome, which involves anti-GQ1b antibodies.
:
Distal paraesthesia and pain
muscle weakness that ascends rapidly from lower to upper limbs
Facial, bulbar & respiratory weakness
Rapid deterioration to respiratory failure can develop within hours.
Examination shows diffuse weakness with loss of reflexes.
Miller Fisher syndrome presents with internal and external ophthalmoplegia, ataxia and areflexia.

• LP - CSF protein
• Electrophysiological changes – reveal conduction block and multifocal motor slowing
• Antibodies to the ganglioside GM1
• Other causes of an acute neuromuscular paralysis should be excluded (e.g., poliomyelitis, botulism,
diphtheria, spinal cord syndromes or myasthenia), via the history and examination rather than investigations .

 Plasma exchange; IVIG therapy

 Supportive measures to prevent pressure sores and DVT.
 Regular monitoring of respiratory function (vital capacity) is needed in the acute phase
 Adverse prognostic features: older age, rapid deterioration to ventilation and evidence of axonal
loss on EMG.
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6) Jacksonian Epilepsy [13]
Ans.
A Jacksonian seizure is a type of focal partial seizure, also known as a simple partial seizure.
The person maintains awareness during the seizure. {awareness is not maintained in complex partial seizures}
Jacksonian seizures are also known as a Jacksonian march. This is because the tingling or twitching begins in a
small area and then "marches" or spreads to a larger area of the body .
: Multiple sclerosis (MS); Age > 65, brain injury, AV malformation etc.
: Jacksonian seizures only affect one side of the body.
 The seizure usually begins with a tingling or twitching sensation in a small area such as: Finger,
Toe, Corner of the mouth.
 The sensation then spreads to a larger area of the body.
 Other symptoms include: Licking lips, Rhythmic hand movements, Eye movement etc.
: Electroencephalogram (EEG); MRI & CT

Surgery for brain lesions

Anti-seizure medications – Valproate; Topiramate
Vitamin B6
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7) Progressive bulbar palsy [13]
Ans.
It comprises 20–30% of ALS, and may have initial bulbar symptoms (unilaterally or bilaterally).
Clinical Features
a) Orbicularis oris muscle is the 1st muscle to be affected.
b) Other muscles affected are muscles of the jaw, other facial muscles, tongue, pharyngeal and
laryngeal muscles.
c) Wasting & fibrillations of tongue, dysarthria and dysphagia and loss of palatal and gag reflexes are
seen.
d) Pyramidal signs may be present
e) Patient dies within 6 months to 21/2 years due to respiratory infections, general weakness and
debility.
{refer MND 6th LQ}
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8) Duchenne muscular dystrophy [11, 08]
Ans.
Definition: Duchenne-type muscular dystrophy is an X-linked recessive disorder resulting from
mutations of dystrophin gene located at Xp21.
Disease mechanism
 DMD encodes dystrophin, a major structural component of muscle
 Dystrophin links the internal cytoskeleton to the extracellular matrix
DMD variants
Becker muscular dystrophy, although a separate disease, is also caused by mutations in the
dystrophin gene
In DMD, there is no dystrophin protein, whereas in Becker muscular dystrophy there is in the
amount or alteration in the size of the dystrophin protein
Clinical presentation
Delayed motor milestones; Speech delay
Muscles affected are proximal and limb girdle
Ambulation is usually lost between the ages of 7 and 13 years
Grossly elevated creatine kinase (CK) levels (in the thousands)
Lifespan is reduced with a mean age of death, usually from respiratory failure, in the mid-twenties
Cardiomyopathy affects almost all boys with DMD and some female carriers.
Management
Genetic counselling is important
There is no specific therapy but physiotherapy and occupational therapy help patients cope with
their disability.
Glucocorticoids – can be tried
Ataluren – to ‘override’ the stop signs in Duchenne, theoretically leading to normalisation of
muscle proteins.
Treatment of associated cardiac failure or arrhythmia – with pacemaker insertion if necessary
Management of respiratory complications (including nocturnal hypoventilation) can improve
quality of life.
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9) "Fall" in the elderly [10, 06]
a. Prevention of Falls in elderly [16]
Ans.
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10) Pseudotumor cerebri [10]
Ans.
Pseudotumor cerebri {aka Idiopathic Intracranial HTN} refers to an ICP in the absence of a tumour
or other diseases.
: It is mostly due to a defect of CSF reabsorption by the arachnoid villi. It can be a/w:
obesity in females & use of drugs like tetracycline, vitamin A & retinoid derivatives.
:
Headache, sometimes accompanied by diplopia and visual disturbance
O/E: papilloedema can be seen.
It is important to record visual fields accurately for future monitoring.
:
 Brain imaging – to exclude a structural or other cause (e.g. cerebral venous sinus thrombosis).
 The ventricles are typically normal in size or small (‘slit’ ventricles).
 The diagnosis can be confirmed by LP, which shows raised normal CSF constituents at increased
pressure (usually > 30 cm H2O CSF).
:
General measures – Weight loss in overweight patients may be helpful if it can be achieved.
Acetazolamide or topiramate – to ICP, the latter perhaps aid weight loss in some patients.
Repeated LP is an effective treatment for headache but may be technically difficult in obese
Patients failing to respond, in whom chronic papilloedema threatens vision, may require optic
nerve sheath fenestration or a lumbo-peritoneal shunt.
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11) Older antiepileptic drugs [10]
a. Benzodiazepines [03]
Ans.
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12) Sensory deficit in syringomyelia [09]
Ans.
Syringomyelia is a neurologic condition caused by the presence of a fluid-
filled cavity within the spinal cord parenchyma or central canal.
This expanding CSF filled "syrinx" compresses the spinothalamic tract
neurons decussating in the anterior white commissure.
The posterior columns are spared as they are located distally.
:
Gradual onset over months or years
Loss of pain and temperature sensation with preserved touch and
vibratory sense (segmental dissociated sensory loss).
There is no sensory loss in segments above and below the lesion; this is described as ‘suspended’
sensory loss – ONLY spinothalamic sensory loss at level of lesion
The upper limbs are preferentially involved in a "cape-like" distribution (sensory loss
predominantly in the shoulder area).
LMN features at level of lesion; UMN features below it
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13) CNS manifestations of tuberculosis [08]
Ans.
The most common presentation of CNS-TB is meningitis, followed by tuberculoma, tuberculous
brain abscess, and Pott's disease.
CNS manifestations of tuberculoma or
tuberculous brain abscess depend largely on
their location.
:
 Patients often present with signs of ICP –
Ex: headache, seizures, papilledema, etc.
 Low grade fever is typically present
 Cranial nerve palsies
  O/E: evidence of meningismus + cranial nerve palsies and other focal deficits.
Hydrocephalus, infarct, ventriculitis etc.
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14) Spino-cerebellar degeneration [07]
Ans.
Spinocerebellar ataxia (SCA) is a progressive neurodegenerative inherited (autosomal dominant)
heterogeneous disease that mainly affects the cerebellum.
Clinical Presentation:
• Involuntary eye movements & Poor hand-eye coordination.
• Problems with balance and coordination.
• Slurred speech; Trouble processing and remembering information (learning disabilities).
• Uncoordinated walking.
Management:
Assistive devices to help people get around, such as crutches or a cane, walker or wheelchair.
Physical therapy to strengthen muscles and improve gait and balance.
Medications to reduce shakiness, stiffness and muscle spasms.
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15) Froin’s syndrome [05]
Ans.
Froin’s syndrome was first described by Georges Froin in 1910 upon performing a lumbar puncture
on a patient with a known spinal cord tumor.
Triad of of elevated protein, xanthochromia, and hypercoagulation of CSF
There is blockage of CSF flow by a spinal cord mass or with meningeal irritation from meningitis.

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16) Lacunar infarct [05]
Ans.
Lacunar infarcts are small deep infarcts secondary to disease of the small perforating vessels
(lenticulostriate arteries) within the brain substance.
Risk factor: Age and hypertension micro-atheroma, lipohyalinosis and dissection of the vessel.
Clinical Features – depending on the site of infarct, it can be – Pure Motor Stroke, Pure sensory
Stroke or both Sensory and Motor Stroke. Examples of infarct locations:
 Thalamus – Pure sensory stroke
 Posterior limb of internal capsule – Pure motor stroke
Diagnosis – CT (for supratentorial lesions) or MRI for both (supra and infratentorial lesions)
 Treatment
Control of hypertension only when the patient stabilizes. Immediate reduction in BP worsens the
condition and hence gradual reduction of BP is advised
Aspirin in a dose of 60 to 150 mg per day
Physiotherapy
Dipyridamole 200 mg bid.
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17) Febrile convulsions [04]
Ans. Febrile seizures are seizures that are caused by a sudden spike in body temperature.
– mostly viral infections – Ex: HHV-6, influenza A virus etc.
: simple febrile seizures or complex febrile seizures.
Simple febrile seizures, lasts less than 15 minutes, and does not recur within 24 hours.
Complex febrile seizures lasts longer than 15 minutes, and recurrence within a 24-hour period.
: Todd's paralysis.
: identify & treat the infection
 Antipyretics & benzodiazepines
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18) Neonatal Seizures [04]
a. Convulsions in young children [03]
Ans.
The neonatal period is defined as the first 28 days of life of a full-term infant.
Neonatal seizures are those that occur from birth to the end of the neonatal period.
Etiology of neonatal convulsions:
– Intrauterine infections, Bacterial meningitis, tuberculous meningitis,
aseptic meningitis, cerebral malaria, tetanus, Reye’s syndrome.
- Dyselectrolytemia (hypocalcemia, hypomagnesemia).
- Neoplasm, brain abscess, tuberculoma, cysticercosis.
- AV malformations, intracranial thrombosis, and hemorrhage.
, sequelae of birth trauma, birth asphyxia, grey matter degeneration,
storage disorders.
- Phenothiazines, salicylate, phenytoin, carbon monoxide, lead.
Five main types of neonatal seizure.
• Subtle seizures (50%)
• Tonic seizures (5%)
• Clonic seizures (25%)
• Myoclonic seizures (20%)
• Non-paroxysmal repetitive behaviours
Management
 Identify & treat the cause of the seizures.
 Phenobarbitone, phenytoin, short-acting benzodiazepines are the most commonly used AEDs.
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19) Multiple Sclerosis – C/F & common presentation [03]
Ans.
Multiple sclerosis is an autoimmune disorder characterized by multiple demyelinating lesions in the
brain and spinal cord; peripheral nervous system is spared.
 Pathologically, the multifocal scarred lesions of MS are termed plaques.
– recurrent attacks of focal neurologic dysfunction, typically lasting weeks or
months, and followed
by variable recovery.
:
Oligoclonal bands + few
lymphocytes in CSF
:
Counselling – about the
nature of disease
For acute attack –
Mostly corticosteroids;
Plasmapheresis & IVIG
To prevent relapses –
Recombinant beta
interferon; Glatiramer acetate (inhibit immune reactions to myelin); Immunosuppressive drugs
(MTX, cyclophosphamide, azathioprine etc.); natalizumab
Symptomatic Therapy – Ex: Spasticity-physiotherapy; Impotence—sildenafil etc.
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20) Wernicke's encephalopathy [02]
Ans.
Wernicke’s Encephalopathy is a common, acute neurologic disorder caused by thiamine deficiency
: Chronic alcoholics; undernutrition (e.g., recurrent dialysis, hyperemesis, starvation,
gastric plication, cancer, AIDS).
: triad of encephalopathy, ocular dysfunction, and ataxia.

Thiamine 100 mg IV or IM, continued daily for at least 3 to 5 days.

Mg sulfate 1 to 2 g IM or IV q 6 to 8 h {since Mg is cofactor in thiamine-dependent enzymes}
Supportive treatment – hydration, correction of electrolyte imbalances & nutritional therapy,
including multivitamins
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21) Absence attacks [02]
Ans.
Absence seizures are brief seizures characterized by sudden discontinuation of the activity being
performed with starring spell, eye fluttering or rhythmic movements.
Etiology: Childhood absence epilepsy (CAE), Juvenile absence epilepsy (JAE), and juvenile
myoclonic epilepsy (JME); Lennox-Gastaut syndrome.
More common in Girls
EEG is the main diagnostic tool – it shows characteristic 3 Hz spike and slow wave discharge
Drug of choice – Valproate (previously Ethosuximide)
Older terms for absence Seizures:
 Pyknolepsy – {pyknos, in Greek means “very frequent”}
 Petit mal seizure
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22) Acute confusional state [01]
a. Give two causes of Delirium [19]
Ans.
Delirium describes cortical dysfunction and replaces the older term
‘acute confusional state’.
Delirium is a syndrome of transient, reversible cognitive dysfunction
that is more common in old age.
Unlike dementia, it is of sudden onset, is characterized by fluctuating
consciousness & inattention.
It is generally manifested in the hours before death. Early recognition
is key because the pt should be encouraged to use the periods of lucidity for final communication
with loved ones.
: Hypoactive, Hyperactive & Mixed
▪ Patients with hyperactive delirium are often agitated and restless,
▪ Hypoactive delirium can present as lethargy and sedation, and
can be frequently misdiagnosed as depression or dementia
: Medications: 👉🏻
 Stop any and all unnecessary medications that may have this side
effect;
 Provide a calendar, clock, newspaper, or other orienting signals;
 Gently correct hallucinations or cognitive mistakes;
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23) Entrapment neuropathies [01]
Ans.
Entrapment neuropathies
refers to compression of
a nerve by hypertrophied
synovium or by joint
subluxation and are the
usual cause of a
mononeuropathy.
: Diabetes,
excess alcohol or toxins,
or genetic syndromes.
– remove the primary cause, either by avoiding the precipitation of activity or by
surgical decompression.
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24) Hydrocephalus [01]
Ans.
 Hydrocephalus is the excessive accumulation of CSF within the brain, and may be caused either by
CSF production, by CSF absorption, or by obstruction of the
circulation.
:
: They range from none to sudden death,
depending on the speed at which and degree to which
hydrocephalus develops.
 Communicating Hydrocephalus – it refers to blockage outside
the ventricular system
 Non-communicating Hydrocephalus – it refers to blockage
within the ventricular system
 Normal pressure hydrocephalus {NPH} – it refers to
intermittent rises in CSF pressure, particularly at night. It is
described in old age as being associated with a triad of Gait
Apraxia, Dementia & Urinary Incontinence.

▪ For obstructive hydrocephalus – Place a shunt to divert the CSF

from the ventricular system to the peritoneal cavity or right
atrium
▪ Lumbar puncture for NPH cases
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25) Electroencephalography [2000]
Ans. The electroencephalogram (EEG) detects electrical activity arising in the cerebral cortex via
electrodes placed on the scalp to record the amplitude and frequency of the resulting waveforms.
Waveforms of EEG:
 With closed eyes, the normal background activity is 8–13 Hz (known as alpha rhythm), most
prominent occipitally and suppressed on eye opening.
 Other frequency bands seen over different parts of the brain in different circumstances are beta
(> 13 Hz), theta (4–8 Hz) and delta (< 4Hz).
Normal EEG patterns evolve with age and alertness – Ex: Lower frequencies predominate in the
very young and during sleep.
Abnormal EEGs patterns – Example:  in fast frequencies (beta) seen with sedating drugs such as
benzodiazepines
EEG in epilepsy is predominantly used for classification and prognostication.
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1. Features of raised intra cranial tension [22]

a. Raised intracranial Tension (ICT) [13]
Ans. In adults, normal intracranial pressure is less than 10–15 mmHg.
Treatment initiated when ICP> 20mmHg
Clinical features:
Headache worse on lying/straining Bradycardia
Vomiting blood pressure
th
Diplopia (6 nerve involvement) Impaired conscious level
Papilloedema
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2. Causes (etiology) of Dementia [21, 17, 15, 12, 09]
Ans.
Dementia is an acquired deterioration in cognitive ability that impairs the successful performance of
activities of daily living. Memory is the most common cognitive ability lost with dementia

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3. Atypical Neuroleptics [20, 18]
Ans.
Atypical antipsychotics {Neuroleptics} or 2nd-generation antipsychotics have become the drugs of
choice for acute psychoses they have fewer side effects regarding extrapyramidal symptoms.
Examples are: Clozapine, Olanzapine, Risperidone, Paliperidone, Iloperidone etc.
Clozapine and Olanzapine
:
Antipsychotic effect is mainly by 5-HT2 blockade. Olanzapine is a Potent anticholinergic.
They have weak D2 blocking effects – low risk of extrapyramidal symptoms, Minimal effect on
prolactin.
:
▪ Sedation, salivation, seizures, weight gain and hypotension.
▪ Precipitation of diabetes
▪ Agranulocytosis, hence regular monitoring of WBC counts is required during clozapine therapy.
▪ Cause Hyperlipidaemia → Incidence of stroke.
▪ Side effects of olanzapine: Dry mouth, constipation and weight gain.
:
Clozapine is the most effective drug in refractory schizophrenia, i.e., patients not responding to
typical neuroleptics may respond to it. It is a reserve drug for the treatment of schizophrenia
because of the risk of agranulocytosis.
Olanzapine is used for the treatment of schizophrenia and mania a/w bipolar disorder.
They suppress both +ve symptoms (thought disorder, hallucinations, delusions, etc.) and
negative symptoms (social withdrawal, lack of motivation) of schizophrenia.
Risperidone
: blocks D2, 5-HT2, α1 & H1 receptors
 for the treatment of schizophrenia & short-term treatment of mania associated with
bipolar disorder.
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4. Coma [20]
a. Nursing of a coma patient [06]
Ans. Coma is defined as a persisting state of deep
unconsciousness, this means a sustained GCS of 8 or less.
: They can be (structural or non-
structural brain disease) & (e.g., type II
respiratory failure) ones.

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5. Diagnosis of brain death [19, 16]
Ans.
Brain death is a state in which cortical and brainstem function is irreversibly lost.

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6. Name four signs of Meningeal irritation [19]
Ans.
Meningismus (stiff neck)
Brudzinski sign – involuntary flexion of the hips with neck flexion
Kernig sign – resistance with knee extension. Patient is supine, with hip & knee flexed to about 90°
Tripod sign or "Amoss's Sign" – Patient is asked to sit up in bed  patient tries to sit up by supporting himself with
his hands placed far behind him in the bed (like a tripod), in order to take the weight off the spine and prevent its flexion
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7. Transient ischaemic Attack (TIA) [17, 13]
Ans.
A transient ischaemic attack (TIA) or "mini stroke" is caused by a temporary disruption in the blood
supply to part of the brain; Symptoms last for <24 hrs.
:
Low flow TIAs: These are brief & recurrent – occurs due to atherosclerotic lesion at the internal
carotid artery (ICA) origin or intracranial portion of ICA, MCA stem, junction of vertebral and
basilar arteries.
Embolic TIAs: These are discrete & single.
Lacunar or penetrating vessel TIAs: This is due to occlusion of small vessels as a result of
lipohyalinosis in response to hypertension or atheroma
Crescendo TIAs are those occurring with frequency & a high likelihood of evolving into stroke
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8. Prion diseases [16]
Ans.
Prion refers to Proteinaceous infectious particle

Prions cause transmissible spongiform encephalopathies.

Human prion diseases are characterised by the histopathological
triad of cortical spongiform change, neuronal cell loss & gliosis.
Prion proteins are not inactivated by cooking or conventional
sterilisation, and transmission occur by consumption of infected CNS tissue or by inoculation (e.g.,
via depth EEG electrodes, corneal grafts, cadaveric dura mater grafts.
The same diseases can occur in an inherited form, due to mutations in the PrP gene.
----------------------------------------------------------------------------------------------------------------------------------------
9. Hemifacial Spasm [16]
Ans.
Hemifacial spasm refers to intermittent twitching around one eye, spreading ipsilaterally to other
facial muscles.
The spasms are exacerbated by talking, eating and stress.
: Idiopathic; similar to trigeminal neuralgia; it has been suggested that it may be due to an aberrant arterial loop irritating
the 7th nerve just outside the pons.
is not effective but injections of botulinum toxin into affected muscles – should
repeat every 3 months or so.
– In refractory cases, microvascular decompression may be considered
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10. Narcolepsy [16, 05]
Ans.
Narcolepsy refers to sudden, irresistible ‘sleep attacks’,
often in inappropriate circumstances such as while eating
or talking.
Etiology: loss of hypocretin-secreting hypothalamic
neurons.
Clinical Features: 👉🏻
Diagnosis requires sleep study with sleep latency testing
(demonstrating rapid onset of REM sleep).
 Treatment: Give stimulants such as modafinil but more severe cases may require sodium oxybate,
dexamfetamine, methylphenidate or SSRIs.
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11. Syncope [15]
Ans. Syncope refers to sudden loss of consciousness due to cerebral perfusion. ‘Presyncope’ refers to
light-headedness, in which the individual thinks he or she may ‘black out’.
Etiology:
Cardiac syncope – due to mechanical cardiac dysfunction or arrhythmia
Neurocardiogenic syncope (aka vasovagal or reflex
syncope) – here, an abnormal autonomic reflex causes
bradycardia and/or hypotension
Postural hypotension – here, physiological peripheral
vasoconstriction on standing is impaired, leading to
hypotension.
Dizziness and presyncope are common in old age
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12. Todd's Paralysis [15]
Ans.
Paresis or paralysis of muscles of affected limb lasting for several hours after prolonged episodes of
seizures is known as Todd’s palsy.
Todd’s palsy is a sign of focal origin of seizure activity.
Typically, this resolves within a few hours, but it may take up to a few days for complete resolution
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13. Mini mental examination [09]
Ans.
The Mini-Mental Status Examination (MMSE) is a useful screening test for dementia.
The goal of MMSE is to evaluate orientation, registration, attention, recall & grasp of general
information.
A score of <24 points (out of 30) indicate a need for more detailed cognitive and physical
assessment.

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14. Cluster headache [08]
Ans.
 Cluster headaches (also known as migrainous neuralgia) are one of the most painful types of
headaches. There is a significant male predominance and onset is usually in the third decade.
:
The cause is unknown but functional imaging studies have suggested abnormal hypothalamic
activity & it differs from migraine in many ways
It is the most common of the trigeminal autonomic cephalalgia syndromes.
Risk Factors: smokers & alcoholics.
:
Patients present with severe, U/L periorbital pain with autonomic features, such as ipsilateral
tearing, nasal congestion and conjunctival injection.
Cluster headache is strikingly periodic, beginning at the same time for weeks at a stretch (the
‘cluster’) followed by remission for months to years
Patients typically are awoken from sleep by symptoms (‘alarm clock headache’).
The pain, though severe, is characteristically brief (30–90 minutes).
Patients are highly agitated during the headache phase {in contrast to those with Migraine}.

For Acute attacks – subcutaneous injections of sumatriptan or inhalation of 100% oxygen.

For Patients with severe debilitating clusters – Lithium therapy
For prophylaxis – verapamil, sodium valproate, or short courses of oral glucocorticoids.
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15. Electroconvulsive therapy [08, 04]
Ans.
Electroconvulsive therapy (ECT) entails producing a convulsion by the brief administration of a
high-voltage direct-current impulse to the head while the patient is anaesthetised and paralysed by
muscle relaxant.
If properly administered, it is remarkably safe, and is of proven efficacy for severe depressive
illness.
: headaches; amnesia for events occurring a few hours before ECT (retrograde)
and after it (anterograde).
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16. Newer anti – epileptics [08]
Ans.
Drugs MOA Uses A/E
Delays the recovery of
As add on drug in refractory Dizziness, diplopia, ataxia,
Lacosamide Na+ channels from
partial seizures and cardiac arrhythmias
inactivation
Increases GABA activity Visual disturbances,
As add on drug in partial
Vigabatrin in brain by inhibiting sedation, confusion and
seizures
GABA transaminase psychosis
Can be used as monotherapy Sedation, ataxia, weight
 Delays the recovery
Topiramate in GTCS, myoclonic and loss, nervousness and
of Na+ channels from
partial (SPS and CPS) seizures confusion
inactivation
Chronic alcoholism
 GABA & glutamate
Reduces the effectiveness
activities Migraine prophylaxis
of oral contraceptives
 As monotherapy or add on
Delays the recovery of Sedation, ataxia, headache,
therapy in GTCS, absence,
Lamotrigine Na+ channels from nausea, vomiting and skin
myoclonic and partial (SPS
inactivation rashes
and CPS) seizures
Other Drugs: Gabapentin, Felbamate, Remacemide etc.
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17. Delirium Tremens [07, 06, 04]
Ans. Delirium Tremens refers to a very severe alcohol withdrawal syndrome characterized by profound
autonomic hyperactivity, extreme confusion, agitation, vivid delusions, and hallucinations (often visual
and tactile) that begins 3–5 days after the last drink.
 Mortality is 5–15%.
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18. Vanilmandelic acid [06]
Ans.
Vanillylmandelic acid (VMA) is an end-stage metabolite of the catecholamines (dopamine,
epinephrine, and norepinephrine).
Urinary VMA is elevated in patients with pheochromocytoma, a tumor of catecholamine-secreting
chromaffin cells.
It can also be used to diagnose neuroblastomas, and to monitor treatment of these conditions.
1. Treatment of Steven Johnson Syndrome [22]
Ans.
Definition: Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe
mucocutaneous reactions, usually to drugs, characterized by blistering and epithelial sloughing.
SJS is the less extensive form and TEN is the more extensive

Withdraw culprit drug

If epidermal loss is >10%  BSA transfer to a specialist unit (ICU or burns unit)
Institute supportive care package:
Heated environment Analgesia
Fluid replacement Preventing/treating infection
Nutritional regimen
Skin handling, topical therapy and dressings:
Necrolytic epidermis readily detaches from underlying dermis
Detached epidermis can be left in situ to act as a biological dressing for the underlying dermis.
Clean the intact skin each day by gentle irrigation with warmed sterile water or spray with a weak
solution of chlorhexidine (1:5000)
Frequent applications of a greasy emollient
Topical antibiotic ointment – on sloughy or crusted areas
Local therapy for care of eyes, mouth & uro‐genital tract
Regular examination & lubricant application.

In the early stages of the acute phase consider using:

(0.5–1 g/kg/day for 3–4 consecutive days)
or
-Prednisolone 0.5–1 mg/kg daily for 10 days, and tapered; or IV Methylprednisolone
500 mg on 3 consecutive days,
or
(3 or 4 mg/kg/day in divided doses for 10 days, and tapered)
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2. Psoriasis – Treatment [21, 19, 17, 10, 09, 04]
a. PUVA therapy [22, 05]
b. Factors causing flare-ups of Psoriasis [17]
c. Types of Psoriasis [13]
Ans.
Psoriasis is a chronic inflammatory,
hyperproliferative skin disease,
characterised by well-defined,
erythematous scaly plaques particularly
affecting extensor surfaces, scalp and nails,
and usually follows a relapsing and
remitting course
Etiopathogenesis: Both genetic and environmental factors are responsible
Occurs equally in both sexes;
Genetic Factors:
 50% cases are the Variants of the HLA-C region within the MHC on chromosome 6
 Other genes involved are IL-13, IL-23, Nuclear Factor kappa B (NFκB) signalling etc.
Environmental factors: (Exacerbating Factors causing flare-ups of Psoriasis) 👇🏻

Exacerbating Factors causing flare-ups of

is the key feature Psoriasis in pre-disposed individuals
It’s thought to be caused by Ex: scratches or surgical wounds (Köbner
Skin trauma
dysregulation of T-Helper cells isomorphic phenomenon)
- β-haemolytic streptococcal throat
 keratinocyte migration time, from
Infection infections  Guttate psoriasis
basal layer to shedding from stratum corneum,
- HIV
from approximately 28 to 5 days  Due to Köbnerisation at sites of sunburn
immature cells reach the stratum Sunlight
or polymorphic light eruption
corneum prematurely excessive Antimalarials, β-blockers, lithium,
accumulation of the stratum NSAIDs and TNF-α inhibitors
corneum Drugs ‘Rebound’ flare of psoriasis {Pustular
psoriasis} may occur after withdrawal
Clinical Features:
of glucocorticoids
Age of onset – bimodal distribution, Psychological
with an early-onset type in the Anxiety and stress
factors
teenage (with family h/o psoriasis) & later-onset type (without family h/o psoriasis) is typically seen between 50
and 60 years.
:
– MC presentation
The lesion is raised, well-demarcated silvery plaque of variable size the bleeds on touch.
MC sites – extensor surfaces (elbows, knees and the lower back)
Other sites: Scalp (mimic seborrheic dermatitis), Nails {‘thimble pitting’, onycholysis},
Flexures (Ex: axillary folds) & Palms (mimic eczema)
: silver/white scale is seen on scraping the
surface, which reveals bleeding points
– MC in children & adolescents. It heralds the
onset of plaque psoriasis in adulthood.
– it’s a medical emergency
– it may be generalised (medical emergency)
or localised (a/w smoking)
– seen in 5-10% cases a/w psoriatic nail disease
Investigations:
Throat swab & skin biopsy
Assess DLQI (Dermatology Life Quality Index) & PASI (Psoriasis
Area and Severity Index).
Tests for HIV & other co-morbidities
Management:
 Counselling the patient & Reassurance is paramount – since Psoriasis impact on all aspects of life
Advice on smoking cessation,  alcohol intake, adequate exercise and a normal BMI
– use topical ointments
– UVB phototherapy / PUVA ± systemic retinoid (Ex: acitretin) or Immunosuppressants
(Ex: MTX or cyclosporine)
– use fumaric acid esters, apremilast and biologics

PUVA is an acronym for Photochemotherapy with Ultraviolet radiation of the A (long-wave) type
A photosensitizing psoralen drug is given orally 2 hours before exposure to . Then, UVA is
supplied by special fluorescent lamps.
Alternatively, the patient bathes in water containing a psoralen and is then exposed to UVR a few
minutes later
Side Effects of PUVA therapy:
Nausea, Pruritus and xeroderma
Burning sensation - Patients who are ‘sensitive to the sun’ such as lupus erythematosus or
porphyria cutanea tarda, should not be treated by PUVA
 risk of squamous cell carcinoma of the skin (10-12 times more risk)
Appearance of ageing and changes in skin elasticity
Cataracts – hence wear UVA protective goggles during exposure and for 24 hours afterwards.
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3. Bullous eruption of skin [19]
a. Pemphigus [09]
Ans.

: 1.
 Miliaria crystallina Epidermolysis bullosa simplex
 Bullous impetigo Thermal injury (some)
 Staphylococcal scalded skin syndrome Erythema multiforme
 Pemphigus foliaceus and variants 2.
 IgA pemphigus ;
 Subcorneal pustular dermatosis
 Erythema toxicum neonatorum
 Transient neonatal pustular melanosis ▪ Bullous pemphigoid
 Acropustulosis of infancy ▪ Mucous membrane
: pemphigoid
Spongiotic dermatitis ▪ Herpes gestationis
Friction blister (may extend into the dermis) ▪ Dermatitis  Bullous SLE
Miliaria rubra herpetiformis  Epidermolysis
Incontinentia pigmenti ▪ Linear IgA bullous bullosa acquisita
IgA pemphigus dermatosis  Epidermolysis
Epidermolytic hyperkeratosis ▪ Porphyria cutanea bullosa
Hailey-Hailey disease tarda dystrophica
▪ Junctional
 Pemphigus vulgaris and variants epidermolysis bullosa
 Paraneoplastic pemphigus ▪ Suction blister
 Darier’s disease ▪ Thermal injury (some)
 PEMPHIGUS
Pemphigus is a group of autoimmune blistering disorders characterized by the intraepidermal split.
Pemphigus can be broadly categorized into:
1) P. vulgaris 4) Paraneoplastic pemphigus (PNP)
2) P. foliaceous 5) Drug-induced pemphigus
3) IgA pemphigus
P vulgaris
It is an autoimmune disorder against Desmoglein (Dsg).
:
Dsg1 – in upper superficial layers of skin
Dsg 3 – in mucous membranes
: Antibodies are formed against both Dsg3 &
Dsg1  Hence, both skin & mucous membranes are involved.
Because the destruction is between epithelial cells (intra-
epidermal), the blister is thin and tears easily (+ve Nikolsky’s Sign)
: Patients presents with asymptomatic vesicles, bullae, erosions or crusted plaques
on the skin, and oral erosions and ulcers.
:
▪ Skin biopsy – reveals a tombstone effect {basement membrane cells remain attached while
epithelial cells split apart from each other}.
▪ Immunofluorescence reveals antibodies on epithelial cells throughout the skin lesion.
: start with systemic steroids  switch to steroid sparing immune modulators
(mycophenolate mofetil, rituximab)
This disease is life-threatening as it involves mucosa, and occurs in people ages 30-50.
P foliaceous
Milder form – Antibodies are formed only against Dsg1
Skin lesions are most common with +ve Nikolsky’s sign
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3. Vitiligo – Treatment [18, 14]
Ans.
Vitiligo is a condition of chronic skin disease in which loss of normal melanocytes results in smooth,
white patches in the midst of normally pigmented skin.
Treatment of Vitiligo:
 Advise to use sunscreen
 Response to treatment varies between individuals
 Topical corticosteroids - E.g., 0.1% betamethasone valerate or 0.05% clobetasol
propionate once daily – with intermittent regimen (e.g. 15 days per month for 6
1st Line
months) to avoid local side effects
 Topical calcineurin inhibitors – pimecrolimus, tacrolimus – on face & neck
nd
2 line Phototherapy – Ex: PUVA & UVB therapy
Grafting techniques
In stable vitiligo (e.g., segmental vitiligo)
3rd line Principle: to transplant autologous melanocytes from a normal pigmented area
Types:
1. Tissue grafts (full‐thickness punch grafts, split‐thickness grafts, suction blister grafts)
 2. Cellular grafts (cultured melanocytes & epithelial sheet grafts and non‐
cultured epidermal cellular grafts).
Depigmenting treatment
 Indicated in extensive vitiligo with only a few residual areas of pigmentation
 Skin bleaching with
- Laser therapy (e.g., Q‐switched alexandrite 755 nm, Q‐switched ruby 694 nm) or
- Cryotherapy or
- Creams (e.g., 20% mono-benzyl-ether of hydroquinone),
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4. Scabies – Complications & Treatment [18, 14, 13, 10, 08, 05, 04]
Ans.
Scabies is a parasitic infection of skin characterised by an intense itching with typical distribution
caused by the mite Sarcoptes Scabei.
Complications
Management:

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5. Systemic Sclerosis (Scleroderma) – C/F & Mx [17]
Ans.
Definition: It is a multisystem autoimmune disease
that causes fibrosis in the skin and internal organs with
associated vascular & inflammatory manifestations.
 2 major subsets of systemic sclerosis are the limited
and diffuse.
Clinical presentation:
Typical presenting features: Raynaud phenomenon,
symptoms of gastro‐oesophageal reflux and swelling
or discomfort in the extremities.
Symptoms of Limited Scleroderma
 GIT – dysphagia & symptoms of gastro‐oesophageal reflux disease
Skin – Non-pitting edema, puffy fingers, tightness, hardening, itching & Raynaud phenomenon
Heart – cardiac myositis & interstitial fibrosis cardiomyopathy & cardiac arrhythmias
Lungs – ILD, pulmonary fibrosis, PAH
Renal – Scleroderma renal crisis
Musculoskeletal – Muscle weakness; Tendon friction rubs
Management

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6. Acne vulgaris [16, 04]
Ans.
Definition - Acne vulgaris refers to chronic, self-limiting, inflammatory disease of the pilosebaceous
unit, manifesting generally in adolescence with pleomorphic lesions like comedones, papules, pustules,
nodules, and cysts and these may lead to scarring.
Etiopathogenesis
Causative Organism:
Cutibacterium acnes
{formerly Proprionibacterium acnes}

Other factors - Diet, Stress

Clinical Types of Acne:
1) Grade I (Mild):
Comedones, occasional papules
2) Grade II (Moderate): Comedones, many papules, few pustules
3) Grade III (Severe): Predominantly pustules, nodules & abscesses also called Acne Conglobata (AC)
4) Grade IV (Cystic): Mainly cysts or abscesses, widespread scarring.
Treatment

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7. Lichen Planus [15]
Ans.
Lichen planus is an idiopathic T cell–mediated chronic inflammatory disease clinically characterised
by pruritic, pink, purple, polygonal, flat-topped papular lesions.

 Clinical
 Histopathology – reveals:
  Basal epidermal keratinocyte damage
 Epidermal changes: hyperkeratosis, hypergranulosis, and elongation of rete ridges that resemble
a sawtooth pattern.
 Dense lympho-histiocytic infiltrate at the DEJ
 Multiple apoptotic cells bodies are seen at the DEJ.
 Separation of the epidermis in small clefts (Max Joseph cleft formation)
----------------------------------------------------------------------------------------------------------------------------------------
8. Atopic Eczema [13, 04]
Ans.
Atopic dermatitis (AD) is a chronic inflammatory skin disease primarily beginning in childhood with a
variable natural course.
 Patients with AD often additionally have atopic comorbidities like allergic asthma & allergic rhinitis
 Itch is the hallmark symptom of the disease.

Scabies, Allergic contact Eczema, Seborrheic dermatitis,

dermatitis psoriasis etc.
----------------------------------------------------------------------------------------------------------------------------------------
9. Dermatomyositis – C/F [13, 01]
Ans.
Dermatomyositis is a rare inflammatory myopathy with characteristic skin manifestations & muscular
weakness.

Site: face, hands and extensor surfaces of the limbs. Typically present as:
Scalp: erythema and a diffuse non‐scarring hair loss
Eyelid erythema is characteristic and pathognomonic: upper eyelids,lilac (or
heliotrope) in colour
Facial dermatosis: Confluent erythema of the whole face, extending onto the
neck and upper chest
Shawl sign - fixed macular erythema on the upper torso, both the ‘V’ of the
chest and across the shoulders
Nail fold changes - periungual erythema, dilated capillary loops in the proximal
nail fold
Skin signs
Gottron’s papules- inflammatory, flat‐topped, lichenoid lesions that occur on
the skin overlying the distal and proximal interphalangeal joints of the fingers
and the metacarpophalangeal joint
Holster sign - erythema over the hips and lateral thighs
Vasculopathic ulcers
Flagellate erythema- multiple, red, macular streaks occurring on the trunk and
proximal limbs aligned diagonally.
Mechanic’s hands’ (or ‘machinist’s hands’) – non‐inflammatory hyperkeratosis
occurring on the hands or feet over the radial surfaces of the fingers and the
outer border of the feet.
proximal myopathy - present with problems climbing stairs, getting out of chairs
Muscle signs
and performing tasks that requiring lifting the hands above the head
Associated
Cardiac abnormalities; ILD; dysphagia; symmetrical arthritis
features
Clinically amyopathic dermatomyositis (CADM) refers to the presence of cutaneous manifestations of
DM in the absence of clinical signs of muscle involvement.
:

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10. Urticaria [07]
Ans.
Urticaria (hives) is a vascular reaction of the skin characterized by formation of erythema, raised
wheals, edema, and itching.
Pathophysiology 👉🏻
Types of urticaria 👇🏻

Investigations
: clinical history + Confirm with IgE, skin prick test, radio-allergo-sorbent tests
(RASTs) etc.
ESR; IgE; Autologous serum skin test (ASST);
Other tests include thyroid autoantibodies, CBP, C-reactive proteins, estimation of ANA,
exclusion of H. pylori infection etc.
Management
Acute Urticaria – Identify & remove
the trigger + Symptomatic Rx.
Chronic urticaria – Stepwise
management .

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11. Erysipelas [06]
Ans.
Erysipelas is a superficial bacterial skin infection that characteristically extends into cutaneous
lymphatics.
Causative organism: Group A streptococci {MC}; Staphylococcus aureus
Clinical Presentation
Common Sites: face, scalp, legs and feet are common sites.
Erysipelas lesions begin as a bright red plaque edematous, and brawny indurated plaques,
which are warm to touch.
There is bacteremia and a/w constitutional symptoms such as fever, malaise, and chills.
Management: Empiric antibiotic therapy directed against streptococcal & staphylococcal species
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12. Skin tuberculosis [05]
Ans.
Tuberculosis of the skin has a worldwide distribution.
DIAGNOSIS
 Tuberculin reaction (Koch phenomenon)
 QuantiFERON-TB gold test: measure specific antigen-driven
interferon-γ synthesis by whole blood cells and was
approved by FDA.
 Histopathology – It reveals accumulation of epithelioid
histocytes & Langhans-type giant cells with a varying amount
of caseation necrosis in the center.
TREATMENT
Anti-tubercular Drugs.
Surgical intervention in Scrofuloderma maybe needed
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13. Erythema multiforme [05]
Ans.
Erythema multiforme is a rare cutaneous or
mucocutaneous eruption characterized by “target”
lesions, predominantly on the face & extensor surfaces
It has a benign course but frequent recurrences,
possible ocular complications.
Based on the degree of mucous membrane
involvement, EM is divided into:
a) EM minus (EMm, also called EM minor) if only the
skin & lips are involved
b) EM majus (EMM, also called EM major) when
mucous membranes are affected.
Clinical features
The typical target lesion is a circular, wheal-like erythematous papule or plaque that persists for
1 week or longer
Symmetric, distribution on the extensor surfaces of the extremities (hands, feet, elbows, and
knees), face, and neck
Lesions often first appear distally and then spread in a centripetal manner.
Management – Treat the cause
 Liquid antacids, topical glucocorticoids & local anesthetics relieve symptoms of painful mouth or
genital erosions.
Eye involvement – ocular lubricant
Systemic corticosteroids – to shorten the duration of fever and eruption
Immunosuppressants – Azathioprine or Mycophenolate mofetil
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14. Isotretinoin and Acyclic retinoids [05]
Ans.
The term “Retinoids” refers to a family of chemical compounds which are derivatives of vitamin A,
or all-trans-retinol
Classification of retinoids:
Isotretinoin – it’s a systemic retinoid; FDA approved
for the treatment of Nodulocystic acne & Resistant
acne with a tendency for scarring
Acyclic retinoids {Ex: Peretinoin} – used in HCC
chemoprevention
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15. Tinea pedis [02]
Ans.
Definition: Dermatophyte infection of the soles of the feet and the
interdigital spaces is known as tinea pedis (aka athlete’s foot)
Etiopathogenesis
 Causative Organisms: T. rubrum, T. interdigitale, & E. floccosum
{T = Trichophyton; E=Epidermophyton}

 Aggravating factors are warmth, humidity, and hyperhidrosis

Clinical Features: 4 clinical variants
Interdigital type: commonest type
 Lateral (3rd & 4th) toe webs are the commonest sites
Chronic hyperkeratotic (papulosquamous, “Moccasin”) type:
▪ Patchy diffuse moccasin-like scaling over the soles
Vesicular (inflammatory, bullous) type – seen with Trichophyton interdigitale
Acute ulcerative type – ulcers on the soles often complicated
by 2° bacterial infection
“Two-feet one-hand syndrome” – bilateral tinea pedis and
unilateral tinea manuum occur simultaneously
Differential Diagnosis: Candidiasis, contact dermatitis, soft
corns, psoriasis, pityriasis rubra pilaris, Reiter’s syndrome etc.
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1. Name 4 drugs causing lupus [22]

Ans.
----------------------------------------------------------------------------------------------------------------------------------------
2. Define Macule and Papule [21]
Ans.
Macule Papule
 A macule is a circumscribed flat lesion (not palpable)
characterized by alteration in skin color, of any size or shape.
 A large macule is called a patch. A papule is an elevated solid
 Depending upon the color of the macules, they may be subclassified as: lesion of the skin, less than 1 cm
 Hypopigmented and depigmented macules in diameter
 Hyperpigmented macules
 Erythematous macules
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3. Causes of dry skin (xerosis) [21]
Ans.
Xerosis refers to generalized dryness of skin which appears as polygonal skin-colored or light brown
scales over legs and trunk
Causes of Dry Skin:
 Elderly
 Systemic causes: DM, thyroid disorders, Vit. A def., chronic renal failure, ionising radiation,
malignancy.
 Dermatological conditions – Atopic eczema, keratoderma, keratosis pilaris,
 Drugs – Retinoids, thalidomide, interferons, chemotherapy drugs
Pathogenesis: Dry skin occurs due to changes in the microcirculation, the nutrient supply of the skin &  in the production
of sweat and oil in the skin.
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4. Allergic contact Eczema [17]
Ans.
It’s a common inflammatory skin disorder which occurs due to allergen-specific T lymphocytes.
Prototype of type IV-cell mediated hypersensitivity
Patch test – GOLD standard for identification of contact allergen.
Differential Diagnosis: Atopic Dermatitis, Nummular eczema etc.
Treatment:
 Identify & avoid allergen
 Topical corticosteroid is the 1st line of treatment
 Abx for 2° bacterial infections
 Anti-histamines – for relief of pruritus
 Supportive care for oozing lesions – Calamine, cold compresses with water or saline etc.
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5. Lymphogranuloma Venereum [17]
Ans.
Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis types L 1, L2 & L3.
Clinical features of LGV – 3 stages:
a) Primary stage
b) Secondary stage (inguinal syndrome) &
c) Tertiary stage (Ano-Genito-rectal syndrome).
Complications of LGV: strictures, fistulae, and lymphatic obstruction
Laboratory diagnosis of LGV: +ve chlamydial serology, isolation of C. trachomatis from the infected
site, and histological identification of Chlamydia in infected tissue.
 Treatment of LGV:
 Tetracycline hydrochloride is the antibiotic of choice.
 Other options: Azithromycin 1 g single dose + Doxycycline 100 mg BD for 7 days orally
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6. Bowen's Disease [16]
Ans.
It is carcinoma-in-situ seen in uncircumscribed elderly men on the shaft of penis or scrotum.
: Arsenic, chemical carcinogens & HPV
: It presents as reddish brown to hyperpigmented scaly sharply demarcated plaque
varying in size from a few millimetres to a few centimeters.
: Ulceration is an ominous sign which indicates beginning of invasive SCC
: cryotherapy, curettage with cautery, excision, 5-fluorouracil (5-FU),
radiotherapy, laser etc.
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7. Mention provoking factors in Erythema Nodosum [13]
Ans.
Erythema Nodosum is a type of panniculitis the hallmark of which is acute onset of tender,
erythematous, non-ulcerative subcutaneous nodules located symmetrically on the shins.

– Notorious Organisms – Streptococcus, Mycoplasma, Mycobacteria, HIV, HBV, Rickettsia,

Chlamydia etc.
- OCPs
– Drugs: Penicillin, Phenytoin, Sulphonylurea, Sulphonamide etc.
– SLE; Sarcoidosis
– Ulcerative Colitis & Crohn’s Disease {Inflammatory Bowel Disorder}
– Malignancy {Lymphoma}
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8. Hypopigmented patch [12]
Ans.
A decrease in the number of melanocytes or melanin results in a hypopigmented macule / patch
It seen in pityriasis alba, pityriasis versicolor, tuberous sclerosis, nevus depigmentosus ,leprosy, and
other disorders.
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9. Larva migrans [12]
a. Cutaneous larva migrans [02]
Ans.
▪ However, the larvae of lower
animal nematodes when
accidentally infect man, they are
not able to complete their normal
development (because humans are
the unusual host for them) and
their life cycle gets arrested. The
larvae wander around aimlessly in
the body. This is called as larva
migrans (LM).
▪ 2 types of larvae migrans exists:
1) Cutaneous larva migrans: aka creeping eruption. Larva
migration occurs in skin and subcutaneous tissue.
2) Visceral larva migrans: Larva migration takes place in
viscera – treat with DEC 300 mg thrice daily for 3 weeks.
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10. Melatonin [10]
Ans.
 Melatonin is a hormone secreted from Pineal Gland
 Hypothalamus is responsible for the circadian fluctuations of melatonin secretion {more in
darkness}
1. Heat stroke [21, 20, 19, 11, 09, 05]
Ans.
Heat stroke occurs when the core body temperature
rises above 40°C and is a life-threatening condition.
Clinical Features:
 The patient’s skin feels very hot but Sweating is
absent due to failure of thermoregulatory
mechanisms
 Headache, nausea and vomiting can also occur.
 CNS: coarse muscle tremor and confusion,
aggression or loss of consciousness.
Complications: hypovolaemic shock, lactic acidosis,
DIC, rhabdomyolysis, hepatic and renal failure, and
pulmonary and cerebral oedema.
Management: Heat stroke is an emergency with a
significant mortality
 Immediate cooling should begin at the scene,
before transfer to hospital.
 Use evaporative or convective cooling
 The aim should be to reduce core temperature by

 Fluid resuscitation with crystalloid IV fluids. Avoid

solutions containing potassium
 IV dextrose (since hypoglycaemia can occur).
 Monitor fluid balance, including central venous pressure – to avoid overaggressive fluid
replacement  pulmonary oedema
 Once emergency treatment is over, shift the patients to ICU & screen for complications.
 Screen for complications: routine haematology and biochemistry, coagulation screen, ALT &
AST, creatine kinase and chest X-ray.
 Advice the patient to avoid heat and heavy exercise during recovery before discharge from
hospital.
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1. Radiation hazards [09, 05]

Ans.
Radiation Hazards 👉🏻
Radiation protection:
Avoid Unnecessary X-ray examinations especially in the
case of children and pregnant women
 Proper use of lead shields and lead rubber aprons by workers regularly associated with X-ray
procedures.
Workers must wear a film badge or dosimeter which shows accumulated exposure to radiation
since last time the instrument was charged.
Besides, periodic medical examinations & regular working hours, holidays must be ensured to
workers to maintain their state of health
----------------------------------------------------------------------------------------------------------------------------------------
2. Selenium [09]
Ans.
Selenium is an inorganic micronutrient
Dietary sources: Fish, wheat grown in selenium-rich soils {North American soil has a higher
selenium content than European and Asian soil}
Enzymes containing Selenium:
i) Glutathione peroxidase – helps in preventing free radical damage to cells
ii) Monodeiodinase – it converts thyroxine to triiodothyronine.
hypothyroidism, cardiomyopathy in children (Keshan’s disease) and
myopathy in adults.
heart disease.
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3. Anti-snake venom [07]
Ans.
• Antivenoms should be administered intravenously by slow infusion, the same dose being given to
children and adults.
• Allergic reactions are frequent, and adrenaline (epinephrine) 1 in 1000 solution should be available.
• In severe cases, the antivenom infusion should be continued even if an allergic reaction occurs,
with subcutaneous injections of adrenaline being given as necessary.
• {refer POISONING}
1. Describe the features of autosomal dominant, autosomal recessive, X-linked and non-germ line
cytoplasmic inheritances. Write diseases that are transmitted in the above patterns [16, 09]
a. Mention Autosomal recessive disorders [12]
b. Y chromosome linked inheritance [07]
Ans.
:
Here, a heterozygous individual who has two different forms (or alleles) of the same gene will manifest
the disease.
The offspring of heterozygotes
have a 50% chance of
inheriting the chromosome
carrying the disease allele.
Some persons who carry an
abnormal gene may not have
signs of the disease. This is due
to reduced penetrance of the
disease. {Penetrance is all or none:
either the person has the disease or does
not}

:
These disorders manifest themselves only when both chromosomes
carry the same gene mutation (homozygous) or two different mutations
in the same gene (compound heterozygote).
The parents are unaffected carriers (heterozygous for the disease allele).
Each offspring of two carriers has a 25% chance of being affected, a 50%
chance of being a carrier, and a 25% chance of being genetically normal.
:
Mutant gene is present on X chromosome
These disorders occur in males & only in homozygous females
X--linked recessive diseases are transmitted by healthy female carriers or
affected males if they survive to reproduce.
Affected father cannot transfer the disease to son as the son’s X
chromosome is from mother.
: These are rare.
Disease will manifest even if single X chromosome has abnormal gene,
hence no carriers
Affected father cannot transfer the disease to son as the son’s X
chromosome is from mother
If mother is affected and father is normal, 50% of both sons and daughters are affected.
Affected males tend to have the disease more severely than the heterozygous female.
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1. Genetic counselling [21, 17, 14, 99]
Ans.
Genetic counselling refers to the process of communicating information about genetic risks
Strict patient confidentiality should be observed at all times
:
 To establish a diagnosis of genetic disease
 To estimate the risks to the individual and other family members.
 To provide information and support.
:
Prospective genetic counselling: This allows for the true prevention of disease.
Screening tests of the population → Identify heterozygous individuals for any particular defect
→ explain them the risk of their having affected children if they marry another heterozygote for
the same gene. Ex: sickle cell anaemia and thalassemia.
Retrospective genetic counselling: i.e., the hereditary disorder has already occurred within the
family (marriage already happened). The methods here are:
(i) Contraception (ii) Pregnancy termination and (iii) Sterilization depending upon the attitudes and cultural
environment of the couples involved.
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2. Human genome project [10]
Ans.
Human genome project (HGP) was an international project to decode all the DNA base pairs
This project began in 1990 and was completed in 2003.
The project involved studying DNA obtained from many individuals
It has produced a reference database of sequence of human genome which is used worldwide in
biomedical sciences. It is available to anyone on the internet
:
Human genome consists of 46 chromosomes (22 pairs of autosomal chromosomes and 1 pair of
sex chromosomes).
Only 1.5% of the total length of human genome encodes proteins & rest of the genome is junk
DNA.
The human genome is estimated to contain 30,000–40,000 genes.

Knowledge of the effects of variation of DNA can revolutionize the ways to diagnose, treat and
even prevent many diseases.
Many questions about the similarities and differences between humans and our closest relatives
(the primates, and other mammals) are resolved by the data from this project.
Improved diagnosis of diseases.
Gene therapy.
Earlier detection of genetic predisposition to disease.
Pharmacogenomics—customized drug therapy to target specific genetic composition to get better
response with minimal side effects.
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3. Polymerase Chain Reaction [07]
Ans. Polymerase chain reaction (PCR) is a laboratory technique for rapidly producing (amplifying)
millions to billions of copies of a specific segment of DNA, which can then be studied in greater detail
 Principle: 3 steps
1) DNA extraction from the organism: lysis of cell (via boiling, adding lysozyme, proteinase etc.) →
release of DNA
2) Amplification of extracted DNA: done in thermocycler. The extracted DNA is subjected to many
cycles of amplification. Each amplification cycle has three steps:
i. Denaturation at 95°C: dsDNA separates into two single strands.
ii. Primer annealing (55°C): Primer anneals to the complementary site on the target ssDNA.
iii. Extension of the primer (72° C): catalysed by Taq Polymerase enzyme → add free nucleotides to
the primer.
3) Gel electrophoresis of amplified product: based on molecular size, the amplified DNA forms clear
bands which can be visualized under UV light.
Applications of PCR:
To amplify very few copies of a specific
organism’s DNA.
To detect the organisms that are highly
fastidious or non-cultivable by
conventional culture methods.
To detect the genes responsible for drug resistance in the organism (Ex: MecA gene detection in
Staphylococcus aureus).
To detect genetic diseases, such as sickle cell anemia, phenylketonuria, and muscular dystrophy.
Modification of PCR:
1) Reverse transcriptase PCR (RT-PCR): useful for detection of RNA viruses.
2) Nested PCR: used for detection of Mycobacterium tuberculosis in samples.
3) Multiplex PCR: can detect many DNA sequences of several organisms in one reaction. Ex: for the
etiological diagnosis, of pyogenic meningitis, different primers targeting the common agents of
pyogenic meningitis, such as pneumococcus, meningococcus and H. influenzae can be added
simultaneously in the same reaction tube.
4) Real-time PCR (rt-PCR): can quantitate the DNA present in the specimen; hence can he used for
monitoring the disease progression in response to treatment, e.g., viral load monitoring in HIV.
----------------------------------------------------------------------------------------------------------------------------------------------
4. SIDS – sudden infant death syndrome [02]
Ans.
Aka Crib death / Cot death – S DS refer to Sudden & unexplained death of an healthy infant
Mostly occur during sleep; in early morning hours
Theories of cause of Death:
Prolonged sleep apnoea – fail to breath during sleep  hypoxia  bradycardia  death.
Airway obstruction – due to anatomical defects, faulty neck position & prone position during
sleep
Respiratory tract obstruction  Narrowing of air passage  hypoxia  bradycardia  death
Damage to brain during pregnancies
Toxic causes, Allergies, Deficiencies of vitamins, antibodies, hormones etc.
Medicolegal importance – charge of infanticide maybe levelled on innocent mother
----------------------------------------------------------------------------------------------------------------------------------------------
5. Phenylketonuria [04, 01]
Ans.
Phenylketonuria is an autosomal recessive metabolic genetic disorder
: Deficiency of hepatic enzyme phenylalanine hydroxylase is the cause for this disease
Phenylalanine cannot be converted to tyrosine  phenylalanine accumulates
So alternate minor pathways are opened to metabolise excess phenylalanine  Phenylketone
(phenylpyruvate), phenyllactate and phenylacetate are excreted in urine
:
The classical PKU child is mentally retarded
Phenylalanine interferes with neurotransmitter synthesis  Agitation,
hyperactivity, tremors and convulsions.
The child often has hypopigmentation {due to activity of tyrosinase}
Mousy body odor – due to phenyllactate in sweat
:
Blood phenylalanine
Guthrie test is a rapid screening test – Bacillus subtilis cannot grow in a medium devoid of
phenylalanine
Ferric chloride test – ferric chloride + phenylketones ➔ blue-green color
DNA probes
:
Provide a diet containing low phenylalanine – Ex: Food based on tapioca (cassava) will have low
phenylalanine content.
Continue this special diet during the 1st decade of life; after which the child can have a normal diet
Female child, on growing to adulthood may become pregnant. Then again special diet is to be
given, because the increased phenylalanine level will affect the brain development of the fetus
----------------------------------------------------------------------------------------------------------------------------------------------
6. Niemann Pick's disease [2000]
Ans. It is a lipid storage disorder
This is an inborn error of meta-bolism due to failure of degradation of sphingomyelin
Etiopathogenesis: The enzyme sphingomyelinase is deficient in this condition
NPC1 {Niemann-Pick disease type C1} protein is involved in cholesterol transport in the secretory pathway.
NPC1 gene when disrupted, leads to severe neurological dysfunction.
Clinical Presentation: Sphingomyelin accumulate in blood
 Severe CNS damage, mental retardation, hepatosplenomegaly & Cherry red spot in macula.
 Death occurs by 2 years of age
Nutritional treatment: Restrict cholesterol; mevinolin
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1. Gene Xpert test [21]

Ans.
Gene-Xpert, a CBNAAT (Cartridge Based Nucleic Acid Amplification Test) is a widely accepted
diagnostic test for Tuberculosis.
This is a rapid diagnostic test for TB detection as well as Rifampicin resistance in direct smear
negative cases.
It uses a sputum sample to detect DNA of TB bacteria and can give a result in less than 2 hours.
----------------------------------------------------------------------------------------------------------------------------------------------
2. Role of genetics in diabetes mellitus [11]
Ans.
– Ex: MODY is an autosomal dominant hereditary disease
– Type 1 is a/w HLA-DR 3 and DR4, whereas type 2 is not a/w HLA
– autoimmunity against islet cells
– esp. central obesity is a/w Type 2 DM
– Offsprings of diabetic pregnancies are at high risk of developing type 2 diabetes at an
early age
1. Oncogenes [19, 16, 05]
a. Tumour suppressor genes [15]
Ans.
 Most tumors exhibit genetic abnormalities such as deletions, inversions, translocations, or
duplications
 Most genetic abnormalities lead to activation of proto-oncogenes to oncogenes or deletion of
tumor suppressor genes—or both. Both these changes cause abnormal cellular proliferation and
cancer formation
Oncogenes
Proto-oncogenes in the normal state stimulate the normal growth of cells.
Activated proto-oncogenes are called oncogenes and are responsible for the development of
cancers
Cause of Activation of proto-oncogenes: point mutation, DNA amplification, chromosomal
rearrangement and viral infections
Point mutations occur due to ionizing radiation, UV rays, and carcinogens
DNA amplification  overexpression of gene product – Ex: ERBB2/HER2 in breast cancers &
NMYC gene in neuroblastoma.
Chromosomal rearrangement – Examples are:
In Burkitt’s lymphoma, the c-myc oncogene is activated by translocation of genetic material
from chromosome 8 to chromosome 14
In CML, reciprocal translocation of the long arms of chromosomes 9 and 22  leads to
generation of a fusion protein (BCR-ABL) with tyrosine kinase activity
Amplification of the HER-2/neu oncogene in breast cancer
Viral infections – The 7 known human oncogenic viruses are , ,
(HCV), (HTLV-1), human papillomaviruses ( ), Kaposi
sarcoma-associated herpesvirus ( ; aka human herpesvirus 8 (HHV-8)) and
(MCPyV)
Tumour suppressor genes
In health: They suppress unwanted cell proliferation
In neoplasia: Their loss of function results in unregulated cell growth & genetic instability leading to
tumor formation. Examples are:
1) Retinoblastoma Gene ➔ Retinoblastoma & osteosarcoma
2) TP53 ➔ Li-Fraumeni syndrome
3) BRCA1 and BRCA2 ➔ Carcinoma of breast
4) WT1 ➔ Wilms Tumor
5) APC gene ➔ Colonic carcinoma
6) NF1 and NF2
7) E-cadherin
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2. Tumour marker [12, 02]
a. Alpha feto-protein [21, 04]
 b. Carcino-Embryonic Antigen (CEA) [14]
Ans.
Tumor markers are products of malignant tumors
that can be detected in the cells themselves or in
blood and body fluids.

:
Detection of cancer, e.g., PSA is used to screen
prostatic adenocarcinoma
Determine the effectiveness of therapy
Detection of recurrence

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3. Vincristine [04, 02]
Ans.
Vinca Alkaloids: Vinblastine and vincristine are derived from the periwinkle plant. They are CCS agents
and act during M phase of cell cycle. Vinblastine
and vincristine have the same MOA but differ in
anti-tumour spectrum and toxicity.

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4. Classify anti-cancer drugs [03]
Ans.

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5. Paraneoplastic syndrome [01]
Ans.
Paraneoplastic syndromes are
symptom complexes in cancer
patients which are not directly
related to mass effects or invasion
or metastasis or by the secretion of
hormones indigenous to the tissue
of origin.
:
May be the first manifestation
of an occult neoplasm.
May be mistaken for metastatic
disease leading to inappropriate
treatment.
May present with fatal clinical
problems.
Certain tumor products causing
paraneoplastic syndromes may
be useful in monitoring
recurrence in patients who had
surgical resections or are
undergoing chemotherapy or radiation therapy.
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6. Acute tumour lysis syndrome [2000]
Ans.
Tumor lysis syndrome refers to a group of metabolic complications due to sudden destruction of
tumor cells
It usually occurs after starting treatment of cancers – commonly seen in lymphomas, leukemias
and multiple myeloma
:
Hyperuricemia  uric acid deposition in kidney  AKI
– Dysuria, oliguria, hematuria
Hyperkalemia  muscle weakness and cardiac
arrhythmias.
Hypocalcemia  tetany, and seizures
:
Hydration with IV fluids + Loop Diuretics – to wash out
the excess uric acid crystals
Urinary alkalinization with Sodium bicarbonate – to
convert uric acid to more soluble urate salt
For Hyperuricemia Allopurinol; Rasburicase; Febuxostat
For Hyperkalemia β2-agonists; Insulin + dextrose infusions & Potassium binding resins
For Hyperphosphatemia: Oral phosphate binders; Insulin + dextrose
For Hypocalcemia – treat with IV infusion of calcium gluconate
In severe cases – start Hemodialysis
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1) Mention '4' immuno suppressive drugs [21, 20, 13]
Ans.
MTX, Cyclosporine, Cyclophosphamide, Azathioprine, Tacrolimus, Sirolimus, Glucocorticoids etc.
----------------------------------------------------------------------------------------------------------------------------------------
2) Mention 4 Oncological Emergencies [21, 18]
Ans.

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3) Acute and late side effects of Radiotherapy [15]
Ans.
– Mucositis, Skin erythema (ulceration in severe cases) & Bone
marrow toxicity.
–
After radiation to head and neck  Hypothyroidism, cataracts and retinal damage.
After radiation to thoracic area  Brachial plexopathy, chronic constrictive pericarditis, and lung
fibrosis
After treatment for bladder cancer  Shrinkage and fibrosis of the bladder.
Risk of secondary cancer induction.
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4) Adverse effects of chemotherapy [13]
a. Complications of chemotherapy in malignancy [96]
Ans.
Most cytotoxics have a narrow therapeutic index. They have various effects on normal cells
(especially rapidly dividing cells) which is responsible for their side effects.
Nausea and vomiting – treat with antiemetics – Ex: ondansetron, domperidone, prochlorperazine;
Diarrhea – esp. seen with fluorouracil – treat with antimotility agents – Ex: loperamide
Alopecia – Psychological support and the use of wigs can be encouraged.
Skin & tissue necrosis – due to extravasation of the drug during i.v. administration.
Bone marrow suppression – Marrow is susceptible because of high number of rapidly dividing cells in it.
Leucopenia leads to various infections, thrombocytopenia bleeding manifestations, and
Anemia leads to easy fatigability.
Mucositis – due to damage to the proliferating cells at the base of the mucosal squamous epithelia
or in the intestinal crypts.
Gonadal dysfunction – Cessation of ovulation and azoospermia infertility.
Consider Sperm banking before treatment
Development of secondary malignancies – Ex: leukemias can happen with alkylating agents.
Other side effects – Ex: hemorrhagic cystitis with cyclophosphamide, peripheral edema with
docetaxel, , etc.
1. Clinical features and management of anaphylaxis [21, 17, 16, 14]
a. Anaphylactic Shock [22]
b. Type I anaphylactic reaction [15, 08, 06]
Ans.
 Anaphylaxis is a potentially life-threatening, systemic allergic reaction
characterised by circulatory collapse, bronchospasm, laryngeal stridor, often
associated with angioedema, and urticaria
 Occurs within minutes of exposure to allergen
 Treatment: Inj. adrenaline (1:1000) 0.3-0.5 mL IM

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2. SLE – C/F, Inv. & Rx [16, 14, 13, 11]
a. Diagnostic criteria of systemic lupus [18, 06]
b. Enumerate systemic manifestations of SLE [10]
c. Drug induced lupus [05]
Ans. Systemic Lupus Erythematosus - SLE is a chronic
autoimmune disease which affects multiple organ systems. It is the most common multisystem connective tissue disease
Etiology: {failure of self-tolerance}
• : Family History, deficiencies of complement & Polymorphism in the inhibitory Fc
receptor → inadequate control of B-cell activation.
• : Exposure to UV rays, Smoking, Sex Hormones & Drugs {hydralazine,
procainamide, isoniazid and D-penicillamine}.
Pathogenesis:
LE Bodies: Nuclei of damaged cells react with ANAs, lose their chromatin
pattern to produce LE bodies or hematoxylin bodies.

Clinical Features:
• It predominantly affects young women, with female-to-male ratio of 9:1.
• Typical presentation: Butterfly rash over the face, fever, pain without deformity
in one or more peripheral joints, pleuritic chest pain and photosensitivity.
 • Valvular endocarditis (Libman-Sacks/nonbacterial verrucous endocarditis)
• SLE patients are susceptible to infections, because of immune dysfunction and treatment with
immunosuppressive drugs.
Laboratory Findings: Test for autoantibodies via IFA,
ELISA (for smith antigen), Multiplex flow cytometry
immunoassay; CBP & urinalysis.
Anti-dsDNA & Anti-Sm antibodies are specific for
SLE
Anti-histone antibody is characteristic of drug-
induced lupus
Diagnostic Criteria of SLE: Revised American College of
Rheumatology (ACR) criteria for SLE: A patient is
classified as having SLE if the patient has biopsy-proven
lupus nephritis with ANA, anti-dsDNA antibodies
if the patient satisfies 4 of the following 11 diagnostic
criteria
Management of SLE:
Educate the patient to avoid sun and UV light exposure
NSAIDs for mild joint pain
Hydroxychloroquine (200–400 mg daily) – it  flares; help in cutaneous and joint symptoms.
High dose steroids (oral prednisolone 40–60 mg daily or IV methylprednisolone 500 mg-1 g) pulse
iv cyclophosphamide is required for life-threatening disease (i.e., renal, cerebral involvement,
systemic vasculitis, diffuse alveolar hemorrhage)
Immunosuppressive drugs (azathioprine, MTX, cyclosporin, tacrolimus, mycophenolate mofetil)
Belimumab –  maturation of B cells into plasma cells – inhibits the production of antibodies
Rituximab can be used in CNS lupus
Anticoagulants—such as warfarin is required lifelong for patients with the antiphospholipid
antibody syndrome with thrombotic events.
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3. The complement system [10, 96]
Ans.
The term 'complement' (C) represents a group of proteins normally found in serum in inactive
form, but when activated they augment the immune responses
The complement system comprises of about 30 serum proteins grouped into complement
components, the properdin system and the regulatory proteins
The complement components are named by numerals. There are 9 components; C1 to C9.
C1 has three subunits-C1q, C1r and C1s
The properdin system and the regulatory proteins are named by letter symbols, e.g., factor-B.
Features of Complements:
Constitute about 5% of normal serum proteins
Antigen nonspecific: Their level does not increase following either infection or vaccination.
Species nonspecific: Complements are present in the sera of all mammals, birds, amphibians and fish. Complements from one species can
react with antibodies from other species
Heat labile: Complements get denatured by heating the serum at 56°C for 30 minutes
Binds to Fc region of antibody: IgM (binds strongly) followed by IgG3 → 1 → 2
Site of Synthesis of Complements: Mainly by liver, also by GIT, macrophage and spleen.
 Complement Pathways: There are three pathways of complement activation:
1) Classical pathway: This is an Ab dependent pathway, triggered by the Ag-Ab complex.
2) Alternative pathway: This is an Ab independent pathway, triggered by the antigen directly.
3) Lectin pathway resembles classical pathway, but it is Ab independent.
All the three pathways differ from each other in their initiation till formation of C3 convertase. Then,
the remaining stages are identical in all the pathways.
Stages of Complement Activation: There are 4 main stages in the activation of any of the
complement pathways:
a. Initiation of the pathway
b. Formation of C3 convertase
c. Formation of C5 convertase
d. Formation of membrane attack complex (MAC): {by binding of C5b with C6, C7, C8 & C9}
Biological Role of Complement
Target cell lysis: MAC makes pores or channels in the target cell membrane
Inflammatory response: Complement by-products such as C3a, C4a and C5a act as anaphylatoxins and
chemotactic.
Opsonization: C3b and C4b act as major opsonins
Mediate hypersensitivity reaction II and III
Removes the immune complexes from blood to spleen- by C3b
Immune adherence: CR2 acts as EBV receptors
Kinin like activity (↑vascular permeability): C2b
Viral neutralization

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4. Graft versus host reaction [09]
Ans.
GVH reaction is a condition, where graft mounts an immune response against the host (i.e.,
recipient) and rejects the host, in contrary to the usual situation where the recipient mounts an
immune response against the graft antigens.
GVH reaction occurs when the following 3 conditions are present:
a) The graft must contain immunocompetent T-cells (e.g., stem cells or bone marrow or thymus transplants)
b) The recipient should possess transplantation antigens that are absent in the graft.
c) The recipient may be immunologically suppressed & therefore cannot mount immune response
against graft.
GVH reaction occurs in 2 forms. Acute or fulminant (occurs < 100 days) & chronic GVH (occurs after 100 days)
 The acute GVH disease is characterized by selective damage to the liver (hepatomegaly), skin
(rash), mucosa, and the intestine (diarrhea) mediated by graft’s immunocompetent T-cell.
Chronic GVH disease also attacks the above organs, but in addition, it cause damage to the
connective tissues and exocrine glands.
Treatment: Glucocorticoids.
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5. Tuberculin test [05]
Ans.
{Mantoux test}
 PPD (Purified protein derivative antigen) – It is a purified preparation of the active tuberculoprotein
 0.1 mL of PPD containing 1 TU is injected intradermally into flexor surface of forearm. [TU=
Tuberculin Unit].
 Reading is taken after 48-72 hours. At the site of inoculation, an induration surrounded by
erythema is produced. If the width of the induration is:
≥ 10 mm: Positive.
6-9 mm: Equivocal/doubtful reaction
< 5 mm: -ve.
 :
▪ +ve in adults: indicates present/past exposure to TB bacilli
▪ +ve in children → indicates active infection and used as diagnostic marker
▪ False-positive: after BCG vaccination & NTM infection
▪ False-negative in early or advanced TB, miliary TB, decreased immunity (HIV-infected people)
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6. Cell mediated immunity [04]
Ans. Cell mediated immunity is provided by T cells, NK cells & Macrophages

1) Effector T cells – 2 types: & .

TH Cells recognize the antigens peptides presented by APCs along with MHC-II molecules → secrete
cytokines to modulate the cellular and Immoral immune responses.
Cytotoxic T cells recognize the intracellular antigens
(e.g., viral antigens or tumor antigens) that are
presented by any nucleated cells along with MHC-I
2) Regulatory T cells (Suppressor T cells):
They provide tolerance to self-antigens (known as
peripheral tolerance).
possess surface markers such as CD4, CD25 and Foxp3
Deficiency of Foxp 3 receptors → IPEX syndrome
{ mmune dysregulation, olyendocrinopathy, nteropathy, -
linked}.
are large granular lymphocytes that constitute 10–15%
of total lymphocytes. Similar to cytotoxic T cells, NK cells also are
involved in destruction of virus infected cells and tumor cells.
 NK cells are cytotoxic but antigen nonspecific.
 They are part of innate immunity, act as first line of defense
and do not require prior contact with the antigen.
 :
 Receptor interaction: When activation receptors (e.g., NKR-P1, CD16) present on NK cells are
engaged with ligands present on the target cells, NK cells become activated.
 Target cell destruction: is similar to that of TC cells, i.e., via secreting perforins and granzymes.
However, the NK cells enzymes are constitutively expressed (i.e., they are cytotoxic all the time,
even without exposure to the antigen).

Macrophages are the principal cells involved in phagocytosis. Macrophages from various tissues are
together called as the mononuclear phagocyte system (or previously known as the reticuloendothelial
system).

Recognition: Microbe attach to toll

like receptors present on
Macrophages.
Engulfment: Microbe is ingested with
subsequent formation of a phagocytic
vacuole (phagosome)
Fusion of lysosome with phagosome to form phagolysosome
Killing or degradation of the ingested microbes is done
by:
Oxygen dependent killing by generating free radicals:
▪ ROS are produced by NADPH oxidase
▪ Myeloperoxidase mediates formation of hypochlorite
from H2O2 & Chloride. Hypochlorite destroys microbes
by halogenation or oxidation of proteins & lipids
Oxygen independent killing- by lysosomal enzymes
----------------------------------------------------------------------------------------------------------------------------------------------
7. Auto antibodies in connective tissue diseases [03]
Ans.

----------------------------------------------------------------------------------------------------------------------------------------------
8. Australia antigen [02]
Ans. Australia antigen aka HBsAG {Hep B Surface Antigen}
first marker to be elevated following infection
Presence of HBsAg indicates onset of infectivity
Anti-HBs (Hepatitis B Surface Antibody): It appears after the clearance of HBsAg. Its presence
indicates recovery, immunity and non-infectivity (i.e., stoppage of transmission). It is also the only
marker of hepatitis B vaccination
----------------------------------------------------------------------------------------------------------------------------------------------
9. Anti-phospholipid antibody syndrome [02]
Ans.
Antiphospholipid antibody syndrome is characterized by
hypercoagulable state due to antiphospholipid antibodies
(especially lupus anticoagulant)
Clinical Presentation:
Results in arterial and venous thrombosis including deep
Venous, hepatic vein, placental (recurrent pregnancy
loss), and cerebral (stroke) thrombosis
a/w SLE {MC}
Treatment: Requires lifelong anticoagulation
 Warfarin – for arterial thrombosis, typically stroke
 Heparin and aspirin – for pregnant females with APS
----------------------------------------------------------------------------------------------------------------------------------------------

1. Causes of Generalised Lymphadenopathy [22]

Ans.

----------------------------------------------------------------------------------------------------------------------------------------------
2. JAK2 Proteins [22]
Ans.
JAK2 gene is present on Chromosome 9
JAK2 makes a protein which promote cell growth – especially
RBCs, WBCs & Platelets
JAK2 mutation  myeloproliferative neoplasm (MPN)
JAK2 mutation mostly seen in polycythaemia rubra vera (PRV)
– almost 90% cases
JAK2 mutation is also seen in 50% of those with essential thrombocythemia & myelofibrosis
----------------------------------------------------------------------------------------------------------------------------------------------
3. GAD antibodies [22]
Ans.
 GAD stands for glutamic acid decarboxylase
 Antibodies to GAD (anti-GAD) are reliable serological
markers of Insulin-dependent diabetes mellitus.
----------------------------------------------------------------------------------------------------------------------------------------------
4. Monoclonal antibodies [21, 17, 15]
Ans.

Monoclonal antibodies are defined as the antibodies derived

from a single clone of plasma cell; all having the same antigen
specificity, i.e., produced against a single epitope of an
antigen.

----------------------------------------------------------------------------------------------------------------------------------------------
5. HLA system [16, 08]
Ans.
Human Leukocyte Antigens (HLA) (aka MHC molecules) serve as a unique identification marker for
every individual as the genetic sequence of MHC genes is
different for every individual.
They also determine the histocompatibility between the
donor graft and the recipient (hence the name MHC).
In humans, HLA complex coding for MHC proteins is
located in short arm of chromosome-6.
The genes are clustered in 3 regions named as MHC
region-I, II and III
MHC I and II help in antigen presentation to T-cells:
 MHC I present intracellular antigen on viral/tumor cells
to cytotoxic T-cells
 MHC II presents extracellular antigen on APCs to helper T-cells
MHC III does not help in Ag presentation, but code for various proteins such as complement factors
(C2, C4, C3 convertase, factor B and properdin), heat shock protein, TNF-α and β and steroid 21-
hydroxylases.

----------------------------------------------------------------------------------------------------------------------------------------------
6. Anti-Nuclear Antibody [14]
Ans.
“These are the antibodies directed against nuclear antigens.”
Significance:
Play a role in the pathogenesis of their associated diseases
 Aid in diagnosis and management of various systemic
autoimmune diseases
Associated disorders: SLE (Antibodies to dsDNA & Smith (Sm)
antigen are diagnostic), Systemic sclerosis, Sjogren syndrome
Categories:
1) Antibodies to DNA
2) Antibodies to histone
3) Antibodies to nonhistone proteins bound to RNA
4) Antibodies to nucleolar antigens
Detection methods: Indirect immunofluorescence; ELISA

----------------------------------------------------------------------------------------------------------------------------------------
7. Mention '4' cytokines [13, 12]
a. Interleukins [09]
Ans.
Cytokines are chemical substances which serve as messengers, mediating interaction and
communication between the various cells of immune system.
Major Classes of Cytokines:
 Lymphokines – produced by lymphocytes
 Monokines – produced by monocytes and macrophages
 Interleukins – produced by WBCs and acting on the same or different WBCs
 Chemokines – Involved in chemotaxis and other leukocyte behaviour.
Major producers of Cytokines are TH cells and macrophages
Functions of Cytokines:
(1) Cytokines promote various responses of innate immunity:
▪ Antiviral activity – By Interferon- α and β
▪ Antitumor activity – By TNF- α and β
▪ Pyrogenic activity – By TNF- α, IL-1 and IL-6
(2) Promote development of cellular and humoral responses of adaptive immunity.
 Cytokines such as IL-2, IL-4, IL-5
 IL: 3 – Mast cell degranulation- ↑ histamine secretion
Use of cytokines (e.g., interferons) as drugs:
Interferon-α is used for the treatment of Hep B, hepatitis C, hairy cell leukemia, multiple myeloma
and CML.
Interferon-β is used for the treatment of multiple sclerosis
Interferon-y is used for the treatment of chronic granulomatous disease
----------------------------------------------------------------------------------------------------------------------------------------------
8. Hypersensitivity reaction [12]
a. Type - IV hypersensitivity reaction [11]
b. Type – lll hypersensitivity reaction [10]
Ans.
Definition: Hypersensitivity refers to the injurious consequences in the sensitized host, following
subsequent contact with specific antigen.
Gell and Coombs Classification of HSN: Following an antigen contact, hypersensitivity may occur
immediately or after a
few days. It may result
either due to humoral
or cell-mediated
immune response.
Based on the above
two features, HSN
Rxns are of 4 types:
👉🏻
1. AIDS – etiology, C/F, Complications & Treatment [20]
a. Four names of Antiretroviral drugs [22]
b. CNS manifestations of HIV [21]
c. Four AIDS defining illness [21]
d. What is HAART? Mention the classes of drugs and their use in clinical practice [19, 16, 09, 05]
e. Opportunistic infections of HIV [17, 15, 12, 03]
f. HIV counselling [16]
g. Mention the drugs and side effects of Protease Inhibitors (PIs) [14]
h. Gastro intestinal complications of AIDS [13]
i. Systemic manifestations of AIDS [10]
j. Nucleoside reverse transcriptase inhibitors [08]
Ans.
AIDS is a viral disease characterized by profound
immunosuppression with opportunistic infections,
secondary neoplasms, and neurologic manifestations.
Etiology: Caused by Human immunodeficiency virus (HIV)
Clinical Features:
Acute HIV Disease or Acute Retroviral Syndrome:
Following infection, HIV is carried to the lymphoid tissues where it
replicates and causes viremia → ↓ CD4 T cells.
Asymptomatic Stage (Clinical Latency): Adequate
immune response develops → viremia drops down and
CD4 T cell count becomes normal → The immune
response cannot clear the infection completely, HIV-
infected cells persist in the lymph nodes, and there is a
high level of ongoing viral replication.
Abnormalities of B-cell Function
- Activation of B-cells → hypergammaglobulinemia → circulating immune complexes.
- Impaired humoral immunity → susceptible to capsulated bacterial infection {S. pneumoniae & H. influenzae}.
Persistent Generalized Lymphadenopathy (PGL): It is a result of HIV replication in lymph nodes.
Symptomatic HIV infection (AIDS-related Complex): After variable period of clinical latency, the
CD4 T cell level starts falling. Eventually patients develop constitutional symptoms of AIDS.
CNS manifestations: Aseptic meningitis, Meningoencephalitis, AIDS-dementia complex, Microglial
Nodule, Non-Hodgkin B-cell lymphoma (primary lymphoma of the brain), Demyelinating lesions of
spinal cord & Peripheral neuropathy
AIDS-Defining illness: These are life-threatening
diseases that occur in HIV-positive people.
 When a person gets one of these illnesses, he or
she is diagnosed with the advanced stage of HIV
infection known as AIDS
 Treatment
ART should be started immediately
for all people with a confirmed HIV
diagnosis regardless of CD4 count
HAART = highly active antiretroviral
therapy – it refers to combination of
3 or more ARTs instead of one
Some of the popular 1st line
regimens are as follows:
Dolutegravir/abacavir/lamivudine
(DAL)
Dolutegravir/tenofovir/emtricitabine
(DET)

Nucleoside reverse transcriptase inhibitors:

Zidovudine is the prototype drug of NRTIs. It protects the uninfected cells from HIV, but has no effect on
HIV-infected cells. Zidovudine is effective against HIV-1 and HIV-2. It can also be used for the prophylaxis
of needle stick injury patients and for the prevention of vertical transmission of HIV from mother to
fetus.

 MOA: Zidovudine itself gets incorporated into the proviral DNA

and terminates chain elongation ➔ prevents infection of new
cells by HIV, but has no effect on proviral DNA that has already
integrated into the host chromosome
 A/E: bone marrow suppression ➔ megaloblastic anemia,
neutropenia and thrombocytopenia (ganciclovir should not be
combined). It is contra-indicated in patient with Hb < 8g%. It
can also cause myopathy. Rifampicin increases the clearance of
this drug. Chronic administration is associated with
lipodystrophy syndrome, nail hyperpigmentation and
lipoatrophy.

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2. Falciparum Malaria – C/F, Lab inv. Complications & Mx [21, 14, 13, 08]
a. Black water fever [22]
b. Cerebral malaria (incl Complications & Treatment) [21, 20, 18, 10, 04, 03]
c. Antimalarial drugs [21]
d. Chemoprophylaxis for Malaria (incl Falciparum) [19, 17]
e. Chloroquine [19, 02]
f. Treatment of Vivax Malaria [15]
g. Resistant malaria [12]
h. Life cycle of plasmodium falciparum. Discuss the Dx & treatment of cerebral Malaria [07]
i. Causes of malaria [07]
Ans.
(malignant Tertian malaria)

Clinical Features:
 The incubation period for falciparum, vivax & ovale infections is 8–24 days
Initial non-specific symptoms – malaise, nausea, vomiting, headache, fatigue, body ache &
In falciparum – recurs every day {malignant malaria}
Children can have febrile convulsions at the time of fever
Severe cases of Falciparum malaria can present with features of sepsis & multiorgan dysfunction
O/E – fever, anemia, jaundice and hepatosplenomegaly
Complications of Type of Malaria Periodicity of fever
Falciparum malaria Benign tertian malaria every 3rd day
occurs due to Malignant tertian malaria every 3rd day
sequestration of the
Ovale tertian malaria every 3rd day
parasite in the blood
vessels of visceral organs Benign quartan malaria every 4th day
like brain, kidney, etc. Quotidian malaria recurs every day
:
It is characterized by blackwater fever, algid malaria and septicemic malaria.
 Black water fever:
 It occurs after quinine treatment to pts previously
infected with P. falciparum & Pts with G-6-PD
deficiency
 Pathogenesis: Antibodies develop against
parasitized and quininized RBCs. With subsequent
infection and quinine treatment, there is
immunocomplex formation followed by
complement mediated massive destruction of
both parasitized and non-parasitized RBCs
 C/F: sudden intravascular hemolysis followed by
fever, hemoglobinuria and dark urine.
 Algid malaria: Characterized by cold clammy skin,
hypotension, peripheral circulatory failure and
profound shock.
 Septicemic malaria: present with high grade fever
with dissemination of the parasite ➔ multi organ
failure.

The WHO defines cerebral malaria as a clinical

syndrome characterized by coma at least 1 hour after termination of a seizure or correction of
hypoglycemia, asexual forms of Plasmodium falciparum parasites on peripheral blood smears and
no other cause to explain the coma.
: P. Falciparum attack RBCs  cytoadherence & sequestration  Parasitized RBCs
block brain capillaries → vascular occlusion  cerebral anoxia  impaired neurogenesis,
neuroplasticity & cell death  short- & long-term neuronal defects.
:
Manifests as encephalopathy ➔ Generalized convulsion; Muscle tone & tendon reflexes.
Brainstem signs (abnormalities in posture, pupil size & reaction, ocular movements or abnormal
respiratory patterns)
 Retinal hemorrhages, Brain swelling, ICP, Impaired
consciousness & coma can occur.
Other systemic complications such as anemia, metabolic
acidosis, electrolyte imbalance and hyperpyrexia or
hypoglycemia and shock are commonly present
Long term sequel – post-malaria neurological syndrome: Acute
psychosis, inappropriate speech & behaviour, hallucinations,
catatonia & convulsions
:
:
:
DOC – Parenteral Artemisinins irrespective of CQ-resistance status – Artesunate/Artemether
i.v. Quinine – used only as an alternative when Artemisinins cannot be used (e.g., during 1st trimester of pregnancy)

Tepid sponging for fever

Sodium bicarbonate to correct acidosis
Intravenous diazepam to control convulsions
10% dextrose to combat hypoglycaemia
Blood transfusion to correct anaemia
: Jaundice, Bleeding, Hypoglycemia & Lactic Acidosis;
Renal failure {RBC sequester in renal microvasculature}; Severe normochromic, normocytic anemia;
Pulmonary edema and ARDS
Management of Falciparum malaria ACT {Artemisinin-based Combination therapy}

1. Artesunate + Mefloquine
or
2. Artemether + Lumefantrine
or
3. Artesunate + Sulfadoxine + Pyrimethamine
or
4. Arterolane (as maleate) + Piperaquine
or
5. Quinine + Doxycycline or Clindamycin
Treatment of Vivax malaria:
Chloroquine is the DOC;
ACT + fluid boluses and steroids are given for treatment of vivax shock
Classification of Antimalarial Drugs – Based on stage of the parasite affected
a. Tissue schizonticidal agents: These act on primary (pre-erythrocytic) and latent tissue forms
(hypnozoites – seen in p. vivax & P. ovale) in the liver, e.g., primaquine is effective against both
forms; atovaquone and proguanil act on primary form
b. Blood schizonticidal agents: These act on erythrocytic stage of Plasmodium. They can be:
- Rapid acting and high-efficacy agents, e.g., chloroquine, artemisinin derivatives, quinine,
mefloquine, atovaquone, amodiaquine, lumefantrine, etc.
- Slow-acting and low-efficacy agents, e.g., proguanil, pyrimethamine + Sulphadoxine,
clindamycin; used always in combination with rapid-acting agents
 c. Gametocidal agents: These kill gametocytes of plasmodia in blood, e.g., artemisinin and
primaquine (active against all species); Chloroquine and quinine (vivax).
 Drugs for suppressive prophylaxis: Suppress erythrocytic phase, thus clinical attack of malaria is
prevented—clinical disease is not manifested, e.g., chloroquine, mefloquine and doxycycline
Chloroquine: It is a rapidly acting blood schizontocide against P. vivax, P. ovale, P. malariae,
chloroquine-sensitive strains of P. falciparum and P. knowlesi. It has no activity against liver forms
(pre-erythrocytic and hypnozoites).
▪ : Chloroquine is a basic drug, which is taken up by the acidic food vacuoles of susceptible
plasmodia and inhibits the conversion of heme to hemozoin. The 'drug-heme' complex is toxic and
kills the parasite by damaging the plasmodial membrane. Resistance to chloroquine is common
with P. falciparum
▪ : MAL-RIA
1) Malaria: Chloroquine is the DOC for the treatment of uncomplicated Malaria
2) It is a very effective chemoprophylactic agent for all types of malaria except that caused by the
resistant strains of P. falciparum
3) Amoebiasis – hepatic stage, as it is highly concentrated in the liver.
4) Lepra reaction – anti-inflammatory effect is useful
5) Rheumatoid arthritis it scavenges-free radicals and stabilizes lysosomal membrane.
6) Infectious mononucleosis
7) Autoimmune disorder – discoid lupus erythematosus
▪ :
Antimalarial doses ➔ nausea, vomiting, skin rashes, itching, headache and visual disturbances.
Parenteral administration ➔ hypotension, confusion, cardiac arrhythmias, convulsions & even
cardiac arrest.
Prolonged administration in large doses, as in rheumatoid arthritis, ➔ irreversible retinopathy
and ototoxicity
Long-term therapy requires ophthalmological examination once in 3-6 months.
It should be avoided in epileptics; It should not be given with mefloquine (can precipitate
seizures).
It is safe in pregnancy
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3. Enteric Fever – etiopath, C/F, inv. Dx, complications & Treatment [19, 12, 11]
a. Two Drugs for Treatment of Enteric Fever [21]
b. Complication of Typhoid fever [18, 14]
c. Typhoid vaccines [10]
d. Laboratory Diagnosis of typhoid fever [06]
e. Widal Test [03]
Ans. Enteric fever, was also called as Typhoid, is a systemic infection caused by
Salmonella typhi or paratyphi A & B (aka Eberthella typhi). Enteric fever is a misnomer
as the manifestations are more extraintestinal than intestinal.

Etiology:
• Salmonella are gram-negative, motile, non-lactose fermenting bacilli – causes only where poor
hygiene and overcrowding exists.
• Males > Female
• Risk factors
• Antigens:
» O: Somatic antigen – specific for group
» H: Flagellar antigen
» V: Capsular antigen – responsible for virulence
Pathogenesis:
Mode of transmission: Feco-oral route, MC through contaminated food or water.
Infective dose: Min. 103–106 bacilli. (Salmonella is Acid-labile unlike Shigella)
Pathogenesis can be divided into 4 stages:
: Salmonella enter M cells of Peyer’s patches phagocytosed by macrophages
: salmonella in macrophages reach the mesenteric lymph nodes & multiply 1°
bacteremia colonize the reticuloendothelial tissue {liver, spleen, lymph nodes and bone
marrow} Patients have no signs or symptoms during till now {incubatory period}
: bacteria now invade the blood stream Massive 2° bacteremia 
elevations of Peyer’s patches due to mononuclear cell infiltration shedding of mucosa oval
typhoid ulcers  fever & abdominal pain appear
Bacteria reach gallbladder via blood stream and multiply  Discharged into the intestine
excreted in stool which can spread to others via contaminated food
Clinical Features:
» Step ladder pattern of Fever – a/w headache, myalgia
st
1 week » GI upset – Constipation {due to swelling of lymphoid tissue around ileocecal junction} is
followed by Diarrhea {“pea soup” appearance of stools}, vomiting
• Rose spots on trunk
• Abdominal distension, Hepatosplenomegaly & mild jaundice
End of 1st week
• GI upset
• Bronchitis, Cough and epistaxis occur
End of 2nd Week Complications, delirium, coma & death (if untreated)
Investigations:

Widal Test:
 Principle: It is an agglutination test where H and O antibodies are detected in the patient’s sera by
using H and O Ag.
Antigens used: Four antigens are used: O antigens of S. Typhi (TO), H antigens of S. Typhi (TH), S.
Paratyphi A (AH) and S. Paratyphi B (BH). (Paratyphoid O Ag are not used as they cross-react with the S. Typhi O Ag.
Results:
1. Compact granular chalky clumps → O Agglutination
2. Large loose fluffy clumps → H agglutination
3. If agglutination does not occur, button formation occurs due to
deposition of antigens
Interpretation:
Significant titer: H agglutinin titer > 200 & O agglutinin titer > 100
O Ab appear early and disappear early and indicate recent infection. H Ab appear late and
disappear late.
O Ab are nonspecific. They are raised in all, i.e., S. Typhi, S. Paratyphi A and B
H Ab are specific. TH, AH and BH antibodies are raised in S. Typhi, S. Paratyphi A and B infections.
Treatment:
– Prevention & Control:
Proper sanitation practices – hand washing techniques & safe disposal of excreta
Safe and clean drinking water & food hygiene practices
Health education for endemic areas
Vaccines for typhoid – for people traveling to endemic area or in contact with case/carrier.

DOC – Fluoroquinolone
Case of MDR – Azithromycin 1g OD for 7 days
Case of Quinolone resistance – Ceftriaxone 1-2g iv/i.m for 10 days
Paracetamol for fever, headache & myalgia
 Severe case of typhoid – Dexamethasone
 Chronic carrier – Antibiotic therapy for 6 weeks [Ampicillin + Probenecid]
Ideal management for carrier: Cholecystectomy + Ampicillin
 Supportive measures – good nutrition & hydration
 Disinfection protocol: 5% cresol x 2 hours
Vaccine Age & Dose
Complications:
>5 yrs & ORAL
1. Ty21a
» Bowel – perforation of typhoid ulcers & hemorrhage usually 3 doses: 1,3,5 days
happens in 3rd week 2. ViCPS
>1 yr. & SC/I.M (0.5ml)
Single dose
» Septic foci  multiorgan involvement – Pneumonia,
>5yrs & Parenteral
myocarditis, cholecystitis, Hepatitis, nephritis, osteomyelitis 3. Vi-rEPA
Two doses
» CNS: Stupor, delirium, convulsions, ataxia, Extrapyramidal
signs, encephalitis, coma, death
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4. Cholera – pathophysiology, diagnosis and treatment [13, 11, 09, 04]
Ans.
Causative Organism: Vibrio are curved GNB that are actively motile by means of single polar flagellum
Pathogenesis of Cholera
1. Mode of transmission: contaminated water or food
2. Infective dose: 108 bacilli {V. cholerae is acid-labile}
3. In the small intestine, vibrios penetrate the mucous layer by secreting
proteolytic enzymes
4. Adhesion and colonization: to the intestinal epithelium by type IV
fimbria called toxin coregulated pilus (TCP).
5. Cholera toxin (CT): consists of 2 peptide fragments: A &B
▫ ‘B’ binds to ganglioside receptors of intestinal epithelium. After that A
fragment is internalized and cleaved into A1 and A2
▫ A2 helps in tethering A and B subunits together
▫ A1 → ADP ribosylation of G protein → ↑ adenylate cyclase activity → ↑
intracellular cAMP → cAMP cause accumulation of NaCl in intestinal
lumen → water moves passively into the bowel lumen to maintain
osmolality → watery diarrhea
6. ToxR gene: It regulates the expression of CT, TCP and other
virulence factors
7. Other virulence factors include:
» Zona occludens toxin: Disrupts tight junctions of mucosal cells
» Siderophore: for iron acquisition
» Endotoxin (LPS): Unlike other GNB, the LPS of V. cholerae does not
contribute to pathogenesis of cholera.
Clinical Manifestations of Cholera:
Asymptomatic infection (75% of cases).
IP: 24 to 48 hours.
In symptomatic cases:
• Watery diarrhea, Rice water stool {non-bilious}
• Vomiting may be present but fever is usually absent
• Muscle cramps may occur due to electrolyte imbalance
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5. Outline the clinical features of herpes zoster. What is the drug treatment? Write the treatment of
post heretic neuralgia? What Is ocular herpes? [10, 04]
a. Post herpetic neuralgia [09]
Ans.
Clinical features of herpes zoster:
Herpes zoster, also known as shingles, is caused by the reactivation of the varicella-zoster virus
(VZV) present in the trigeminal ganglia
Seen mainly inn adults
Vesicular rashes are confined to the innervated skin
MC nerve involved is ophthalmic branch of trigeminal nerve
Complications of herpes zoster: Post herpetic Neuralgia, Zoster ophthalmicus {uveitis, keratitis and
corneal perforation} & Ramsay Hunt syndrome
Treatment of Herpes zoster:
▪ Antivirals – acyclovir or famciclovir or valacyclovir
▪ For the pain – NSAIDs & opioid analgesics + neuron modulators {carbamazepine, gabapentin,
amitriptyline and lidocaine patches}
Post herpetic Neuralgia
It refers to persistence of pain and burning sensation along the involved nerve {esp. ophthalmic branch of
trigeminal nerve} for 1–6 months or longer, following healing of the herpes rash.
 Clinical Presentation: continuous burning pain along the affected nerve territory, with marked
sensitivity to light touch (allodynia).
Management:
Aggressive analgesia + amitriptyline 25–100 mg daily, gabapentin (commencing at 300 mg daily and building slowly to 300 mg
twice daily or more) or pregabalin (commencing at 75 mg twice daily and building up to 100 mg or 200 mg 3 times daily if tolerated).

Capsaicin cream (0.075%) may be helpful.

Prednisone + antiviral therapy – Indicated only for healthy elderly persons with moderate or
severe pain at presentation
Ocular herpes – seen in HSV infections – Severe conjunctivitis, dendritic ulcers of cornea & Corneal
blindness
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1) Treatment of Kala-Azar (Visceral ·Leishmaniasis) [22, 18, 07, 06]

Ans.
– Ex: Correction of pancytopenia by blood transfusion.

Pentavalent antimonial – DOC; Dose for VL is 20 mg/kg by rapid IV or IM injection, and therapy continues
for 28–30 days till smear microscopy is negative
Amphotericin B – used in antimonial resistance areas like Bihar; it is also the DOC for HIV/VL co-
infection
Other antileishmanial drugs – Paromomycin & Oral Miltefosine
– Post-kala azar dermal leishmaniasis – Extended course of antimonial is given for
a period of 2–4 months
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2) Corona Virus – C/F & Mx [22]
a. Novel corona virus [21]
Ans.
Coronaviruses are RNA viruses whose name derives from their
characteristic crown-like appearance in electron microscope
:
Incubation period is within 14 days
The clinical spectrum of COVID-19 varies from asymptomatic cases to severe pneumonia
characterized by respiratory failure, to multiorgan failure and death.
Mild disease presents with symptoms of an upper respiratory tract viral infection –
▪ mild fever, cough (dry), sore throat, nasal congestion, malaise, headache, and muscle pain.
▪ new loss of taste and/or smell, diarrhea, and vomiting are usually present.
Severe disease manifests as pneumonia characterized by fever, fatigue, dry cough, dyspnea, low
oxygen saturation (SpO2 <94%), and bilateral infiltrates on chest imaging.
Children seem to be less affected than adults.
Complications: respiratory failure, thrombotic complications, septic shock, multi-organ failure etc.
Complications and death rate are more among elderly people and those with comorbid illness such
as diabetes mellitus, hypertension, heart disease, and pre-existing lung diseases.

h/o recently travelled to China or who have had recent close contact with a confirmed or
suspected case of COVID-19.
 Supportive care for sepsis and ARDS
Steroids – Ex: Dexamethasone (6 mg per day for up to 10 days) for patients who are on mechanical
ventilator or require oxygen.
Remdesivir injection is also recommended for 5 days in patients who require oxygen (O2 saturation
<94% on room air).
Anticoagulant therapy for all admitted patients
Consider ECMO for patients with severe respiratory failure
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3) IRIS (Immune Reconstitution Inflammatory Syndrome) [22]
Ans.
IRIS refers to a collection of inflammatory disorders associated with paradoxical worsening of pre-
existing infectious processes following the initiation of antiretroviral therapy (ART) in HIV patients

ART  immune-function improves  inflammatory reactions occur at the sites of pre-existing

infections.
The syndrome appears to result from an unbalanced immune reconstitution of effector and
regulatory T cells in patients receiving ART.
Main Risk Factor: Presence of opportunistic infection at the time of initiation of ART

Patient presents with worsening or appearance of new clinical or radiological features.

Manifestations depend on the underlying opportunistic infection.
Mycobacterium tuberculosis (TB) is the most common pathogen associated with IRIS.

Treat opportunistic infections

NSAIDs – for milder cases of IRIS
Steroids – for severe cases. ART should be continued unless there is life threatening IRIS.

Initiate ART before the onset of severe immunodeficiency and after the treatment of opportunistic
infections.
In the case of HIV-TB co-infection  treat TB first and after 2 to 4 weeks, start ART.
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4) KFD – Kyasanur Forest Disease [22]
Ans.

Kyasanur Forest Disease

Causative Agent: KFD virus (member of Flaviviridae)
Vector: Hard ticks (Haemaphysalis spinigera)
Mode of transmission: bite of infective ticks
Incubation Period: between 3 and 8 days
Hosts: Monkeys, rodents and squirrels are common hosts. Man is an incidental host and
considered as dead end.
In monkeys: KFD virus cause high fatality in primates especially in monkeys, hence known as
Monkey's disease
Seasonality: KFD is increasingly reported in dry months (January-June) which coincides with human
activity in forest
Clinical Manifestation in Humans:
• 1st stage – hemorrhagic fever
• 2nd stage – meningoencephalitis.
Laboratory Diagnosis
Diagnosis is made by virus isolation from blood or by IgM antibody detection by ELISA.
Recently, nested RT-PCR and real time RT-PCR have been developed detecting viral RNA in serum
samples
Non-specific findings such as leukopenia, thrombocytopenia and ↓ hematocrit, albuminuria and
abnormal CSF are found in second stage.
Killed KFD Vaccine: A formalin-inactivated chick embryo vaccine has been developed for KFD
 Schedule: Two-doses at interval of 2 months, followed by booster doses at 6-9 months and then
every 5 years
 Target area: KFD vaccine is recommended in endemic areas of Karnataka (villages within 5 km of
endemic foci).
Treatment:
 Only symptomatic and supportive measures are required.
 The condition usually resolves without any sequelae – hence, no specific treatment is needed
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5) Mumps – C/F & Complications [21, 17, 14, 10]
Ans. Mumps is an acute, communicable, systemic viral infection whose most distinctive feature is
swelling of parotid glands
: Mumps is caused by mumps virus (paramyxovirus group; RNA virus)

Incubation period is 2–3 weeks.

Starts with a prodrome of fever, malaise, myalgia, and anorexia  then Parotitis develop 
swollen and tender parotid
Parotid glands (MC) > submaxillary > sublingual glands (rare).
Gland swelling increases for a few days and then gradually subsides within a week.
Other than parotitis, orchitis is the most common manifestation  swollen & tender testis.
 Testicular atrophy can develop; sterility is rare.
 Oophoritis can occur in women but less common than orchitis and does not lead to sterility.
Aseptic meningitis of mumps – may lead to cranial nerve palsies. Rarely, encephalitis can occur,
which presents as high fever with altered sensorium.
Other CNS problems occasionally seen are cerebellar ataxia, facial palsy, transverse myelitis,
Guillain-Barré syndrome, and aqueductal stenosis leading to hydrocephalus.
Other clinical manifestations are pancreatitis, myocarditis, mastitis, thyroiditis, nephritis, arthritis,
and thrombocytopenic purpura.
: other causes of parotid swelling - Influenza, parainfluenza and coxsackie virus infections; Parotid
tumor; Sjögren’s syndrome etc.
:
Symptomatic treatment – Analgesics for pain; Antipyretics for fever; Cold compresses for parotid
swelling.
For orchitis also - treat symptomatically with bedrest, NSAIDs, support of the inflamed testis and
ice packs
Patients with meningitis or pancreatitis require hospitalization.
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 6) Dengue Fever [21]
a. Dengue hemorrhagic fever – C/F & Mx [17, 15]
b. Complications of dengue fever [13]
c. Symptoms of Dengue fever [11]
Ans.
Dengue fever is an Acute viral infection caused by dengue virus {ssRNA; Flaviviridae}

 Primary dengue infection occurs when a person is infected with dengue virus for the first time
 Secondary dengue infection: a more severe form of dengue may appear due to infection with
another serotype.
 Antibody Response Against Dengue: 2 types
of Abs – neutralizing and non-neutralizing
antibodies.
» The neutralizing antibodies neutralize the
infective serotype
» The non-neutralizing antibodies are
produced following the 1st serotype
infection, can bind to a 2nd serotype during
secondary dengue infection; but instead of neutralizing, it protects it from immune system by
inhibiting the B cell activation against the 2nd serotype. This phenomenon is called Antibody Dependent
Enhancement (ADE).
WHO classification and grading of the severity of dengue infection
Stages Clinical Features Lab Findings
1. Dengue fever Fever with 2 or more of the following: ▪ Leucopenia (WBC <
(DF) Rash 3
5000 cells/mm ),

Headache, Retro-orbital pain ▪ Thrombocytopeni

(aka biphasic Myalgia a (platelets< 150,000
cells/mm3)
fever, break bone Arthralgia
fever or saddle Haemorrhagic manifestations ▪ ↑haematocrit by
back fever) No evidence of plasma leakage 5-10%
Criteria of DF +
2. Dengue
 +ve tourniquet test (>20 petechial spots per sq. inch
hemorrhagic
in cubital fossa)
fever (DHF)
 Plasma leakage (Rising hematocrit, Pleural effusion,
Grade 1:  Thrombocytopeni
ascites/ Hypoproteinaemia)
a: Platelets <
DHF Grade 1 +
100,000/cu.mm
Evidence of spontaneous bleeding (black tarry stools,
3. DHF Grade 2:
epistaxis, bleeding from gums, etc) and  Haematocrit rise
Abdominal pain 20% or more
DHF Grade 2 + circulating failure (weak rapid pulse,
4. DHF Grade 3
hypotension, presence of cold clammy skin and restlessness)
5. DHF Grade 4 DHF Grade 3 + profound shock with undetectable BP or pulse
DHF III & IV are Dengue Shock Syndrome
» Among all the serotypes combinations, ADE is remarkably observed when serotype 1 infection is
followed by serotype 2.
 The course of dengue illness can be divided into 3 phases – Febrile phase, Critical phase & Recovery
phase.
 : CBP of the patient should be done at 1st visit.
 Management of Dengue Fever:
 Give fluids – Ex: ORS with electrolytes & sugar to replace losses from fever and vomiting.
 Give paracetamol for high fever. Tepid sponge if the patient still has high fever . Do not give Aspirin,
Ibuprofen or other NSAIDs as these drugs may aggravate gastritis or bleeding.
 Instruct the care-givers that the patient should be brought to hospital immediately if there is no improvement.
Management of DHF Grade I & II: Hospitalize the patient & Look for signs of shock. Give IV fluid
therapy.
Management of DHF Grade III & IV: same as DHF II + Oxygen should be given to all patients in shock.

Loss of blood (overt blood) ≥ 10 %

Refractory shock despite adequate fluid administration and declining haematocrit.
If fluid overload is present packed cells are to be given.
In case of massive bleeding, Prolonged shock etc.
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7) Bioterrorism [21]
Ans.
Bioterrorism is terrorism by intentional release or dissemination of biological (bacteria, viruses, or
toxins) or chemical agents.

Biologic Agents – Ex: Anthrax {spores were in letters}, smallpox, botulinum toxin, bubonic plague,
brucellosis, glanders, Vibrio cholerae, viral hemorrhagic fever and tularemia.
Chemical Agents – Ex: Nerve agents (sarin, soman, tabun), arsine, hydrogen cyanide, phosgene,
mustard gas, lewisite, etc.

Surveillance – for early detection.

Public health response: State and local health departments should work along with law
enforcement agencies.
Confirmation of the etiologic agent is important for planning preventive and treatment plans.
Decontamination of clothing and personal items.
Methods of Decontamination – Regular soap and water; 2 % chlorhexidine gluconate & 0.5 %
hypochlorite solution.
Chemoprophylaxis & Vaccines should be given to all exposed persons.
Infection control—via isolation of infected patients, etc.
If the agent is unknown, symptomatic treatment and treatment of coexisting injuries should follow
standard guidelines. If the etiologic agent is known, then specific treatment should be instituted
against that agent.
Psychological support—panic among public should be allayed by assurance and educating the
public about disease course and outcome.
Prevention of Bioterrorism:
Physicians must maintain a high index of suspicion especially when there are clustering of cases
of a rare disease
Many countries are creating specially trained forces to deal with bioterrorism
Examples of early detection methods: electronic chips, fibreoptic tubes, ultraviolet avalanche
photodiodes etc. to detect agents of bioterrorism
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 8) Amoebiasis (incl Treatment) [20, 16]
a. Extra intestinal amoebiasis [13]
b. Chronic amoebiasis [12]
Ans.
: Trophozoites invade the
colonic mucosa by secreting the proteolytic enzymes→ Amoebic
ulcer - flask-shaped and profuse bloody diarrhoea (amoebic
dysentery).
:
a) Severe amoebic colitis: due to necrosis of large intestine, seen
in immunocompromised pts.
b) Amoebic appendicitis: if appendix is involved
c) Intestinal perforation: Occurs when the ulcer progresses
beyond the serosa
d) Toxic megacolon and intussusception
e) Amoeboma (amoebic granuloma): pseudotumor; mass of
granulomatous tissue found in rectosigmoid region.
f) Chronic amoebiasis: It is characterized by thickening, fibrosis, stricture formation with scarring and amoeboma
formation.
erosion and necrosis of small
intestine → trophozoites enter portal veins → multiply & occlude the hepatic venules → anoxic
necrosis of the hepatocytes ➔ Inflammatory response → formation of abscesses
➢ : abscess may grow in various directions & rupture.
Right sided liver abscess may rupture:
1. externally to skin → Cutaneous amebiasis
2. into lungs→ pulmonary amoebiasis with trophozoites in
sputum
3. into the right pleura → amoebic pleuritis
4. below the diaphragm → subphrenic abscess and
generalized peritonitis
Left sided liver abscess may rupture into stomach or left pleura
or pericardial cavity (amoebic pericarditis)
Hematogenous spread can occur from liver to brain (Cerebral amebiasis), spleen (Splenic abscess)
and genitourinary organs (Genitourinary amebiasis).
:
Metronidazole 400 mg thrice a day for 7 days is effective; Alternative: Tinidazole can also be used.
Add luminal amebicides like diloxanide furoate
or iodoquinol or Paromomycin
Increase the dose if Liver abscess is found 
aspirate under ultrasound guidance by
introducing a pig-tailed catheter. Chloroquine
can be used for patients with hepatic amebiasis.
Treatment of Complications – perforation, toxic
megacolon and stricture require appropriate
surgical treatment.
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9) Chickenpox [20]
Ans.
Chickenpox is an infectious disease causing a mild fever and a rash of itchy inflamed pimples which
turn to blisters and then loose scabs
Caused by Varicella‐zoster virus (VZV, aka HHV-3). It is a DNA virus belonging to herpes viridae family
Pathogenesis & Clinical Features:
Virus Enters through the upper respiratory mucosa or the conjunctiva → replicates in the regional
lymph nodes → spills over into the blood stream (primary viremia) → spreads to the liver and
spleen, and multiplies → again enters bloodstream (secondary viremia) → VZV present in the
infected mononuclear cells are transported to:
Skin→ typical vesicular rashes - appears 1st on the face & trunk then spreads to other body parts
Rashes are pruritic and centripetal with relative sparing of the peripheries
Vesicles become pustules which later form crusts
Respiratory tract → shed in the respiratory secretions.
Neurons: VZV gains access to neurons of trigeminal ganglia and undergoes latency  Years later it
may be reactivated vesicular eruption in the relevant sensory dermatomes which is known as
herpes zoster (shingles)
Chickenpox is the primary infection, and usually occurs in childhood
Treatment
 Most people recover with supportive treatment.
 Antiviral agents – acyclovir, famciclovir and valacyclovir.
 Antibiotics may be used for secondary bacterial infection of skin lesions.
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10) Genital Herpes Simplex [19]
Ans.
The causative organism is herpes simplex virus (HSV) type 1 and 2.
Mode of transmission: sexually by an infected partner or orogenital contact
Incubation period is 2–14 days
:
Initially, red painful inflammatory area appears on the clitoris, labia, vestibule, vagina, perineum,
and cervix.
There may be vulvar burning, pruritus, dysuria, or retention of urine.
Multiple vesicles  multiple shallow ulcers ultimately heal up spontaneously by crusting. It takes
about 3 weeks to complete the process.
Inguinal lymphadenopathy occurs.
Constitutional symptoms: fever, malaise, and headache.
First episodes are severe compared to the recurrent disease.

 Virus tissue culture and isolation — confirmatory.

 Detection of virus antigen by ELISA or immunofluorescent method.
 PCR test to identify the HSV DNA is the rapid, specific, and most accurate test.
:
Psychological trauma may precipitate recurrence.
During pregnancy – risks of miscarriage and pre-term labor.
Transfer of infection from mother to neonates during vaginal delivery
Baby may suffer from damage to CNS. Anomaly scan should be done at 20 weeks gestation.
 Deliver by cesarean section for primary genital herpes infection near term.

Rest and analgesics; Saline bath may relieve local pain

Acyclovir – Inhibits the intracellular synthesis of DNA by the virus – given orally in doses of 200 mg
5 times a day for 5 days.
Alternative: Valaciclovir 500 mg BID for 5 days or Famciclovir 250 mg orally thrice daily for 5 days
can be used alternatively.
To recurrences – daily suppressive therapy is given with valacyclovir-500 mg daily, at least for a
year, when recurrences are >9 episodes per year
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11) Leptospirosis – etiology, C/F, Dx, Complications & Mx [17, 16, 15, 14, 12, 11, 08]
a. Weil's Disease [18]
Ans. Leptospirosis is aka Field fever, pretibial fever, rat catcher's yellows & Weil's disease
Epidemiological determinants
 Agent factors
a) L. Interrogans is the causative agent.
b) Source of Infection: Leptospira are excreted in the urine of infected animals
c) Animal Reservoirs: rodents such as rats, mice & domestic animals like cattle, sheep, goats, buffalo,
pigs & horses
 Host factors
1. Age & Sex: 20-45 years; Males > Females
2. Occupation: e. g, Farmers, Veterinarians, meat handlers, veterinarians etc. ➔ ↑ exposure to the
urine of infected animals
3. Poor Immunity
 Environmental factors:
▪ Leptospira shed in the urine → environmental contamination.
▪ Other Factors: poor housing, limited water supply, inadequate method of waste disposal.
Mode of transmission
1) Direct Contact: with urine of infected animal
2) Indirect Contact: with contaminated soil, water, vegetation
3) Droplet Inhalation: Ex: when milking infected goats by breathing air polluted with droplets of urine
Incubation period: Usually 10 days with a range of 4 to 20 days
Clinical types:
1. Anicteric leptospirosis: It is the milder form of the disease – without
jaundice
2. Icteric leptospirosis: It is the severe form of leptospirosis – with jaundice
Diagnosis:
 Can be made by dark-field examination of the patient's blood or by culture on
a semisolid medium. Culture takes 1-6 weeks to become positive.
 ELISA & PCR.
 Now Leptodipstick test is also available.
Treatment & Control:
(1) Antibiotics: Penicillin is the DOC in severe cases.
(2) Environmental Measures: to control rodents, proper disposal of wastes and health education etc.
Vaccination: Immunization of farmers & pets prevent disease.
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12) Giardiasis [17, 15, 13, 09]
Ans.
Habitat: Duodenum and upper part of
jejunum.
Morphology: It occurs in two forms:
(1) trophozoite and (2) cyst.
Life Cycle:
» Host: 1 {man}.
» Infective form: Mature cyst.
» Mode of transmission: Ingestion of food and water contaminated with mature cysts.
Pathogenicity
Mechanism: → Trophozoites adhere to the duodenal mucosa →
disruption of the intestinal epithelial brush border → malabsorption
Malabsorption:
 of fat (steatorrhea): foul smelling profuse frothy diarrhea
 of vitamin B12 and folic acid
 Disaccharidase deficiencies (lactate, xylose) ➔ lactose intolerance
 Protein losing enteropathy.
Antigenic variation: due to a cysteine rich protein on its surface called
variant surface protein (VSP) → evasion of the host immune system.
Clinical Features: 3 stages:
1) Asymptomatic carriers: harbour the cysts and spread the
infection
2) Acute giardiasis:
→ Symptoms: diarrhea, abdominal pain, bloating, belching,
flatus and vomiting
→ Diarrhea is often foul smelling with fat and mucus but no
blood.
3) Chronic giardiasis:
→ Symptoms: recurrent episodes of foul smelling diarrhea, foul flatus, sulfurous belching with
rotten egg taste, and profound weight loss leading to growth retardation.
→ Uncommon symptoms —fever, presence of blood and/or mucus in the stools, and other signs
and symptoms of colitis
Treatment: Metronidazole; Tinidazole (2 g once orally) is more effective than metronidazole.
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13) Botulism [17, 09]
Ans.
Botulism is a paralytic disease caused by botulinum toxin, which is produced by C. botulinum.
C. botulinum is an anaerobic gram-positive organism that forms subterminal spores.
It is found in soil and marine environments throughout the world.
Botulinum toxin is the most potent bacterial toxin known – can be used as an agent of bioterrorism

Under anaerobic conditions, the spores germinate bacteria multiply release the exotoxin.
Botulinum toxin inhibits release of acetylcholine at the NMJ  flaccid paralysis.
Botulism occurs in one of 3 forms: Food-borne botulism, infant botulism, or wound botulism.
  Food-borne botulism is caused by ingestion of preformed toxin present in canned foods.
 Infant botulism occurs due to the practice of feeding honey (contain botulinum) to infants.
 Wound botulism occurs due to contamination of wound with organisms.

Symmetric descending paralysis is characteristic; starts in the extraocular muscles  spreads to the
pharynx, larynx, and respiratory muscles  generalised flaccid paralysis.
Patient may have symptoms like ptosis, blurred vision, diplopia, pooling of secretions, dysphagia,
Paralytic ileus and breathlessness.
Nausea, vomiting and diarrhea (if the source of toxin is intestine).
Patient is conscious, mentally intact, WITHOUT sensory deficits & WITHOUT fever.
Sensory findings are usually absent.
Respiratory paralysis may lead to death in untreated cases.

Toxin can be identified in serum, stool, vomitus, gastric aspirate, and suspected foods.
C. botulinum may be grown on selective media from samples of stool or foods.
Wound cultures that grow C. botulinum suggest wound botulism.

i.v. Botulinum antitoxin ASAP.

Penicillin G or metronidazole – esp. for wound botulism along with incision and thorough
debridement of the infected wound.
Close monitoring for respiratory failure is important.
If respiratory failure develops, endotracheal intubation and mechanical ventilation should be
started. Tracheostomy is required if the patient needs mechanical ventilation for a long time.
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14) Nosocomial infection [16, 13]
Ans.
Hospital acquired infections or nosocomial infections can be defined as: the infections
acquired in hospital by a patient:
a. Who was admitted for a reason other than that infection
b. In whom the infection was not present or incubating at the time of admission
c. This includes infections acquired in the hospital but appearing after discharge, and also
occupational infections among staff of the hospital care facility.

—They are the multidrug resistant isolates present in a hospital, such as

nterococcus faecium, taph. aureus, lebsiella pneumoniae, cinetobacter baumannii, seudomonas
aeruginosa, nterobacter species.
common infections that can spread in hospitals include:
 Escherichia coli, Nosocomially acquired M. tuberculosis, Legionella, Candida albicans
 Clostridium difficile diarrhea
 Blood borne infections (BBIs) transmitted through contaminated needle prick injury or
mucocutaneous exposure of blood include - HIV, hepatitis B and C viruses.
In any hospital, the 4 most common HAIs encountered are (33%),
(15%), (15%) and (13%)

Standard (Routine) Precautions: (indicated while handling all patients, specimens, and sharps):
 Hand hygiene
 Personal protective equipments (PPEs): Gloves, mask, gown, shoes, eye cover
 Spillage cleaning by 10% sodium hypochlorite
 All sharps should be handled with extreme care
Specific Precautions: are needed for preventing specific modes of transmission, such as Airborne
precautions, Droplet precautions and Contact precautions.
The Hospital Infection Control Committee (HICC) maintains surveillance of hospital
acquired infections. The 4 key parameters used for HAI surveillance are:
▪ CA-UTI (Catheter associated urinary tract infection)
▪ CLABSI (central line associated bloodstream infection)
▪ VAP (ventilator associated pneumonia)
▪ SSI (surgical site infections).
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15) Lepra reaction [15, 12, 03, 02]
a. Type-II lepra reaction [11]
b. Dapsone [09]
c. Treatment of multibacillary leprosy [08, 03]
Ans. Multi-Drug therapy is used in treatment of Leprosy
:
Prevent the development of drug-resistant bacilli
Prevent relapse
Shorten the duration of effective therapy
Make the patient non–contagious as early as possible by
killing the dividing bacilli
:
: Dapsone is structurally similar to PABA, hence
competitively inhibits folate synthetase enzyme and prevents
the formation of THFA (tetrahydrofolic acid). Thus, dapsone
produces leprostatic effect.
: dose-related haemolytic anaemia particularly in patients
with G6PD deficiency. Other side effects are anorexia, nausea,
vomiting, fever headache, allergic dermatitis, itching and
peripheral neuropathy. Methaemoglobinaemia can also occur.
Dapsone may cause exacerbation of lesions – “
” which is characterized by fever, dermatitis, pruritis, lymphadenopathy,
methaemoglobinaemia, anemia & hepatitis.
:
These are immunologically-mediated reactions that occur during the course of Leprosy.
 The exact cause of such reactions is not clear and is usually precipitated by infection, trauma,
mental stress, etc.
There are 2 types of reactions:
(Erythema Nodosum Leprosum)
(Reversal Reaction)
It is a delayed type of hypersensitivity It is a type-III hypersensitivity reaction to antigens released
reaction from the dying lepra bacilli
Seen in both multibacillary and
Seen in cases of lepromatous leprosy
paucibacillary cases
There are signs of inflammation in the
There is erythema nodosum - red, painful, tender nodules
skin lesions
Treatment: Thalidomide (DOC);
Treatment: clofazimine or prednisolone
Alternatives: clofazimine, prednisolone, aspirin & chloroquine
:
It is a phenazine dye and has leprostatic activity against lepra bacilli. It has anti-inflammatory
effect, hence is also useful in the treatment of type-2 lepra reaction.
MOA: Clofazimine binds to mycobacterial DNA to inhibit its template function. It also has activity
against dapsone–resistant organism.
A/E: reddish–black discolouration of the skin on exposed parts. It can cause pigmentation of the
conjunctiva and cornea, discolouration of hair, tears, sweat, urine, etc. Nausea, vomiting,
diarrhoea, and abdominal pain are its other side effects. It is contraindicated in pregnancy.
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16) Congenital Syphilis [15, 02]
Ans.
Congenital Syphilis:
: Maternal primary or secondary syphilis. T. pallidum can cross placenta and spread from infected mother to the
fetus

Intrauterine death and perinatal death.

Early (infantile) syphilis: It occurs in the first 2 years of life
▪ Bullous rash of hands & feet and around mouth & anus → epidermal sloughing
▪ Skeletal abnormalities:
- Syphilitic osteochondritis → saddle nose deformity.
- Syphilitic periostitis → excessive new bone formation on the anterior surfaces → anterior bowing, or saber shin.
- Diffuse fibrosis in the liver called as hepar lobatum
- Diffuse interstitial fibrosis in lungs → appear pale and airless (pneumonia alba).
 Late (tardive) syphilis:
Manifests 2 years after
birth. Manifestation is
Hutchinson’s triad which
are:
a) Interstitial keratitis
b) Hutchinson’s teeth {like
small screwdrivers with
notches on enamel}
c) 8th-nerve deafness

Aqueous penicillin
50,000 units/ kg IV q 12 h for the
first 7 days of life and q 8 h
thereafter for a total of 10 days.

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17) Pneumocystis jirovecii [15]
Ans.
 Like protozoa, Pneumocystis exists in cyst and trophozoite forms.
 Cysts are found in environment, whereas in human tissues both cysts & trophozoites are found.
 Inhalation of Cysts → Cysts transform into trophozoite in lungs → trophozoites induce an
inflammatory response & recruit plasma cell → frothy exudate fills the alveoli. Hence, this
condition is also called plasma cell pneumonia.
Lab Dx
Specimen: lung tissue or fluids obtained by bronchoscopy, bronchial lavage, or open lung biopsy.
Gomori's methenamine silver (GMS) staining: to demonstrate the cysts of P. jirovecii which
resemble black colored crushed ping-pong balls, against the green background.
Pneumocystis is not cultivable and there is no serological test available
Detection of 1, 3 β-D-glucan in serum.
PCR assays to detect P. jirovecii specific genes.
Treatment: DOC: Cotrimoxazole (trimethoprim/sulfamethoxazole) for 14 days in non-HIV patients and 21 days in patients
with HIV
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18) Cysticercosis [15]
a. Treatment of Neurocysticercosis [18, 11]
Ans.

Caused by Taenia Solium

: Subcutaneous tissue, skeletal muscle, eyes & CNS
Subcutaneous cysticercosis: manifest as palpable nodules
Muscular cysticercosis: manifest as muscular pain & weakness
Ocular cysticercosis: Can involve eye lids, conjunctiva and sclera. Common symptoms like
proptosis, diplopia, loss of vision and slow growing nodule with focal inflammation
 Neurocysticercosis is the MC parasitic CNS infection of man and the most common cause of adult-
onset epilepsy
Based on the site of involvement, NCC is of two types:
Parenchymal: Involves brain parenchyma
Extra parenchymal sites: meninges, ventricles and spinal cord
Manifestations: Asymptomatic; Seizures (MC manifestation), Hydrocephalus (MC extra
parenchymal feature),  ICP and HTN – presented as
headache, vomiting and vertigo, Chronic meningitis &
dementia
NCC exists in 4 morphological stages: vesicular form 
necrotic  nodular  calcified stage
:
 Albendazole or Praziquantel.
+
Symptomatic Treatment: antiepileptics, VP shunting (to  ICP)
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19) Hyperpyrexia [14]
Ans. Hyperthermia (hyperpyrexia).

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20) Treatment of syphilis [14]
a. Tertiary syphilis [16]
b. Jarisch-Herxheimer reaction [06]
c. Endemic Syphilis [02]
Ans.
Syphilis is a chronic STD Caused by spirochete Treponema pallidum → passes from the site of
inoculation to regional lymph nodes → systemic circulation.
Route of transmission: Sexual & transplacental
Pathogenesis:
TH1 response is seen with production of IFN-γ which mediates macrophage activation and killing of
bacteria.
Production of treponeme-specific antibodies activate complement cascade → opsonization of
bacteria by macrophages
TprK, a protein in the outer membrane facilitates the persistence of bacteria.
Stages: The course of acquired syphilis is divided into 3 stages: Primary, secondary & tertiary syphilis.
1) : Seen 3 weeks after infection.
• Clinical Picture:
 Primary Chancre
Sites: Penis or scrotum in males; vulva or cervix in females.
Plenty of treponemes can be demonstrated in the chancre via silver stains or
immunofluorescence.
Painless, non-tender & with serous discharge on manipulation.
Regional Lymphadenitis
• Morphology: Proliferative endarteritis with rich infiltrate of plasma cells
2) : seen 2–10 weeks after the primary chancre in untreated patients.
Mucocutaneous Lesions:
Skin lesions:
▪ Rashes: Red-brown macules on the palms of the hands, or soles of the feet.
▪ Condylomata lata: broad-based, elevated plaques seen in moist areas of the skin on inner
thigh, anogenital region or axilla
Mucosal Lesions: in the mucous membranes of oral cavity or vagina as silvery-gray superficial
erosions. These lesions contain numerous T. pallidum and are the highly infectious
Painless Lymphadenopathy
3) After a latent period of 5 or more yrs spirochetes → obliterative endarteritis.
Focal lesions are called gumma.
: Gummas are seen as single or multiple, gray-white & rubbery nodular
lesions at various sites. e.g., Bone/joints (pain, swelling or fracture); Skin/Mucus membranes
(nodular lesions); Liver involvement seen with scarring is known as hepar lobatum.
Microscopy: Coagulative necrosis is seen in the center with palisading macrophages & fibroblasts in
the periphery surrounded by plasma cells.
:
 Syphilitic aortitis
 Saccular aneurysm {in asc. aorta} and aortic valve insufficiency
 On gross examination, the aortic intima appears rough and pitted (tree-bark appearance).
 Myocardial ischemia due to narrowing of the coronary artery.
It may be asymptomatic or symptomatic.
Asymptomatic neurosyphilis: CSF shows antibodies, pleocytosis (increased numbers of
inflammatory cells), ↑ protein levels, or ↓ glucose.
Symptomatic disease:
▪ Chronic meningitis
▪ Tabes dorsalis {due to demyelination of posterior column & dorsal root}.
▪ General paresis of insane
Treatment of Syphilis:
The treatment of choice in all stages of syphilis is long-acting preparation of penicillin (benzathine
penicillin) except in neurosyphilis where aqueous penicillin is used.
 Benzathine penicillin 2.4 million units IM (1.2 million units to each buttock) cures primary, secondary, and
early (<1 year) latent syphilis.
 Additional doses of 2.4 million units should be given 7 and 14 days later for late (>1 year) latent syphilis.
 :
Penicillin injected in pts with secondary syphilis  shivering, fever, myalgia, exacerbation of
lesions, even vascular collapse {due to sudden release of spirochaetal lytic products};
Lasts for 12–72 hours.
It does not recur and does not need interruption of therapy.
 It is treated with Aspirin and corticosteroids
Neurosyphilis should be treated with i.v. aqueous Penicillin G (3 to 4 million units IV Q 4h for 10 to 14 days)
followed by Benzathine penicillin 2.4 million units deep IM once a week for 3 weeks.
Congenital syphilis: Aqueous penicillin 50,000 units/ kg IV q 12 h for the first 7 days of life and q 8 h thereafter
for a total of 10 days.
For penicillin allergic patients – Doxycycline 100 mg BD for 1 month should be given.
▪ Doxycycline is contraindicated in pregnant women and children. In such cases penicillin should
be administered after desensitization.
▪ Alternative: Ceftriaxone 1 gm daily IM/IV for 8 to 10 days.
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21) Shigellosis – causative agent, epidemiology & C/F [14]
Ans.
It is a necrotizing infection of the distal small bowel and colon caused by Shigella.
Pathogenesis
Mode of transmission: via ingestion of contaminated food & water (most common). It can also be
transmitted sexually (homosexuals)
Shigella ingestion → reaches the stomach → resistant to acid in the stomach → reach colon →
penetrate the intestinal mucous epithelium and are taken up by M or microfold epithelial cells →
proliferate inside the cytoplasm of these epithelial cells → penetrate into the lamina propria →
phagocytosed by macrophages → Shigella induces apoptosis of macrophages → causes
inflammatory reaction → loosen the intercellular barriers and damages surface epithelium →
leading to superficial ulcers → allows entry of Shigella in the intestinal lumen to the colonocyte
basolateral membrane.
Exotoxin: Shiga toxin is a cytotoxin, produced by S. dysenteriae → inhibits protein synthesis by inhibiting 60S
ribosomes
Endotoxin: LPS induces intestinal inflammation and ulcerations.
Clinical manifestations:
1) : watery diarrhea with fever, anorexia and vomiting
2) : passage of bloody mucopurulent stools with abdominal cramps.
3) : It is commonly seen with children less than 5 years age:
a. Intestinal complication such as toxic megacolon, perforations and rectal prolapse
b. Metabolic complications, such as hypoglycemia,
hyponatremia, and dehydration.
c. Ekiri syndrome (toxic encephalopathy): It is a metabolic
complication of shigellosis
d. Hemolytic Uremic Syndrome: It is due to toxin secreted
by Shigella organism
4) : Patients expressing HLA-B27, develop
an autoimmune reaction months after S. flexneri infection;
characterized by reactive arthritis, ocular inflammation and
urethritis. It is seen only in 3% of cases).
Lab Dx:
 Culture:
▪ Enrichment broth: Uniform turbidity appears in 24 h
▪ DCA agar: colonies appear like to those on MacConkey
▪ XLD agar: red colonies without black center
▪ SS agar (Salmonella Shigella agar)
  Shigella is nonmotile, non-capsulated and non-sporing
 Biochemical Rxns:
1. Oxidase test is negative for all species
2. All are urease and citrate negative
3. TSI shows alkaline/acid, no gas and no H2S
4. All species ferments mannitol except S. dysenteriae
5. Decarboxylase test: All shigellae are negative for lysine, arginine and ornithine except S. sonnei
which decarboxylates ornithine
 Antimicrobial susceptibility testing is done on Mueller Hinton agar by disk diffusion test.
Treatment: ORS; Ciprofloxacin is the DOC; (Alternatives: Ceftriaxone, Azithromycin); Avoid loperamide
Prevention:
 Handwashing after handling of children's feces and before handling of food
 Stool decontamination (e.g., with sodium hypochlorite)
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22) Diphtheria [13]
Ans. C. Diphtheriae is a Gram +ve, non-capsulated, non-sporing, non-motile, club shaped rod. 2
characteristic features of this bacteria are: Cuneiform arrangement {V or L-shaped} & Metachromatic
granules
Virulence Factors (Diphtheria Toxin): DT is a polypeptide with 2 fragments: A (active) & B (binds to
host cell receptors and helps in entry of fragment A)
▪ A goes into the cell → ADP ribosylation of elongation factor 2 (EF-2) → inhibition of EF-2 →
inhibition of translation → Host cell’s Death
Pathogenicity and Clinical Manifestations: Bacilli secrete the toxin
→ toxemia → manifestations.
MC form of diphtheria.
➢ DT inhibit protein synthesis  Necrosis of the Epithelium of the
tonsils & pharynx  form mucosal ulcers, lined by a tough,
leathery, greyish white pseudo-membrane coat; It is named as
pseudomembrane because it is adherent to the mucosal base and bleeds on removal, in
contrast to the true membrane which can be easily separated
➢ In severe cases, pseudo-membrane extends into the larynx →
fatal airway obstruction → asphyxia.
➢ There may be massive tonsillar swelling and neck edema in
some pts {Bull-neck appearance}.
: presents as punched-out ulcerative
lesions with necrosis, or rarely pseudo-membrane formation. It is due to the organism itself & not
toxin-mediated.
Systemic Complications: toxin-mediated
DT will Damage the myelin of Cranial Nerves
Myocarditis: a/w arrhythmias and dilated cardiomyopathy.
Others: pneumonia, renal failure, encephalitis, cerebral infarction, and pulmonary embolism.
Treatment:
1) Antidiphtheritic Serum (ADS – Antitoxin)
2) Penicillin or Erythromycin is the DOC
Immunisation:
Diphtheria toxoid is used for vaccination. Vaccine is not effective for:
 a. Prevention of cutaneous diphtheria
b. Elimination of carrier state
Pertussis component (in DPT) acts as adjuvant
Administration of DPT:
✓ Schedule: 5 doses → 3 doses at 6, 10 and 14 weeks + 2 booster doses at 16- 24 months and 5
years
✓ Site: IM at anterolateral aspect of thigh, (gluteal region is not preferred as fat may inhibit DPT absorption).
AEFI of DPT:
 Mild: Fever and local reaction (swelling & indurations).
 Severe: Whole cell killed vaccine of B. pertussis is encephalitogenic. Hence, DPT is not recommended after 6 years of age.
Contraindication to DPT: Hypersensitivity to previous dose & Neurological disorders
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23) Pertussis [12]
Ans. Bordetella causes a paroxysmal productive cough in children called as whooping cough or 100
days fever.
Virulence Factors – Toxins:
 Pertussis toxin (PT) expressed only by B. pertussis, similar to
cholera toxin in its structure and function (↑cAMP)
 Other toxins: Tracheal cytotoxin, adenylate cyclase toxin and Endotoxin
Clinical Manifestations: 3 stages
1. Catarrhal phase: characterized by common cold like
nonspecific symptoms.
2. Paroxysmal phase: specific symptoms such as: Whooping cough, Post tussive vomiting.
3. Convalescent stage: Antibodies appear in serum
Complications:
Malnutrition can occur due to prolonged disease
Respiratory complications: Otitis media, pneumonia due to B. pertussis itself or secondary bacterial infection,
atelectasis, emphysema, bronchiectasis, pneumothorax and pneumomediastinum.
Severe cough increase in pressure in various body compartments  epistaxis; retinal,
subconjunctival and intracranial hemorrhage; inguinal hernia; rectal prolapse; rupture of the
diaphragm; rib fracture
Neurological complications: Seizures and encephalopathy.
Management – Macrolide antibiotics (azithromycin, clarithromycin) are the DOC for pertussis.
Alternative: Trimethoprim-sulfamethoxazole for individuals allergic to macrolides.
Supportive measures – adequate nutrition and hydration; Avoid factors aggravating cough such as
excessive crying.
Complications are managed as per standard guidelines.
Prophylaxis:
: Erythromycin is DOC.
:
1) Whole-Cell Pertussis Vaccines: It is given along with DPT to children < 5 years age.
2) Acellular Pertussis Vaccine: It is composed of pertussis toxoid and ≥ 2 other bacterial components
such as pertactin or fimbriae. Though the efficacy is same as WC vaccine, it is associated with fewer
side effects and safely given after 5–6 years.
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24) Food poisoning [12, 09]
Ans.
Food poisoning is an acute gastroenteritis caused by ingestion of contaminated food or drink
The condition is characterized by:
▪ History of ingestion of a common food
▪ Attack of many persons at the same time, and
▪ Similarity of signs and symptoms in the majority of cases.
Types of food poisoning: Food poisoning may be of two types: non-bacterial and bacterial.
: Caused by chemicals such as arsenic, cadmium, mercury, fertilizers, pesticides etc.
: Caused by the ingestion of foods contaminated by living bacteria or their toxins.
Types of
Incubation Mechanism Of
Bacterial food Agent Source Other features
Period Food Poisoning
poisoning
farm animals and
S. poultry - via
Salmonella Organisms multiply in the intestine
typhimurium, contaminated 12 to 24
food meat, milk and milk
and give rise to acute enteritis and
S. enteritidis hours
poisoning products; human colitis
etc.
carriers
Cows suffering
Enterotoxins of from mastitis have toxin is heat- Unlike salmonella
Staphylococcal certain strains of been responsible food poisoning,
resistant & act
food coagulase positive for outbreaks of 1- 8 hours staphylococcal food
Staphylococcus food poisoning directly on the poisoning rarely
poisoning
aureus involving milk and intestine and CNS causes fever
milk products
Toxin is heat-labile,
acts on
Botulism differs
Home-canned parasympathetic
from other forms of
Exotoxin of vegetables, nervous system →
18 to 36 food poisoning in
Botulism Clostridium smoked or pickled dysphagia, diplopia,
that the GI
botulinum fish, homemade hours. ptosis, dysarthria,
symptoms are very
cheese etc. blurring of vision,
slight
muscle weakness and
even quadriplegia
spores survive cooking
→ germinate →
Clostridium Ingestion of meat,
6 to 24 organism produce Recovery is rapid
Cl. perfringens perfringens meat dishes and
hours toxins → diarrhoea, (within one day)
(welchii) poultry
abdominal cramps and
little or no fever
Emetic form
spores survive cooking
(1-6 hours);
→ germinate →
B. cereus food Raw, dried and Recovery is rapid
B. cereus organism produce
poisoning processed foods Diarrhoeal (within one day)
toxins → emesis /
form (12-24
diarrhoea
hours)
Differential Diagnosis: Food poisoning may be mistaken for cholera, acute bacillary dysentery and
chemical (arsenic) poisoning.
Investigation of Food Poisoning:
1. Secure complete list of people involved and their history – Ex: foods eaten during the previous 2 days,
and place of consumption; time of onset of symptoms; etc.
2. Lab investigations – to identify the causative agent from stool, vomit or remnants of food.
3. Animal experiments – Ex: feed rhesus monkeys with the remnants of food –useful in the case of
botulism.
4. Blood for antibodies: This is useful for retrospective diagnosis.
5. Environmental study: This includes inspection of the eating place(s), kitchen(s), and questioning of
food handlers regarding food preparation.
Prevention and Control
Food sanitation:
Meat inspection: The food animals must be free from infection.
Personal hygiene: among individuals engaged in the handling & preparation of food is needed.
Food handlers: Those suffering from infected wounds, boils, diarrhoea, dysentery, throat infection,
etc should be excluded from food handling.
Food handling techniques:
• The handling of foods with bare hands should be reduced to a minimum.
• Milk, milk products and egg products should be pasteurized.
• Food must be thoroughly cooked.
Sanitary improvements: Sanitization of all work surfaces, utensils and equipments must be ensured.
Health education: Food handlers should be educated in matters of clean habits and personal
hygiene, such as frequent and thorough hand washing.
Refrigeration: Foods not eaten immediately should be kept in cold storage to prevent bacterial
multiplication and toxin production. ·'Cook and eat the same day" is a golden rule. Cold is bacteriostatic
at temperature below 4 °C.
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25) Anthrax [12]
a. Cutaneous lesion in anthrax [07]
Ans.
Caused by Bacillus anthracis which is a
G+ve, large rectangular rods, arranged
in chains, non-motile and capsulated
bearing non-bulging oval spores
Virulence Factors & Pathogenesis:
Anthrax Toxin – contains 3 fragments;
1. Edema factor: It is the active fragment; acts as adenylyl cyclase
and increases host cell cAMP → edema.
2. Protective factor: binds to host cell receptors and facilitates the entry of other fragments into the
host cells. Features Cut. Anthrax Pulm. Anthrax
3. Lethal factor: It causes cell Aka Hide porter's disease Wool sorter's disease
death; acts by cleaving host cell Transmission Spores enter Via abraded Inhalation of spores
MAP-Kinase (mitogen-activated skin
protein kinases) Characterized by Malignant pustule: Hemorrhagic pneumonia:
Papule → painless vesicle Bacilli spread by lymphatics
Anthrax Capsule – polypeptide
→ black, necrotic eschar or blood, leading to
(polyglutamate). It inhibits (anthrax) surrounded by Hemorrhagic mediastinitis,
complement mediated non-pitting indurated Bacteremia & meningitis
phagocytosis. edema
Treatment: Occupational Dock worker, butcher,
Workers of wool factory
exposures abattoir and farmer
✓ DOC: 1st Choice – Ciprofloxacin
Occurrence Most common (95%) Rare
(FQ); 2nd Choice – Doxycycline
a/w Bioterrorism No Yes
 ✓ Raxibacumab: is a monoclonal antibody that neutralizes anthrax toxin (protective antigen).
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26) Albendazole [10, 04, 02]
Ans. Anthelmintic agent
MOA is similar to mebendazole.
 MOA: It binds to β-tubulin and inhibits microtubule polymerization. It also blocks glucose transport
into the parasite. As a result, intestinal parasites are immobilized or die slowly
 It has broad spectrum of anthelmintic activity.
Pharmacokinetics: fatty food increases its absorption; It produces an active metabolite, albendazole sulphoxide, which is
widely distributed into various tissues including hydatid cyst
Uses:
Against Intestinal Nematodes: roundworm, hookworm, whipworm, pinworm, threadworm and
also in mixed worm infestations. It is more effective than mebendazole in trichinosis.
Neurocysticercosis: Both albendazole and praziquantel are highly effective but albendazole is
preferred to praziquantel, because it is cheaper, less toxic, duration of treatment is shorter, it
reaches high concentration in brain and CSF.
Hydatid disease – as DOC
Filariasis
Cutaneous larva migrans.
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27) Western Blot Test [10]
Ans.
In Western blot, antibodies to multiple specific proteins are detected.
Procedure:
Microbial protein is run on gel electrophoresis to separate the ligands, which are then
transferred on to a nitrocellulose membrane strip.
Patient’s serum is added to this nitrocellulose strip. If there are antibodies to a specific
microorganism, they bind to antigens present on the strip.
Enzymatically labelled anti-immunoglobulins can be added now which bind to the antibodies and
visualised by the addition of an enzyme substrate to produce coloured bands.
This test is commonly used to confirm the diagnosis of HIV infection
Western Blot detects individual antibodies in serum separately against various antigenic fragments
of HIV.
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28) Differences between amoebic dysentery and bacillary dysentery [10]
Ans. Bacillary dysentery is caused by Shigella

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29) Yellow fever vaccine [09, 07]
Ans.

It is a live attenuated vaccine, which is prepared in allantoic cavity of chick embryo (hence, it is
contraindicated in people having allergy to egg).
In India: It is prepared in Central Research Institute (CRI), Kasauli
Strict cold chain has to be maintained during the transport with a temperature range of –30°C to
+5°C
It is available in lyophilized form and has to be reconstituted before use
 Reconstitution is usually done with diluents such as physiological saline.
 Once reconstituted, it should be used within ½ hour
Dosage: Single dose, given subcutaneously
For international travel – Yellow fever vaccine certificate is issued after 10 days of vaccination and
renewed (i.e., reimmunization) every 10 years.
Precaution: Cholera and yellow fever vaccine interact with each other, hence should not be given
together (3 weeks gap to be maintained)
Contraindications of yellow fever vaccine:
▪ People with allergy to egg
▪ Children <9 months, (<6 months during epidemic)
▪ Pregnancy (except during outbreak)
▪ HIV-infected people.
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30) Difference between lepromatous and non-lepromatous leprosy [08]
a. Physical signs in lepromatous leprosy [06]
Ans.
TYPE OF LEPROSY
Features
Tuberculoid (Paucibacillary) leprosy Lepromatous (Multibacillary) leprosy:
▪ Asymmetric neuronal involvement
with nerve degeneration causes skin
anaesthesia with atrophy of skin and
Weak cell mediated immunity presents
Pathogenesis: muscle.
with heavy bacterial burden
▪ Strong TH1 response → produce IFN-γ
→ macrophage activation and killing
of bacteria.
Bact. Index 0-1 + 4-6 +
Many symmetrical lesions with Irregular
One or few asymmetrical lesions with margins are seen
sharp margins are seen. Skin: Hypoesthetic or anaesthetic
macular, papular or nodular lesions
Gross
Lesions are Hypopigmented, annular Leonine facies: Nodular lesions coalesce
macules with tendency towards central giving lion-like appearance
clearing Loss of eyebrows, Pendulous earlobes,
Claw-hands, saddle nose
Noncaseating granulomas composed of 1) Lepra cells: large aggregates of lipid-
epithelioid cells and giant cells laden macrophages, filled with masses
Micro
(globi) of acid-fast bacilli.
Grenz/clear zone is absent 2) Grenz (clear) zone: uninvolved dermis.
 Langhans
Seen Not seen
Giant cells
Nerve Seen, but with less severe sensory loss
Common with sensory disturbances
involvement than tuberculoid
Lepromin test Positive (Normal CMI) Negative (Low CMI)
Humoral
Normal Exaggerated
Immunity

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31) Ainhum [07]
Ans.
Ainhum also known as 'dactylolysis spontanea' is a painful constriction of
the base of the 5th toe frequently (occasionally other toes also) followed
by bilateral spontaneous autoamputation a few years later.
Grooving  pain  constriction deepens  tendon, nerve & vessel involvement  bone gets cut
spontaneously without any bleeding (auto-amputation) in many (2-5) years.
:
 Commonly affects males & Common in blacks, in Negroes.
 History of running barefoot in childhood is common.
 Fifth toe is commonly affected; (Gangrene of little toe). Often it can be bilateral.
: It is early "Z" plasty later amputation. Most often autoamputation occurs.
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32) Imidazole [07]
Ans.
Imidazoles are a group of drugs used in Anaerobic infections
Examples of Imidazoles: Metronidazole, tinidazole
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33) Treatment of guinea-worm infection [06]
Ans.

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34) Moraxella catarrhalis infection [05]
Ans. Moraxella catarrhalis is a harmless commensal of upper respiratory tract and genital tract
It is a Gram-negative diplococci
Pathogenesis: It causes opportunistic lower respiratory tract infections, especially in adults with
COPD. It has also been isolated in cases of otitis media, less commonly in meningitis, endocarditis
and sinusitis
Identification is confirmed by automated systems such as MALDI-TOF or by culture & various
biochemical reactions
Treatment: Amoxicillin-clavulanate, 2nd- and 3rd-generation oral cephalosporins, and trimethoprim-
sulfamethoxazole (TMP-SMZ) are the most recommended agents
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35) Neonatal Tetanus – Prevention [05]
Ans. Neonatal Tetanus occurs due to infection of the umbilical stump after birth, the first symptom being
seen about the 7th day. Therefore, tetanus is known as "8th day disease”
 Clean delivery practices – educate pregnant women about the "5 cleans" - clean hands, clean delivery
surface & clean cord care i.e. clean blade for cutting the cord, clean tie for the cord
 Training of birth attendants alone can reduce death due to neonatal tetanus by 90%.
 Tetanus toxoid will protect both the mother and her child.
 According to the National Immunization Schedule, 2 doses of TT should be given to pregnant women
between 16-36 weeks of pregnancy, allowing an interval of 1-2 months between the 2 doses.
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36) Types of Rickettsial Fevers [03]
a. Scrub Typhus [16]
Ans.

is caused by Orientia tsutsugamushi

: It is transmitted by the bite of infected trombiculid mites
:
 Triad of an eschar (at the site of bite), regional lymphadenopathy and maculopapular rash.
 Non-specific manifestations may appear early, such as fever, headache, myalgia, cough, and
gastrointestinal symptoms
: encephalitis and interstitial pneumonia may occur rarely (due to vascular injury).
 :
 Weil-Felix test: Nonspecific
 Indirect immunofluorescence antibody (IFA): It is specific, considered as the gold standard
serological test
 ELISA – cost-effective and considered as alternative to IFA for diagnosis
 Molecular test – Ex: PCR
: Doxycycline is the DOC; {Alternative – Chloramphenicol or azithromycin}
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37) Paul Bunnell Test [02]
Ans. Done for EBV
Heterophile Agglutination Test (Paul-Bunnell test): It is a tube agglutination test that uses sheep
RBCs to detect heterophile antibodies in patient's serum.
Procedure: Serial dilutions of inactivated (56°C for 30 minutes) patient's serum are mixed with
equal volumes of 1 % sheep RBCs, and then the tubes are incubated at 37°C for 4 hours
Result: Agglutination titer of >256 is considered as significant
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38) Amphotericin B [02]
Ans.
Amphotericin B is a fungicide
MOA: Fungal cell membrane contains a sterol which resembles cholesterol and is called 'ergosterol'.
A/E: AMB is the most toxic of all anti-fungals.
 fever, chills, headache, dyspnoea, gastrointestinal
disturbances, phlebitis at the site of injection, etc.
 Anaemia and electrolyte disturbances.
 Nephrotoxicity with azotaemia
 Hepatotoxicity can occur occasionally.
 Headache and convulsions may occur on intrathecal administration
Formulations of Amphotericin B: AMB is poorly water soluble, hence intravenous preparation is made
with deoxycholate.
Uses. Azoles (fluconazole and itraconazole) have replaced AMB in the treatment of many fungal diseases.
1. Intravenous AMB is the DOC for mucormycosis. It is also useful for aspergillosis, cryptococcosis,
sporotrichosis, histoplasmosis and blastomycosis.
2. It is useful for esophageal candidiasis, cryptococcal and Coccidioides meningitis.
3. Others: It is useful in leishmaniasis.
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39) Congenital Rubella syndrome [02]
Ans.
Congenital Rubella Syndrome: Rubella is teratogenic {one of the agents in 'TORCH complex}
- maximum if the mother acquires the infection during first trimester, risk is negligible
th
after 5 month.
Classical triad consists of:
 Ear defect: Sensory neural deafness (MC)
 Ocular defects: Salt‐and‐pepper retinopathy & cataract
 Cardiac defect: Patent ductus arteriosus (PDA), pulmonary artery stenosis & ventricular septal
defect.
Transient Congenital Changes: Hepatosplenomegaly, bone lesion, intrauterine growth retardation
(IUGR), thrombocytopenia with petechiae (Blueberry muffin syndrome)
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1. Post-Exposure Prophylaxis of Rabies [22]

Ans. Postexposure prophylaxis (PEP) = local wound care + both active and passive immunization.
Local Treatment: clean the wound, scrub with soap and water and apply antiseptics. Bite wounds are
not sutured immediately.
Passive Immunization: Human rabies immune globulin (HRIG) & Equine rabies immunoglobulin (ERIG)
Active Immunization (Rabies Vaccine): 2 types of Vaccines – Neural & non-neural.
: They are poorly immunogenic and encephalitogenic; hence not used.
Cell line derived, they are the recommended vaccine currently:
 Purified Vero cell (PVC)
 Human diploid cell (HDC).
National Guideline on Rabies Prophylaxis: Regimens:
Site of Injection:
1) Deltoid region is ideal site. Gluteal region is not recommended because fat retards the absorption of antigen

2) Infants and young children: Anterolateral part of the thigh is the preferred site
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2. Four examples of cephalosporins [21]
a. Third generation Cephalosporins [05]
Ans.

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3. Hemorrhagic viral fevers [20, 04]
Ans.
Mosquito-transmitted: Dengue Viruses, Zika Virus & Yellow fever virus
Tick-transmitted: Kyasanur Forest Disease (KFD) Virus
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4. Clinical features of Tetanus [19]
a. Tetany [08]
b. Tetanus Toxoid and its significance. [11]
Ans. TETANUS is an acute bacterial disease characterized by muscular rigidity & painful paroxysmal spasms
of muscles
Clinical Manifestations
 Muscles of face & jaw are affected first (shorter distances for the toxin to reach the presynaptic
terminals)
 1st Symptom: Increase in the masseter tone {trismus or lock jaw}
 In neonates, difficulty in feeding is the usual presentation.
 As the disease progress, generalized painful muscle spasm  leads to descending spastic paralysis.
 Hands, feet are spared & Deep tendon reflexes are exaggerated.
Complications:
a. Risus sardonicus: sustained spasm of the facial muscles that appears to produce grinning.
b. Opisthotonos position: occurs due to generalized spastic contraction of the extensor muscles.
c. Respiratory muscles spasm → May cause airway obstruction
Tetanus Toxoid is a preventive active immunisation vaccine which is available either as:
i. Monovalent vaccine {prepared by incubating toxin in formalin}.
ii. Combined vaccine: DPT
In children: Total 'seven doses' are given; 3 doses of pentavalent vaccine (DPT, hepatitis B and Hib) at
6, 10 and 14 weeks of birth, followed by 2 booster doses of DPT at 16-24 weeks and 5 years followed by
2 additional doses of TT at 10 years and 16 years.
Site: IM at anterolateral aspect of thigh (children) and in deltoid (adults).
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5. Weil-Felix Test [19]
Ans.
Weil-Felix test is done for typhus fever.
It is a heterophile antigen detection test
Here, Abs against rickettsial antigens are detected by using cross reacting Proteus antigens
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6. Prevention & Treatment of Filariasis [18, 16, 05]
a. Diethyl carbamazine citrate [10]
Ans.

 For chemotherapy and prophylactic therapy – DOC is

Diethylcarbamazine (DEC) given at the rate of 6 mg/kg
 –
 MDA (Mass Drug Administration) – it is done annually
Drugs given: DEC (6 mg/kg) + Albendazole
 DEC-medicated salt: Started in Maharashtra; Common salt medicated with 1-4 g of DEC per kg
 Vector control
Antilarval measures – Ex: Mosquito larvicidal oil (MLO), Pyrosene oil, organophosphorus
larvicides (e.g., temephos, fenthion).
Anti-adult measures – Ex: DDT, lindane, malathion
Removal of aquatic plants (Ex: Pistia plant) – to control breeding of Mansonia mosquitoes
Minor environmental measures – such as filling up of ditches,
drainage of stagnant water, adequate maintenance of septic
tanks and soakage pits, etc.
 Personal prophylaxis – to avoid mosquito bites → clothing minimizing skin exposure, use of
repellents, mosquito nets & window screens
 Diethylcarbamazine (DEC) – DOC for treatment of filariasis – can kill both adult worms &
microfilariae. However, adults are cleared slowly. Dose: 6 mg/kg daily for 12 days
Alternative: Albendazole 400 mg twice daily for 21 days;
Ivermectin: 400/kg single dose can kill the microfilariae but has no effect on adult worms
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7. Granuloma inguinale – causative organism, Genital lesions & Treatment [18, 05]
Ans.
Granuloma inguinale aka Donovanosis is a chronic, progressively destructive bacterial infection of
the genital region.
: It is a sexually transmitted infection. It is caused by a Gram-negative intracellular
bacterium, Klebsiella granulomatis.

Incubation period is 1 to 4 weeks.

Genitals & perianal region are the common sites.
The primary lesion is a painless nodule  enlarges  produce bright-red ulcers with pearly rolled
edges. Ulcer bleeds easily.
The lesions progress slowly and heal with fibrosis. There is NO lymph node involvement.
Extragenital lesions – seen in oral cavity, lips, and bones.
: Use either trimethoprim/sulfamethoxazole or doxycycline for 3 to 5 weeks
Alternatives: ciprofloxacin, erythromycin, or azithromycin.
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8. Brucellosis & it’s Treatment [18, 13]
Ans. Brucellosis is a zoonotic infection transmitted to human beings from infected animals (sheep,
goats, camels, cattle or buffalo, swine, dogs).

The incubation period varies from 1 week to several months.

Acute or insidious onset fever – characteristically undulant, i.e. it may disappear and again appear.
Brucellosis is a multisystem disease and affects almost all the organs. Clinical features depend on
the system involved
Constitutional symptoms: anorexia, asthenia, fatigue, weakness, and malaise, and weight loss.
Lymphadenopathy and splenomegaly are seen in 50% of the cases

The “gold standard” for the treatment of brucellosis in adults is IM streptomycin + doxycycline.
The alternative regimen (current WHO recommendation) is rifampicin + doxycycline for 6 weeks.
For patients in whom tetracyclines are contraindicated (children, pregnant women)  Use
trimethoprim sulphamethoxazole.
Surgery – If abscesses develop, they need to be drained.
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9. Complications of Hepatitis B [16]
Ans.
Hepatic complications: fulminant hepatitis/ cirrhosis/ hepatocellular carcinoma
Extrahepatic complications: During the prodromal phase, a serum sickness-like syndrome
characterized by arthritis, rash, angioedema, and rarely, hematuria and proteinuria may develop.
This is due to immune complex deposition.
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10. Ascariasis [15]
Ans. It is a parasitic disease caused by infestation of Ascaris Lumbricoides

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11. Molluscum Contagiosum [15]
Ans. Molluscum contagiosum virus is an obligate human poxvirus.
Transmission: Direct and indirect contact (e.g. by barbers, common use of towels, swimming pools)
Rarely sexual transmission has been reported in young adults.
Clinical manifestations:
 Skin: pink wart-like lesions with a dimple at center (umbilicated). Lack of associated inflammation
and necrosis
 Self-limiting: Lesions disappear in 3-4 months.
 In HIV-infected patients: Disease is more generalized, severe and persistent.
Lab Diagnosis: Molluscum bodies are the intracytoplasmic eosinophilic inclusions seen in skin
scrapings stained with histopathological stains. It cannot be propagated in tissue culture, egg or in
animals
TREATMENT: Surgical removal of the lesions by ablation.
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12. Treatment of Gonorrhoea [11]
Ans.

Adequate therapy for gonococcal infection and meticulous follow up are to be done till the patient
is declared cured.
Treat adequately the male sexual partner
simultaneously. Use condom till both the sexual
partners are free from disease
To avoid multiple sex partners.
:
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13. Influenza Vaccine [10]
Ans.
 Types: Both injectable (inactivated/killed) and nasal spray (live attenuated) vaccines are available.
 Injectable Vaccines: Most widely used; 3 types:
a) Inactivated Influenza Vaccine (IIV), e.g., Fluzone: It is prepared by growing the vaccine strains in
allantoic cavity of embryonated chick eggs.
b) Cell Culture-based Inactivated Influenza Vaccine; e.g., Flucelvax: It is prepared in Madin-Darby
Canine Kidney (MDCK) cell line.
c) Recombinant Influenza Vaccine (RIV); e.g., FluBlok: Contains recombinant influenza HA antigens.
RIV does not contain any egg protein.
Dose: 0.5 ml for adults and children over 3 years and 0.25 ml for children from 6 months to 3
years of age
Route of Administration: IM
Timing of vaccination: Optimally before onset of influenza season, i.e., by end of October.
Side Effects: fever, local inflammation at the site of injection, and very rarely Guillain-Barre
syndrome (an ascending paralysis). Persons allergic to eggs may develop symptoms and signs of
hypersensitivity.
Indications:
➢ All persons aged ≥ 6 months.
➢ If traveling to an area of increased influenza activity; preferably ≥ 2 weeks before departure.
Contraindications: IIV should not be administered to
➢ People who have allergy to eggs or have history of hypersensitivity to previous dose of vaccine.
➢ People who developed Guillain-Barre syndrome (GBS) within 6 weeks of getting an influenza vaccine.
➢ Children less than 6 months of age (inactivated influenza vaccine is not approved for this age group).
 Live Attenuated Influenza Vaccine (LAIV): nasal spray
 It can grow in upper respiratory tract (at 33°C) but not in lower respiratory tract (at 37°C) → may
cause mild flu like symptoms but never infect lower respiratory tract, hence never cause serious
adverse effects.
 Route of Administration: Intranasal Spray
 Indication: all healthy persons of 2-49 years age (except in pregnancy), but is not given to high-
risk groups
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14. Ulcer over penis [07]
Ans.

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15. Brugia malayi [07]
Ans.
It causes Lymphatic filariasis along with Wuchereria bancrofti and Brugia timori.
Features of Brugia malayi:
Periodicity – Nocturnal
Vector – Mosquitoes
Dwelling place of adult worm - Lymphatic vessels
Dwelling place of microfilariae – Blood
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16. Itching around anus [07]
Ans.

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17. Fluconazole [07]
Ans.
 MOA Azoles impair ergosterol synthesis by inhibiting 14 α-demethylase enzymes. It is a water-soluble
triazole. Fungicidal concentrations are achieved in nails, vagina and saliva. It is the preferred azole for fungal meningitis because of good
penetration into brain and CSF. Dose reduction is needed in renal impairment (since it’s excreted in urine).
 Spectrum: Cryptococcosis, Candidiasis & Coccidioidomycosis, and mucosal (oropharyngeal, vaginal)
Indications, coccidioidal meningitis and some tinea infections.
 A/E: nausea, vomiting, abdominal pain, rash and headache. It does not inhibit steroid synthesis in
man. Fluconazole is not recommended in pregnant and lactating women.
 Uses:
 Cryptococcal meningitis
 Candida esophagitis.
 Vaginal candidiasis, oropharyngeal candidiasis in both
normal and immunocompromised patients.
 Most tinea infections including pityriasis versicolor involving large area of skin and cutaneous
candidiasis
 An eye drop is useful in Fungal keratitis
 For disseminated candidiasis, cryptococcal or coccidioidal meningitis and other systemic fungal
infections
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18. MMR- mumps measles rubella vaccination [06]
Ans.

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19. Auto-hyper-infections in Strongyloides stercoralis [06]
Ans.
 In Strongyloides stercoralis, sometimes, the L1 larvae released in the human intestine don’t pass in
the feces but develop into filariform larvae that eventually penetrate the intestinal wall or perianal
skin, enter the venous circulation and reach lungs.
 This means that the parasite never reaches the soil; instead, it re-enters the host via enteral
circulation (endoautoinfection) or perianal skin (exoautoinfection).
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20. Drug treatment of Tape worm [06]
Ans.
For T. saginata (beef tapeworm) & T. solium (pork tapeworm) – Praziquantel, given as a single dose
(10 mg/kg) is effective against this tapeworm. Niclosamide (2 g) is an alternative.
For Hymenolepis nana (dwarf tapeworm) – Praziquantel, 5 to 10 mg/kg as a single dose is highly
effective. Niclosamide (2 g) is an alternative
For Echinococcosis (dog tapeworm) (hydatid cyst) – Albendazole + PAIR + Surgery
1. Obesity – Define, C/F, Dx, Complications & Mx. Outline weight reduction methods. Define BMI
(Body Mass Index). [21, 16, 11, 10]
a. Two conditions causing Obesity [21]
b. Causes of Obesity [17]
c. Mention four complications of obesity [15, 14]
d. Hazards of obesity [10, 09]
e. Diagnosis of Obesity [04]
Ans. Obesity is defined as an excess of adipose tissue
Etiology: Obesity is the result of an imbalance between daily energy intake and energy expenditure
resulting in excessive weight gain. There are multiple factors which can cause obesity:
Sedentary lifestyle.
Dietary factors: Overeating, high fat diet.
Endocrine disorders: hypothyroidism, Cushing’s syndrome, PCOD, hypogonadism etc.
Social factors: Low socioeconomic status;
Psychiatric disorders like Night eating syndrome, binge-eating.
Genetic factors.
Drugs: Steroids, clozapine, amitriptyline, cyproheptadine, thiazolidinediones.
Clinical Features & Complications of Obesity
Digestive tract diseases (gallstones, reflux esophagitis) – overeat due to leptin resistance
Non-alcoholic steatohepatitis (NASH)
Obstructive sleep apnoea.
Respiratory failure (Pickwickian syndrome).
CVS – Hypertension; Coronary artery disease
Metabolic – Hyperlipidaemia; Type 2 DM (insulin resistance) – occurs due to adipokines from adipose tissues
Degenerative joint disease (osteoarthritis).
Thromboembolic disorders & Varicose veins
incidence of cancers (colon, rectum, and prostate in men; uterus, biliary tract, breast, and ovary
in women).
Psychosocial problems (low self-esteem, depression)
Clinical Assessment
History Physical Examination
Age of onset, recent weight changes.
Family history of obesity. Degree and distribution of body fat,
Cigarette and alcohol use. overall nutritional status
Complete nutrition history. Look for signs of secondary causes of
Physical activity. obesity.
Sleep patterns. Look for any complication of obesity such
History of any depression and eating disorders. as hypertension, atherosclerosis, etc.
Use of any drugs and nutritional supplements.

Investigations: Blood sugar, Lipid profile, Urea, creatinine, Electrolytes, Thyroid function tests and
other endocrine work up, if necessary, ECG to look for evidence of coronary artery disease
Treatment – Obesity needs multiprong treatment strategies and may require lifelong treatment.

• Low-fat, high-complex carbohydrate, high-fiber diet.

• Avoid foods with high calories without other nutrients, i.e., fat, sucrose, and alcohol.
Aerobic Exercise + diet results in greater weight loss than diet alone.
esp. for those with a BMI > 30.
 Appetite-suppressing medications – Ex: phentermine, diethylpropion, mazindol, lorcaserin and
phentermine/ topiramate.
 Gastrointestinal fat blockers (e.g., orlistat) – Dose of orlistat is 120 mg t.i.d with meals.
Removal of subcutaneous fat by aspiration after injection
of saline
Bariatric surgery for patients with severe obesity (BMI > 40, or
>35 with comorbidities). These are as follows: –
Gastric banding—restrictive procedure; it compartmentalizes the upper
stomach by placing a tight, adjustable prosthetic band around the
entrance to the stomach.
Roux-en-Y gastric bypass (RYGB)—here a small proximal
gastric pouch is created and connected to the rest of the
GIT via a tight stoma and a Roux-en-Y small bowel
arrangement. RYGB results in substantial amounts of
weight loss.
Vertical banded gastroplasty {stomach stapling operation}—
restrictive procedure; here, the upper part of the stomach
is partitioned by a vertical staple line with a tight outlet wrapped by a prosthetic mesh or band.
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2. Protein Energy Malnutrition – types, C/F, biochemical anomalies & Mx [16, 01]
a. Grading of Malnutrition [03] ➔ refer pg. no. 16 Paeds notes
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1. Fat soluble vitamins [21]

a. deficiency [22, 17, 13, 05, 02]; Rickets [18] ➔ refer pg. no. 18 Paeds notes; Cholecalciferol [07]
b. Sources & deficiency manifestations [15, 09, 02]; Bitot Spots [18]; Retinoic acid [10]
c. [12, 11]
Ans.
Fat soluble vitamins – ADEK

: Vit A is lipid soluble and is obtained from diet in 2 forms:

 Preformed vitamin A (retinol and retinyl ester) - derived from animal sources – Ex: meat, dairy
products, and fish liver oils (cod liver oil and shark liver oil)
 Provitamin A (beta-carotenoid) - derived from plant sources – Ex: Carrot, Papaya, mango etc
:
1) Effects in the eye:
• Night blindness {since Vitamin A is a component of rhodopsin}
 • Xerophthalmia (dry eye) –> keratinisation of cornea → Bitot spots → Erosion of corneal surface
(keratomalacia), scarring and irreversible blindness {since Vit A is necessary for maintaining the
differentiation of epithelial cells}
2) Effects on other epithelia: lining of the upper respiratory passage & urinary tract also undergoes
squamous metaplasia
3) Urinary Tract: Desquamation of keratin debris in kidneys →stone formation
4) Skin: Follicular hyperkeratosis
5) Immune deficiency: Increased risk of developing infections e.g., measles, pneumonia & infectious
diarrhea.
(dry eye) refers to all the ocular
manifestations of vitamin A deficiency in man.
The younger the child, the more severe the disease.
of xerophthalmia
1) Short-term action: administration of large doses of vitamin A orally. Under National
Immunization Schedule, Vitamin A is given as:
 1 lac IU at 9 months age (along with measles vaccine)
 2 lac IV every six months thereafter, till the age of 5 years (at 18, 24, 30, 36, 42, 48, 54, 60 months)
2) Medium-term action: promote regular and adequate intake of vitamin A enriched foods
3) Long-term action: These are measures aimed at elimination of factors contributing to ocular
disease, e.g., persuading people to consume green leafy vegetables or other vitamin A rich
foods; promotion of breast-feeding for as long as possible; etc.

The nutritionally important forms of Vitamin D in man are Calciferol (Vitamin D 2) & Cholecalciferol
(Vitamin D3).
: Exposure to sunlight produces cholecalciferol (from cholesterol in skin); fish
liver oil, fish, egg yolk & Milk are good sources of the vitamin.

Rickets is characterized by expansion of the hypertrophic

chondrocyte layer of the growth plate in Children. Skeletal
changes in rickets:
1) During the non-ambulatory stage of Infancy
a) Head:
• Craniotabes: skull appears square and box-like; Parietal bones are soft,
• Delayed closure of anterior fontanelle
• Frontal bossing & flattening of occipital bones
b) Chest
 Rachitic rosary: Overgrowth of cartilage or osteoid tissue
at the costochondral junction.
 Pigeon chest: anterior protrusion of the sternum (pectus carinatum)
 Harrison’s sulcus/groove: It is due to indrawing of ribs on inspiration
2) In Ambulatory Child: Lumbar lordosis & Bowing of the legs
Osteomalacia: Vitamin D deficiency in adults → ↑ risk of fractures affecting vertebral bodies &
femoral necks
include – educate parents to expose their children regularly to sunshine;
vitamin D fortification of foods, especially milk etc.
 : An excessive intake is harmful and may result in hypercalcaemia → anorexia, nausea,
vomiting, thirst, and drowsiness. The patient may lapse into coma, while cardiac arrhythmias and
renal failure may occur.

Of these α-tocopherol is biologically the most potent – act as antioxidant.

Sources of Vit E: vegetable oils, cotton-seed, sunflower seed, egg yolk and butter.
Foods rich in PUFA are also rich in vitamin E.
Recently the cytotoxic effect of vitamin E on human lymphocytes at high concentrations has been
reported. Hence, caution should be exercised against the mega-dose consumption of vitamin E in
clinical practice.

Sources: Green leafy vegetables, intestinal bacterial synthesis etc.

RDA of Vit K: 50–100 mg/day
Vitamin K is stored in the liver.
Function of vitamin K: It act as a cofactor for the post-translational carboxylation of certain
coagulation factors (II, VII, IX, X, proteins C and S).
Causes of Vit K deficiency: Inadequate diet, use of broad-spectrum Abx, liver & pancreatic disorders
Clinical Manifestations of Vitamin K deficiency: ↑blood clotting time & Prothrombin content of blood;
» There are no specific clinical features. Bleeding can occur at any site.
» Newborn infants tend to be deficient in vitamin K due to minimal stores of prothrombin at birth
and lack of an established intestinal flora.
» Soon after birth, all infants or those at increased risk should receive a single IM dose of a
vitamin K preparation (0.5 mg of vitamin K1) by way of prophylaxis – to prevent hemorrhagic
disease of the newborn
Investigations:
 In mild vitamin K deficiency only, the PT is prolonged.
 In severe Vit K deficiency both PT and aPTT are prolonged.
Treatment: Replace Vit K parenterally either subcutaneously or intravenously.
A single dose of 15 mg will completely correct laboratory abnormalities in 12–24 hours
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2. Clinical features of B12 Deficiency [21, 20]
a. Oral absorption of cyanocobalamin [07, 06]
Ans.

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3. Total Parenteral Nutrition [21, 08, 04] ➔ refer pg. no. 48 Surgery – Paper 1 notes
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4. Antioxidants [16, 09]
Ans:
The body has several mechanisms to counteract
oxidative stress by producing antioxidants,
either naturally generated in situ (endogenous
antioxidants), or externally supplied through
foods (exogenous antioxidants)
Antioxidants neutralize the excess of free
radicals, to protect the cells against their toxic
effects and to contribute to disease prevention
Some Examples of Anti-oxidants are:
 Vit A supplementation has been shown to  incidences of leukoplakia, lung cancer etc.
 Vit C help in infertility, mood disorders, longevity, cataract formation, blood pressure, etc.
 Vit E supplementation can symptoms of intermittent claudication, rheumatoid arthritis & parkinsonism
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5. Frailty Syndrome [16]
a. Define frailty. Write the difference between frailty and disability? [14]
Ans:
It is a distinct clinical syndrome
meeting >3 of five phenotypic
criteria: weakness, slowness, low
level of physical activity, self-
reported exhaustion, and
unintentional weight loss.
Frailty is defined as the loss of an
individual’s ability to withstand
minor stresses because the reserves
in function of several organ systems are so severely reduced that even a trivial illness or adverse
drug reaction may result in organ failure and death
Frailty Disability
Frailty indicates increased vulnerability
Disability indicates established loss of function
to loss of function
Frailty doesn’t arise from a single Disability may arise from a single pathological event
pathological event (such as a stroke) in an otherwise healthy individual.
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6. Scurvy [15, 10, 03]
a. Sources & deficiency manifestations of Vit C [18]
Ans. Vitamin C (ascorbic acid) is a water-soluble vitamin.
It is the most sensitive of all vitamins to heat.
Man, monkey and guinea pig are perhaps the only species known to require vitamin C in their diet.
of Vit C:
Fruits – Ex: Amla, Guava, Lime & Orange
Vegetables – Ex: Cabbage, Cauliflower, Spinach etc.
:
Vitamin C is a potent antioxidant; supports immune function
It is needed for the formation of collagen, which accounts for 25 % of total body protein.
 Vitamin C, by reducing ferric iron to ferrous iron, facilitates the absorption of iron from
vegetable foods.
It inhibits nitrosamine formation by the intestinal mucosa.
Vitamin C also plays a role in wound healing and facilitates recovery from burns
for vitamin C is 40 mg per day for adults
Causes of Vit C Deficiency
 Infants fed exclusively on boiled milk;
 Lack of dietary fruit and vegetables >2 months; severely malnourished individuals,
 Drug and alcohol abusers, Extreme poverty, Smoking
Clinical Picture of Deficiency – SCURVY
Defective collagen formation poor wound healing,  platelet adhesiveness & capillary
hemorrhage  swollen & bleeding gums, subcutaneous bruising or bleeding into the skin or joints
Eventually, teeth become loose and avulsed
Other Hemorrhagic manifestation include – petechiae and purpura, splinter hemorrhages,
hemarthroses, and subperiosteal hemorrhages. Intracerebral hemorrhage can cause death
Anaemia and weakness.
Diagnosis is based on clinical features; there will be  Serum ascorbic acid levels of <0.2 mg/dL
Treatment – Scurvy is treated with 300–1000 mg of ascorbic acid orally per day.
Eating raw fruits and vegetables especially citrus fruits.
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7. Pellagra [10, 97]
a. Niacin (Vitamin-B3) [19, 13]
Ans. Niacin & Nicotinic acid are synonyms. It is also called as Pellagra preventing factor of Goldberger
Co-enzyme forms of niacin (NAD+, NADP+) help in cellular respiration
Niacin is Synthesized from Tryptophan
Causes for Niacin Deficiency: tryptophan, pyridoxine, Hartnup disease, intake of INH, Carcinoid
syndrome etc.
Deficiency of Niacin  PELLAGRA
Pellagra is seen among people whose staple diet is maize & sorghum (jowar or guinea corn)
– (meaning “raw skin”) is characterized by 3 Ds: ermatitis, iarrhea, and ementia.
Dermatitis—it appears as erythema resembling severe sunburn, symmetrically over the areas of
the body exposed to sunlight – dorsum of hands and feet, and neck (Casal’s necklace).
Skin lesions are dark, dry, and scaling.
Diarrhea—a/w glossitis, stomatitis & dysphagia – indicate the presence of inflammation throughout the GIT.
Dementia— seen in chronic cases
it begins with lethargy, insomnia and irritability, and progresses to confusion, memory loss,
hallucinations, and psychosis.

Nicotinamide – dose of 100 mg 8th hourly by mouth or by the parenteral route for 5 days.
Diet rich in niacin such as meats, milk, peanuts, green leafy vegetables, whole or enriched grains,
and brewers’ dry yeast.
Toxicity of Niacin: Niacin cause histamine release  vasodilatation  itching, burning and tingling.
Excess intake of 50 mg/day may lead to liver damage
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8. Thiamine deficiency [08]
 a. Clinical features of Beri-Beri [22, 19]
Ans.

 Thiamine is needed in carbohydrate metabolism – Thiamine pyrophosphate (TPP) helps in the

conversion of pyruvate to acetyl CoA. This is the bridge between glycolysis and the tricarboxylic acid (Krebs) cycle.
 TPP is also the co-enzyme for transketolase of the PPP {Pentose Phosphate Pathway}.
 Thiamine is also important for nerve impulse conduction.

Cause of deficiency: chronic alcoholics; poor diet; people eating mainly polished rice
Cells cannot metabolize glucose aerobically  accumulation of pyruvic and lactic acids 
vasodilatation & increased cardiac output. There is also less ATP generation.
Clinical Features
Infantile beriberi – seen in exclusively breastfed
infants of thiamine-deficient mothers
Dry beriberi – mainly affects nervous system
Wet beriberi – mainly affects heart
Treatment
Thiamine is given at a dose of 50 to 100 mg for 7 to 14
days IV or IM. Then an oral dose of 10 mg per day is
given until full recovery is achieved.
Korsakoff’s psychosis is irreversible and does not respond to thiamine treatment.
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9. Weaning [03]
Ans.
Weaning is a gradual withdrawal process starting around the age of 6 months, because the mother's
milk alone is not sufficient to sustain growth beyond 6 months.
It should be supplemented by foods rich in protein and other nutrients – Ex: cow's milk, fruit juice, soft
cooked rice, suji, dhal and vegetables.
The weaning period is the most crucial period in child development, for during the weaning process
children are particularly exposed to the deleterious synergistic interaction of malnutrition and
infection.
Weaning, if not done properly, is followed by diarrhoea and months of growth failure → kwashiorkor,
marasmus and immunodeficiency → recurrent and persistent infections w
At the age of 1 year, the child should receive solid foods consisting of cereals, pulses, vegetables &
fruits.
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1) Selenium deficiency [17]

Ans:
The family of seleno-enzymes includes:
Glutathione peroxidase – prevent free radical damage to cells
Monodeiodinase – converts thyroxine to triiodothyronine
Selenium deficiency can cause hypothyroidism, cardiomyopathy in children (Keshan’s disease) and
myopathy in adults. {Excess selenium can cause heart disease}
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2) Folic Acid deficiency [14]
Ans.
Folate deficiency cause 3 major birth defects (spina bifida, anencephaly and encephalocele) – occur
due to imperfect closure of the neural tube
Folate deficiency – in adults  megaloblastic anemia, heart disease, dementia and cancer.
All women planning a pregnancy are advised to include good sources of folate in their diet {Liver,
leafy vegetables}, and to take folate supplements (5 mg) throughout the first trimester
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3) Enumerate functions of Vitamin B6 [10]
Ans.

 Active form of pyridoxine {Vitamin B6} is pyridoxal

phosphate (PLP)
 PLP acts as co-enzyme for many reactions in protein
metabolism

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4) Abuse of the elderly [10]
a. Geriatric abuse [05]
Ans.
1. Psychosis – classify & Mx. Mention the difference between psychosis and neurosis. [22]
a. Major depression [21]; Depression [11, 06, 05]; Diagnosis of depression [05, 04]
b. Tricyclic Antidepressants [21, 19]; Antidepressants [11]
c. Schizophrenia [17, 14, 13, 10]; Two Drugs for treatment of Schizophrenia [21]; Paranoid schizophrenia [08];
Catatonia [02]
d. Bipolar Disorder [16, 15]; Manic depressive psychosis [01, 97]
e. Behaviour therapy [09, 05]
Ans.

Psychosis is defined as a severe mental condition in which thought and emotions are so affected
that contact is lost with external reality.
Psychotic disorders are characterized by delusions, hallucinations, disorganized thinking, motor
behaviour abnormalities (including catatonia), and negative symptoms.
If psychotic symptoms last more than 1 month, then it is called schizophrenia.
: Antipsychotic drugs {neuroleptics}– Examples: risperidone, olanzapine, clozapine, etc.
Features Psychosis Neurosis
Mental illness with
A reaction to a stressful
Cause underlying organic
condition
disease
Severity Major Minor
Empathy Absent Present
Contact
Absent Present
with reality
Insight Absent Present

 Depression is characterized by persistent low mood and loss of interests/pleasure.

 Prolonged depression is called dysthymia.
 Depression may be mild, moderate or severe, and episodic, recurrent or chronic.
 – Genetic predisposition;  serotonin & norepinephrine in the brain;
Adverse life events and emotional deprivation early in life.
Abnormal hypothalamo-pituitary-adrenal axis (HPA) regulation  cortisol levels that do not
suppress with dexamethasone.
Medical conditions: Hypothyroidism, severe anemia, hyperparathyroidism, Cushing’s disease,
Addison’s disease, tuberculosis, HIV, dementia, post-traumatic brain injury syndromes,
malignancy, SLE, etc.
Drugs: Alcohol, beta-blockers, withdrawal from cocaine and amphetamines.
 – For diagnosis, ≥5 of the following must be present nearly every day during same 2-
week period:
Depressed mood most of the day.
Markedly diminished interest or pleasure in all or almost all activities for most of the day.
Significant (>5%) weight gain or loss or decreased or increased appetite.
 Insomnia (often sleep-maintenance insomnia) or hypersomnia.
Psychomotor agitation or retardation observed by others (not self-reported).
Fatigue or loss of energy.
Feelings of worthlessness or excessive or inappropriate guilt.
Diminished ability to think or concentrate or
indecisiveness.
Recurrent thoughts of death or suicide, a suicide
attempt, or a specific plan for committing suicide.

Diagnosis is mainly based on clinical criteria.
Investigations are mainly done to exclude conditions that
can cause depression – CBC, TSH levels, and routine
electrolyte, vitamin B12, and folate levels; Test for illicit
drug use if suspected.

👉🏻
– Both cognitive behavioural therapy and interpersonal therapy are as
effective as antidepressants for mild to moderate depression.
(electroconvulsive therapy) – can be required for severe depression

Schizophrenia is a psychotic disorder that impacts thought processes, emotions & behaviour.

Genetic factors
Environmental factors—advanced paternal age, perinatal insults like viral infection, starvation,
toxic exposure, anoxia and birth trauma.
Exposure to psychoactive drugs in adolescence and young adulthood.
Psychological stresses like adverse life events & highly emotional family environment
Structural abnormalities of the brain - schizophrenic brains are smaller than normal brains, with
enlarged ventricles.
Schizophrenia can be associated with temporal lobe epilepsy, Huntington’s chorea, cerebral tumors
and demyelinating diseases. This is known as symptomatic schizophrenia.
:
Positive Symptoms
Negative Symptoms
(First-rank Symptoms) – synonymous with psychosis – ABCD.
: Auditory hallucinations.
Flattened (blunted) affect— loss of
Broadcasting, insertion/withdrawal of
capacity to express feelings  monotonous
thoughts belief that their thoughts are
voice, and absence of meaningful gestures.
being broadcast to others and others
Apathy and loss of drive (avolition)
thoughts are being ‘inserted’ into their
Social inattention
mind.
Poverty of speech
: Control of feelings, impulses or acts by
Poor self-care.
others.
: Delusions.
Catatonia—this refers to adoption of awkward postures for prolonged periods
 : DSM-5 criteria for the diagnosis
of schizophrenia are as follows.

bock D2 receptors in the brain

Conventional (typical, or 1st generation) drugs –
chlorpromazine and haloperidol
Newer (atypical, or second generation) drugs –
clozapine, olanzapine, quetiapine and risperidone.
• Newer drugs also block 5-HT2 receptors and are less
likely to produce extrapyramidal side-effects
• Clozapine can cause agranulocytosis and requires regular monitoring of WBC count.
support for the patient and family education.
• Cognitive behavioural therapy may help patients to cope with their symptoms and also to
adhere to treatment with antipsychotic drugs.
: After symptoms of schizophrenia have been controlled by drugs, social and
occupational rehabilitation is required to obtain employment and to re-establish a social network.

Bipolar disorders are characterized by alternating episodes of mania and depression

Genetic factors; Dysregulation of serotonin and norepinephrine
Triggers of Bipolar disorders: Stressful life events; physical illness & Drugs (e.g., cocaine,
amphetamines), alcohol, and certain antidepressants (e.g., tricyclics, MAOIs).

Manic Episodes:
Abnormally elevated mood lasting for at least 1 week.
Inflated self-esteem or grandiosity; More talkative than usual
Racing thoughts or flight of ideas.
Decreased need for sleep
Increase in goal-directed activity.
Excessive involvement in pleasurable activities like spending money or sexual indiscretion.
Hypomania refers to a less severe level of symptoms
Depressive Episodes – {refer pg. no. 122}
– done to rule out hyperthyroidism & stimulant drug abuse which can mimic
bipolar disorder.

Drugs for bipolar disorder – Mood stabilizers & 2ndgeneration antipsychotics.

Mood stabilizers – Ex: lithium, sodium valproate, and lamotrigine.
2nd-generation antipsychotics – Ex: olanzapine, aripiprazole, risperidone, lurasidone etc.
Antidepressants (e.g., SSRIs) can added for severe depression
Electroconvulsive therapy (ECT) – in refractory cases.
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1) Anxiety neurosis [22, 17, 16, 13, 12]

Ans.
Anxiety is a distressing, unpleasant emotional state of nervousness and uneasiness.
 Initial manifestations appear at the age of 20–35 years, and it is more common in women.
Symptoms: excessive worry about a number of events or activities, irritability, difficulty in
concentrating, and insomnia for at least 6 months.
Somatic manifestations – heart rate, palpitations; S.O.B., rapid breathing; chest pain or pressure;
choking sensation; dizziness; sweating; dyspepsia; trembling; tingling or numbness in arms and
legs; faintness; and dry mouth.
:
Generalized anxiety disorder Panic disorder
Separation anxiety Substance/medication-induced anxiety
Specific phobia disorder
Social anxiety Anxiety disorder due to medical conditions

Antidepressants such as escitalopram and venlafaxine are effective in anxiety disorder.

Alternatives: benzodiazepines and buspirone.
Psychotherapy (cognitive-behavioural therapy), relaxation and biofeedback may be of some help.
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2) Substance abuse [20]
a. Addiction [04]
Ans:
Substance abuse refers to excess use of a substance despite social, health & occupational problems
Substance dependence (addiction) refers to substance use a/w psychological dependence
(craving), physiologic dependence (withdrawal symptoms on stopping the drug) & tolerance.
Substance abuse & dependence are more common in men
Etiology – peer pressures; Easy availability of a drug; Psychiatric problems such as depression.
Diagnosis – it is based on history & examination.
Physical examination—needle marks in IV drug users; evidence of localized or systemic infections;
staining of teeth, respiratory problems in inhalation drug abuse.
Drug screening of samples of urine or blood.
Management
 Psychological counselling.
 Harm minimization—for example, advice to use clean needles.
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3) Post-Traumatic Stress Disorder [19, 17, 15]
Ans:
PTSD is recurring, intrusive recollections of an overwhelming traumatic event (e.g., rape, severe burns,
accident, military combat).

Risk factors: genetic influence, past psychiatric history and personality characteristics of high
neuroticism and extroversion
In PTSD, there is norepinephrine in response to stress
– Women are more affected than men
PTSD usually starts within 6 months after the traumatic event.
Feelings of fear, helplessness, or horror evoke PTSD.
 Typical symptoms are recurrent intrusive memories (flashbacks) of the traumatic event, as well as
sleep disturbance, nightmares (usually of the traumatic event) from which the patient awakes in a
state of anxiety, symptoms of autonomic arousal, and emotional blunting.
Patients often actively avoid stimuli that precipitate recollections of the trauma.

 Psychotherapy (exposure therapy) – Here the person is exposed to situations which he avoids
because they may trigger recollections of the trauma. Repeated exposure in fantasy to the
traumatic experience itself usually lessens distress after some initial increase in discomfort.
 Selective serotonin reuptake inhibitors (SSRI) such as sertraline are also effective in PTSD.
 Most patients recover within 2 years.
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4) Obsessive compulsive Neurosis [18, 14, 12]
a. Obsessive Compulsive Disorder (OCD) [19]
Ans:
Obsessions are persistent intrusive thoughts. Compulsions are intrusive behaviours.
:
In the obsessive-compulsive reaction, an irrational idea or impulse persistently intrudes into the
mind, leading to repetitive actions (Ex: washing the hands many times).
These patients are usually predictable, orderly, and intelligent.
Highest prevalence is in the young, divorced, separated, and unemployed.
Under extreme stress, these patients may exhibit paranoid and delusional behaviours, which
can mimic schizophrenia.
: two-thirds of OCD patients will develop major depression during their lifetime.

Exposure & ritual prevention therapy – It involves gradually exposing patients to situations or
people that trigger obsessions and rituals while requiring them not to perform their rituals.
Antidepressants – SSRIs and clomipramine are also effective in OCD.
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5) Melancholia [18]
Ans.
The word ‘melancholia’ means feeling intensely sad and hopeless.
It is a type of depression.
– are similar to the general symptoms of depression but are more severe.
Movements, thoughts and speech can be very slow. Less commonly, agitation can be seen.
Symptoms are worse in the morning
: Antidepressants + psychotherapy
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6) Lithium [10, 07, 04]
Ans:
MOA of Lithium:
Lithium reduces the release of IP3 & DAG, which are 2nd
messengers for both α-adrenergic and muscarinic transmission.
Lithium block action of ADH on collecting duct  nephrogenic diabetes insipidus
Inhibits the release of thyroid hormones
Increases total WBC count (leukocytosis)
Uses of Lithium:
a) As a prophylactic agent for bipolar disorder.
b) Lithium has a slow onset of action, hence, not useful for acute mania.
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7) Anorexia nervosa [04, 02]
Ans:
: Anorexia nervosa is an eating disorder characterized by restriction of energy intake relative
to requirements, leading to a significantly low body weight.
– Exact etiology is unknown, but a combination of genetic, environmental, psychological and
social factors (ex: Social pressure on women to be thin) play a role.
It is common in women.
Patients avoid high calorie foods leading to significant weight loss.
Some patients may eat and use purging to control their weight (via self-induced vomiting, use of
laxatives and diuretics).
Downy hair (lanugo) may develop on the back, forearms and cheeks.
Associated anxiety and depressive symptoms are common.
Extreme starvation affects multiple organ systems, especially heart and skeletal system.
Amenorrhea is also common
– Rule out other causes of weight loss such as:
Malabsorption syndromes (e.g. due to inflammatory bowel disease or celiac disease)
New-onset type 1 diabetes
Adrenal insufficiency, and cancer.
Amphetamine abuse may cause similar symptoms.

Goals of treatment:
To ensure patient’s physical well-being –
To maintain normal body weight,
To correct the psychological disturbances –
▪ Cognitive behavioural therapy to manage the anxiety related to eating and poor body image.
▪ Family therapy – encourage family members to refeed patients at home
▪ Psychotropic drugs – if there is associated depression.
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8) Juvenile delinquency [04]
Ans.
Juvenile means a boy of < 16 years and a girl of < 18 years.
The Children Act, 1960 in India defines delinquent as "a child who has committed an offence".
Causes of Juvenil delinquency:
1. Biological causes: The XYY men suffer from severe disturbance of the whole personality.
2. Social causes: Broken homes, e.g., death of parents, separation of parents, step mothers & Disturbed
home conditions, e.g., poverty, ignorance about child care, too many children, etc.
3. Other causes: Absence of recreation facilities, cheap recreation, sex-thrillers, urbanization and
industrialization, cinemas and television, slum-dwelling, etc.
Preventive measures:
1) Improvement of family life: A well-adjusted family can stem the tide of delinquency. Parents should be
prepared for parenthood. The needs of children should be appreciated and met.
2) Schooling: There should be a healthy teacher-pupil relationship. The school teacher can detect early
signs of maladjustment.
3) Social welfare services: recreation facilities, parent- counselling, child guidance, educational facilities
and adequate general health services.
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1. Somatization Disorders [19]

Ans:
Aka Somatic symptom disorder is characterized by an extreme focus on physical symptoms — such
as pain or fatigue — that causes major emotional distress.
Somatic symptom disorders include Factitious disorder, Conversion disorder, Psychological factors
affecting a medical condition etc.

Most patients have multiple somatic symptoms such as pain, headache, etc.
The somatic symptoms are not explained by a medical condition and are also not part of depressive
or anxiety disorder.
Symptoms persist for a long time & disrupts daily life.
When physical complaints accompany another medical disorder, patients over-respond to the
implications of the medical disorder; for example, patients who have had an MI may constantly
worry about having another MI or think themselves as unfit.

 Cognitive-behavioural therapy.
 Treatment of concurrent mental disorders (e.g., depression).
 SSRIs & serotonin-norepinephrine reuptake inhibitors (SNRIs)
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2. Side effects of anti-psychotic drugs [17]
Ans.Dose-Dependent extrapyramidal symptoms (EPS).
Parkinsonism: They are tremor, rigidity, hypokinesia, etc. Centrally acting anticholinergics
(benzhexol, benztropine and antihistamines like promethazine, diphenhydramine, etc.) are effective in controlling
these symptoms.
Acute dystonias: Uncontrolled muscular movements involving the face, tongue, neck, etc.
Akathisia: Feeling of restlessness- the person cannot sit at a place & has a desire to move about.
Neuroleptic malignant syndrome: characterised by muscular rigidity, hyperpyrexia, mental
confusion and coma. It is treated with i.v. dantrolene.
Tardive {late occurring} dyskinesia: involuntary
movements of the mouth, tongue and the upper
limbs.
Hyperglycaemia and precipitation of diabetes can
occur with chlorpromazine.
Hypersensitivity reactions can occur - skin rashes,
itching, dermatitis, leucopenia and rarely obstructive
jaundice

Antimuscarinic property may worsen delirium and dementia

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3. Dissociate personality [04]
Ans:
Dissociative disorder (aka hysteria; Conversion disorder).
 It consists of neurologic symptoms that develop unconsciously without a definable organic cause.
 “Conversion” is characterized by conversion of psychic conflict into physical symptoms.
Clinical Features – It is more common in young & uneducated poor women.
Onset can be linked to a stressful event.
Patients present neurologic symptoms – Ex: impaired coordination, weakness, paralysis of an arm
or a leg, seizures, blindness, etc.
There is apparent unconcern (La belle indifference) even in the face of gross physical disability.
Clues pointing towards conversion disorder are:
H/o similar episode in the past and a temporary “solving of the problem” by the conversion
Presence of a serious precipitating emotional event, presence of associated depression, etc.
A complete physical and neurological examination is important to rule out physical causes.
Treatment
Reassurance – Explain the physiological mechanism for the symptom that emphasizes the link with
psychological factors such as stress.
Advice on how to cope with stress and relaxation techniques.
Antidepressant drugs & Cognitive behavioural therapy can be helpful
1) Infective Endocarditis – etiopath, C/F, Complications, Dx, Mx & Prevention [22, 18, 17, 14, 09, 03]
a. Four Clinical features of Infective Endocarditis [21]
Ans. Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart.
Etiology:
» Causative Organism: > 90% of IE is caused by streptococci and staphylococci.
▪ Staph. aureus: in i.v. drug abusers.
▪ Coagulase-negative staphylococci (e.g., S. epidermidis) – MCC for prosthetic valve endocarditis.
▪ Streptococcus viridans: causes endocarditis of previously damaged or abnormal valves.
▪ Commensals in the oral cavity: HACEK group (Haemophilus, Actinobacillus, Cardiobacterium,
Eikenella, and Kingella) & Enterococci.
» Predisposing Factors- 3 factors ➔ Bacteremia;
Underlying heart disease & Low Immunity.
Pathogenesis: 👉🏻👉🏻👉🏻👉🏻👉🏻👉🏻👉🏻👉🏻👉🏻👉🏻
• Valves affected: Aortic and mitral valves (MC) &
valves of right heart (esp. tricuspid) in IV drug
abusers.
• Organisms that cause endocarditis usually enter
the bloodstream from mucosal surfaces, skin, or
sites of focal infection
Clinical Picture: Fever, chills, weakness, fatigue,
loss of weight & a flu like syndrome;
Murmurs
Investigations: Biopsy; Blood culture;
ECG.
Diagnostic criteria: Modified Duke’s
Criteria

Complications of Infective Endocarditis - These may

be divided into cardiac and extracardiac.
Cardiac Complications – Ring abscess; Myocardial
abscess; Perforation and rupture; Suppurative
pericarditis; Valvular dysfunction {Stenosis or
insufficiency}.
 Extracardiac Complications:
Embolic complications (due to septic emboli):
 Septic infarcts (e.g., spleen, kidney or brain)
 Small emboli (microthromboemboli) may produce tiny haemorrhagic lesions namely:
(1) Subungual hemorrhages and
(2) Janeway lesions which are nontender, hemorrhagic lesions on the palms or soles.
Immunological phenomena
 Focal segmental glomerulonephritis: Grossly, the outer surface of kidney
develops a flea-bitten appearance due to patchy haemorrhagic foci
involving the glomeruli.
 Osler nodes: small, tender subcutaneous nodules in the pulp of digits and
persist for hours to several days.
 Roth spots are retinal hemorrhages with white or pale centres
composed of fibrin.
Management
Antibiotic Regimens for Infective Endocarditis:
Vancomycin and gentamicin ( ) – For Native valve endocarditis {cover MRSA & Strep}
Linezolid or daptinomycin can be used if vancomycin is contraindicated
Vancomycin, Gentamicin and rifampicin ( ) – for Prosthetic valve endocarditis {cover MRSA,
coagulase-negative staphylococci}
Rifampin can penetrate the biofilm of most of the pathogens that infect these devices
Indications of Surgery: Prosthetic valve dysfunction, badly damaged valve, CCF, Large vegetations
(>10 mm) on echo, recurrent embolic events
Prevention: prevention of bacteremia by the administration of antibiotics prior to any procedure
can prevent the occurrence of infective endocarditis
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2) Acute Ml – Definition, Mechanism, Etiology, Risk Factors, C/F, Complications, inv. & Mx [22, 21, 18,
13, 12, 06]
a. Treatment of Acute Myocardial Infarction [14, 11]
b. Arrhythmias in myocardial Infarction [12]
c. Serum markers in acute myocardial infarction [08]
Ans.
Death of cardiac muscle secondary to prolonged ischemia of the coronary arteries.
Etiopathogenesis:
Risk factors: Advancing age, atherosclerosis, middle aged males, post-menopausal women.
Coronary Atherosclerosis: seen in 90% of MI cases;
Complete occlusion results in ischemic coagulative
necrosis of the area supplied by the particular coronary
artery. The anatomic area supplied by that artery is
called as the area at risk
Nonatheromatous Causes of MI:
Coronary Vasospasm without coronary atherosclerosis
Coronary Emboli: due to atrial fibrillation, Vegetations of IE, Intracardiac prosthetic material etc.
Vasculitis, Amyloid deposition in vascular walls, Hematologic disorders like sickle cell disease,
Vascular dissection, Lowered systemic blood pressure (e.g., shock).
 Arterial trunks involved:
a) Left anterior descending coronary artery – MC
b) Right coronary artery
c) Left circumflex coronary artery
Clinical Feature:
Precipitating factors: vigorous physical exercise,
emotional stress etc.
Chest pain for >30 min, crushing or squeezing in
nature; radiates to the neck, left shoulder & left arm.
N/V; Dyspnea; epigastric discomfort
O/E: Rapid, weak pulse; , diaphoresis;
rd th
3 + 4 heart sound, B/L basal crepitations (due to
pulmonary edema) can be heard on auscultation 👉🏻
Investigations:
: Cardiac specific troponins (T & I); CK-MB; Myoglobin
rises within 1-3 hrs & return to normal in 24 hrs
rise within 2–4 hours of the onset of MI, and returns to normal within 3
days
Cardiac troponins begin to rise in 2 to 4 hours & returns to normal in 5 to 10 days
: It not specific marker. It starts rising after 24–48 hours. It returns to normal in
7–14 days
:
 ST elevation is seen
with transmural infarct
{STEMI}
 No ST elevation seen with subendocardial infarct {NSTEMI}
 T wave inversions
: reveals Hypokinesia or akinesia of ventricular wall due to ischemia or infarction
(CAG) – to identify the site of block and allow percutaneous coronary
intervention.
– CBP, RFT, serum electrolytes, glucose, and lipid profile etc.
Management of MI:
– don’t delay – More delay means more myocardial damage.
Oxygen (2–4 litres/min for 6–12 hours after infarction).
Aspirin 300 mg oral + clopidogrel 300 mg oral + IV heparin
To relieve chest pain & anxiety – Sublingual glyceryl trinitrate 0.4 mg; IV morphine 2–5 mg
To sympathetic overactivity &  myocardial oxygen demand – IV β-blocker, e.g., metoprolol, 5
mg every 2 to 5 min for a total of 3 doses {avoid β-blockers in AV block, hypotension & in COPD}
– reperfusion can be done by 2 ways
 Fibrinolysis – should be done within 12 hours of STEMI – Streptokinase, tissue plasminogen
activator (tPA) – they activate plasminogen to plasmin which breaks down the thrombus
 Percutaneous Coronary Intervention (PCI) – includes angioplasty & stenting –
used in patients who have contraindications to fibrinolytic therapy
(CABG) – done in patients with left main stem
or triple vessel disease with impaired left ventricular function.
 Complications of MI:
1) Left ventricular failure and cardiogenic shock
2) Myocardial rupture: → result in hemopericardium and
cardiac tamponade.
3) Dilatation of ventricular chamber
4) Ventricular aneurysm: It develops as a late complication
of large transmural infarcts.
5) Extension of infarct: new areas of repeated necrosis can occur adjacent to an existing myocardial
infarct causing extension of infarct.
6) Arrhythmias – These include sinus bradycardia, tachycardia, ventricular tachycardia, and
ventricular fibrillation. In inferoseptal infarcts → partial or complete heart block
7) Progressive late heart failure (chronic IHD): Usually develops due to the functional
decompensation of hypertrophied noninfarcted myocardium.
8) Mural thrombus: Infarct  myocardial contractility (causing stasis) and endocardial damage
(creating a thrombogenic surface) which favour mural thrombosis → left-sided thromboembolism.
They may also develop within ventricular aneurysms
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3) Acute Rheumatic fever – Etiopath, C/F, Diagnostic Criteria, Mx & Prophylaxis [Aug-21, 16, 08]
a. Acute Pancarditis - etiology, clinical features and management [18]
b. Sydenham's chorea [17]; Rheumatic chorea [03, 97] ➔ refer CNS
c. Duckett Jones Criteria [17, 04]
d. Rheumatic Carditis [03, 97]
Ans.
Acute Rheumatic fever is a febrile disease affecting connective tissues initiated by infection of the
throat by group A beta haemolytic streptococci.
of rheumatic heart disease: -
 Acute rheumatic fever develops after a latent period of 2 to 6 weeks following an episode of
pharyngitis or tonsillitis by group A – β- hemolytic streptococci.
 Antibodies produced by B-cells against the M proteins of streptococci cross-react with self-antigens
in the myocardial cells and glycoproteins of the valves in the heart (type II hypersensitivity
reaction).
 Cytokines produced from stimulated T cells activate
macrophages, which are seen in lesions of rheumatic
fever.
:
 Acute rheumatic Carditis: Pericardial friction rubs,
tachycardia, and arrhythmias.
 Chronic RHD:
Murmurs; Cardiac
hypertrophy &
dilation; Heart
failure &
arrhythmias.

:
  Major: Migratory polyarthritis of the large oints; ancarditis; Subcutaneous odules; rythema
marginatum; ydenham chorea
 Minor: Fever; Arthralgia; WBC, ↑ acute phase reactants in blood; 1st degree AV block;
: Evidence of a preceding Group A streptococcal infection, with 2 major or 1 major & 2
minor manifestations
aims of management are to limit
cardiac damage and relieve symptoms
Bed rest – to joint pain; &  cardiac workload
Antibiotics – single dose of benzathine
penicillin or a 10-day course of penicillin-V (or
erythromycin if penicillin allergic) to eliminate
any residual streptococcal infection
Aspirin or Glucocorticoids – to relieve arthritis
Treatment of cardiac failure: medical
treatment  valve replacement or pacemaker insertion
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4) Describe Congestive Cardiac Failure – Etiology, C/F, Inv. & Treatment. Write in brief on heart failure
with preserved ejection fraction [May-21, 19, 17, 13, 11, 08]
a. Left Ventricular failure [14]
b. Heart failure – etiology, Dx & Mx [04]
Ans.
Congestive Cardiac Failure {Heart failure}: is defined as a complex clinical syndrome that can result
from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or
eject blood
- Heart failure can be due to the following factors:
1) Intrinsic pump failure {weak myocardium} – Myocarditis, MI, Cardiomyopathies, Arrhythmias etc.
2) Increased Workload on the Heart –
 Pressure overload – hypertension, Stenotic valves & COPD
 Volume overload – High output states (thyrotoxicosis, anemia, AV shunts, beriberi), ASD, VSD,
Valvular insufficiency (MR & AR)
3) Impaired Filling of Cardiac Chambers - Constrictive pericarditis; Cardiac tamponade
: mostly these are due to perfusion
Symptoms Signs
Dyspnea – it can be on exertion, Vital signs – low BP; PR & RR
on lying down (Orthopnoea) & General examination – Patient is dyspneic and orthopnic;
Paroxysmal nocturnal dyspnea JVP; Pitting pedal edema
Fatigue, nausea, anorexia, and CVS:
pain abdomen  Cardiac enlargement (apex beat shifted down and out)
Oliguria during daytime  MR, TR  Pansystolic murmur
Noturia – due to shift of fluid  3rd & 4th heart sounds are often audible
from the extravascular to the RS –due to pulmonary edema – Tachypnea; B/L fine basal
intravascular compartment  crepitations and rhonchi
excretion of sodium and water Abdomen – liver maybe enlarged & tender;
nocturia. CNS: Confusion, memory disturbances {brain perfusion}
 :
 Chest X-ray – to detect cardiomegaly & pulmonary edema;
 ECG: It can show cardiac rhythm, identify ischemia, prior or recent MI, and detect evidence of left
ventricular hypertrophy. It also shows conduction defects and electrolyte disturbances.
 Echocardiography – to confirm the presence of heart failure
 Radionuclide studies –non-invasive – for accurate measurement of wall motion abnormalities,
ventricular volume and ejection fraction
 serum levels of ANP (atrial natriuretic peptide) and
BNP (brain natriuretic peptide)
 Coronary angiogram can identify the extent of
coronary artery disease.
:
 Treat both the underlying and precipitating causes
 Non-pharmacological Measures: Adequate rest; Diet
low in salt & oils;
 Drug therapy: There are two distinct goals of drug
therapy in heart failure:
, this can be achieved by:
lnotropic drugs – Digoxin, dobutamine/ dopamine, inamrinone/milrinone
Diuretics – Furosemide, thiazides, metolazone
RAS inhibitors – ACE inhibitors/ARBs
Vasodilators – Hydralazine, nitrate, nitroprusside
Synthetic BNP – Nesiritide
β blocker- Metoprolol, bisoprolol, carvedilol,
nebivolol
and prolongation of
survival. This is possible with:
ACE inhibitors/ ARBs.
β blockers
Aldosterone antagonist – Spironolactone,
eplerenone
Neprilysin inhibitor – Sacubitril
 Circulatory Assist Devices/Cardiac Transplantation – for Class IV heart failure
 : It is a clinical
syndrome in which patients have
features of HF as the result of high left
ventricular (LV) filling pressure despite
normal ejection fraction

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5) HTN – Causes, Clinical Signs & Symptoms, End Organ Manifestations, Complications & Mx [20, 15, 10]
a. Secondary hypertension {incl. causes} [22, 16, 13, 08]
b. Retinal changes in hypertension [10]
c. Target organ damage in hypertension [08]
d. Hypertensive Left Ventricular Failure – C/F, inv. & Tt [03]
Ans.
Clinically significant hypertension is defined as DBP >90mm Hg or SBP >140mm Hg.
Pathogenesis of Essential or Primary Hypertension – MC type of HTN
Genetic factors: Polymorphisms in vasomotor tone or
blood volume regulation.
Reduced renal sodium excretion – increases fluid
volume & BP
Increased vascular resistance with vasoconstriction or
structural changes in vessel walls
Environmental factors: Stress, obesity, smoking,
physical inactivity, heavy salt consumption
Clinical features:
Symptoms Signs
BP is elevated (systolic ≥140 mmHg and
 Mostly asymptomatic – Hypertension is a “silent killer”
diastolic ≥90 mmHg).
 Headache.
Signs of an underlying cause – Ex:
 Attacks of sweating, headache & palpitations Radio-femoral delay in coarctation of the aorta.
(seen in pheochromocytoma).
Bruit may be heard over the abdomen in lumbar
 Breathlessness may be present due to left
area in renal artery stenosis
ventricular hypertrophy, diastolic dysfunction, Cushingoid features (lemon on stick appearance)
or heart failure. Cardiac examination reveals left ventricular
 Angina & leg claudication {due to atherosclerotic hypertrophy and a loud A2.
narrowing of coronary and lower limb arteries}.
Optic fundus should be examined in all
 Malignant hypertension presents with severe patients for hypertensive retinopathy
headache, vomiting, visual disturbances, seizures,
changes.
altered sensorium, or symptoms of heart failure.
In malignant hypertension, there is papilledema.
Complications of Hypertension:
CVS complications – Left ventricular hypertrophy; CAD (Angina, MI); Aortic dissection; Heart failure;
 CNS complications – TIA, stroke, Intracerebral hemorrhage, Subarachnoid hemorrhage &
Hypertensive encephalopathy
Renal Complications: Proteinuria; CKD; Hypertensive
nephrosclerosis.
Ophthalmic Complications
Malignant Hypertension – characterized by very high BP
with papilledema and end organ damage

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6) Classify congenital heart diseases. Write Fallot’s Tetralogy – C/F, inv., complications & Mx [18, 15, 11, 08]
a. Name two congenital heart diseases [20]
Ans.
 MC cyanotic congenital heart disease with right to left
shunt.
 The 4 components of tetralogy of Fallot (TOF) are:
1) VSD
2) Overriding aorta
3) Right ventricular out flow tract obstruction
4) Right ventricular hypertrophy (RVH)

Mild (RVOT) obstruction—Often presents with an

isolated murmur (Pink tetralogy).
Severe obstruction (PS) presents with cyanosis, left lower parasternal heave, S 2—loud and single
(due to anterior position of the aorta and soft closure of the pulmonary valve).
Intensity of the murmur is inversely proportional to the degree of obstruction
Pan digital clubbing
– seen in TOF in children < 2 years of age.
 ▪ Events like waking up in the morning or exertion (excessive crying/straining for defecation) which
decreases the systemic vascular resistance, initiates the spell.
▪ Child Starts crying → becomes more hyperpneic and restless → deepening of cyanosis
(disappearance of heart murmur) → Gasping respiration → syncope may follow → severe spells
can lead to convulsions or hemiparesis. This vicious cycle continues if not intervened
▪ Toddlers assume squatting to relieve these symptoms

Hypoxic spells and Squatting.

Cerebral abscesses from septic emboli, cerebral thrombosis/stroke due to dehydration
and bacterial endocarditis may occur.
Polycythemia {erythropoietin stimulation due to low arterial oxygen saturation.} Though they
have polycythemia, smear shows microcytic RBCs due to relative iron deficiency.
Bleeding disorder, gout.

For cyanotic spells – Knee-chest position, vasoconstrictors

Correct iron-deficiency anemia

▪ Corrective Surgery: Patch closure of the VSD and RV muscle bundle resection + trans pulmonary
valve annulus patch or pulmonary valvotomy at 6–12 months of life.
▪ Palliative Surgery – Blalock–Taussig shunt

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7) Angina Pectoris – Risk Factors, C/F & Mx [15]
a. Unstable angina [02]
b. Prinzmetal’s angina [2000]
Ans.
 Angina pectoris is defined as a discomfort in the chest and/or adjacent area associated with
myocardial ischemia but without myocardial necrosis.
 It is a common presenting symptom among patients with coronary artery disease (CAD).
:
Stable angina
Unstable angina is diagnosed when a patient has new-onset
angina, worsening angina, or angina occurring at rest.
Prinzmetal’s angina is due to coronary vasospasm occurring at
rest.
Decubitus angina

History Physical Examination

General examination – reveals the following:
Angina usually builds up within 30 seconds ▪ Signs of generalized atherosclerosis like
and disappears in 5 to 15 minutes. tendon xanthoma, xanthelasmas,
The discomfort is most commonly thickening of Achilles tendon, locomotor
midsternal and radiates to the neck, left brachialis and corneal arcus.
shoulder, and left arm. ▪ Signs of PVD – Ex: absent peripheral
The clenching of the fist over the sternum pulses.
while describing the pain (Levine’s sign) ▪ Heart rate & BP.
Pain may be associated with sweating, ▪ Excessive sweating may be noted.
palpitations, dizziness and dyspnea. Systemic examination –
There may be history of other comorbid 3rd and 4th heart sounds;
conditions like diabetes and hypertension. Mitral regurgitation murmur,
Smoking history may be positive. Paradoxical splitting of S2, Bilateral basal
crepitations may be heard during ischemia.

Resting ECG: During an attack, ST depression and T wave inversions in the leads corresponding to
ischemic areas may be seen.
Exercise ECG (Stress Test): Patient is asked to walk on a treadmill and ECG is recorded
continuously. Patient may experience chest discomfort during exercise and if ECG shows ST
depression of >1 mm, it suggests myocardial ischemia.
Cardiac Scintigraphy: Myocardial perfusion scans at rest and after stress (i.e., exercise or
dobutamine), is a sensitive indicator of ischemia and useful in deciding if a stenosis seen at
angiography is giving rise to ischemia.
Echocardiography: Ischemic or infarcted ventricular wall does not move properly. This is called
regional wall motion abnormality (RWMA) and reflect ischemia or previous infarction
Coronary Angiography (CAG): It is always done in patients being considered for revascularization
(i.e., coronary artery bypass grafting or coronary angioplasty).

Give reassurance – advice to stop smoking; regular exercise and low-fat

diet; Treat Comorbid conditions such as anemia, hyperthyroidism, diabetes, HTN, &
hypercholesterolemia.

Glyceryl trinitrate (GTN) & Long-acting nitrates (e.g. isosorbide dinitrate and mononitrate)
 Antiplatelet agents: Aspirin, Clopidogrel
Beta-blockers: atenolol, metoprolol, carvedilol, and nebivolol
Angiotensin-converting enzyme (ACE) inhibitors
Statins
Calcium channel blockers: diltiazem and verapamil, amlodipine, felodipine, nifedipine
: Percutaneous transluminal coronary
angioplasty (PTCA) is the technique of dilating coronary
stenosis by passing and inflating a balloon inside the
stenosis.
CABG is indicated
when patients remain symptomatic despite optimal
medical therapy and whose disease is not suitable for
PTCA.
)
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8) Mitral Stenosis – etiology, symptoms, signs, complications and management [11, 10, 04]
a. Clinical features of Mitral Stenosis [22]
Ans.
Mitral valve stenosis — sometimes called mitral stenosis — is a
narrowing of the valve between the two left heart chambers
:
Almost always rheumatic in origin
Other rare causes: congenital mitral
stenosis & heavy calcification of the
mitral valve in old age
Atrial dysrhythmias,
thromboembolism, CCF, pulmonary
infarcts, hemoptysis, Infective
endocarditis, pulmonary infections, etc.
:
Medical management – for mild symptoms
Anticoagulants to risk of systemic embolism
Digoxin, β-blockers or calcium
antagonists – to control ventricular
rate
Diuretic to control pulmonary
congestion.
Antibiotic prophylaxis against
infective endocarditis
Surgical Intervention – if the patient
remains symptomatic despite medical
treatment or if pulmonary hypertension
develops. The options are:
Mitral balloon valvuloplasty is the treatment of choice if specific criteria are fulfilled
Alternative: mitral valvotomy.
Valve replacement is indicated if there is mitral reflux or if the valve is rigid and calcified
----------------------------------------------------------------------------------------------------------------------------------------
9) Draw a diagram of the conducting system of the heart. Write the various atrioventricular (A.V.)
blocks. Draw illustrative electro cardiograms [09]
a. P-R Interval [19]
b. Wenckebach's phenomenon [18]
c. Complete Heart Block [14]
Ans.
Heart block conduction block
can occur at any level in the
conducting system
 Atrioventricular (A.V.) blocks –
refers to block in either the AV
node or the His bundle
 Bundle branch block – refers to block lower in the conduction
system
PR interval = Atr depolar + AVN delay
Atrioventricular (A.V.) blocks
AV block is defined when some or all impulses are delayed or
do not reach the ventricle during normal sinus rhythm
Conduction through AV node may be Delayed (First-Degree
AV Block), Intermittent (2nd-degree AV block) or absent (3rd-degree AV block).
1st Just delay in the AV node;
degree PR interval >0.2 sec
Mobitz Progressive prolongation of PR
type I interval until a P wave fails to
block conduct
{Wenckebach
Usually, it does NOT progress to complete AV block.
2nd phenomenon}

degree Here the conduction fails

Mobitz suddenly and unexpectedly
type II without a preceding change in PR
block intervals.
It can progress to complete AV block

Complete AV Block –
3 rd
▪ ECG shows constant P-P & R-R intervals
degree but with complete AV dissociation, i.e.,
atria and ventricles beat independently
Management of AV Block:
In most cases, the AV block will resolve within 7–10 days.
Asymptomatic 1st-degree or Mobitz type-I 2nd-degree AV
block (Wenckebach phenomenon) does not require
treatment
For Symptomatic 2nd- or 3rd-degree AV block – Atropine
(0.6 mg IV, repeated as necessary) or, if this fails, a
temporary pacemaker.
If the patient presents with asystole, start IV atropine (3 mg) or IV isoprenaline (2 mg in 500 mL
5% dextrose, infused at 10–60 mL/hr) until a pacemaker can be inserted
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10) Classify cardiomyopathy. What are the clinical features each type? Outline the treatment [07]
a. Ischemic cardiomyopathy [22]
b. Cardiomyopathy [20]
Ans. Cardiomyopathies are primary diseases of the myocardium, which are classified according to their
effects on cardiac structure and function
Type of CM Clinical Features Treatment
▪ Autosomal dominant transmission
▪ Dilation of all the 4 chambers
▪ Results in systolic dysfunction (ventricles Treatment is symptomatic until
Dilated CM
cannot pump), leading to biventricular CHF; a heart transplant is made
▪ Chest pain {mimic ACS}
▪ Cardiac Ejection Fraction will be < 25%
 Autosomal dominant transmission
▪ Beta-blockers, calcium
antagonists & disopyramide
▪ Amiodarone for
Hypertrophic
arrhythmias
CM
▪ To relief outflow
obstruction – myectomy or
septal ablation can be done

 Autosomal dominant transmission

 It is characterised by replacement of  Treat the right-sided cardiac
patches of the right ventricular myocardium failure with diuretics
with fibrous and fatty tissue  Cardiac arrhythmias with β-
Arrhythmogenic
 Ventricular arrhythmias, sudden death and blockers
ventricular CM
right-sided cardiac failure can occur  Implantable defibrillator –
 ECG typically shows broadened QRS In patients at high risk of
complex and inverted T waves in the right sudden death
precordial leads.
Ventricular filling is impaired because the
Restrictive CM Treatment is symptomatic until
ventricles are ‘stiff’ (due to infiltration) high atrial
(Obliterative CM) a heart transplant is made
pressures & atrial hypertrophy
Acute left ventricular outflow obstruction
characterised by dilatation of the left
ventricular apex a/w stress. {Broken heart syndrome}
▪ Presents with chest pain, breathlessness
 β-blocker – to prevent
and sometimes cardiac failure
arrhythmia
Takotsubo CM ▪ Women > men
 ACE inhibitor – to treat left
▪ Echocardiography then shows characteristic
ventricular dysfunction
‘apical ballooning’ of the LV
▪ The dilated apex and narrow outflow of the
LV resemble a Japanese octopus trap, or
takotsubo
Amyloidosis; Sarcoidosis; Storage diseases {glycogen, hemochromatosis, Niemann-Pick disease};
Secondary
endocrine diseases; Nutritional deficiencies; Autoimmune diseases;
Causes of CM
neuromuscular diseases {Friedreich’s ataxia} & Drugs {heavy metals}
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11) Write the anatomy of pericardium. What are the clinical features and treatment of pericardial
effusion? [06]
Ans.
Anatomy of pericardium:
The pericardium is a fibroserous sac which encloses the heart and
the roots of its great blood vessels
Site: The pericardium lies within the middle mediastinum,
posterior to the body of the sternum and 2nd–6th costal cartilages
and anterior to the middle four thoracic vertebrae (i.e., from T5 to T8).
Sinuses of the pericardium – 2 – Transverse sinus & Oblique
sinus; - they are formed due to the reflection of visceral
layer of pericardium around the great vessels of the heart
Functions of the pericardium:
▪ Restricts excessive movements of the heart
▪ Serves as a lubricated container in which heart can
contract and relax smoothly
▪ Limits the cardiac distension
Clinical features of pericardial effusion
Sharp retrosternal and left precordial pain sometimes referred to back and left shoulder.
Pain is exacerbated by movement, respiration and lying down. It is typically relieved by sitting
forward.
Pericardial friction rub heard best at the end of expiration with the patient leaning forward.
Pericardial rub becomes quieter as fluid accumulates and separates the layers of the pericardium.
Apex beat is obscured
Ewart’s sign – pericardial effusion compresses the base of the left lung, producing an area of
dullness to percussion below the angle of the left scapula
Cardiac tamponade maybe present
Treatment of pericardial effusion:
Identify & treat the cause
Pericardiocentesis is indicated to relieve the pressure if there is tamponade
Recurrent effusions (commonly due to malignancy) may require pericardial fenestration
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12) Discuss the role of risk factors and life style modification in ischaemic heart disease [05]
Ans.
– Cigarette smoking, High BP, ↑serum cholesterol, DM, Obesity, Stress etc.
– Age, Sex, Family history, Genetic abnormality etc.
Smoking – Nicotine stimulates adrenergic drive → ↑BP & myocardial oxygen demand;
Hypertension: accelerates the atherosclerotic process.
↑Low-density lipoprotein (LDL) cholesterol. HDL cholesterol is protective against the development of CHD.
Diabetes: The risk of CHD is 2-3 times higher in diabetics than in non-diabetics.
A family history of CHD is known to increase the risk of premature death.
Hormones – Ex: ↑estrogen.
Oral contraceptives – ↑risk of myocardial infarction in women
Alcohol: High alcohol intake is an independent risk factor for all cardiovascular diseases.
 Prevention of ischaemic heart disease:
 Specific interventions like:
 Dietary changes:
▪ ↓ fat intake to 20-30 % of total energy intake
Population strategy –
▪ Saturated fats must be limited to < 10 % of total energy intake;
▪ ↑ in complex carbohydrate consumption (i.e., vegetables, fruits,
The aim is to change the
whole grains and legumes)
community as a whole,
▪ Reduction of salt intake to 5 g daily or less
not the individual
 Avoid alcohol consumption
subjects living in it
 Achieve a smoke-free society
 ↓ Mean population BP levels (by ↓salt intake, ↓Alcohol)
 Regular physical activity
Identifying those at High risk – By means of simple tests such as BP &
serum cholesterol measurement
High risk strategy Specific advice: Having identified those at high risk, the next step will be
to bring them under preventive care and motivate them to take positive
action against all the identified risk factors
▪ e.g., cessation of smoking, control of hypertension and diabetes, healthy
Secondary prevention –
nutrition, exercise promotion etc. (same as above)
▪ Secondary prevention must be seen as a continuation of primary
The aim is to prevent the
prevention
recurrence &
▪ Much research is in progress for Secondary prevention – Ex: drug trials,
progression of CHD
coronary surgery, use of pace makers)
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1. Atrial Fibrillation {incl Mx} [21, 20, 19, 15, 17, 14, 06, 04, 03, 02]
a. Difference between atrial flutter and atrial fibrillation [11]
Ans.
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial
activation with consequent deterioration of mechanical atrial function.
AF is the most common arrhythmia in adults.
– 3 types – paroxysmal, persistent or chronic
 Paroxysmal AF refers to an episode that terminates
spontaneously or with intervention in < 7 days.
 Persistent AF refers to episode sustained for more than
7 days, or AF that terminates only with cardioversion.
 Chronic or permanent AF is the one that is
unresponsive to cardioversion.

Symptoms Signs
Can be asymptomatic. Irregularly irregular pulse which is usually 100–150 per minute.
Patients may complain of Varying volume of pulse.
anxiety, palpitations, Apex pulse deficit.
fatigue and dyspnea. Loss of ‘a’ wave in JVP due to absent atrial contraction.
Patients may also present Variable intensity S1.
with stroke due to Signs of cardiac failure – B/L basal lung crepitations
systemic embolism. Features of underlying disease-causing atrial fibrillation.
 :
There is no coordinated mechanical contraction of atria giving rise to turbulence and stasis of blood
in the atria leading to clot formation  Thromboembolism
Syncope, Hypotension, Pulmonary edema, Angina & Cardiac failure

ECG shows varying RR intervals. P waves are absent

Echocardiogram can detect underlying condition such as mitral stenosis, atrial dilatation and clot
Routine tests include complete blood count (to identify anemia), thyroid function tests (to identify
hyperthyroidism), serum electrolytes (to identify electrolyte imbalance) and chest X-ray (to identify
pneumonia, COPD).

Identify & treat the cause accordingly

If patient is hemodynamically unstable  start anticoagulants & electrical cardioversion (DC shock
with 100 to 200 joulesif fails  try with 360 J) + IV procainamide.
For hemodynamically stable patients, treatment depends on the duration of AF
If AF duration is less than 48 hours  anticoagulants & cardioversion can be attempted.
If AF duration is ≥48 hours  only anticoagulants; Cardioversion is risky, because clot formation
can occur in the atria, which can be dislodged by cardioversion.
i.v. β-blockers (esmolol, metoprolol) or CCB (verapamil or diltiazem) – to control ventricular rate
Chronic anticoagulation is required for these patients to prevent clot formation.
AV node ablation & pacemaker implantation – for patients with poor rate control despite optimal
medical therapy
Atrial flutter Atrial fibrillation
Atrial flutter is an organized atrial Atrial fibrillation (AF) is a supraventricular tachyarrhythmia
rhythm with an atrial rate between 250 characterized by uncoordinated atrial activation with
and 350 beats per minute consequent deterioration of mechanical atrial function
In atrial flutter, the atria beat regularly,
In atrial fibrillation, the atria beat irregularly.
but faster than usual
ECG shows regular sawtooth-like atrial
ECG shows varying RR intervals. P waves are absent and
flutter waves (F waves) between QRS
there may be undulating baseline instead of P waves
complexes
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2. Treatment of Digitalis Toxicity [19]
a. Digitalis [08, 05]
Ans.
Digitalis lanata is the source of Digoxin, the only glycoside that is currently in use. Others like Digitoxin (from
Digitalis pupurea) and Ouabain (from Strophanthus gratus), etc. are no longer clinically used or marketed

Pharmacological Actions: Cardiac & Extracardiac.

: Digitalis has direct and indirect actions on the heart.
 Direct action by inhibiting Na+-K+-ATPase.
 Indirect action by stimulating vagus (vagomimetic effect).
Myocardial contractility: Digitalis ↑the force of contraction of the myocardium (positive
inotropic effect) → complete emptying of the ventricles during systole → ↓pulmonary
congestion and systemic venous pressure. The diastolic size of the heart is reduced. When the
size of the heart is reduced, muscle fibre length is also reduced, thereby, decreasing the oxygen
 requirement of myocardium. The digitalised heart, thus, can do more work for the same energy.
Therefore, digitalis is called as 'cardiotonic’.
Heart rate: In small doses, digitalis ↓heart rate by stimulation of vagus. In toxic doses, it can
increase sympathetic activity thus increasing heart rate.
Electrophysiological actions: At therapeutic concentrations, digoxin increases resting membrane
potential by vagal action in atria and AV node. It also prolongs effective refractory Period (ERP)
and decreases conduction velocity in AV node. This may lead to bradycardia and AV block. At
higher concentrations, digoxin can increase automaticity in cardiac tissue by direct action as well
as by increasing sympathetic activity. This can result in atrial and ventricular arrhythmias
ECG: Digitalis produces prolongation of P-R interval, inversion T wave and depression of ST
segment.

GIT: Digitalis can produce anorexia, nausea, vomiting and

occasionally diarrhoea.
Kidney: In patients with CCF, digitalis causes diuresis
(increased urine output).
CNS: In high doses, it can cause central sympathetic
stimulation, confusion, blurring of vision, disorientation, etc.
Adverse Effects: Digoxin has a narrow margin of safety.

GIT: anorexia, nausea and vomiting, which are due to GI

irritation and CTZ stimulation.
CNS effects: headache, confusion, restlessness, disorientation, weakness, visual disturbances,
altered mood and hallucinations.
Skin rashes and gynaecomastia can occur occasionally.

Factors Affecting Digitalis Toxicity:

 Age: Elderly patients are more susceptible to digitalis toxicity due to declining renal & hepatic functions
 Route: Intravenous digitalization carries more risk than oral route
 Hypokalaemia increases the binding of digoxin to Na+ K+ ATPase and enhances its toxicity
 Hypercalcaemia and hypomagnesaemia enhance digoxin toxicity
 Hypothyroidism, hyperthyroidism, hypoxia, renal failure and myocarditis are predisposing factors
to digitalis toxicity
Treatment of Digoxin Toxicity
 Shift the patient to ICU
 Stop digoxin and potassium depleting diuretics (thiazides/loop diuretics)
 Potassium chloride orally or intravenously is the DOC for tachyarrhythmias (if K+ levels are low)
 Intravenous lignocaine is the DOC for ventricular arrhythmias
 Supraventricular arrhythmias are treated with oral or intravenous Propranolol
 AV Block & Bradyarrythmias are treated with atropine and Cardiac pacing
 Digoxin antibodies (Digibind): neutralises the circulating digoxin/digitoxin & rapidly reverses
toxicity, but it is expensive.
Uses of Digitalis
: Digitalis is useful in patients with low output failure especially when
a/w atrial fibrillation. It is ineffective in high output failure associated
with severe anaemia, thyrotoxicosis and AV shunt. The beneficial effects
of digoxin are due to its action on:
 Myocardium (+ve inotropic effect);
 Venous system.
 Kidney.
: It is the most common cardiac arrhythmia. In atrial
fibrillation, the atria beat at a rate of 350-600/minute. Digitalis has both
direct and indirect (vagomimetic) actions on AV node. It depresses AV
node by increasing ERP and decreasing conduction velocity, thus reduces
the ventricular rate.
: In atrial flutter, the atria beat rapidly at a rate of about
300/minute. Digitalis controls ventricular rate by depressing AV
conduction
(PSVT): In PSVT, the heart rate is about 140-220/minute. The preferred drug for PSVT is
adenosine. Digoxin is preferred in PSVT, if there is associated heart failure. It terminates the arrhythmia by increasing the vagal tone.
----------------------------------------------------------------------------------------------------------------------------------------
3. Pre-excitation syndromes [18]
Ans.
Pre-excitation syndromes occur due to accessory pathways between the
atria and the ventricle that avoid the conduction delay of the AV node  earlier activation (pre-
excitation) of the ventricles  Short PR.
:
Lown-Ganong-Levine syndrome Wolff-Parkinson-White (WPW) syndrome
 It the MC accessory pathway SVT
 Here the accessory pathway may be wholly
 Here the accessory pathway (Kent bundles)
or partly within the node (Mahaim fibers).
directly connects the atria and ventricle
 The QRS complex is normal, since ventricular
 QRS complex will be abnormal, since
activation is via the normal conduction
ventricular activation is via both the AV &
pathway (His Purkinje system)
accessory conduction pathway
: ECG, Electrophysiological studies

Vagotonic maneuvers during SVT.

Drug therapy – These drugs increase the refractory period of accessory pathway and conduction
rate through it:
Adenosine for emergency management of SVT.
Verapamil or diltiazem if narrow QRS complex (antegrade conduction through AV node).
Wide QRS complex tachycardia (antegrade conduction through accessory pathway) – found a/w
AF – If hemodynamically compromised, immediate cardioversion is indicated; otherwise, treat
with IV procainamide or ibutilide
For frequent recurrence, radiofrequency catheter ablation of accessory pathway is done.
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4. TEE (Trans Esophageal Echocardiography) [16]
Ans. In TEE, an ultrasound probe is passed into the esophagus and placed behind the left atrium. It can
obtain clear images of cardiac structures especially valves and left atrium.
Uses of TEE
It is useful to pick up vegetations in infective endocarditis which may not be detected by surface
echocardiography.
 It is also useful for investigating patients with prosthetic (especially mitral) valve dysfunction,
congenital abnormalities (e.g., ASD), aortic dissection, and systemic embolism.
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5. Cardio pulmonary Resuscitation (CPR) [16]
Ans.
Immediate CPR increases the survival after cardiac arrest.
The sooner it is initiated the better is the prognosis.
Goals of CPR are:
(1) Restoring a spontaneous circulation as quickly as possible;
(2) maintaining continuous artificial circulatory support until
return of a spontaneous circulation has been achieved.
CPR consists of 4 main parts:
1. Circulation (C)
2. Airway (A)
3. Breathing (B)
4. Defibrillation (D)
As per new American Heart Association guidelines, the sequence of CPR is CAB and not ABC.

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6. Pericarditis [15]
a. Signs of Constrictive Pericarditis [19, 02]
Ans.
Pericarditis is inflammation of the pericardium.
Pericarditis can be classified as acute (<6 weeks), subacute (6 weeks to 6 months) and chronic
(>6months).
Constrictive Pericarditis – Here the pericardium
becomes thick, fibrous and calcified, which interferes
with relaxation of the heart during diastole

Ascites, dependent edema, hepatomegaly, and

raised JVP {due to  ventricular filling}
ventricular filling cardiac outputfatigue, hypotension, and reflex tachycardia
Pulmonary venous congestion produces dyspnea, cough, and PND
Kussmaul’ s sign and pulsus paradoxus
A ‘pericardial knock’ may be heard in early diastole at the lower left sternal border due to rapid
ventricular filling.
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7. Pulsus paradoxus [13, 05]
Ans.
BP normally falls (less than 10 mmHg) during inspiration but rises during expiration.
Pulsus paradoxus is an exaggeration of the normal phenomenon leading to exaggerated fall in BP
{>10 mmHg fall during inspiration} during inspiration. Hence, the name "paradoxus" is a misnomer
Causes of Pulsus Poradoxus: Constrictive pericarditis; Cardiac tamponade; Restrictive
cardiomyopathy; COPD; Severe asthma & Tension pneumothorax

Reverse Pulsus Paradoxus – This refers to inspiratory rise in arterial pressure – seen in
hypertrophic cardiomyopathy, positive pressure ventilation and AV dissociation
----------------------------------------------------------------------------------------------------------------------------------------
8. Ventricular ectopics [11]
a. ECG in ventricular ectopic beat [10, 07]
Ans.
Also known as ventricular premature complexes (VPC), or ventricular premature beat.
Etiology – Idiopathic, MI, Drug toxicity (e.g. digitalis intoxication), Electrolyte disturbances (e.g.
hypokalemia), Coronary artery disease, Heart failure; Hypertension; Valvular heart disease.
Characteristics of VPCs:
Single VPCs may occur sporadically or as bigeminy (every other beat is a VPC), trigeminy (every
third beat is a VPC), or higher order periodicities
Two consecutive VPCs are termed a couplet.
Three or more consecutive VPCs at a rate of 100 beats per minute or more are termed
ventricular tachycardia (VT).
Clinical Features:
 can be asymptomatic
The pulse is irregular due to premature beats;
Patient may complain of extra beats, missed beats or heavy beats because it may be the
premature beat, the post-ectopic pause or the next forceful sinus beat that is noticed by the
patient
ECG in ventricular ectopic beat
Broad (>0.12 s) and bizarre QRS complex, not preceded by P waves.
If the VPC comes early (‘R on T’ ventricular premature beat occurring simultaneously with the
upstroke or peak of the T wave of the previous beat), it may induce ventricular fibrillation in
patients with heart disease
Treatment:
 Identify & treat the underlying cause
 No treatment required for asymptomatic patients
 Symptomatic patients are treated with betablockers or amiodarone
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9. DC Cardioversion [11]
Ans.
 Cardioversion is the delivery of electrical shock that is synchronized to the R wave of QRS complex
 The machine used for cardioversion is called defibrillator
Indications: Atrial fibrillation, Atrial flutter, Supraventricular tachycardia, VT (ventricular tachycardia)
& VF (ventricular fibrillation).
Method – There are two electrodes in the defibrillator.
One is applied below the right clavicle. Another is applied on the lower part of left axilla.
Required amount of energy is selected.
After clearing everybody from the patient, shock is delivered by pressing the shock button.
Complications
Skin burns.
ECG changes (ST segment and T wave changes).
Precipitation of new arrhythmias.
Embolization – esp. in patients with AF who have not been anticoagulated prior to cardioversion.
Myocardial dysfunction and necrosis.
Transient hypotension & Pulmonary edema.
----------------------------------------------------------------------------------------------------------------------------------------
10. Angiotensin receptor blocker [09, 05]
Ans. Angiotensin Receptor Blockers (ARBs) or Angiotensin Receptor Antagonists:
ARBs competitively inhibit the binding of angiotensin-II to AT1-receptor and block its effects.
ARBs produce effects similar to those of ACE inhibitors but do not affect bradykinin production.
headache, hypotension, weakness,
rashes, nausea, vomiting and teratogenic
effects. They may cause hyperkalaemia in patients with renal failure or in patients
on K+-sparing diuretics.
ARBs are used in HTN, CCF, MI & Diabetic nephropathy. Like ACE inhibitors,
ARBs Prevent/delay the development of renal complications in diabetics. ARBs are
mainly indicated in patients who develop cough & are intolerant with ACE inhibitors.
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11. Signs in aortic aneurysm [05]
Ans.
Abdominal Aorta Aneurysm Thoracic Aorta Aneurysm
• Pain in the hypogastrium or
• Pain in the chest or back.
lower back. Pain is steady
• Symptoms due to compression of adjacent structures:
gnawing type and may last
 Hoarseness of voice due to compression of
for hours to days.
• Examination reveal a
 Diaphragmatic paralysis due to compression of
pulsatile mass at or above
 Wheezing, cough, hemoptysis, dyspnea, or pneumonitis
the umbilicus.
due to compression of the
• An arterial bruit may be
 Dysphagia due to compression of
heard over the abdomen if
 Superior vena cava syndrome due to compression of .
there is atherosclerotic
• Tracheal tug is descent of trachea with every heartbeat. It is
narrowing.
seen in arch of aorta aneurysm due to pulsatile pressure on
• When the aneurysm
the left bronchus.
ruptures, patient presents
• Ascending aorta aneurysms – heart failure due to aortic
with abdominal pain,
regurgitation from aortic root dilatation and myocardial
hypotension and a pulsatile
infarction due to compression of a coronary artery.
abdominal mass.
----------------------------------------------------------------------------------------------------------------------------------------
12. Non-invasive Cardiac Imaging [03]
Ans. Non-invasive cardiac imaging is used for the diagnostic and prognostic assessment of patients
with heart diseases
Examples of Non-invasive Cardiac Imaging:
▪ Exercise ECG;
▪ Stress Echocardiography
▪ Cardiac MRI
▪ MPI – Myocardial Perfusion Imaging
▪ CCTA – Coronary CT Angiography
{refer each section appropriately}
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13. Apical impulse [02]
Ans.

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1) Cardiac Tamponade – Clinical Signs [22]
Ans.

----------------------------------------------------------------------------------------------------------------------------------------
2) Sick Sinus Syndrome [22]
Ans. Sick Sinus Syndrome refers to episodes of sinus bradycardia, sinoatrial block, or sinus arrest
It is caused by idiopathic fibrosis of the sinus node.
Other causes are ischemic heart disease, cardiomyopathy, myocarditis and drugs.
Clinical Presentation: Patient experiences a combination of symptoms (dizziness, confusion,
fatigue, and syncope) – due to cerebral hypoperfusion & Cardiac output.
Management: Usually these episodes are intermittent. If the symptoms are recurrent, permanent
pace maker insertion is required.
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3) Austin Flint Murmur [22]
Ans.
This is a mid-diastolic, low-pitched, rumbling murmur heard over the apex in severe aortic regurgitation
: It is due to the aortic regurgitant jet impinge on anterior mitral leaflet causing it to vibrate.
It may be confused with mid-diastolic murmur (MDM) of mitral stenosis.
MDM of mitral stenosis is characterized by loud S1, opening snap, and presystolic accentuation. All these features
are absent in Austin Flint murmur.
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4) Collapsing Pulse [21, 12]
a. Water hammer pulse [05]
Ans.
Collapsing Pulse is
characterized by a rapid upstroke, a rapid down stroke and a high volume.
The rapid upstroke is due to increased stroke volume.
Rapid downstroke is due to either diastolic leak back into left ventricle (e.g. aortic regurgitation) or
rapid run off to the periphery due to low systemic vascular resistance (e.g. AV fistula).
Causes of water hammer pulse:
Aortic regurgitation
Ruptured sinus of Valsalva
Patent ductus arteriosus
Mitral regurgitation
Hyperkinetic circulatory states (anemia, hyperthyroidism, beriberi, Paget's disease, and
arteriovenous fistula)
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5) Anti-arrhythmic drugs [21, 03]
Ans.
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6) Calcium channel blockers (with Doses) [21, 13]
Ans.
Verapamil: 40–160 mg TDS oral
Diltiazem: 30–60 mg TDS–QID oral
Nifedipine: 5–20 mg BD–TDS oral
Felodipine: 5–10 mg OD
Amlodipine: 5–10 mg OD
Benidipine: 4–8 mg OD

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7) Name four β Blocker drugs [19, 12, 08]
Ans.

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8) Treatment of Paroxysmal Super-Ventricular Tachycardia (PSVT) [18]
Ans. In PSVT, there is rapid regular palpitations, usually with abrupt onset
If Patient is hemodynamically unstable (e.g., hypotension, pulmonary edema) emergency
cardioversion.
If Patient is hemodynamically stable – do vagal maneuvers – Ex: right carotid massage, Valsalva
maneuvers, and facial immersion in cold water.
If maneuvers are not successful – then use drugs
Drugs used in PSVT: Adenosine, Verapamil, Diltiazem, Esmolol, Digoxin etc.
DOC is adenosine (i.v. 6 mg fast bolus).
Alternatives: Verapamil 5–10 mg IV over 5–10 minutes, IV diltiazem, or beta-blockers (esmolol,
propranolol, metoprolol).
Radiofrequency catheter ablation of accessory pathway can cure SVT
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9) Risk factors for atherosclerosis [17]
Ans.

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10) Supraventricular Tachycardia [14]
Ans.
Supraventricular tachycardias (SVTs) are tachyarrhythmias which arise above the ventricle, i.e.,
from the atrium or the atrioventricular junction.
Since the conduction is via the His-Purkinje system, QRS shape is normal (narrow QRS complex).
Following is a list of supraventricular tachycardias:
 Sinus tachycardia
 Paroxysmal supraventricular tachycardias (PSVTs) (AV nodal re-entry tachycardia & AV
reciprocating tachycardia)
 Atrial fibrillation
 Atrial flutter
 Atrial tachycardia
 Multifocal atrial tachycardia
 Accelerated junctional tachycardia
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11) Clinical features of Marfan's syndrome [14]
Ans.
Marfan’s syndrome is an autosomal dominant inherited disorder of connective tissue.
Etiology: mutation of FBN1 gene, which encodes fibrillin, an extracellular matrix protein
Clinical features of Marfan's syndrome:
HEART – aortic aneurysm and dissection, mitral valve prolapse; AR, MR)
Eye – dislocated lenses, retinal detachment
SKELETON – tall, thin body build with long arms, legs and fingers {arachnodactyly}; scoliosis, pectus
excavatum & a high-arched palate.
Skin laxity and joint hypermobility
 risk of pneumothorax.
For clinical diagnosis, two out of three major systems should be affected
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12) Mention the drugs and side Effects of ACE (Angiotensin Converting Enzyme)
inhibitors [14]
Ans. Adverse Effects {CAPTOPRIL} & Contraindications
1. Cough (dry cough) is due to increased bradykinin levels in the lungs {ACEI inhibit
the degradation of bradykinin}.
2. Angioedema — swelling in the nose, lips, mouth, throat, larynx and glottis. There can be airway
obstruction —If required, adrenaline, glucocorticoids and antihistamines should be administered.
3. Proteinuria can occur rarely. The drug should be discontinued.
4. Teratogenic effect (growth retardation, foetal hypotension, renal failure and neonatal death)—
hence contraindicated in pregnancy.
5. HypOtension may occur following the 1st dose of ACEI
6. NeutroPenia is rare.
7. Rashes.
8. Itching
9. Loss of taste sensation (dysgeusia).
10. ACEI are contraindicated in patients with B/L renal artery stenosis as acute renal failure can be
precipitated
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13) Atrial Flutter [10]
Ans.
Atrial flutter is an organized atrial rhythm with an atrial rate between 250 and 350 beats per minute.
: Emotional stress or following surgery, exercise, excessive caffeine use, smoking, and acute
alcoholic intoxication, RHD, HTN, HF, COPD etc.
: Patients complain of palpitations.
 Very fast heart rate due to 1: 1 AV response may cause angina and hemodynamic instability.
– ECG shows regular sawtooth-like atrial flutter waves (F waves) between QRS complexes.

Electrical cardioversion – for acute symptomatic attack

Anti-arrhythmic drugs (amiodarone) – to recurrence
For persistent recurrent atrial flutter – use AV nodal blocking agents – Ex: CCB or radiofrequency
catheter ablation.
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14) Medical closure of PDA (Patent Ductus Arteriosus) [07]
Ans.
For Premature infants  indomethacin closes PDA by inhibiting prostaglandin production
• In other cases, PDA can be closed surgically or via transcatheter methods. Surgery should be done as soon as
possible and before the age of 5 years. Closure should not be done if Eisenmenger syndrome has developed.