ADrPlexus – Digital Strides 2017
NIMHANS MOCK 3
1. A 45-year-old man presented with diplopia,
dysarthria and difficulty with swallowing. Over the
next few days he developed weakness of the upper and
lower limbs. On day 4 he was unable to walk unaided.
He denied any sensory symptoms or bladder
disturbances. His previous medical history is
unremarkable. He is a non-smoker, does not drink
alcohol excessively. He does not take any drugs On
examination he was apyrexial. His general medical
examination was normal. His higher mental function
was unremarkable. There were no signs of meningism.
Cranial nerve examination showed bilateral dilated
and fixed pupils. He had binocular diplopia but no
obvious ophthalmoplegia. He was dysarthric with
weak cough. His vital capacity was 3.15 standing and
2.00 lying flat. He had lower motor neuron
tetraparesis of power 3/5. He was hyporeflexic with
normal sensation. He was unable to walk unaided.
Blood tests including FBC, U+Es, LFTs, TFTs, Ca,
Autoantibody screen, ESR, CRP were normal. ECG and
CXR were unremarkable. CT brain was normal. Nerve
conduction studies and EMG were normal. What is the
most likely diagnosis?
1. Guillain Barre Syndrome
2. Lyme disease
3. Myasthenia gravis
4. Botulism
Ans. 4
The clinical presentation of descending weakness with
autonomic dysfunction (fixed dilated pupils) is typical of
botulism. It is a neuromuscular junction disorder and
therefore nerve conduction studies and EMG are normal.
Repetitive nerve stimulation showing incremental
responses, which is diagnostic of Botulism. CSF analysis is
usually normal.
2. The following are features of Marasmus except
1. Fatty liver
2. Hypoplastic bone marrow
3. Thymic atrophy
4. Lymphoid atrophy
Ans. 1
fatty liver
Robbin’s 8th edition Page no 429
The central anatomic changes in PEM are
(1) growth failure,
(2) peripheral edema in kwashiorkor, and
(3) loss of body fat and atrophy of muscle, more marked in
marasmus.
The liver in kwashiorkor, but not in marasmus, is enlarged
and fatty; superimposed cirrhosis is rare.
1
In kwashiorkor (rarely in marasmus) the small bowel
shows a decrease in the mitotic index in the crypts of the
glands, associated with mucosal atrophy and loss of villi
and microvilli. In such cases concurrent loss of small
intestinal enzymes occurs, most often manifested as
disaccharidase deficiency. Hence, infants with kwashiorkor
initially may not respond well to full-strength, milk-based
diets. With treatment, the mucosal changes are reversible.
The bone marrow in both kwashiorkor and marasmus may
be hypoplastic, mainly as a result of decreased numbers of
red cell precursors. The peripheral blood commonly
reveals mild to moderate anemia, which often has a
multifactorial origin; nutritional deficiencies of iron, folate,
and protein, as well as the suppressive effects of infection
(anemia of chronic disease) may all contribute. Depending
on the predominant factor, the red cells may be microcytic,
normocytic, or macrocytic.
The brain in infants who are born to malnourished
mothers and who suffer PEM during the first 1 or 2 years
of life has been reported by some to show cerebral
atrophy, a reduced number of neurons, and impaired
myelinization of white matter.
Many other changes may be present, including (1) thymic
and lymphoid atrophy (more marked in kwashiorkor than
in marasmus), (2) anatomic alterations induced by
intercurrent infections, particularly with all manner of
endemic worms and other parasites, and (3) deficiencies of
other required nutrients such as iodine and vitamins.
3. The most common form of vascular ectasia is
1. Nevus Flammeus
2. Spider Telangiectasia
3. Osler Weber Rendu disease
4. Bacillary Angiomatosis
Ans. 1
Nevus Flammeus
Robbin’s 8th edition Page no 520
Vascular ectasias
Nevus flammeus
Spider telangiectasia (arterial spider)
Hereditary hemorrhagic telangiectasis (Osler-Weber-
Rendu disease
Reactive vascular proliferations
Bacillary angiomatosis
Nevus flammeus is the ordinary “birthmark” and is the
most common form of ectasia; it is characteristically a flat
lesion on the head or neck, ranging in color from light pink
to deep purple. Histologically, there is only vascular
dilation; most ultimately regress.
The so-called port wine stain is a special form of nevus
flammeus; these lesions tend to grow with a child, thicken
the skin surface, and demonstrate no tendency to fade.
Such lesions in a trigeminal nerve distribution are
occasionally associated with the Sturge-Weber syndrome Investigations of choice in respiratory system
(also called encephalotrigeminal angiomatosis). Sturge- Disease Investigation
Weber syndrome is a rare congenital disorder associated o Intersitial lung disease HRCT
with venous angiomatous masses in the cortical o Bronchiectasis HRCT (1stchoice)
leptomeninges and ipsilateral facial port wine nevi; mental Bronchography (2nd
retardation, seizures, hemiplegia, and skull radioopacities choice)
also occur. o Pulmonary embolism CT with i.v. Contrast (1st
choice)
4. Compliment dependent cytolysis is an example of o Solitary pulmonary V/Q scan (2nd choice)
which type of HSR nodule
1. Type I HSR o Calcification CT scan
2. Type IV HSR o Pulmnnary malignancy CT scan
3. Type III HSR o Superior sulcus or CT scan (except in superior
4. Type II HSR pancoast tumor sulcus or pancoast tumor)
MRI
Ans. 4
TYPE II HSN : 7. The diagnostic test based on Antigen – Antibody
1.Compliment depd cytolysis – Transfusion reaction, reaction which result in insoluble precipitate
erythroblastosis fetalis, AI hemolytic anemia 1. WIDAL
2.Compliment depd inflammation (C3a,C5a) – GoodPasteur 2. Lancefield grouping (Streptococcus)
syndrome, Pemphigus vulgaris, Bullous pemphigous, 3. Tuberculin test
rheumatic fever , vasculitis 4. Ames test
3. Compliment depd phagocytosis
Ans. 1
5. Succinylcholine is used with caution in all Antigen Antibody Reaction
except - Precipitation –
1. Mysthenia gravis  Definition- {Soluble Antigen + Antibody} → insoluble
2. Burns precipitate / floccules
3. Crush injury  Ring test –
4. Tachycardia o Ascoli thermo precipitation test ( anthrax) ,
o Lancefield grouping (Streptococcus)
Ans. Is '4' i.e.. Tachycardia  Slide flocculation test – VDRL, RPR
 Sch is the only muscle relaxant that causes vagal  Tube flocculation test – Kahn test, standardization of
stimulation  Causes bradycardia, (attenuates toxin
tachycardia & hypertension).  Immuno-diffusion ( In gel) –
 In bums, crush injury and mysthenia gravis can cause o Elek gel precipitation (C diphtheriae toxigenicity
severe hyperkalemia, testing),
 Succinylcholine can cause dangerous hyperkalemia in o Eiken(E.coli)
patients with; -
□ Burn □ Rhabdomyolysis 8. Ritter’s disease is caused by
□ Massive trauma □ Severe Parkinsonism 1. Pseudomonas auroginosa
□ Crush injury □ Tetanus 2. Streptococcus pneumonia
□ Severe intra-abdominal infection □ Polyneuropathy 3. Bacillus anthracis
□ Spinal cord injury □ Closed head injury 4. Staphylococcus aureus
□ Hemiplegia/Paraplegia □ Stroke
□ Muscular dystrophy □ Encephalitis Ans. 4
□ GB syndrome □ Mysthenia gravis Epidermolytic toxin (Exfoliative toxin) by Staphylococcus
responsible for Ritter disease. Epidermolytic toxin
6. Best imaging modality in bronchogenic carcinoma (Exfoliative toxin) Mainly belong to phage group II
1. CT Two types of toxin : A: heat stable, chromosomal gene, B:
2. MRI heat labile, Plasmid controlled
3. Bronchoscopy Presentation: Scalded skin syndrome, Severe- Ritter
4. None disease (newborn), TEN (adult)
Milder- Pemphigus neonatorum, bullous impetigo
Ans. is ‘1’ i.e., CT
 CT scan is the investigation of choice for pulmonary 9. Which test is performed to detect reversible
malignancy except for superior sulcus or pancoast myocardial ischemia?
tumor, where MRI is the investigation of choice. 1. Coronary angiography

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2. MUGA scan
3. Thallium scan 11. Neurofibroma is -
4. Resting echocardiography 1. Autosomal dominant
2. Autosomal recessive
Ans. is ‘3' i.e., Thallium scan 3. X-linked recessive
 Thallium is used for perfusion scan to sec the viability 4. X-linked dominant
(reversibility) of myocardium.
Radionuclide scanning Ans. is '2' i.e., Autosomal recessive
 There are two main forms of cardiac scanning with  Neurofibromatosis comprises of two distinct
radionuclides: - A) Myocardial imaging; and B) Nuclear disorders
angiography o Neurofibromatosis I
A) Myocardial imaging: - Myocardial imaging can be o Neurofibromatosis II
achieved in two ways: -  The genes for these are located on different
1) Infarct scanning: - Uses an isotope (pyrophosphate) chromosomes.
which accumulates in damaged myocardium. The Area  Both are inherited in an autosomal dominant pattern.
of infarct appears as Hot spot. o NF-1: Neurofibroma gene on chromosome 17.
2)Perfusion scanning:- Perfusion scan looks at the blood o NF-2; Neurofibroma gene on chromosome 22.
(lowing through the coronary arteries and is useful Neurofibromatosis type I (Von-Recklinghewsen
in the diagnosis of coronary artery disease. It can also be disease)
used to identify areas of reversibility following a o NF-1 is diagnosed when any two of the following
MI. A radioisotope, most commonly thallium is injected seven signs are present.
into a peripheral vein. It travels to the coronary 1. Six or more cafe-au-lait macules
arteries and images arc taken with a special gamma o >5 mm in prepupertal individuals
camera of the heart. Other isotopes used tor perfusion o >15 mm in postpuberal individuals
scanning are technetium and M1B1 (2-mcthoxy Iso-Butyl o Cafe-au-lait spots are the hallmark of
Isonilrite). The area appears as cold spot because neurofibromatosis and are present in almost
radionuclide binds to viable area. 100% of the patient.
B) Nuclear angiography: - Nuclear angiography can also 2. Axillary or inguinal freckling
be done on two different ways: - 3. Two or more Lisch nodules.
1) First pass technique: - It involves rapid i.v. injection of o Lisch nodules are hamartomas located within the
a bolus of a simple radionuclide (Tc-99 pertechnetate). iris.
Its passage through the cardiac chambers is then recorded. 4. Two or more neurofibroma or one plexiform
The method is most useful for the study of intracardiac neurofibroma.
shunts. o Typically involve the skin, but may be situated
2. Multigated equilibrium studies (MUGA): - A along peripheral nerves and blood vessels.
radioactive isotope (technetium) is injected into a o They are small, rubbery lesions with a slight
peripheral vein. The gamma camera is able to detect purplish discoloration of the overlying skin.
technetium labelled RBC and produces moving images of a 5. A distinctive osseous lesion.
heart.A MUGA scan can assess the degree of damage to the o Sphenoid dysplasia or cortical thinning of long
myocardium following a ML More importantly, it can bones.
give an accurate and reproducible assessment of left 6. Optic glioma
ventricular function. It is used in patients undergoing 7. A first degree relative with NF-I
chemotherapy (e.g., anthracyclin) to assess whether the o Other findings are: -
drugs are having an adverse effect on cardiac function. o Pseudoarthrosis of tibia.
o Scoliosis is the most common orthopaedic
10. Pfeiffer’s bacillus is problem in NF-1, but is not specific enough to be
1. Haemophillus infuenzae included as a diagnostic criterian.
2. Haemmophihlus aegypticis o Short stature
3. C.diphtheriae o Mental retardation, epilepsy
4. Burkholderia pseudomallei o Hypertension
o Aqueductal stenosis with hydrocephalus
Ans. 1 o Meningiomas, ependynomas, Astrocytomas,
phcochromocytomas.
 Kleb-Loeffler bacilli– C.diphtheriae o NF-I is caused by mutation in NF-1 gene on
 Preisz Nocard bacilli – C.pseudotuberculosis chromosome 17 which encodes protein
 Koch Week bacilli – H.aegypticis neurofibroma I.
 Whitmore bacilli – Burkholderia pseudomallei Neurofibromatosis type-2
 Pfeiffer’s bacilli – Haemophillus infuenzae

3
o NF-2 may be diagnosed when one of the following
two features arc present.
1. Bilateral ocoustic neuroma - Most distinctive feature
2. A parent, sibling or child with NF-2 and cither
unilateral eighth nerve masses or any two of the
following Neurofibroma, meningioma, glioma,
Schwannoma or juvenile post subcapsular cataract.
NF-2 is cause by mutation in NF-2 gene on
chromosome 22 that encodes for
proteinneurofibromin 2, Schwannomin or merlin.
12. Most common benign heart tumor is-
1. Rhabdomyoma
2. Hemangioma
3. Lipoma
4. Myxoma
Ans. is ‘4’ i.e., Myxoma
o The most frequent cardiac tumor for all age groups is -
Metastasis.
o The most frequent primary cardiac tumor for all age
groups is - Myxoma.
o The most frequent primary cardiac tumor in infants
and children is - Rhabdomyoma.
Cardiac myxoma
o This is the most common primary tumor of heart
o Most commonly seen in left atrium.
o More common in females.
o Myxoma may be of two types
1. Sporadic myxomas
o These are the usual form of myxomas (more than 90%
of myxomas are sporadic)
o Mean age is 56 years.
o Most sporadic myxomas aresolitary.
2. Familial myxomas
o Constitute less than 10% of all myxomas.
Occurs at younger age.
o Myxomas are bilateral and multiple.
o Myxomas may occur in locations other than atria.
o Some patients with cardiac myxoma have a syndrome,
i.e. carney syndrome that consists of: -
i) Myxoma ii) Spotty pigmentation
iii) Endocrinopathy
Morphology
o The region of the fossa ovalis in the atrial spetum is
the favored site of origin.
o Myxoma may be pedunculated or sessile.
o Pedunculated myxoma can move and obstruct the AY
valve.
o Myxomas are gelatinous structures consisting of
myxoma cells (lepidic cells), endothelial and smooth
muscle cells embedded in a stroma rich in
glycosamincglycans.
13. Paraffin baiting mixed culture is done for
1. Botryomycosis
2. Actinomyces
3. Nocardiosis
4. Madurellosis
Ans. 3
Nocardia
 Strictly aerobic , acid fast, urease+ve,
exogenous infection
 Nocardia – grow on Sabouraud’s dextrose
agar, brain heart infusion agar
 For isolation of Nocardia from soil, paraffin
bait technique used.
14. True statement about clostridium perfringens all
except
1. It is the commonest cause of Gas gangrene
2. It can be detected by Nagler's reaction
3. The food poisoning spores of clostridium perfringens
are heat sensitive
4. The major enzyme secreted is hyaluronidase
Ans. 4
Hyaluronidase( "spreading factor" ) -Breaks down
hyaluronic acid, enabling the bacteria to spread between
cells produced by Staphylococcus aureus and streptococci.
Enzyme responsible for gas gangrene in C.perfringens will
be lecithinase
15. Not a feature of HELLP syndrome -
1. Haemolysis
2. Elevated liver enzymes
3. Low platelet count
4. Renal failure
Ans. is ‘4’ i.e., Renal failure
HELLP syndrome
o It is an acronym for Haemolysis(H), Elevated liver
enzyme(E) (AST & ALT> 70IU/L, LDH> 600IU/L), Low
platelet cout(L)(<100000/mm3).
o It is a rare complication of pre-eclampsia but may
develop even without hypertension.
o Manifested by nausea, vomiting, epigastric or right
upper quadrant pain.
16. Dohle bodies are seen in -
1. Multiple myeloma
2. May-Hegglin anomaly
3. Waldenstorm Macroglobulinemia
4. Lymphoma
Ans. is '2' i.e., May-Hegglin anomaly
Dohle bodies
 Dohle bodies are light blue gray, bosophilic inclusions
in the peripheral cytoplasm of neutrophils,
 They are thought to be remnants of the rough
endoplasmic reticulum containing RNA.
 They are seen in: Burns, Infections, Physical trauma,
Neoplastic diseases, Wissler's disease, May-Hegglin
anomaly, Chcdiak-Steinbrinck-Higashi's syndrome.

4

17. The following are true of ovarian choriocarcinoma
except
1. Are usually found in association with other germ cell
tumours
2. Is extra-embryonic differentiation of malignant germ
cells.
3. Ovarian primaries are indolent tumours
4. They elaborate high levels of chorionic gonadotropins
Ans. 3
ovarian primaries are indolent tumours
Robbin’s 8th edition Page no 1049
More commonly of placental origin, the choriocarcinoma,
like the endodermal sinus tumor, is an example of extra-
embryonic differentiation of malignant germ cells. It is
generally held that a germ cell origin can be confirmed
only in the prepubertal girl, because after this age an origin
from an ovarian ectopic pregnancy cannot be excluded.
Most ovarian choriocarcinomas exist in combination with
other germ cell tumors, and pure choriocarcinomas are
extremely rare. They are histologically identical to the
more common placental lesions, described later. The
ovarian primaries are aggressive tumors that generally
have metastasized widely through the bloodstream to the
lungs, liver, bone, and other viscera by the time of
diagnosis. Like all choriocarcinomas they elaborate high
levels of chorionic gonadotropins, which is sometimes
helpful in establishing the diagnosis or detecting
recurrences. In contrast to choriocarcinomas arising in
placental tissue, those arising in the ovary are generally
unresponsive to chemotherapy and are often fatal.
18. The following are variants of papillary carcinoma
of thyroid except
1. Tall cell variant
2. Diffuse sclerosing variant
3. Follicular variant
4. Anaplastic variant
Ans. 4
Anaplastic variant
Robbin’s 8th edition Page no 1122
Papillary carcinomas are the most common form of
thyroid cancer. They occur throughout life but most often
between the ages of 25 and 50, and account for the
majority of thyroid carcinomas associated with previous
exposure to ionizing radiation. The most common variant,
and the one most liable to misdiagnosis, is the follicular
variant, which has the characteristic nuclei of papillary
carcinoma but has an almost totally follicular architecture.
A tall-cell variant is marked by tall columnar cells with
intensely eosinophilic cytoplasm lining the papillary
structures. An unusual diffuse sclerosing variant of
papillary carcinoma occurs in younger individuals,
including children. The tumor demonstrates a prominent
papillary growth pattern, intermixed with solid areas
containing nests of squamous metaplasia. There is
5
extensive, diffuse fibrosis throughout the thyroid gland,
often associated with a prominent lymphocytic infiltrate,
simulating Hashimoto thyroiditis. Lymph node metastases
are present in almost all cases. The papillary
microcarcinoma, which is defined as an otherwise
conventional papillary carcinoma less than 1 cm in size,
and usually confined to the thyroid gland.
19. Elution mechanism due to
1. Haemagglutinin
2. Neuraminidase
3. Glycoprotein
4. Protein matrix (NS 1)
Ans. 2
 Myxovirus (Influenza)
 Elution (d/t neuraminidase)– only in Myxovirus
(except RSV & Measles)
20. A newborn presents with excessive frothing. CXR
given below
Which of the following statements are not correct?
1. Polyhydramnios
2. Absent stomach bubble
3. Type C is commonest
4. Associated with dextrocardia
Ans. 4. Associated with dextrocardia
21. Tumor that follows rule of 10 is -
1. Pheochromocytoma
2. Oncocytoma
3. Lymphoma
4. Renal cell carcinoma
Ans. is ‘1’ i.e., Pheochromocytoma
o Pheochromocytomas usually subscribe to a convenient
"rule of 10s":-
 10% of pheochromocytomas arise in association
with one of several familial syndromes. These
include the MEN-2 A & MEN-2B syndromes, type I
neurofibromatosis, von Hippel-Lindau syndrome
& Sturge-Weber syndrome
 10% of pheochromocytomas are extra-adrenal,
occurring in sites such as organ of Zuckerkandl &
carotid body, where these chromaffin-negative
 tumors arc usually called paragangliomas to
distinguish them frompheochromocytomas.
 10% of nonfamilial adrenal pheochromocytomas
are bilateral; this figure may rise to 70% in cases
that are associated with familial syndromes.
 10% of nonfamilial adrenal pheochromocytomas
are bilateral: this figure may rise to 70% in cases
that areassociated with familial syndromes,
 10% of adrenal pheochromocytomas arc
biologically malignant, although the associated
hypertension represents a serious & potentially
lethal complication of even "benign" tumors,
 10% of adrenal pheochromocytomas arise in
childhood, usually the familial subtypes, and with
a strong malepreponderance. The nonfamilial
pheochromocytomas most often occur in adults
between 40 & 60 years of age, with a slight female
preponderance.
22. The following are false of thymomas except
1. Equal sex incidence
2. Neoplastic cells are thymic epithelial cells and
thymocytes
3. They are common in posterior mediastinum
4. Tumors that have a substantial proportion of
medullary-type epithelial cells are usually invasive.
Ans. 1
Equal sex incidence
Robbins 8th edition Page no 636
The designation “thymoma” is restricted to tumors of
thymic epithelial cells. Such tumors typically also contain
benign immature T cells (thymocytes). The tumors usually
occur in adults older than 40 years of age; thymomas are
rare in children. Males and females are affected equally.
Most arise in the anterior superior mediastinum, but
sometimes they occur in the neck, thyroid, pulmonary
hilus, or elsewhere. They are uncommon in the posterior
mediastinum. Macroscopically, thymomas are lobulated,
firm, gray-white masses of up to 15 to 20 cm in size. They
sometimes have areas of cystic necrosis and calcification.
Most are encapsulated, but 20% to 25% of the tumors
penetrate the capsule and infiltrate perithymic tissues and
structures. Noninvasive thymomas are most often
composed of medullary-type epithelial cells or a mixture of
medullary- and cortical-type epithelial cells. The
medullary-type epithelial cells are elongated or spindle-
shaped. There is usually a sparse infiltrate of thymocytes,
which often recapitulate the phenotype of medullary
thymocytes. In mixed thymomas there is an admixture of
polygonal cortical-type epithelial cells and a denser
infiltrate of thymocytes. The medullary and mixed patterns
together account for about 50% of all thymomas. Tumors
that have a substantial proportion of medullary-type
epithelial cells are usually noninvasive.
23. Sildenafil acts by inhibiting -
1. Phosphodiesterase - 2
2. Phosphodiesterase - 5
6
3. Adenyl cyclase
4. Guanyl cyclase
Ans. is ‘2’ i.e., Phosphodiesterase – 5
o Sildenafil is used to treat Erectile Dysfunction
o Mechanism of action:
Nitic Oxide(NO)
Activation of Guanylyl PDE- 5  Sildenafi
cyclase ↓
↓
GTP cGMP → Degraded product
Reduction of intracellular
calcium
↓
Smooth muscle relaxation
o Penile tumescence during sexual arousal is improved,
but it has no effect on penile tumescence in the
absence of sexual activity, because sexual stimulation
results in smooth muscle relaxation of the copus
cavernosum, increasing the inflow of blood.
o Sildenafil in addition, weakly inhibits the isoenzyme
PDE-6 which is involved in photoreceptor
transduction of retina  impairment in colour vision
especially blue green discrimination
24. Not true about Wilson’s disease
1. Defect in ATP7B
2. Serum ceruloplasmin is increased
3. Kayser Feischer ring pathognomonic
4. Penicillamine is used in treatment
Ans. 2. Serum ceruloplasmin is increased
Wilson’s disease
Autosomal recessive; Liver symptoms first, neurologic
symptoms later
Dystonia, tremors, basal ganglia problems
Kayser-Fleischer rings-pathognomonic
MRI shows lesions in thalamus and basal ganglia
Best screen-serum ceruloplasmin (decreased)
Increased urinary Cu excretion
Confirm with liver biopsy-increased Cu content
Treatment
- Chelation with penicillamine (slows progression)
- Definitive treatment with liver transplant
25. A ex-preterm infant who has lower limb weakness
has the following picture in MRI. What does the
neonate have?
 B. Inspiratory reserve volume-2 L
C. Expiratory reserve volume-1 L
D. Air left in the lungs after a maximal expiratory effort is
the residual volume-1.3L. This is 20% of total lung
capacity

28. "Menke's disease" is a disease of -

1. Impaired zinc transport
2. Impaired copper transport
3. Impaired magnesium transport
1. Periventricular leukomalacia 4. Impaired molybdenum transport
2. Canavan disease
3. Duchene’s muscular dystrophy Ans. is '2' i.e., Impaired copper transport
4. Neuronal ceroidlipofuscinosis Menke's disease is caused due to defect in the copper
transport.
Ans. 1. Periventricular leukomalacia  There is defect in the transport of copper present in
PVL the intestinal mucosa to the blood stream.
PVL refers to injury of the cerebral white matter, generally  The mucosal lining of intestine contains high level of
more severe in the deep that in superficial white matter, copper bound to metallothionein protein.
and exists in 2 major forms:  Rather than being transporated to bloodstream, the
 cystic copper remained in the mucosa and was lost when
 diffuse Typically cystic PVL (cPVL) is located deep in intestinal cells were naturally soughed off.
the cerebral white matter (WM), usually dorsal and Menkes disease is caused due to defect in the "MNK"
lateral to the external angles of the lateral ventricles). gene.
(ref: Volpe JJ. The encephalopathy of prematurity — brain  The protein normally Junction by moving copper from
injury and impaired brain development inextricably the intestinal mucosal cells into the blood stream,
intertwined. SeminPediatr Neurol. 2009 Dec; 16(4): 167– where
78.) it is bound by proteins such as albumin and
transported to organs and tissues.
26. Which cell serves as progenitor cell following lung Serum copper is critical for the functioning of several
injury for repair? enzymes
1. Merkel cells  Lysyl oxidase → is important for the cross linking of
2. Airway epithelial cells collagen and elastin such that deficiencies lead to
3. Clara cells problems in connective tissues such as bones
4. Neuroepithelial bodies  Cytochrome oxidase → Involved in temperature
maintenance
Ans. 3  Tyrosinase → Necessary for pigmentation
Ganong review of medical Physiology 24th ed p.621 Clinical features of menkes disease
Conducting airways  Growth retardation
A. First 16 generations starting from trachea  Coarse hair, brittle and ivory white (result of
B. Ciliated- “Mucociliary escalator”. beat at rates of 10–15 depigmentations). The hair fibres are twiisted and
Hz. Moves 16 mm/min broken helically (kinky hair),
C. Basal cells-progenitor cells following injury is present  Seizures
D. Clara cells- nonciliated, secrete defense markers, serve  Cerebral and cerebellar degeneration (postmortem
as progenitor cells after injury analysis)
E. Epithelial cells-lung defense- IgA, collectins,defensins  Hypothermia
 Thrombosis
27. Value of residual volume in lung is  Poor bone development
1. 1000 ml  Increased tendency towards aneurysms
2. 2000 ml
3. 3000 ml 29. The Diagnosis of this disorder
4. 1300 ml

Ans. 4
Ganong review of medical Physiology 24th ed p.629
Lung volumes
A. Amount of air that moves into the lungs with each
inspiration-Tidal volume(500-750 ml)

7
 5 days

31. Contraction stress test false is -

1. Oxytocin not used
2. Invasive method
3. Detects fetal well being
4. Negative test is associated with good fetal outcome

Ans. is '1' i.e., Oxytocin not used

Contraction stress test (CST) (syn : Oxytocin challenge
test)
 It is an invasive test to asses fetal respiratory well
being during pregnancy.
 It detects alteration in FHR in response to uterine
1. Normal X ray contraction induced by oxytocin indicating hypoxia,
2. Duodenal atresia  Interpretations
3. Jejunal Atresia  Negative test indicated good outcome
4. Malrotation  Positive test is associated with increased incidence of
IUD, fetal distress & low Apgar score,
Ans: 2.  There is 50% chance of false positive results.
Double bubble- Duodenal atresia
Triple bubble- jejunal atresia 32. Maximum chance of transmission during delivery-
1. HSV
2. CMV
30. Emergency contraceptive should must be started 3. VZV
with in how much time after unprotected intercourse- 4. Rubella
1. 24 hrs
2. 48 hrs Ans. is ‘1’ i.e., HSV
3. 72 hrs "Transplacental infection by HSV is not usual. The
4. 96 hrs fetus becomes affected by virus shed from the cervix
or lower genital tract during vaginal delivery."
Ans. is ‘3’ i.e., 72 Hrs.  Overall most common congenital infection is CMV.
Emergency contraception (post coital contraception)  But most common congenital infection during delivery
Indications is HSV.
o Unprotected intercourse
o Condom rupture 33. Drug causing abruption placenta –
o Missed pill 1. Methadone
o Delay in taking POP for more than 3 hours 2. Cocaine
o Sexual assault or rape & first time intercourse. 3. Amphetamine
"Morning after pill: ethinyl-estrediol 2.5 mg, premarin 15 4. Fluoxetine
mg, the drug is taken orally twice daily for 5 days.
Beginning soon after exposure but not later than 72 hrs.” Ans. is ‘2’ i.e., Cocaine
Etiology of abruptio placenta
Post-coital contraceptives Risk factors
Drug Dose Pregnancy  Multigravida
rate(%)  Advancing age of mother
Levonorgestrel 75 mg stat & after 0-1  Poor socioeconomic status
12 hrs  Malnutrition
Ethynyl estradiol 2 tab stat & 2 0-2  Smoking
50 mcg+ days after  Hypertension
norgestrel 0.25 Causes
mg  Trauma
Conjugated 15 mg BD for 5 0-0.6  Sudden uterine decompression eg:- following delivery
estrogen days of the 1st baby of twins, sudden escape of liquor amnii
Ethinyl estradiol 2.5 mg BD for 5 0-0.6 in hydramnios, PROM,
days  Short cord
Mifepristone 10 mg single dose 0-0.6  Supine hypertension syndrome
Copper IUDs Insertion within 0-0.1  Placental anomalies
8
 1 Sick placenta
 Folic acid deficiency
 Uterine factors like septate uterus or a submucous
fibroid
 Torsion of uterus
 Cocaine abuse
 Thrombophillias
 Prior abortion
34. Peritonitis in acute appendicitis is caused by -
1. Early rupture of appendix
2. Late rupture of appendix
3. Fecolith
4. Old age
Ans. is ‘1’ i.e., Early rupture of appendix
 Perforation of appendix in acute appendicitis
commonly leads to an abscess cavity walled off by the
small bowel loops and the omentum, forming a
phlegmon. Rarely the appendix may perforate freely
into the peritoneal cavity and cause generalized
peritonitis. This usually occurs in cases of early
rupture of the appendix as inflammatory process did
not get time to be localized by the omentum and bowel
loops.
 Usually the rupture of appendix is a late sequelae of
appendicitis, usually occurring 48 to 72 hours from
the onset of symptoms.
Also know:
 The site of rupture is commonly just beyond the point
of obstruction, along the antimcsenteric border of
appendix.
 Fecaliths are the most common cause of appendiceal
obstruction.
 Lets also see the management of appendicitis:
Management of appendicitis:
 The treatment of appendicitis is appendectomy. (It can
be done open or laparoscopically)
 Prophylactic antibiotics are indicated preoperatively.
Postoperative antibiotic coverage is of no use in
simple (uncomplicated) acute appendicitis. If
perforated or gangrenous appendicitis is found,
antibiotics are continued until the patient is afebrile
and has a normal white blood cell count.
Perforated Appendicitis
 Rupture is suspected in the presence of fever with a
temperature of >39°C (102°F) and a white blood cell
count of >18,000cells/mm3.
 The management of perforation depends on the
nature of the perforation.
 If the perforation is free causing intraperitoneal
dissemination of pus and fecal material, urgent
laparotomy is done for appendectomy and irrigation
and drainage of the peritoneal cavity,
 If the perforation is contained it would result in an
appediceal mass or abscess. This is managed as
descnbed under.
9
 Patients who present late in the course of appendices
with a palpable or radiographic ally documented
mass(abscess or phlegmon) are treated with- (abscess
or phlegmon) are treated with-
 Conservative therapy and interval appendectomy 6 to
10 weeks later.(conservative management includes
intravenous antibiotics and fluids as well as bowel
rest.)
 Patients with large abscesses, greater than 4 to 6 cm in
size, and especially those patients with abscess and
high fever, benefit from abscess drainage.
35. Champagne bottle appearance is seen in -
1. Varicose veins
2. DVT
3. Lipodermatosclerosis
4. Venous ulceration
Ans. is ‘3’ i.e., Lipodermatosclerosis
 Lipodermatosclerosis refers to a skin change of lower
legs that often occurs in patients who have chronic
venous insuficiency. This is a type of panniculitis
(inflammation of subcutaneous fat),
 Inverted champagn bottle or bowling pin appearence
is seen,
 This is also seen in "Charcot-Marie-Tooth disease
36. Bismuth classification in which class, hepatic
duct confluence is involved -
1. I
2. II
3. III
4. IV
Ans. is ‘2’ i.e., Type II
Bismuth - Corlette classification is used to classify
cholangiocarcinoma.
Type I - Common hepatic duct involvement,
Type II - CHD + bifurcation/confluence of hepatic ducts,
Type III - a) Extension to right secondary intrahepatic duct.
b) Extension to left secondary intrahepatic duct.
Type IV - Involving both right and left secondary
intrahepatic ducts.
37. Parathyroid glands are removed by surgery, for
recurrence investigation of choice-
1. Technetium scan
2. SPECT
3. MRI
4. Neck ultrasound
Ans. is '1' i.e., Technetium scan
 Preoperative localisation tests for parathyroid glands
are –
1. Tc 99m labeled sestamibi scan (>80% sensitive)
2. Single positron emission computed tomography
(SPECT).
3. CT and MRI scan.
4. Neck ultrasound.
38. True about her2/neu overexpression in Carcinoma
breast -
1. Responds well to taxanes
2. Good prognosis
3. Responds well to monoclonal antibodies
4. Seen only in breast cancer
Ans. is ‘3’ i.e., Responds well to monoclonal antibodies
Prognostic markers of breast cancer
A. Indices of proliferation (PCSA, Ki-67)
 PCNA & Ki-67 expression are poor prognostic markers
 PCNA (proliferating cell nuclear antigen) and Ki-67
expression arc positively correlated with p53
overexpression, high s-phase fraction, aneuploidy.
high mitotic index, and high histologic grade in human
breast cancer specimens, and arc negatively correlated
with estrogen receptor content.
B. Indices of Apoptosls (bcl-2 and box: bell ratio)
 Overexpression of bcl-2 and reduced box : bc12 ratio
are poor prognostic markers
 Bcl-2 is the only oncogene that acts by inhibiting
apoptosis rather than by directly increasing cellular
proliferation. 9 Rax is death-signal protein and inhibits
the anti-apoptotic actions of bcl-2.
 Overexprcssion of bcl-2 and a decrease in the bax : bcl-
2 ratio correlates with high histologic grade, the
presence of axillary lymph node metastases, and
reduced disease-free and survival rates.
C. Indices of angiogenesis (VEGF A angiogenesis index)
 Angiogenesis is necessary for the growth and
invasiveness of cancer and promotes cancer
progression through several different mechanisms.
VEGF stimulates the growth of new blood vessels.
 Overexpression of VEGF (vascular endothelial growth
factor) is poor prognostic marker.
 Bevacizumab is a monoclonal antibody that blocks
vascular endothelial growth factor. Bevaci/umab is the
first clinically available angiogenisis inhibitor and is
used for metastatic breast cancer (Anliangiogenesis
breast cancer therapy)
D. Growth factor receptors
 HER 2/neu o: EGFr overexpression are poor
prognostic markers.
 Patients whose tumors ovcrexprcss HER-2/ncu are
given anti-l IER-2'neu therapy - Trastuzumab
(Hcrceptin). It is a recombinant humanized
monoclonal antibody directed against HER-2/neu.
E. p53
 p53 overexpression is poor prognostic marker
F. Steroid hormone receptors (ER, PR)
 Patients with hormone receptor positive tumor show
good response to hormone therapy.
 Tumors positive for estrogen or progesterone
receptors have a higher response rate to endocrine
therapy than tumors that do not express estrogen or
progesterone receptors. Tumors positive for one
10
receptor and not the other have an intermediate
response rate.
 The HER2 receptor (previously called HER2/neu, or
ERBB-2 receptor) belongs to the epidermal growth
factor receptor (EGFR) family of receptors, which are
critical in the activation of subcellular signal
transduction pathways controlling epithelial cell
growth and differentiation and possibly angiogenesis.
 Amplification of HER2 or overexpression of its protein
product is observed in 18 to 20 percent of human
breast cancers.
 HER2 overexpression is also noted in other tumors
such as esophagogastric tumors, lung, ovary & head
and neck squamous cell ea. (In all of these sites, HER2
overexpression has been identified as a negative
prognostic factor.)
Following points arc to be noted about HKR2
overexpression in breast ca;
 Prognostic value of H ER2 — HER2 overexpression is a
poor prognostic marker. HER2 overexpression is
associatedwith high rates of disease recurrence and
death in the absence of adjuvant systemic therapy.
 Predictive value of HER2 — MLR2 status predicts
response to specific therapies:
 Patients with high levels of HER2 expression benefit
from treatment with agents that target HER2, such as
trustuzumab (a monoclonal antibody) and lapatinib.
 HER2 status appears to predict resistance or
sensitivity to different types of chemotherapeutic
agents, including anthracyclines and taxanes.
 Women whose rumors overexpress HER2 appear to
derive greater benefit from anthracycline-based
adjuvant therapy than from adjuvant therapy that is
alkylating agent-based, such as CMF
(cyclophosphamide,methotrexate, fluorouracin.
 Relationship between HER2 overexpression and
taxanes is still under study with various studies giving
conflicting reports.
 HER-2 positivity is associated with resistance to
endocrine therapies.
39. True about achalasia cardia is -
1. Dysphagia is a presenting symptom
2. The cause is the absence of Auerbach'splexes
3. Esophagectomy is the treatment
4. Motilily-improving agents are used in treatment
Ans. ‘1’ i.e., dysphagia is a presenting symptom
Achalasia
 Achalasia cardia is a motor disorder of the esophageal
smooth muscle in which the LES does not relax
normally with swallowing, & the esophageal body
undergoes nonperistaltic contractions. (Primary
peristalsis is absent or reduced).
 The pathogenesis of achalasia is poorly understood.
It involves:
 Neurogenic degeneration either idiopathic or due to
infection. The degenerative changes are either
 intrinsic (degeneration of ganglion cells of Aurebach’s transmitted inhibitory effect of CCK is absent owing to
myentric plexus) or extrinsic (extraesophageal vagus the loss of inhibitory neurons.
nerve or the dorsal motor mucleus of vagus). Also know
 Pharmacologic studies suggest dysfunction of  Schwartz writes-"Although complete absence of
inhibitory neurons containing nitric oxide and peristalsis in the esophageal body has been proposed
vasoactive as the major abnormality, present evidence indicates
intestinal polypeptide in the distal esophagus (LBS). achlasia is a primary disorder of the LES”. The LES fails
The clolinergic innervation of the LES is intact or to relax on deglutition, elevation of intraluminal
affected only in advanced disease, esophageal pressure esophageal dilatation subsequent
 As a result of the abnormality, the LES fails to relax, loss of primary peristalsis in the body of esophagus,
primary peristalsis is absent in esophagus which  Other options are described ahead,
dilates. As  Over 20 year period a patient will have upto 80% risk
the disease progresses the esophagus becomes of esophageal CA. Sq. cell CA is the most frequent type
massively dilated and tortuous. seen
Clinical findings
 Both sexes arc equally affected 40. A new born with respiratory distress from day 1
 May develop at any age but peak years are from 30 to has this X-ray. Identify
60.
 Classical clinical symptom is progressive dysphagia for
both solids and liquids. Dysphagia is worsened by
emotional stress and hurried eating,
 Regurgitation and Pulmonary aspiration occur
because of retention of large volumes of saliva and
ingested food in the esophagus.
 Esophagitis with ulceration may occur with chronic
retention of food.
 Pain is infrequent in classical achlasia but a variant
called vigrous achlasia is characterized by chest pain
and esophageal spasms that generate non-propuloine
high-pressure waves in the body of the esophagus.
Diagnosis
 Chest x-ray - shows absence of gastric air bubble, an 1. CCAM
air-fluid level in the mediastinum in the upright 2. Congenital lobar emphysema
position representing retained food in oesophagus, 3. Pneumothorax
 Barium swallow - Shows dilated esophagus with 4. CDH
tapering narrowing in the terminal end of esophagus
describe as 'birds beak1 appearance. Fluoroscopy Ans. 2. Congenital lobar emphysema
shows loss of normal peristalsis in the lower two Congenital lobar emphysema
thirds of esophagus. The most common site of involvement for congenital lobar
 Endoscopy may be done to rule out any secondary emphysema is
cause of achlasia eg. carcinoma, stricture at LES. 1. Left upper lobe (40% to 50%)
Manometry 2. Right middle lobe (30% to 40%)
 It's the most vonfrmatory investigation. 3. Right upper lobe (20%)
 It is able to distinguish between various forms of 4. Lower lobes (1 %), and multiple sites for the
motor disorders of esophagus remainder.
 Manometric characteristics of Achlasia 5:1 male predominace
‐ Incomplete lower esophageal sphincter relaxation (<
75% relaxation) Chest x ray findings
‐ Elevated LES pressure Lobar inflation
‐ LOSS of primary peristaltic waves in the esophageal Mediastinal shift
body, hut disorganized muscular activity may he Atelectasis of adjacent lungs
present. Ipsilateral hemidiaphram flattening
‐ Increased intraesophageal baseline pressure relative Mimic tension pneumothorax
to gastric baseline. D/D:
 Cholecystokinin (CCK) which normally causes a fall in Pneumothorax
the sphincter pressure, paradoxically causes Pneumatocoele
contraction of the LES (the CCK test). This paradoxical Giant CCAM
response occurs because, in achlasia the neurally
41. Most common type of intussusceptions-
11
1. Multiple 2. It is a spinal reflex
2. Colocolic 3. It is usually present at birth
3. Honleal 4. Its disappearance is essential for the child to be able to
4. Ileocolic turn over

Ans. is '4' i.e., Ileocolic Ans. 4. Its disappearance is essential for the child to be
Types of intussusception in decreasing order able to turn over
 Ileocolic (-77%) ATNR (Asymmetric tonic neck reflex is a brain stem
 Ileoileo-colic(~12) reflex)
 Ueoileai(~5%) How to elicit?
 Colocolic(-2%)  Baby to be lying supine, head in mild line, awake or
 Multiple (1%) light sleep.
 Retrograde  Shoulder horizontal
Intussusception  Head turned to right till jaw over right shoulder
 Intussusception is the telescoping of one pon  Held for 15 sec and released.
childhood (3 months to 6 years)
 It is the most common cause of intestinal obstruction
ear
 An intussusception is composed of three parts.
‐ The entering or inner tube - intussusception
‐ The returning or middle tube
‐ The sheath or outer tube - intussuscipiens.

Clinical features
 Intussusception classically produces severe cramping
abdominal pain in an otherwise healthy child. The
child often draws his or her legs up during the pain
episodes and is usually quite during the intervening
periods.
 Vomiting is almost universal Normal response:
 Initially the passage of stools may be normal while  Passive reflex elicited
later on blood mixed with mucus is evacuated – red  Mental extension, occipital flexion
currant jelly stool  Arm and leg on the mental side extend
 An abdominal mass may be plapated – a sausage  Arm and leg on the occipital side flexes.
shaped mass, which may increase in size and firmness  If it occurs spontaneous, it is an active reflex.
during the paroxysms of pain.
 It I usually present from 1 month age
 There may be an associated feeling of emptiness in the Abnormal response:
right fossa(Sign of Dance)
 Sustained or exaggerated response –
 On rectal examination, blood-stained mucus may be
 Consistent failure to move an extremity
found on the finger. Occasionally in extensive ileocolic
 Persistence of this reflex beyond 6 months.
or colocolic intussusception, the apex may be palpable
 Obligatory ATNR
or even protrude from the anus.
Clinical implication:
 Diagnosis can be made on:
 In severe spastic cerebral palsy this reflex persists and
 Barium enema which shows characteristic
may increase.
‐ Claw sign
 This persistence of the reflex prevents child rolling
‐ Coiled spring sign
from prone to supine or vice versa.
 On ultrasound which shows
(M Singh, Clinical methods in Pediatrics)
‐ Target sign
‐ Pseudokidney sign
43. A 1-month-old fair-haired, fair-skinned baby
 When the clinical index of suspicion is high, presents with projectile vomiting of 4 days' duration.
hydrostatic reduction by contrast agent or air enema
Physical exam reveals a baby with eczema and a musty
is the diagnostic and the therapeutic procedure of
odour. Whichscreening test would most likely be
choice. Hydrostatic reduction is contraindicated in
abnormal?
peritonitis or hemodynamic instability.
1. Ferric chloride test
2. Benedict test
42. Which of the following is true regarding
3. Rothera Test
Asymmetric tonic neck reflex?
4. Diazo test
1. Persistence beyond 6 months is normal
12
 Erythema nodosum
Ans. 1. Ferric chloride test • Erythema nodosum in itself is not a disease
Phenyl Ketonuria • Associated with many infections (e.g., group A
• Defect in Phenylalanine hydroxylase streptococcal infection, tuberculosis, Yersinia
• Mental retardation, vomiting, growth retardation, infection,histoplasmosis, coccidioidomycosis)
hyperactive, hepatomegaly, vomiting, purposeless • Inflammatory states (e.g., inflammatory bowel disease,
movements, athetosis, seizures systemic lupus erythematosus, juvenile rheumatoid
• Exam: Fair hair, fair skin, blue eyes, rash, tooth arthritis, sarcoidosis)
abnormalities, microcephaly • Administration of drugs (e.g., sulfonamides, phenytoin,
• Normal at birth , progressive MR oral contraceptives)
Treatment
• Cofactor tetrahydrobiopterin(BH4) administration can 46. A newborn being evaluated for hyperammonemia
reduce phenylalanine levels has elevated orotic acid but decreased/absent
• Abnormal urinary metabolites are detected by citrulline. What is the most likely diagnosis?
Guthrie or ferric chloride test 1. Citrillinemia
• Mental retardation can be prevented by restriction of 2. Arginosuccinic aciduria
phenylalanine in the diet right from birth which 3. OTC deficiency
should continue for 8-10 year 4. CPS deficiency
Urine Odours in IEMs
Musty-PKU Ans. 3. OTC deficiency
Cabbage-Tyrosinemia Urea Cycle
Maple syrup-MSUD
Sweaty feet-Isovaleric acidemia, glutaric acidemia type II
Cat urine-3-methylcrotonylCoA carboxylase and multiple
carboxylase deficiencies

44. Which of the following is not a feature of erb’s

palsy?
1. Inability to abduct shoulder
2. Inability to externally rotate shoulder
3. Loss of grasp
4. Inability to supinate forearm

Ans. 3. Loss of grasp

Erb’s palsy

Flow chart differentiating Hyperammonemia

Police man receiving tip position – C5, C6 root injury

Klumpke’s – C7, C8, T1 injury

45. Erythema nodosum is associated with all of the

following except
1. Sarcoidosis
2. Yersinia infection
3. Pseudotumour cerebri
4. Inflammatory bowel disease

Ans. 3. Pseudotumour cerebri

13
 Neonatal hyperammonemia

Symptoms in first 24hr life Symptoms after 24hr life

Premature Full term Acidosis No acidosis

THAN IEM OA or PC deficiency Organic Urea cycle

acidemias defects

Plasma AA

Absent citrulline Cit.moderately Cit. highly Elev;

Elev; ASA No ASA present
present

Urine Orotic acid Argininosuccinic Citrullinemia

aciduria

Low Elev

CPS deficiency OTC deficiency

Urea cycle defects basis. He is diabetic and takes an oral hypoglycemic.

Urea cycle defect: after the introduction of feeds and no
acidosis
Mx – Nil oral. Sodium Benzoate and arginine, Peritoneal
dialysis
Autosomal recessive , risk in each pregnancy is 25 %
his blood sugars have been slightly higher than
normal. Exam reveals a tender RUQ, positive Murphy's
sign

47. Which one of the following is not considered as

firstrank symptom of schizophrenia?
1. Auditory hallucinations
2. Insertion of thoughts
3. Delusional perceptions
4. Compulsive acts that relieve the tension

Ans. Is '4' i.e., Compulsive acts that relieve the tension

Schneider's first rank symptoms
1. Hallucinations:- Audible thoughts, voices
commenting on one's action, voices heard arguing two
or more hallucinatory voices discussing the subject in 1. Gas in gall bladder wall
third person (third person hallucination). 2. Gall stone ileus
2. Thought attention phenomena:- Thought insertion, 3. Aortic aneurysm
thought withdrawal, thought broadcasting. 4. Liver abscess
3. Passivity phenomena:- Made feeling (affect), made
impulse, mode volition (acts), somatic passivity. Ans. 1. Gas in gall bladder wall
4. Delusional perceptions (Primary delusions).
49. Max duration of time spent is in NREM stage –
48. A 55 year old male presents to the ER with 1. I
complaints of RUQ pain, fever and chills. He says he 2. II
has not been feeling well for the past 3 days. He had 3. III
similar pain 3 months ago but it subsided with some 4. IV
zantac. he denies any trauma and drinks on a social
14
Ans. is ‘2' i.e., II
 REM sleep ocupies 20-30% of total steep and NREM
sleep ocupies 60- 70% (state I: 5-10%, stage II: 40-
50% stage III & IV: 15-20%).
Stages of Sleep
o Sleep is basically divided into two phases : -
A) Non-REM (NREM) or slow-wave sleep: - It is called
Non-REM sleep because no rapid eye movement (REM) is
there on eletrooculogram, rather there is slow or quiscent
eye movement. It is also referred as S-sleep (synchronized
sleep) or quiet sleep or orthodox sleep because there
diminished physiological functions and a low level of
overall activity. It is further divided into: -
1. Stage 1: - It is a transition from wakefulness to sleep
and is characterized by disappearance of alpha activity
and appearance of theta activity. There is slow eye
movements.
2. Stage 2: - It is characterized by typical EEG activity i.e..
Sleep spindles and 'K-complex'. No eye movement
occurs.
3. Stage 3 & 4: - Stage 3 & 4 are stages of deep sleep.
These are also called slow wave sleep as these stages
are characterized by slow delta waves. Delta wave
appearance starts in stage 3 and dominated in stage 4.
B) REM sleep: - The REM sleep is so named as there is
rapid roving movements of eye, i.e., rapid eye movement
(REM)on electro-oculogram. It is also called paradoxical
sleep because there is a paradoxical elevation of brain
activity & metabolism and physiological activity. The high-
amplitude slow waves seen in stage 3,4 of REM sleep
is replaced by rapid low voltage activity (beta wave).
Features of REM sleep are: -
i. EEG  Beta wave, Reappearance of alpha wave,
Saw-tooth wave (low voltage fast activity), Ponto-
genitai-occipital spikes.
ii. Dreaming
iii. Other features: - Generalized muscular atony,
Penile erection, autonomic hyperactivity
(Increased pulse rate & BP) and intermittent
movement of small muscle groups.
 The NREM (with its four stages) and REM sleep repeat
several times a night in cyclic manner, 4-6 times
depending on the length of sleep. A typical cycle starts
with stage I of the NR£M sleep which is followed by
second, third and fourth stages. After this the sleep
returns to stage 3 and 2. The first REM sleep occurs
now, 70-90 minutes after the the commencement of
sleep (Note: - Stage 1 NREM sleep occurs only once at
the start of the sleep as this is only a transition phase
between wakefulness and sleep. Once the sleep starts
the cycle rotates between stage 2,3, 4 NREM and REM
sleep). REM sleep occupies 20-30% of total sleep and
NREM sleep occupies 60-70% (Stage-1 -> 5-10%;
Stage 2 -> 40-50%; Stage 3 & 4 -H5-20%).
50. All are associated with Wernicke's encephalopathy
except -
1. Cog wheel rigidity
15
2. Alteration in menial function
3. VIth nerve palsy
4. Ataxia
Ans. is ‘1' i.e., Cog-wheel rigidity
 Wernicke's encephalopathy is characterized by a triad
of global confusion (alteration in mental
function),Ophthalmoplegia (Bilateral 6th nerve palsy)
and ataxia.
Wernicke's encephalopathy
 It is an acute neurological disorder characterized by a
classical triad of ataxia, ophthalmoplegia and
confusion. The clinical findings include : -
1. Ocular: - Nystagmus, hi lateral lateral rectus palsy,
conjugate gaze palsies. The most common ocular
abnormality is nystagmus, not complete
ophthalmoplegia. Less frequently noted are pupillary
abnormalities such as sluggishly reactive pupil, ptosis,
scotomas, and anisocoria.
2. CNS (encephalopathy): - Global confusion, disinterest,
inattentiveness or agitation. Rarely stupor and coma
mayoccur.
3. Gait ataxia
4. Peripheral polyneuropathy: - Weakness, foot drop,
decreased proprioception.
5. Other symptoms: - Autonomic dysfunction
(tachycardia & postural hypotension). If there is
coexisting cardiovascular beriberi; hypothermia;
abdominal symptoms (nausea, vomiting, abdominal
pain).
51. A 40 year old female developed persistent oral
ulcers followed by multiple flaccid bullae on trunk and
extremities. Direct examination of a skin biopsy
immunofluorescence showed intercellular IgG
deposits in the epidermis and suprabasal split with
acantholytic cells. The probable diagnosis is:
1. Pemphigus vulgaris
2. Pemphigoid.
3. Erythema multiforme.
4. Dermatitis hepetiformis
Ans. 1. Pemphigus vulgaris
Reference
Pemphigus Vulgaris
1. It is an Auto Immune Mediated blistering skin
diseasefother immune mediated blistering skin
diseases are Pemphigus Foliaceus, Bullous
Pemphigoid, Cicatrical Pemphigoid, Dermatitis
Herpetiformis, Epidermolysis Bullosa Acquista and
Linera IgA disease)
2. HLA-DR4 and DRW6
3. Acantholyssis and Intraepidermal L\Blisters are
haracteristic features
4. Acantholytic cells are Round cells with
hyperchromatic nucleus and Perinuclear Halo
5. Nikolsky's Sign is seenfOther diseases with Nikolsky's Pemphigus is seen after administration of
Sign are Pemphigus, Pophyria, Steven Johnson's Toxic Penicillamine and Captopril
Epidermal Necrolysis, Staphylococcal Scalded Skin • Pemphigus Vegitans is the least common
Syndrome) Nikolsky's Sign is negative in Pemphigoid
6. Tzanck's Test is used. Let us see the differences between Pemphigus and
7. Tzanck's Cell is Keratinocyte Phempigoid
8. IgG antibodies are seen
9. Row of Tombstones appearance is present in Features Pemphigus Pemphigoid
PemphigusVulgaris Age 40-60 60-80
HPE-Row of Present Absent
Explanation Tombstones Present Absent
1. Pemphigus vulgaris presents with Acantholysis and Nikolsky's Sign Intraepidermal Sub Epidermal
Intraepidermal Bullae. Bulla Location Flacced Tense
2. Pemphigoid presents with subepidermal bullae IgG Bulla Features Involved Not involved
Antobodies are present against Basement Membrane Mucosa (eg Oral) Present Absent
and usually affect the elderly in 60 - SO years and Acantholysis
Mucosal Involvement is rare. There is no statistical
association with internal malignancy and HLA and 52. MRI in a patient demonstrates periventricular
Direct Immunonoflourescence reveals IgG and C3 high–signal intensity lesions. What is your diagnosis
deposits.
3. Erythema multiforme is usually due to Viral (Herpes)
or other Bacteria and Fungus. Lesions come in crops
and last for 2 ot3 weeks, and commonly affect the face,
dorsal surface of hand and feet and ecxtensor sirface
of forearm and legs, palms and soles. Target Lesions
(Bullet's Eye lesions) are specific and they consist of 3
conventric zones of color changes and are mostly
found acrally on the hand and feet in Erythema
Multiformae Minor
4. Dermatitis herpetiformis presents as intensely
pruritic, chronic, papulovesicular lesions that are
symmetrically distributed over extensor surfaces.
Associate with gluten sensitive Enteropathy. More
than 90 % express HLA B8 HLA DRW3 and HLA
DQW2. Subepidermal Blisters with Neutrophils ar
seen and Granular IgA deposits are seen in the dermal
papillae. The IgA antibodies are against Gliadin.
Treatmetn is with Dapsone and if the patient cannot
tolerate Dapsone, Sulphapyridine is substituted. Diet 1. Multiple Sclerosis
should exclude Gluten which is present in Barley ,Rye 2. Toxoplasmosis
and Wheat. Oats are tolerated and Gluten is not seen 3. Periventricular leukomalacia
with Rice. 4. Hypertensive Encephalopathy

Tips Answer 1. Periventricular plaques, head MRI

• PemphiguS has Superficial (Intra epidermal) blisters This radiology finding is characteristic for multiple
• PemphigoiD has Deep (Sub Epidermal) blisters sclerosis. Neural inflammation increases the permeability
• And among Pemphigus of the blood brain barrier, which allows IV contrast
o P.Erythematosus and P.Foliaceous show material to accumulate in the periventricular region.
intraepidermal Acantholytic Split in Stratum
Granulosum (Pnemonic EFG)and 53. All are grave sign of GERD in child except?
o P.Vulgaris and P.Vegetans show Intraepidermal 1. Heartburn
Acantholytic split in between the Basal layer and the 2. Dysphagia
Prickle cell layer 3. Odynophagia
• The Nikolsky sign is positive in pemphigus and more 4. Jaundice
rarely toxic epidermal necrolysis.
• Pemphigus Vulgaris is due to autoimmunity directed Ans. 1. Heartburn
against Cadherin This is one of the most frequent, early and constant feature
• Pemphigus Foliaceus is due to autoimmunity directed of GERD.
against Desmoglein and this Drug induced
16
Once alarm factors are excluded, patients with typical
GERD do not need further evaluation and are treated
empirically. Upper endoscopy is indicated to exclude
mucosal injury in cases with atypical symptoms, symptoms
unresponsive to acid suppressing drugs, or alarm factors.
Odynophagia
Unexplained weight loss
Recurrent vomiting
Occult or gross gastrointestinal bleeding
Jaundice
Palpable mass or adenopathy
Family history of gastrointestinal malignancy
Odynophagia
Upper endoscopy is performed as the initial diagnostic test
in patients with unexplained dyspepsia who are >55 years
old or who have alarm factors because of the elevated risks
of malignancy and ulcer in these groups. The management
approach to patients <55 years old without alarm factors
is dependent on the local prevalence of H, pylori infection.
Alarm Symptoms that Indicate the Need for Upper
Endoscopy
Weight loss
Recurrent vomiting
Dysphagia
Bleeding
Anemia
54. Which of the following is not a major prognostic
factor in multiple myeloma?
1. Beta 2 microglobulin
2. Labelling Index
3. Hypercalcemia
4. Elevated CRP
Ans. 3. Hypercalcemia
Most other guides have gone wrong with the answer.
This is a key question, and one of the most vital updates
that has been incorporated into Harrison's "18thEd.
Until Harrison's 17th Ed, Salmon-Durie Prognostic System
was in use, which included Hb, serum calcium, Skeletal
survey (lytic lesions), Serum M protein, Urinary light chain
excretion and serum creatinine levels.
Going with previous editions, the answer so far has been
cRP, since this was the only, minor (placed under ''Other
Factors") prognostic marker. All other options were
specifically mentioned as important prognostic
determinants. But, Harrison's 18th has dropped this
system, and adopted International Staging System(ISS).
Thus, the answer too has changed. With Salmon-Durie
System being scrapped, Serum Calcium level loses its
status as a major determinant of disease progression: all
other options, except serum Ca++ has been categorically
mentioned as vital prognostic determinants in Harrison's
"18th, thus this is the current answer.
17
International Staging System
Stage Median Survival, Months
2M < 3.5, alb 3.5 I (28%) 62
2M < 3.5, alb < 3.5 II (39%) 44
or 2M = 3.5-5.5
2M > 5.5 III 29
(33%)
Note: (#), % patients presenting at each stage.
Abbreviations: 2M, serum 2-microglobulin in mg/L; alb,
serum albumin in g/Dl
Serum 2-microglobuliu is the single most powerful
predictor of survival and can substitute for staging. 2-
Microglobulin is a protein of 11,000 mol wt with
homologies to the constant region of immunoglobulin’s
that is the light chain of the class I major histocompatibility
antigens (HLA-A, -B, -C) on the surface of every cell.
Patients with 2-microglobulin levels <0.004 g/L have a
median survival of 43 months and thosewith levels >0.004
g/L only 12 months. Serum 2-microglobulin and albumin
levels are the basis for a three-stage International Staging
System (ISS). It is also felt that once the diagnosis of
myeloma is firm, histologic features of atypia may also
exert an influence on prognosis. High labeling index and
high levels of lactate dehydrogenase are also associated
with poor prognosis.
Other factors that may influence prognosis are the
presence and number of cytogenetic abnormalities,
hypodiploidy, chromosome 13q and 17p deletion,
translocations t(4;14) and t(14;16); circulating plasma
cells; performance status; as well as serum levels of
soluble IL-6 receptor,C-reactive protein, hepatocyte
growth factor, C-terminal cross-linked telopeptide of
collagen I, transforming growth factor (TGF)-, and
syndecan-1. Microarray profiling and comparative
genomic hybridization have formed the basis for RNA-and
DXA-based prognostic staging systems, respectively. The
ISS system is the most widely used method of assessing
prognosis.
Durie-Salmon staging system
First published in 1975, the Durie-Salmon staging system
is still in use:
• stage I: all of
o Hb>10g/dL
o normal calcium
o Skeletal survey: normal or single plasmacytoma or
osteoporosis
o Serum paraprotein level <5 g/dL if IgG, < 3 g/ dL if
IgA
o Urinary light chain excretion < 4 g/24h
 stage II: fulfilling the criteria of neither I nor III
 stage III: one or more of
o Hb<8.5g/dL
o high calcium > 12 mg/ dL
o Skeletal survey: Three or more lytic bone lesions
o Serum paraprotein > 7g/dL if IgG, > 5 g/dL if IgA
 o Urinary light chain excretion > 12g/24h
 Stages I, II, and III of the Durie-Salmon staging system
can be divided into A or B depending on serum
creatinine:
• A: serum creatinine < 2 mg/dL (< 177 umol/L)
• B: serum creatinine > 2 mg/dL (> 177 umol/L)
55. Dengue Hemorrhagic Fever presents with all
except:
1. Capillary leak
2. Thrombocytopenia
3. Elevated hematocrit
4. Hypoproteinemia
Ans. 4. hypoproteinemia
Dengue Hemorrhagic Fever/Dengue Shock Syndrome
Dengue HF is identified by the detection of bleeding
tendencies (tourniquet test, petechiae) or overt bleeding in
the absence of underlying causes such as preexisting
gastrointestinal lesions. Dengue shock syndrome, usually
accompanied by hemorrhagic signs, is much more serious
and results from increased vascular permeability leading
to shock. In mild DHF/DSS, restlessness, lethargy,
thrombocytopenia(<100,000/L), and hemoconcentration
are detected 2-5 days after the onset of typical dengue
fever, usually at the time of defervescence. The
maculopapular rash that often develops in dengue fever
may also appear in DHF/DSS. In more severe cases, frank
shock is apparent, with low pulse pressure, cyanosis,
hepatomegaly, pleural effusions, ascites, and in some cases
severe ecchymoses and gastrointestinal bleeding. The
period of shock lasts only 1 or 2 days, and most patients
respond promptly to close monitoring, oxygen
administration, and infusion of crystalloid or— in severe
cases — colloid. The case-fatality rates reported vary
greatly with case ascertainment and the quality of
treatment; however, most DHF/DSS patients respond well
to supportive therapy, and the overall mortality rate at an
experienced center in the tropics is probably as low as 1%.
The induction of vascular' permeability and shock depends
on multiple factors, including the following:
1. Presence of enhancing and nonneutralizing
antibodies — Transplacental maternal antibody may
be present in infants <9 months old, or antibody
elicited by previous heterologous dengue infection
may be present in older individuals. T cell reactivity is
also intimately involved.
2. Age—Susceptibility to DHF/DSS drops considerably
after 12 years of age.
3. Sex—Females are more often affected than males.
4. Race — Whites are more often affected than blacks.
5. Nutritional status — Malnutrition is protective.
6. Sequence of infection — For example, serotype 1
followed by serotype 2 seems to be more dangerous
than serotype 4 followed by serotype 2.
7. Infecting serotype — Type 2 is apparently more
dangerous than other serotypes.
18
56. A reticulocyte count >10% will be seen in all of the
following except:
1. Acute hemorrhage
2. Thallassemia
3. Immune Hemolytic anemia
4. Rh Incompatibility
Ans. 2. Thallassemia
Reduced Reticulocyte Count in Beta Thalassemia
Two major features contribute to the pathogenesis of
sequelae of β-thalassemia: inadequate β -globin gene
production, leading to decreased levels of normal
hemoglobin (Hb A), and an imbalance in α- and β -globin
chain production. Selected features of the thalassemias can
be seen in Table 462-6 . In bone marrow, thalassemic
mutations disrupt the maturation of red blood cells,
resulting in ineffective erythropoiesis; the marrow is
hyperactive, but the patient has relatively few
reticulocytes and severe anemia. In β -thalassemias, there
is an excess of α-globin chains relative to β - and y-globin
chains; α-globin tetramers (α 4) are formed, and these
inclusions interact with the red cell membrane and
shorten red cell survival, leading to anemia and increased
ervthroid production. The γ-globin chains are produced in
increased amounts, leading to an elevated Hb F (α2γ2)- The
6-globin chains are also produced in increased amounts,
leading to an elevated Hb A2(α2δ2) in β -thalassemia.
The infant is born only with Hb F or, in some cases, Hb F
and Hb E (heterozygosity for β°-thalassemia). Eventually,
patients with p-thalassemia have severe anemia, few
reticulocytes, numerous nucleated red cells, and
microcytosis, with almost no normal-appearing red cells
on the smear. The hemoglobin level falls progressively to
<5.0 g/dL unless transfusions are given. The reticulocyte
count is commonly <8% and is inappropriately low
compared with the degree of anemia because of ineffective
erythropoiesis. The unconjugated serum bilirubin level is
usually elevated, but other chemistry values may be
normal at anearly stage. Even if the patient is
untransfused, eventually there is iron accumulation, with
an elevated
serum ferritin level and saturation of transferrin. Bone
marrow hyperplasia can be seen on radiographs.
Laboratory Investigations and Diagnosis of Paroxysmal
Nocturnal Hemoglobinuria (PNH)
The most consistent blood finding is anemia, which may
range from mild to moderate to very severe. The anemia is
usually normo-macrocytic, with unremarkable red cell
morphology; if the MCV is high, it is usually largely
accounted for by reticulocytosis, which may be quite
marked (up to 20%, or up to 400,000/L). The anemia may
become microcytic if the patient is allowed to become
iron-deficient as a result of chronic urinary blood loss
through hemoglobinuria. Unconjugated bilirubin is mildly
or moderately elevated, LDH is typically markedly elevated
(values in the thousands are common), and haptoglobin is
usually undetectable. All these findings make the diagnosis prolonged epistaxis requiring medical attention.
of HA compelling. Menorrhagia is a common manifestation of VWD.
Menstrual bleeding resulting in anemia should warrant an
General examination Jaundice, pallor evaluation for VWD and, if negative ,functional platelet
Other physical finding Spleen may be enlarged; disorders . Frequently ,mild type 1 VWD first manifests
bossing of skull in severe with dental extractions, particularly wisdom tooth
congenital cases extraction ,or tonsillectomy.
Hemoglobin level From normal to severely
reduced Laboratory Diagnosis of von Willebrand Disease
MCV, MCH Usually increased Type aPTT VWF VWFAc FVIIIAc Multimer
Reticulocytes Increased Antige tivity tivity
Bilirubin Increased (mostly un n
conjugated) 1 Nor ↑ ↓ ↓ ↓ Normal distribution,
LDH Increased (up to 10x decreased in
normal with intravascular quantity
hemolysis) 2A Nor ↑ ↓ ↓↓ ↓ Loss of high- and
Haptoglobin Reduced to absent (if intermediate-MW
hemolysis is part multimers
intravascular)_ 2Ba Nor ↑ ↓ ↓↓ ↓ Loss of high-MW
multimers
57. Laboratory finding consistent with von Willebrand 2M Nor ↑ ↓ ↓↓ ↓↓ Normal distribution,
Disease: decreased in
1. Prolonged aPTT quantity
2. Prolonged PT 2N ↑↑ Nor ↓b Nor ↓b ↓ ↓ Normal distribution
3. Bleeding tendency is a must 3 ↑↑ ↓↓ ↓↓ ↓↓ Absent
4. Thrombocytosis
58. Transmural involvement not seen in:
Ans. 1. Prolonged aPTT 1. Ulcerative colitis
Elevated constantly in all forms of vWD. PT is not altered. 2. Crohn's Disease
3. Mesenteric arterial occlusion
von Willebrand Disease 4. Necrotizing enterocolitis
VWD vvVis the most common inherited bleeding disorder.
Estimates from laboratory data suggest a prevalence of Ans. 1. Ulcerative colitis
approximately 1%, but data based on symptomatic UC doesn't involve muscularis propria, and never extends
individuals suggest that it is closer to 0.1% of the beyond mucosa.
population. VWF serves two roles: (1) as the major
adhesion molecule that tethers the platelet to the exposed The distinction between ulcerative colitis and Crohn
sub endothelium; and (2) as the binding protein for FVIII, disease is based, in large part, on the distribution of
resulting in significant prolongation of the FVIII half-life in affected sites and the morphologic expression of disease at
circulation. The platelet-adhesive function of VWF is those sites. Ulcerative colitis is a severe ulcerating
critically dependent on the presence of large VWF inflammatory disease that is limited to the colon and
multimers, while FVIII binding is not. Most of the rectum and extends only into the mucosa and submucosa.
symptoms of VWD are "platelet-like" except in more In contrast, Crohn disease, which has also been referred to
severe VWD when the FVIII is low enough to produce as regional enteritis (because of frequent ileal
symptoms similar to those found in Factor VIII deficiency involvement) may involve any area of the GI tract and is
(hemophilia A). typically transmural.

VWD has been classified into three major types, with four
subtypes of type 2. By far the most common type of VWD is
type 1 disease, with a parallel decrease in VWF protein,
VWF function, and FVIII levels, accounting for at least 80%
of cases. Patients have predominantly mucosal bleeding
symptoms, although postoperative bleeding can also be
seen. Bleeding symptoms are very uncommon in infancy
and usually manifest later in childhood with excessive
bruising and epistaxis. Since these symptoms occur
commonly in childhood, the clinician should particularly
note bruising at sites unlikely to be traumatized and/or

19
 Drowsiness Drowsiness
Disorientation Confusion
Dizziness Headache
Headache Coma
Coma
Cardiovascular
↓ Wood pressure ↓ Blood pressure
Ventricular fibrillation Dysrhythmias (related to
(related to hyperkalemia hyperkalemia from
from compensation) compensation))
Warm, flushed skin (related Warm, flushed skin (related
Features That Differ between Crohn Disease and to peripheral vasodilation) to peripheral vasodilation)
Ulcerative Colitis Gastrointestina
Feature Crohn Disease Ulcerative No significant findings Nausea, vomiting, diarrhea,
Colitis Neuromuscular abdominal pain
MACROSCOPIC Seizures
Bowel region Ileum ± colon Colon only Respiratory No significant findings
Distribution Skip lesions Diffuse Hypoventilation with
Stricture Yes Rare hypoxia (lungs are unable Deep, rapid respirations
Wall appearance Thick Thin to compensate when there (compensatory action by
MICROSCOPIC is a respiratory problem) the lungs)
Inflammation Transmural Limited to
Pseudo polyps Moderate mucosa 60. Insulin does not cause:
Ulcers Deep, knife-like Marked 1. Gluconeogenesis in the liver
Lymphoid reaction Marked Superficial, 2. Protein synthesis
Fibrosis Marked broad-based 3. Cellular transport of glucose
Serositis Marked Moderate 4. Hypokalemia
Granulomas Yes (-35%) Mild to none
Fistulae/ sinuses Yes Mild to none Ans. 1. Gluconeo gene sis in the liver
No Principal Actions of Insulin.
No
CLINICAL Rapid (seconds)
Perianalfistula Yes (in colonic No Increased transport of glucose, amino acids, and K+ into
Fat/ vitamin disease; No insulin-sensitive cells
malabsorption Yes Yes Intermediate (minutes)
Malignant potential With colonic No Stimulation of protein synthesis
Recurrence after involvement Yes Inhibition of protein degradation
surgery Common Activation of glycolytic enzymes and glycogen synthase
Toxic megacolon No Inhibition of phosphorvlase and gluconeogenic enzymes
Delayed (hours)
59. Increased irritability of the skeletal muscles is Increase in mRN'As for lipogenic and other enzymes
classically seen in The actions of insulin on adipose tissue; skeletal, cardiac,
1. Metabolic acidosis and smooth muscle; and the liver are summarized:
2. Metabolic alkalosis
3. Respiratory acidosis Effects of Insulin on Various Tissues
4. Respiratory alkalosis Adipose tissue
Increased glucose entry
Ans. 2. Metabolic alkalosis Increased fatty acid synthesis
Metabolic alkalosis Increased glycerol phosphate synthesis
• pH greater than 7.45 Increased triglyceride deposition
• PC02 normal or may be inc. b/c of compensating Activation of lipoprotein lipase
• HC03 greater than 26 Inhibition of hormone-sensitive lipase
• urine PH greater than 6 Increased K+ uptake
Muscle
Lewis's Medical Surgical Nursing By Chintamani Increased glucose entry
writes: Increased glycogen synthesis
Respiratory (↑ PaCO2) Metabolic (↓HCO3- ) Increased amino acid uptake
Neurologic Increased protein synthesis in ribosomes

20
Decreased protein catabolism
Decreased release of gluconeogenic amino acids
Increased ketone uptake
Increased K+ uptake
Liver
Decreased keto genesis
Increased protein synthesis
Increased lipid synthesis
Decreased glucose output due to decreased
gluconeogenesis, increased glycogen synthesis, and
increased glycolysis
General
Increased cell growth
Ref: review of Medical physiology 23Ed Ganong
61. Which is the commonest area of intracranial
hypertensive bleed?
1. Basal ganglia
2. Brain stem
3. Subdural hemorrhage
4. Cerebellum
Ans. 1. Basal ganglia
Hypertensive Intraparenchymal Hemorrhage
Pathophysiology
Hypertensive intraparenchymal hemorrhage
(hypertensive hemorrhage or hypertensive intracerebral
hemorrhage) usually results from spontaneous rupture of
a small penetrating artery deep in the brain. The most
common sites are the basal ganglia (especially the
putawen), thalamus, cerebellum, and pons. When
hemorrhages occur in other brain areas or in
nonhypertensive patients, greater consideration should be
given to hemorrhagic disorders, neoplasms, vascular
malformations, and other causes. The small arteries in
these areas seem most prone to hypertension-induced
vascular injury.
The hemorrhage may be small or a large clot may form and
compress adjacent tissue, causing herniation and death.
Blood may dissect into the ventricular space, which
substantially increases morbidity and may cause
hydrocephalus.
Most hypertensive intraparenchymal hemorrhages
develop over 30-90 min, whereas those associated with
anticoagulant therapy may evolve for as long as 24-48 h.
Within 48 h macrophages begin to phagocytize the
hemorrhage at its outer surface. After 1-6 months, the
hemorrhage is generally resolved to a slitlike orange cavity
lined with glial scar and hemosiderin-laden macrophages,
cause the greatest difficulty in coma diagnosis.
The most common categories are:
(1) Basal ganglia and thalamic hemorrhage (acute but not
instantaneous onset, vomiting, headache, hemiplegia,
and characteristic eye signs);
(2) Pontine hemorrhage (sudden onset, pinpoint pupils,
loss of reflex eye movements and corneal responses,
ocular bobbing, posturing, hyperventilation, and
excessive sweating);responses, ocular nobbing,
posturing, Hyperventilation, and excessive sweating);
21
(3) Cerebellar hemorrhage (occipital headache, vomiting,
gaze paresis, and inability to stand);
(4) Basilar artery thrombosis (neurologic prodrome or
warning spells, diplopia, dysarthria, vomiting, eye
movement and corneal response abnormalities, and
asymmetric limb paresis); and
(5) Subarachnoid hemorrhage (precipitous coma after
headache and vomiting).
62. A 14 year old boy fell off a bicycle and injured his
head. However, he had a good Glasgow Coma
Scalelevel when he was admitted for observation. 3
hours after admission, he became non-responsive to
pain and unconscious. What is the possible diagnosis?
1. Extradural hemorrhage
2. Subdural hemorrhage
3. Subarachnoid hemorrhage
4. Intracerebral hemorrhage
Ans. 1. Extradural hemorrhage > B. Subdural hemorrhage
EDH is safer option, though data provided here seems
insufficient to differentiate thes two etiologies. A CT Scan
is mandatory.
A "lucid interval" of several minutes to hours before coma
supervenes is most characteristic of epidural hemorrhage
(i.e. Extradural hemorrhage), but have been described
frequently for Subdural hemorrhage with up to one-third
of patients have a lucid interval.See below:
Acute subdural hematomas typically arise from venous
sources, often the bridging veins locatedimmediately
under the dura mater. As the brain volume decreases with
age, traction on these venousstructures increases and even
minor head trauma in the elderly can lead to a subdural
hematoma.
Approximately 33% of patients with an acute subdural
bleed will experience a lucid interval after theevent, which
is followed bit obtundation. Subdural bleeding is typically
slower than epidural bleeding due to their different
sources .Small subdural bleeds are asymptomatic and
often do not require evacuation.
Diffuse Axonal Injury
A special type of deep white matter lesion consists of
widespread mechanical disruption, or shearing, of axons at
the time of impact. Most characteristic are small areas of
tissue injury in the corpus callosum and dorsolateral pons.
The presence of widespread axonal damage in both
hemispheres, a state called diffuse axonal injury (DAI), has
been proposed to explain persistent coma and the
vegetative state after closed head injury, but small
ischemic-hemorrhagic lesions in the midbrain and
thalamus are as often the cause. Only severe shearing
lesions that contain blood are visualized by CT, usually in
the corpus callosum and centrum semiovale; however,
selective imaging sequences of the MRI can demonstrate
such lesions throughout the white matter.
Diagnosis
CT without contrast initially shows a low-density mass shifts; this circumstance in an older patient is suggested by
over the convexity of the hemisphere (Fig. 378-5). a "hypernormal" CT scan with fullness of the cortical sulci
Between 2 and 6 weeks after the initial bleeding the and small ventricles. Infusion of contrast material
hemorrhage becomes isodense compared to adjacent brain demonstrates enhancement of the vascular fibrous capsule
and may be inapparent. Many subdural hematomas that surrounding the collection. MRI reliably identifies
are several weeks in age contain areas of blood and subacute and chronic hematomas.
intermixed serous fluid. Bilateral chronic hematomas may
fail to be detected because of the absence of lateral tissue
63. Atonic bladder is seen in
1. Spinal shock
2. Spinal injury above the level of sacral segments
3. Brainstem injury
4. Transection of the afferent nerves from the bladder

Ans. 1. Spinal shock

Sacral Cord/Conus Medullaris
The conus medullaris is the tapered caudal termination of
the spinal cord, comprising the lower sacral and
singlecoccygeal segments. The distinctive conus syndrome
consists of bilateral saddle anesthesia (S3-S5), prominent
bladder and bowel dysfunction (urinary retention and
incontinence with lax anal tone), and impotence. The
bulbocavernosus (S2-S4) and anal (S4-S5) reflexes are
absent (Chap. 367). Muscle strength is largely preserved.
By contrast, lesions of the cauda equina, the nerve roots
derived from the lower cord, are characterized by low back
and radicular pain, asymmetric leg weakness and sensory
loss, variable areflexia in the lower extremities, and
relative sparing of bowel and bladder function.
Immediate after effects of acute spinal cord injury
During the immediate after effects of acute spinal cord
injury, there is a state of spinal shock; during spinal shock
the patient has a flaccid paralysis below the level of the
spinal lesion; no reflexes are obtained, sensation is not
perceived and the bladder loses its capacity to contract
and is in a state of retention overflowing when fully
stretched; this is an atonic bladder and may last for days,
weeks or months
1. this occurs because the inhibiting effects of the higher
central nervous system has been cut off from the
lower cord
2. as spinal shock passes off, reflexes return (flexor
reflexes of skeletal muscle return first in 3 days to 3
weeks following injury) and become hyperactive;
spasticity sets in and the bladder begins to show
evidence of contractions even when the bladder isn't
full
Human infection begins when a female anopheline
mosquito inoculates plasmodial sporozoites from its
salivary gland during a blood meal. These microscopic
motile forms of the malarial parasite are carried rapidly
via the bloodstream to the liver, where they invade hepatic
parenchymal cells and begin a period of asexual
reproduction. By this amplification process (known as
intrahepatic or preerythrocytic schizogony or merogony),
a single sporozoite eventually may produce from 10,000 to
>30,000 daughter merozoites. The swollen infected liver
cell eventually bursts, discharging motile merozoites into
the bloodstream. These merozoites then invade the red
blood cells (RBCs) and multiply six- to twentyfold every
48-72 h. When the parasites reach densities of ~50/~ L of
blood (~100 million parasites in the blood of an adult), the
symptomatic stage of the infection begins. In P. vivax and
P, ovale infections, a proportion of theintrahepatic forms
do not divide immediately but remain dormant for a
period ranging from 3 weeks to a year or longer before
reproduction begins. These dormant forms, or hypnozoites
, are the cause of the relapses that characterize infection
with these two species.
Characteristics of Plasmodium Species Infecting
Humans

64. Infective stage of malaria to human?

1. Sporozoite
2. Trophozoite
3. Schizont
4. Gametocytes

Ans. 1. Sporozoite

22
Finding for Indicated Species
Characteristic P. P. vivax P. P.
falcipar ovale malariae
um
Duration 5.5 8 9 15
ofintrahepatic
phase(days)
Number 30,000 10,000 15,000 15,000
ofmerozoitesrele
ased
perinfectedhepat
ocyte The C wave may reflect the carotid pulsation in the neck
Duration 48 48 50 72 and/or an early systolic increase in right atrial pressure as
oferythrocytic the right ventricle pushes the closed tricuspid valve into
cycle(hours) the right atrium (bulging/ coving up).
Red cell Younger Reticulocy Reticul Older cells
preference cells tes and ocytes The venous waveform is divided into several distinct
(but cells peaks. The a wave reflects right atrial presystolic
can up to 2 contraction and occurs just after the electrocardiographic
invade weeks old P wave, preceding the first heart sound (S1).
cells
of all  A prominent a wave is seen in patients with reduced
ages) right ventricular compliance; a cannon a wave occurs
Morphology Usually Irregularl Infecte Band with atrioventricular (AV) dissociation and right atrial
only y derythr orrectang contraction against a closed tricuspid valve. In a
ring shapedlar ocytes, ular patient with a wide complex tachycardia, the
Formsb; ge rings enlarge forms
banana- andtropho d and oftrophoz appreciation of camion a waves in the jugular venous
Shapedg zoites; ovalwit oites waveform identifies the rhythm as ventricular in
ametocy enlarged h tufted common origin. The a wave is not present with atrial
tes erythrocyt ends; fibrillation.
es; Schuffn  The x descent defines the fall in right atrial pressure
Schuffner’ er’s after inscription of the a wave.
s dots dots  The c wave interrupts this x descent and is followed by
Pigment color Black Yellow- Dark Brown- a further descent.
brown brown black  The v wave represents atrial filling (atrial diastole)
Ability to cause No Yes Yes No and occurs during ventricular systole. The height of
relapses the v wave is determined by right atrial compliance as
well as the volume of blood returning to the right
65. C wave in JVP is caused by: atrium either antegrade from the cavae or retrograde
1. Atrial contraction through an incompetent tricuspid valve. In patients
2. Buldging of the Tricuspid Valve with TR, the v wave is accentuated and the subsequent
3. Filling of the Blood against closed valve fall in pressure (y descent) is rapid. With progressive
4. Idioventricular rhythm degrees of TR, the v wave merges with the c wave, and
the right atrial and jugular vein waveforms become
Ans. 2. Buldging of the Tricuspid Valve "ventricularized."
 The y descent, which follows the peak of the v wave,
can become prolonged or blunted with obstruction to
right ventricular inflow, as may occur with tricuspid
stenosis (TS) or pericardial temponed.

66. Tetany is seen in all of the following except:

1. Hypocalcemia
2. Hypomagnesemia
3. Hypoparathyroidism
4. Metabolic acidosis

Ans. 4. metabolic acidosis

23
All other options execp metabolic acidosis has certain • Infiltration by metastases or systemic diseases
association with hypocalcemia/ tatany. Alkalosis of nil • Autoimmune
types, hyperaldosteronism, hypocalcemia, and Reduced parathyroid function
hypokalemia may present with tetani. • Hypomagnesaemia
• Activating CaSR mutations
Clinical and Laboratory Findings of Metabolic High Parathyroid Hormone Levels (Secondary
Alkalosis Hyperparathyroidism)
With metabolic alkalosis, changes in CXS and peripheral Vitamin D deficiency or impaired 1,25(OH)2D
nervous system function are similar to those of production/action
hypocalcemia; symptoms include mental confusion; • Nutritional vitamin D deficiency (poor intake or
obtundation; and a predisposition to seizures, paresthesia, absorption)
muscular cramping, tetany, aggravation of arrhythmias, • Renal insufficiency with impaired 1,25(OH)2D
and hypoxemia in chronic obstructive pulmonary disease. production
Related electrolyte abnormalities include hypokalemia and • Vitamin D resistance, including receptor defects
hypophosphatemia. Parathyroid hormone resistance syndromes
• PTH receptor mutations
Clinical and Laboratory Findings of Respiratory • Pseudohypoparathyroidism (G protein mutations)
Alkalosis Drugs
• (From, Harrison's Principles Of internal Medicine 18th • Calcium chelators
Edition) • Inhibitors of bone resorption (bisphosphonates,
The hyperventilation syndrome may be disabling. plicamycin)
Paresthesia; circumoral numbness; chest wall • Altered vitamin D metabolism (phenytoin,
tightness or pain; dizziness; inability to take an ketoconazole)
adequate breath; and, rarely, tetany may be Miscellaneous causes
sufficiently stressful to perpetuate the disorder. • Acute pancreatitis
• Acute rhabdomyolysis
• (From, Davidson's Principles and Practice of Medicine • Hungry bone syndrome after parathyroidectomy
21st Ed) • Osteoblastic metastases with marked stimulation of
Clinical features are those associated with the cause, bone formation (prostate cancer)
but there is frequently also agitation associated with Abbreviations: CaSR, calcium sensor receptor; PTH,
perioral and digital tingling, due to a reduction in parathyroid hormone.
ionised calcium concentration caused by increased
binding of calcium to albumin in the alkalotic ECF. In Causes of Hypercalcemia
severe cases, Trousseau's sign and Chvostek's sign Excessive PTH production
maybepositive ,and tetany or seizures may • Primary hyperparathyroidism (adenoma, hyperplasia,
develop(p.766). rarely carcinoma)
• Tertiary hyperparathyroidism (long-term stimulation
Causes of Tetany of PTH secretion in renal insufficiency)
• The usual cause of tetany is lack of calcium. An excess • Ectopic PTH secretion (very rare)
of phosphate (high phosphate-to-calcium ratio) can • Inactivating mutations in the CaSR (FHH)
also trigger the spasms. Milk-and-alkali tetany is an • Alterations in CaSR function (lithium therapy)
example of this imbalance. Hypercalcemia of malignancy
• Under function of the parathyroid gland can lead to • Overproduction of PTHrP (many solid tumors)
tetany. • Lytic skeletal metastases (breast, myeloma)
• Low levels of carbon dioxide cause tetany by altering Excessive l,25(OH)2D production
the albumin binding of calcium such that the • Granulomatous diseases (sarcoidosis, tuberculosis,
ionised (physiologically influencing) fraction of silicosis)
calcium is reduced; the most common reason for • Lymphomas
low carbon dioxide levels is hyperventilation. • Vitamin D intoxication
• Low levels of magnesium can lead to tetany. Primary increase in bone resorption
• Hyperthyroidism
Low Parathyroid Hormone Levels • Immobilization
(Hyperparathyroidism) Excessive calcium intake
Parathyroid agenesis • Milk-alkali syndrome
• Isolated • Total parenteral nutrition
• DiGeorge syndrome Other causes
Parathyroid destruction • Endocrine disorders (adrenal insufficiency,
• Surgical pheochromocvtoma, VIPoma)
• Radiation
24
Medications (thiazides, vitamin A, antiestrogens) In untreated patients or in patients in whom therapy has
not adequately controlled virus replication, after a variable
67. In view of ART therapy all are true except: period, usually measured in years, the CD4+ T cell count
1. ART started when CD4 count <200/µL in adults falls below a critical level (<200/L) and the patient
2. ART started when CD4+ T cell count <500/ µL in becomes highly susceptible to opportunistic disease. For
adults this reason, the CDC case definition of AIDS includes all
3. ART initiation is independent of CD4 count in infants HIV-infected individuals with CD4+ T cell counts below
4. ART is indicated in pregnant women with HIV this level (Table 189-1). Patients may experience
constitutional signs and symptoms or may develop an
Ans. 1. ART started when CD4 count <200/µL in adults opportunistic disease abruptly without any prior
Indications for the Initiation of Antiretroviral Therapy in symptoms, although the latter scenario is unusual. The
Patients with HIV Infection depletion of CD4+ T cells continues to be progressive and
I. Acute infection syndrome unrelenting in this phase. It is not uncommon for CD4+ T
II. Chronic infection cell counts inthe untreated patient to drop as low as 10/L
A. Symptomatic disease (including HIV- or even to zero. In countries where cART and prophylaxis
associated nephropathy) and treatment for opportunistic infections are readily
B. Asymptomatic disease accessible to such patients, survival is increased
1. CD4+ T cell count <500/ La dramatically even in those patients with advanced HIV
2. Pregnancy disease. In contrast, untreated patients who progress to
III. Post exposure prophylaxis this severest form of immunodeficiency usually succumb
'This is an area of controversy. Some experts would treat to opportunistic infections or neoplasm’s (see below).
everyone regardless of CD4+ T cell count.
Source :Guidelines for the Use of Antiretroviral Agents in Abbreviation; PGL, progressive generalized
HIV-infected Adults and Adolescents, USPHS. lymphadenopathy
Clinical Categories of HIV Infection
Clinical Categories Category A: Consists of one or more of the conditions
listed below in an adolescent or adult (>13 years) with
CD4+ T A B C AIDS- documented HIV infection. Conditions listed in categories
Cell Asymptomatic, Symptomatic, Indicator B and C must not have occurred.
Categories Acute Not A or C Conditions Asymptomatic HIV infection
(Primary) HIV Conditions Persistent generalized lymphadenopathy
or PGL Acute (primary) HIV infection with accompanying illness
>500/ L Al Bl CI or history of acute HIV infection
200-499/ A2 B2 C2 Category B: Consists of symptomatic conditions in an HIV-
L infected adolescent or adult that are not included among
<200/L A3 B3 C3 conditions listed in clinical category C and that meet at
least one of the following criteria:
In Pediatric HIV, (1) The conditions are attributed to HIV infection or are
Initiation of Therapy indicative of a defect in cell-mediated immunity ;or
HIV-infected children with symptoms (clinical category A, (2) the conditions are considered by physicians to have a
B, or C) or with evidence of immune dysfunction (immune clinical course or to require management that is
category 2 or 3) should be treated with anti-retroviral complicated by HIV infection. Examples include, but are
therapy, regardless of age or viral load. not limited to, the following:
Children <1 yr of age are at high risk for disease Bacillary angiomatosis
progression, and immunologic and virologic tests to Candidiasis, oropharyngeal (thrush)
identify those likely to develop rapidly progressive disease Candidiasis, vulvovaginal; persistent, frequent, or poorly
are less predictive than in older children. Therefore, such responsive to therapy
infants should be treated with anti-retroviral agents as Cervical dysplasia (moderate or severe)/cervical
soon as the diagnosis of HIV carcinoma in situ
infection has been confirmed, regardless of clinical or Constitutional symptoms, such as fever (38.5°C) or
immunologic status, or viral load. diarrhea lasting >"1 month
Hairy leukoplakia, oral
Data surest that HIV-infected infants who are heated Herpes zoster (shingles), involving at least two distinct
before the age of 3 months control their HIV infection episodes or more than one dermatome
better than infants whose anti-retroviral therapy started Idiopathic thrombocytopenic purpura
later than 3 mo of age. Listeriosis
Pelvic inflammatory disease, particularly if complicated by
Advanced HIV Disease tuboovarian abscess

25
Peripheral neuropathy 68. Prophylaxis of Pneumocystis carnii pneumonia
Category C: Conditions listed in the AIDS surveillance case includes:
definition. 1. Clotrimoxazole
Candidiasis of bronchi, trachea, or lungs 2. Penicillin
Candidiasis, esophageal 3. Vancomycin
Cervical cancer, invasive 4. Fluoroquinolones
Coccidioidomycosis, disseminated or extrapulmonary
Cryptococcosis, extrapulmonary Ans. 1. Clotrimoxazole
Cryptosporidiosis, chronic intestinal (>1 month's Pathogenesis and Pathology Pneumocystis Infection;
duration) Studies over the past several years have shown that
Cytomegalovirus disease (other than liver, spleen, or Pneumocystis commonly colonizes patients who are
nodes) immune suppressed or who have chronic obstructive
Cytomegalovirus retinitis (with loss of vision) pulmonary disease. This colonization elicits an
Encephalopathy, HIV-related inflammatory response and is associated with a decline in
Herpes simplex: chronic ulcer(s) (>1 month's duration); or lung function.
bronchitis, pneumonia, or esophagitis
Histoplasmosis, disseminated or extra pulmonary The host factors that predispose to the development of PcP
Cryptosporidiosis, chronic intestinal (>1 month's include defects in cellular and humoral immunity. The risk
duration) of PcP among HIV-infected patients rises markedly when
Cytomegalovirus disease (other than liver, spleen, or circulating CD4+ T cell counts fall below 200/ L. Other
nodes) persons at risk for PcP are patients receiving
Cytomegalovirus retinitis (with loss of vision) immunosuppressive agents (particularly glucocorticoids)
Encephalopathy, HIV-related for cancer and organ transplantation; those receiving
Herpes simplex: chronic ulcer(s) (>1 month's duration); or biologic agents such as infliximab and etanercept for
bronchitis, pneumonia, or esophagitis rheumatoid arthritis and inflammatory bowel disease;
Histoplasmosis, disseminated or extrapulmonary children with primary immunodeficiency diseases; and
Isosporiasis, chronic intestinal (>1 month's duration) premature malnourished infants.
Kaposi's sarcoma
Lymphoma, Burkitt's (or equivalent term)
Lymphoma, primary, of brain
Mycobacterium avium complex or M. kansasii,
disseminated or extrapulmonary
Mycobacterium tuberculosis, any site (pulmonary or
extrapulmonary)
Mycobacterium, other species or unidentified species,
disseminated or extrapulmonary
A B
Pneumocystis jiroveci pneumonia
Pneumonia, recurrent Prevention for Pneumocystis Infections
Progressive multifocal leukoencephalopathy Prophylaxis is indicated for HIV-infected patients with
Salmonella septicemia, recurrent CD4+ T cell counts of <200/(µL or a history of
Toxoplasmosis of brain oropharyngeal candidiasis and for both HIV-infected and
Wasting syndrome due to HIV non-HIV-infected patients who have recovered from PcP.
Prophylaxis may be discontinued in HIV-infected patients
Mechanisms of CD4+ TCell Dysfunction and Depletion once CD4+ T cell counts have risen to >200/ µL and
Direct Mechanisms Indirect Mechanisms remained at that level for 3 months. Primary prophylaxis
Loss of plasma Aberrant intracellular' signaling guidelines for immune compromised hosts not infected
membrane integrity due events with HIV are less clear.
to Autoimmunity TMP-SMX is the drug of choice for primary and secondary
viral budding Innocent bystander killing of prophylaxis (Table 207-2). This agent also provides
Accumulation of viral antigen-coated protection against toxoplasmosis and some bacterial
unintegrated viral DNA cells infections. Alternative regimens are available for
Interference with cellular Apoptosis individuals intolerant of TMP-SMX (Table 207-2). Although
RXA processing Inhibition of lymphopoiesis there are no specific recommendations for preventing the
Intracellular gp120-CD4 Activation-induced cell death spread of Pneumocystis in health care facilities, it seems
autofusion events Elimination of HIV-infected cells prudent to prevent direct contact between patients with
Syncytia formation by virus-specific PcP and other susceptible hosts.
immune responses

26
Prophylaxis of Pneumiocytosis
Drug(s), Dose, Route Comments
•First Choice
TMP-SMX, 1 DS tablet or 1 SS tablet qd PO TMP-SMX can be safely reintroduced for treatment of some
patients who have had mild to
moderate side effects.
•Other Agents
Dapsone, 50 mg bid or 100 mg qd PO -
Dapsone, 50 mg qd PO; plus pyrimethamine, 50mg weekly Leucovorin prevents bone marrow toxicity from
PO; plus leucovorin, 25 mg weeklyPO pyrimethamine.

Dapsone, 200 mg weekly PO; plus
pyrimethamine, 75 mg weekly PO; plus
leucovorin, 25 mg weekly PO
Pentamidine, 300 mg monthly via Respirgard IInebulizer
Atovaquone, 1500 mg qd PO
TMP-SMX, 1 DS tablet three times weekly PO
Leucovorin prevents bone marrow toxicity from plus
pyrimethamine.
Adverse reactions include cough and bronchospasm.
-
TMP-SMX can be safely reintroduced for treatment of some
patients who have had mild tomoderate side effects.

Treatment of Pneumocystosis
Drug(s), Dose, Route Adverse Effects
• First Choice
TMP-SMX (TMP: 5 mg/kg; SMX: 25 mg/kg)q6-8h PO or IV Fever, rash, cytopenias, hepatitis, hyperkalemia, GI
disturbances
• Other Agents
TMP, 5 mg/kg q6-8h; plus dapsone, 100 mg qd PO Hemolysis (G6PD deficiency), methemoglobinemia, fever, rash,
GI disturbances
Atovaquone, 750 mg bid PO Rash, fever, GI and hepatic disturbances
Clindamycin, 300-450 mg q6h PO or 600 mg q6-8h IV; plus Hemolysis (G6PD deficiency), methemoglobinemia,
primaquine, 15-30 mg qd PO rash,colitis, neutropenia
Pentamidine, 3-4 mg/kg qd IV Hypotension, azotemia, cardiac arrhythmias, pancreatitis,
dysglvcemias, hypocalcemia, neutropenia, hepatitis
Trimetrexate, 45 mg/m2 qd IV; plus leucovorin/ 20 mg/kg Cytopenias, peripheral neuropathy, hepatic disturbances
q6h PO or IV
• Adjunctive Agent
Prednisone, 40 mg bid x 5 d, 40 mg qd x 5 d, 20mgqdxlld; PO Immunosuppression, peptic ulcer, hyperglycemia, mood
or lV changes, hypertension

69. A 3 day old infant was brought in with complaints of being restless and feed intolerant. He has a heart rate of 250
beats per minute, and ECG shows a QRS complex of duration 0.07 sees, with no discernible p waves. Which of the
following is a likely diagnosis?
1. SVT
2. PSVT with aberrant conducting channels
3. Ventricular Tachycardia
4. Atrial fibrillation

Ans. 2. PSVT with aberrant conducting channels

Rate beyond 200 bpm, narrow QRS, and "absent" (undermined) P waves, all suggest Reentrant SIT.
AF does show P (f) waves: VT will have wide QRS complexes. SVT (in general) will have definite P waves.

ECG Findings in AVNodal Reentrant Tachycardia

27
The APC initiating AVXRT is characteristically followed by a long PR interval consistent with conduction via the slow pathway.
AVXRT is manifest typically as a narrow QRS complex tachycardia at rates that range from 120 to 250 beats/min. The QRS-P
wave pattern associated with typical AVXRT is quite characteristic, with simultaneous activation of the atria and ventricles
from the reentrant AV nodal circuit.
The P wave frequently is buried inside the QRS complex mid either will not be visible or will distort the initial or terminal
portion of the QRS complex. Because atrial activation originates in the region of the AV node, a negative deflection will be
generated by retrograde atrial depolarization when recording ECG leads II, III, or AVF.

Ventricular Tachycardia
ECG showing AV dissociation (arrows mark P waves), wide QRS >200 ms, superior frontal plane axis, slurring of the initial
portion of the QRS, and large S wave in V-all clues to the diagnosis of ventricular tachycardia.

ECG Clues Supporting the Diagnosis of Ventricular Tachycardia

AV dissociation (atrial capture, fusion beats)

QRS duration >140 ms for RBBB type V1> morphology; V1>160 ms for LBBB type V1 morphology
Frontal plane axis -90° to I800
Delayed activation during initial phase of the QRS complex
LBBB pattern-R wave in V1, V2>40 ms
RBBB pattern— onset of R wave to nadir of S >100 ms
Bizarre QRS pattern that does not mimic typical RBBB or LBBB QRS complex
Concordance of QRS complex in all precordial leads
RS or dominant S in V6 for RBBB VT
Q wave in V6 with LBBB QRS pattern
Monophasic R or biphasic qR or R/ S in V1 with RBBB pattern

Atrial Fibrillation

Ventricular rate vary between 120 and 160 beats per minute, in some patients it can be >200 beats per
minute.
Counterclockwise right AFLrepresents -80% of all AFL withsuperiorly directed activation of theinteratrial septum, which
producesthe saw-toothed appearance of the P waves in ECG leads II, III, and aVF. Clockwise rotation of the same right atrial
circuit producespredominantly positive P waves in leads II, III, and aVF (Fig. 233-4). Macro reentrant left AFL also
maydevelop, albeit much less commonly.
28
The mechanism for AF initiation and maintenance, although still debated, appears to be a complex interaction between drivers
responsible for the initiation and the complex anatomic atrial substrate that promotes the maintenance of multiple wavelets of
(Micro)re-entry. The drivers appear to originate predominantly from the atrialized musculature that enters the pulmonary
veins and represent either focal abnormal automaticity or triggered firing that is somewhat modulated by autonomic
influences. Sustained forms of micro reentry as drivers also have been documented around the orifice of pulmonary veins;

70. Limiting factor to ORS stool output is

1. 5 ml/kg/hr
2. 10 ml/kg/hr
3. 15 ml/kg/hr
4. 20 ml/kg/hr

Ans. 1. 5ml/kg/hour, probably

Truly speaking, I didn't quite get, what exactly has been asked?
Is it asking about the rate of stool output, beyond which ORS is risky (i.e. IV fluid becomes mandatory) or it simply asked the
maximum allowable dose of ORS in diarrhoea?
You can go through Dr. OP Ghai 7th Ed page-265
Or, check IAP Book, which says 5ml/kg/hr is the highest rate at which ORS can be safe, beyond which, superadded IV fluid is
necessary. It writes:

Deficit fluid therapy for Severe Dehydration'(Plan C)

Infants (<1 year) Older child (>1 year)
Volume of Ringer's lactate 30 ml/kg body wt. within first I hour, 30 ml/kg body weight within hour,
followed by 70 ml/kg body weight over followed by 70 ml/kg body ' weight
next 5 hours over next 2 ½ hours
Monitoring Assess for improvement every 1-2 hours:
• If not improving, give IV infusion more rapidly
• Encourage oral feeding by giving ORS 5 ml/kg/hour, along with IV fluids, as soon
as the child is able to drink
Reassess hydration status:
• After 6 hours (infants) and 3 hours (Older children) assess hydration status and
choose appropriate plan

71. A child can make of tower of three cubes at:

1. 12 months
2. 15 months
3. 18 months
4. 24 months

Ans. 2. 15 months
Builds tower of 2-3 cubes (Uses objects in combination) by 15 months
Builds tower of 6 cubes (Requires visual, gross, and fine motor coordination) by 22 months
• 15 MO Motor: Walks alone; crawls up stairs Adaptive: Makes tower of 3 Cubes; makes a line with crayon; inserts raisin in
bottle
• 18 MO Motor: Runs stiffly; sits on small chair; walks up stairs with one hand held; explores drawers and wastebaskets
Adaptive: Makes tower of 4 Cubes; imitates scribbling; imitates vertical stroke; dumps raisin from bottle
• 24 MO Motor: Runs well, walks up and down stairs, one step at a time; opens doors; climbs on furniture; jumps Adaptive:
Makes tower of 7 Cubes (6 at 21 mo); scribbles in circular pattern; imitates horizontal stroke; folds paper once imitatively
• 30 MO Motor: Goes up stairs alternating feet Adaptive: Makes tower of 9 Cubes; makes vertical and horizontal strokes, but
generally will not join them to make cross; imitates circular stroke, forming closed figure
• 36 MO Motor: Rides tricycle; stands momentarily on one foot Adaptive: Makes tower of 10 Cubes; imitates construction of
"bridge'' of 3 cubes; copies circle; imitates cross.

Developmental Milestones in the First 2 Yr of Life

MILESTONE AVERAGE AGE DEVELOPMENTAL IMPLICATIONS

OFATTAINMENT(MO)

29
GROSS MOTOR
Holds head steady while sitting 2 Allows more visual interaction
Pulls to sit, with no head lag 3 Muscle tone
Brings hands together in midline 3 Self-discovery of hands
Asymmetric tonic neck reflex gone 4 Can inspect hands in midline
Sits without support 6 Increasing exploration
Rolls back to stomach 6.5 Truncal flexion, risk of falls
Walks alone 12 Exploration, control of proximity to parents
Runs 16 Supervision more difficult
FINE MOTOR
Grasps rattle 3.5 Object use
Reaches for objects 4 Visuomotor coordination
Palmar grasp gone 4 Voluntary release
Transfers object hand to hand 5.5 Comparison of objects
Thumb-finger grasp 8 Able to explore small objects
Turns pages of book 12 Increasing autonomy during book time
Scribbles 13 Visuomotor coordination
Builds tower of 2 cubes 15 Uses objects in combination
Builds tower of 6 cubes 22 Requires visual, gross, and fine motor coordination
COMMUNICATION AXD LANGUAGE
Smiles in response to face, voice 1.5 More active social participant
Monosyllabic babble 6 Experimentation with sound, tactile sense
Inhibits to "no" 7 Response to tone (nonverbal)
Follows one-step command withgesture 7 Nonverbal communication
Follows one-step commandwithout gesture 10 Verbal receptive language(e.g./'Give it to me")
Says “mama” or “dada” 10 Expressive language
Points to objects 10 Interactive communication
Speaks first real word 12 Beginning of labeling
Speaks 4-6 words 15 Acquisition of object and personal names
Speaks 10-15 words 18 Acquisition of object and personal names
Speaks 2-word sentences(e.g./'Mommy 19 Beginning grammaticization, corresponds with50+
shoe") word vocabulary
COGNITIVE
Stares momentarily at spot whereobject 2 Lack of object permanence (out of sight, out ofmind)
disappeared [e.g., yam ball dropped]
Stares at own hand 4 Self-discovery, cause and effect
Bangs 2 cubes 8 Active comparison of objects
Uncovers toy (after seeing it hidden) 8 Object permanence
Egocentric symbolic play (e.g./pretends to 12 Beginning symbolic thought
drink from cup)
Uses stick to reach toy 17 Able to link actions to solve problems
Pretend play with doll (e.g., gives 17 Symbolic thought
doll bottle)

72. Which is the least common complication of acute post streptococcalglomerulonephritis in child?
1. Heart failure
2. Encephalopathy
3. Hyperkalemia
4. Bleeding diathesis

Ans. 4. Bleeding diathesis

Complications of Acute Rheumatic Endocarditis
Severe mitral insufficiency may result in cardiac failure that may be precipitated by progression of the rheumatic process, the
onset of atrial fibrillation, or infective endocarditis. The effects of chronic mitral insufficiency may become manifest after many
years and include right ventricular failure and atrial and ventricular' arrhythmias.

30
Renal failure, consequent hyperkalemia and • Amino acid and organic acid disorders (eg, maple
encephalopathy are also widely recognized complications. syrup urine disease, propionic acidemia,
methylmalonic acidemia, tyrosinosis, glutaric aciduria,
Scute Rheumatic Carditis (Pancarditis) is now history. 3-hydroxy-3-methylglutaric aciduria)
There is conspicuous evidence that, it's primarily an  Systemic disease (eg, sepsis, burns, cardiogenic shock,
endocarditis only. Resultant myocardial failure (so-called respiratory distress syndrome)
"Myocarditis") resolves instantly with valve prosthesis).
74. Nuchal translucency is seen in
73. Neonatal hypoglycemia is associated with 1. Open neural tube defects
1. Adrenal Insufficiency 2. Trisomy 21
2. Glucocorticoid exces 3. Trisomy 13
3. Pancreatic aplasia 4. Trisomy 15
4. Postmaturity
Ans. 2. Trisomy 21
Ans. 1. Adrenal Insufficiency Increased Nuchal translucency/ fold thickness is most
Both Adrenal (Medulla) insufficiency and Congenital commonly associated with Down's syndrome; but, is also
Adrenal Hyperplasias (Cortex) may lead to Neonatal found in Turner syndrome, Trisomy IS, Trisomy 13 and
hypoglycemia. Triploidy. So, Trisomy 21 has to be the pick.
Other options do not decrease serum glucose level. So,
itsthe answer of exclusion. Nuchal translucency
SYMPTOMS OF HYPOGLYCEMIA The translucent area measured (the nuchal translucency)
• Jitteriness is due to a blockage of fluid in the developing fetal
• Tremors lymphatic system. Progressive increase in the width of the
• Apnea translucent area during the 11 to 14 week measurement
• Cyanosis period is thus indicative of congenital lymphedema
• Limpness/ lethargy
• Seizures Fetuses at risk of Down's syndrome tend to have a higher
INFANTS AT RISK FOR HYPOGLYCEMIA amount of fluid around the neck.
Diminished production
 Limited glycogen This is only useful to measure between 11 and 14 weeks of
• SGA gestation, when the fetal lymphatic system is developing
• Prematurity and the peripheral resistance of the placenta is high.
• Birth stress
• Glycogen storage disorders After 14 weeks the lymphatic system is likely to have
 Limitedgluconeogenesis developed sufficiently to drain away any excess fluidand
• SGA changes to the placental circulation will result in a drop in
• Inborn errors peripheral resistance. So after this time any abnormalities
Increased utilization causing fluid accumulation may seem to correct
 Hyperinsulinism themselves and can thus go undetected by nuchal
• IDM scanning.
• Beckwith-Wiedemann syndrome
• Nesidioblastosis or pancreatic adenoma Other chromosomal defects that cause a thicker nuchal
• Erythroblastosis fetalis translucency are
• Exchange transfusion, chlorpropamide, • Turner syndrome
benzothiazides, • Trisomy 18
• I2-sympathomimetics, malpositioned UA catheter • Trisomy 13
Unknown Mechanism • Triploidy
 LGA infants who are not IDM
 Sepsis
 Polycythemia or hyperviscosity syndrome
 Congenital hypopituitarism
The causes of hypoglycemia in older infants, children, and
teenagers include:
• Poisonings/drugs (eg, ethanol, isoniazid, insulin,
propranolol, salicylates, oral hypoglycemics,
pentamidine, quinine, disopyramide, unripe ackee
fruit, Vacor).
• Liver disease (eg, Reye syndrome, hepatitis, cirrhosis,
hepatoma)
31
 Abdominal and particularly vaginal sonography are useful
diagnostic techniques for evaluating endometrium.
Endometrial thickness can be measured and the echo
pattern of the different parts of endometrium analysed.
During normal cycles a triple line sign is typical for the late
proliferative and periovulatory phase. In the secretory
phase the endometrium is echogenic and posterior
enhancement of echoes can be seen. It is also useful to
control the effects of hormonal treatments or the
endometrium using sonography. In postmenopausal
women endometrial thickness of 4-5 mm or more is
abnormal andfurther evaluations are indicated. In
endometrial cancer sonography is a reliable way to
estimate myometrial invasion.

The signs of secretory endometrium included absent

Nuchal fold thickness
triple-line sign, hyper echoic functional layer, and strong
A nuchal scan is a sonographic prenatal screening scan
posterior acoustic enhancement. When all of these US
(ultrasound) to help identity higher risks of chromosomal
signs were clearly depicted in combination, the accuracy of
defects including Down's syndrome in a fetus, particularly
diagnosis was 93% (30 patients). The accuracy of
for older women who have higher risks of such
diagnosis for all patients in the study was 76% (73
pregnancies. High thickness measurements are also
patients). The relative distributions of each US sign in
associated with congenital heart defect
proliferative and secretory endometrium were compared.
Despite complicating extrinsic factors such as uterine
75. Triple line sign is seen in the endometrium in
leiomyomas and intrinsic factors such as the transition
which of the following phase?
period between endometrial phases, US staging of the
1. Secretory phase
endometrium is a useful diagnostic technique that allows
2. Proliferative phase
serial examinations of the endometrium.
3. Endometriosis
4. Endometrial carcinoma
76. First changes occurs during treatment with iron
deficiency anemia
Ans. 2. Proliferative phase
1. Reticulocyte count increase
Ultrasound evaluation of the Endometrium
2. Hemoglobin increase
• After menstruation the endometrium is demonstrated
3. Ferritin level
as a single echogenic line.
4. RBC indices
• The estrogen biosynthesis by the dominant follicle
leads to stimulation of the endometrium with growth
Ans. 1
of the glands and stroma (i.e. Proliferative Phase). This
Causes of iron deficiency
change is visualized as the "triple-line". The interface
Increased demand for iron and/or hematopoiesis
between the two leaves of the endometrium is the
• Rapid growth in infancy or adolescence
central echogenic line. The two outer lines represent
• Pregnancy
the basalis of the developing endometrium.
• Erythropoietin therapy
• The endometrium appears hypoechoic compared to
Increased iron loss
the echogenic lines. The thickness of the endometrium
• Chronic blood loss
can reach 6 to 10 mm, around the time of ovulation,
• Menses
which represents a two to three fold increase in its
• Acute blood loss
original thickness.
• Blood donation
• Phlebotomy as treatment for polycythemia vera
Decreased iron intake or absorption
• Inadequate diet
• Malabsorption from disease (sprue, Crohn's disease)
• Malabsorption from surgery (postgastrectomy)
• Acute or chronic inflammation

Generic name Tablet (iron Elixir (iron content),

An ultrasound image of a thin endometrium portraying a content), mg mg in 5 mL
single echogenic line and Visualization of the triple-line
Ferrous sulfate 325 (65) 300 (60)
sign of the endometrium at the period ovulation
195 (39) 90(18)
32
Extended release 525 (105)  Thymoma (MC)
325 (107)  Teratoma
 Lymphoma
Ferrous fumarate 195 (64) 100 (33)
 Thyroid lesions
Ferrous 325 (39) 300 (35)
 Parathyroid tumors.
gluconate 150 (150) 100(100)
Posterior mediastinum
Polysaccharide 50(50) 100(100)
 Neurogenic tumors (schwannoma, neurofibroma)
iron
(MC)
 Lymphoma
77. A 30 Year Old Patient comes to casualty with  Gastroenteric hernia.
nausea,hematemesis, diarrhea. Chest X-Ray finding is Middle mediastinum
given below. On Evaluation patient is found to have  Bronchogenic cyst
metabolic acidosis. What is your diagnosis  Pericardial cyst
 Lymphoma.

79. Adenoma sebaceum in aldolescent is seen in

1. Neurofibromatosis
2. Tuberous sclerosis
3. von Hippel-Lindau syndrome
4. All of them

Ans. 2
Tuberous Sclerosis (Bourneville's Disease)
 Tuberous sclerosis is characterized by triad of
cutaneous lesions seizures and mental retardation.
 The cutaneous lesions include adenoma sebaceum
(facial angiofibromas), ash leafshaped hypopigmented
macules (best seen under ultraviolet illumination with
1. Aspirin Toxicity
a Wood’s lamp), shagreen patches (yellowish
2. Iron Toxicity
thickenings of the skin over the lumbosacral region of
3. Lead Toxicity
theback) and depigmented nevi.
4. Alcoholic Toxicity
 Tuberous sclerosis patients are at increased risk of
developing ependymoma childhood astrocytomas, of
Ans. 2. Iron poisoning, abdominal x-ray
which >90% are subependymal giant cell
Iron poisoning presents with GI symptoms (nausea,
astrocytomas. These are benign neoplasms that may
vomiting, hematemesis, diarrhea) due to the iron induced
develop in the retina or along the border of the lateral
damage to the GI mucosa. Toxic iron levels also cause
ventricles. They may obstruct the foramen of Monro
hypoperfusion (veno/capillary dilation) and mitochondrial
and produce hydrocephaly Rhabdomyomas of the
damage, both causing a metabolic acidosis. Since iron
myocardium and angiomyomas of the kidney, liver,
tablets are radio-opaque they can be seen in the stomach
adrenals and pancreas may also occur.
on AXR. Diagnosis with serum iron levels and treat with an
 Treatment is symptomatic. Anticonvulsants for
iron chelator such as deferoxamine.
seizures, shunting for hydrocephalus, and behavioral
and educational strategies for mental retardation are
78. Tumor commonly seen in the anterior
the mainstays of management. Severely affected
mediastinum
individuals generally die before age 30.
1. Neurofibroma
 Mutations in either the TSC-1 gene at 9q or the TSC-2
2. Metasatic carcinoma
gene at 16p are associated with tuberous sclerosis.
3. Teratoma
These genes encode tuberins, proteins that modulate
4. Schwannoma
the GTPase activity of other cellular signaling proteins.
Ans. 3
80. Treatment of choice in cryptococcal meningitis
Common Mediastinal Tumors
1. Fluconazole
Superior mediastinum
2. Nystatine
 Lymphoma
3. Amphotericin B
 Thymoma
4. Clotrimazole
 Thyroid lesions
 Metastatic carcinoma
Ans. 3
 Parathyroid tumors.
Amphotericin B and other polyenes, such as nystatin, bind
Anterior mediastinum
to ergosterol in fungal cell and increase membrane
33
permeability. The imidazoles and triazoles, such as palsy region
itraconazole and fluconazole, inhibit 14-α-sterol
demethylase, prevent ergosterol synthesis and lead to the 83. AIHA and pernicious anemia are example of which
accumulation of 14-α-methylsterols. The allylamines, such type hypersensitivity?
as naftifine and terbinafine, inhibit squalene epoxidase 1. Type 1
andp;revent ergosterol synthesis. The echinocandins (e.g. 2. Type 2
capofungin) inhibit the formation of glucans in the fungal 3. Type 3
cell wall. 4. Type 4

81. Which is not seen with scarcoidosis? Ans. 2. Type 2

1. Hypercalcemia
2. Osteomalacia Ref—Ananthanarayan and Paniker 9th ed, p. 166; Robbins
3. Diabetes insipidus 9th ed, p. 202-203
4. Addison’s disease AIHA and pernicious anemia are example of type 2
hypersensitivity reaction.
Ans. 2 It was asked from our explanation part of question no 62
 Sarcoidosis is an inflammatory disease characterized (2014 paper) of Sure Success in
by the presence of noncaseating granulomas. The WBPGMEE book so go through the chart carefully.
disease is often multisystem and requires the presence
of involvement in two or more organs for a specific 84. False positive D-xylose test is seen in all except
diagnosis. The finding of granulomas is not specific for 1. Ascites
sarcoidosis, and other conditions known to cause 2. Renal failure
granulomas must be ruled out. These conditions 3. Hepatic failure
include mycobacterial and fungal infections, 4. Blind loop syndrome
malignancy and environmental agents such as
beryllium. Ans. 3
 Respiratory complaints including cough and dyspnea False positive D-xylose test seen in the following condition
are the most common presenting symptoms. 1. Third space collection (ascites/ pleural effution)
 Symptoms related to cutaneous and ocular disease are 2. Delayed gastric emptying
the next two most common complaints. Skin lesions 3. Rapid intestinal transit
are often nonspecific. 4. Renal insufficiency
 Nonspecific constitutional symptoms include fatigue, 5. Bacterial overgrowth
fever, night sweats and weight loss. Fatigue is perhaps 6. Vomiting
the most common constitutional symptom that affects 7. Blind loop syndrome
these patients.
Schilling test
82. Which of these is pathognomonic for motor neuron Part 1 test result Part 2 test result Diagnosis
disease? Normal - Normal or
1. Extensor plantar response vitamin B12
2. Sensory loss deficiency
3. Fasciculation Low Normal Problems with IF
4. Bowel and bladder involvement production, e.g.
pernicious
Ans. 3 anemia
Type UMN LMN Low Low Malabsorption
degeneration degeneration (terminal ileum)
Amyotrophic Yes Yes
lateral sclerosis 85. Revised criteria for rheumatoid arthritis include
(ALS) the following except
Primary lateral Yes No 1. Morning stiffness
sclerosis (PLS) 2. Asymmetrical arthritis
Progressive No Yes 3. Rheumatoid nodule
muscular atrophy 4. Arthritis of three or more joints
(PMA)
Progressive No Yes, bulbar Ans. 3
bulbar palsy region Classification criteria for rheumatoid arthritis
(PBP) Score
Pseudobulbar Yes, bulbar No Joint involvement 1 large joint 0
34
 (shoulder, elbow, (%) (range),
hip, knee, ankle) years
2-10 large joints 1 Esophagus 57 0.5 67
1-3 small joints 2 Stomach 213 29 30.1 (10-61)
(MCP, PIP, thumb Small 520 13 41.7 (21-84)
IP, MTP, wrists) intestine
4-10 small joints 3 Colon 84 39 45.8 (27-71)
>10 joints (at 5 Pancreas 132 36 40.8 (16-60)
least 1 small Lung 17 15
joint) Testis 4.5 9 8.6 (3-20)
Serology Negative RF and 0 Breast 15.2 54 37(9-48)
negative ACPA Uterus 16 9
Low-positive RF 2 Ovary 27 21 28(4-57)
or low-positive Cervix 1.5 10 34.3 (23-54)
anti-CCP
antibodies (3
times ULN) Size of polyp and malignancy
High-positive RF 3 Size of polyp Malignant potential
or high-positive < 1.5 cm Negligible
anti0CCP 1.5-2.5 cm Intermediate
antibodies (>3 >2.5 cm Substantial
times ULN)
Acute-phase Normal CRP and 0 88. BPH is most commonly involved which lobe of the
reactants normal ESR prostate?
Abnormal CRP or 1 1. Anterior
abnormal ESR 2. Posterior
Duration of <6 weeks 0 3. Median
symptoms 4. Lateral
≥6 weeks 1
Ans. 3
86. Scirrhous carcinoma of stomach is best diagnosed Lobes
by? The "lobe" classification is more often used in anatomy.
1. CT Anterior lobe (or isthmus) Roughly corresponds to
2. Ba meal part of transitional zone
3. Endoscopy Posterior lobe Roughly corresponds to
4. Clinical examination peripheral zone
Lateral lobes Spans all zones
Ans. 3 Median lobe (or middle Roughly corresponds to
Symptom’s of gastric carcinoma lobe) part of central zone
S-Slient Endoscopy with multiple
O-Obstruction biopsy and brush cytology
L-Lump is the investigation of • BPH most commonly arise from median lobe
I-Incidious onset choice for all type of gastric • Carcinoma prostate most commonly affects posterior
D-Dysphagia carcinoma lobe.
87. A girl presented with pigmentation of lip with The common drugs used in BPH and their side effects
intestinal polyp. Her younger sister suffers from same Drug Dosage Mechanism Side effect
disease. Most common diagnosis:
Finast 5 mg 5a-reductase Impotence,
1. Villous adenoma
eride once inhibitor decreased libido,
2. Peutz-Jeghers syndrome
daily decreased semen
3. Carcinoid
quantity at
4. Melanoma
ejaculation,
decreased semen
Ans. 2
prostate specific
Risk ratio compared to the general population,
antigen,
lifetime frequency, mean age and age range of
gynecomastia
malignancies related to Peutz-Jeghers syndrome
(rare)
Organ Risk ratio Frequency Mean age
35
Dutast 0.5 mg 5a-reductase Impotence,
eride once inhibitor decreased libido, 90. Thyroid surgery not indicated in:
daily decreased semen 1. Thyroid carcinoma
quantity at 2. For cosmesis
ejaculation, 3. Pain
decreased semen 4. Toxic goiter
prostate specific
antigen, Ans. 3
gynecomastia AMES classification of thyroid cancers
(rare) Low mortality High mortality
Teraz 1 mg α1,-adrenergic Asthenia, risk risk
osin once receptor hypotension, A:Age Men; <41 years of Men: >41 years of
daily to antagonist dizziness, age age
start; somnolence Women: <51 Women: >51
may years of age years of age
increase M: Metastases Absence of Presence of
up to 10 distant distant
mg/day metastases metastases
Doxaz 1 mg 1-adrenergic Orthostatic E: Extent of Intrathyroidal Extrathyroidal
osin once receptor hypotension, primary tumor papillary cancer papillary cancer
daily to antagonist fatigue, dyspnea (confined to Follicular cancer
start; thyroid) with major
may Follicular cancer capsular
increase with minor involvement
up to 8 capsular
mg once involvement
daily S: Size of tumor Primary tumor Primary tumor 5
Tams 0.4/0.8 α1-adrenergic Dizziness, rhinitis, <5 cm in cm in diameter
ulosin mg once receptor abnormal diameter (regardless of
daily antagonist ejaculation extent of disease)
Alfuzo 2.5 mg α1-adrenergic Fatigue, edema,
sin tid/5 receptor rhinitis, headache, 91. A 23 year old female was worked up for infertility
mg antagonist upper respiratory Below is the USG finding. What is ur diagnosis
bid/10 tract infection
mg once
daily
Saw 160 mg Mixed Aggravate chronic
palme twice gastrointestinal
tto daily disease such as
peptic ulcer

89. In blunt trauma abdomen organ most commonly

suffered:
1. Spleen
2. Liver
3. Cecum
4. Pancreas

Ans. 1
Blunt Trauma Abdomen
Solid organs usually involved 1. Müllerian agenesis
1. Spleen (most common) 2. Uterus didelphys
2. Liver 3. Bicornuate uterus
3. Kidney 4. Septated uterus
In addition to these organs, blunt force to the upper
abdomen may fracture the pancreas. Answer 3. Bicornuate Uterus
Which is susceptible to injury because of its position
overlying the vertebral column. Class I: Müllerian agenesis (absent uterus).

36
Uterus is not present, vagina only rudimentary or absent.
The condition is also called Mayer-Rokitansky-Kuster-
Hauser syndrome. The patient with MRKH syndrome will
have primary amenorrhea.
Class II: Unicornuate uterus (a one-sided uterus).
Only one side of the Müllerian duct forms. The uterus has a
typical "penis shape" on imaging systems.
Class III: Uterus didelphys, also uterus didelphis (double
uterus).
Both Müllerian ducts develop but fail to fuse, thus the
patient has a "double uterus". This may be a condition with
a double cervix and a vaginal partition (v.i.), or the lower
Müllerian system fused into its unpaired condition. See
Triplet-birth with Uterus didelphys for a case of a woman
having spontaneous birth in both wombs with twins.
Class IV: Bicornuate uterus (uterus with two horns).
Only the upper part of that part of the Müllerian system
that forms the uterus fails to fuse, thus the caudal part of
the uterus is normal, the cranial part is bifurcated. The
uterus is "heart-shaped".
Class V: Septated uterus (uterine septum or partition).
The two Müllerian ducts have fused, but the partition
between them is still present, splitting the system into two
parts. With a complete septum the vagina, cervix and the
uterus can be partitioned. Usually the septum affects only
the cranial part of the uterus. A uterine septum is the most
common uterine malformation and a cause for
miscarriages. It is diagnosed by medical image techniques,
i.e. ultrasound or an MRI. MRI is considered the preferred
modality due to its multiplanar capabilities as well as its
ability to evaluate the uterine contour, junctional zone, and
other pelvic anatomy. A hysterosalpingogram is not
considered as useful due to the inability of the technique to
evaluate the exterior contour of the uterus and distinguish
between a bicornuate and septate uterus.
92. Sistrunk’s operation is done in
1. Thyroglossal cyst
2. Dermoid cyst
3. Thyroid nodule
4. Branchial cleft cyst
Ans. 1
Anatomical clues to the diagnosis of neck masses
Location/morphology of Possible cause
mass
Midline Thyroglossal duct cyst,
dermoid, teratoma
Anterior to Branchial cleft remnant
sternocleidomastoid muscle anomalies
Posterior to Lymphangioma/cystic
sternocleidomastoid muscle hygroma
Near thyroid Diffuse thyroid enlargement
or thyroid nodule
Preauricular Parotid or submandibular
gland pathology
Lymph node clusters Inflammatory or neoplastic
lymphadenopathy
37
93. Projectile vomiting is seen in
1. Hypertrophic pyloric stenosis
2. Esophageal atresia
3. Intussusception
4. Cholera
Ans. 1
 Cholera is characterized by an acute onset of copious
watery diarrhea and vomiting without abdominal
cramps or fever.
 The stools are colorless with small flecks of mucus
("rice-water") and are sometimes described as having
a fishy odor.
 At first, children may be restless or extremely thirsty,
but if fluid and electrolyte losses are not replaced, they
may become lethargic or unconscious.
 Other signs of dehydration may rapidly manifest,
including poor skin turgor, sunken eyes, dry mouth
and tongue, no urine output, delayed capillary refill,
rapid or weak pulse and low blood pressure.
 Severe dehydration, metabolic acidosis, and
hypokalemia can occur in 4-12 h.
The fluid losses may be so rapid that the child quickly
develops hypovolemic shock, hypoglycemia, coma and
seizures and is at risk of dying within a few hours of
onset
Treatment—ORS (with rice)
94. Comprehensive neck dissection refers to
1. Radical neck dissection
2. Extended neck dissection
3. Posterior triangle dissection
4. Selective neck dissection
Ans. 1
Neck dissection operations are classified according to the
cervical lymphatic regions that are resected.
Selective neck dissection (SND) is done for NO necks (no
clinical evidence of neck nodes) or for very limited cervical
metastases. Central neck dissection encompasses only
level VI.
Comprehensive or therapeutic neck dissection involves
surgical clearance of levels I-V and may either be a radical
(RND) or modified (MND) neck dissection. RND includes
resection of sternocleidomastoid muscle (SCM) and
accessory nerve (XIn) and internal jugular vein (IJV). MND
preserves SCM and/or XIn and/or IJV. MND type I entails
preservation of 1/3, usually XIn; MND type II entails
preservation of 2/3, usually XIn and IJV; with MND type III
all 3 structures are preserved. MND type II is most
commonly done, and is oncologically acceptable in the
absence of adherence of cervical nodal metastases to XIn
or IJV.
Extended neck dissection includes additional lymphatic
groups (parotid, occipital, level VI, mediastinal,
retropharyngeal) or nonlymphatic structures (skin,
muscle, nerve, blood vessels, etc.) not usually included in a 2. Brochial asthma
comprehensive neck dissection. 3. Wheal and flare reaction aftering of antigen
- The neck is conventionally divided into 6 levels; level VII 4. Aspergillus culture +ve from sputum
is in the superior mediastinum.
- Level 1 is bound by the body of the mandible above, the Ans. 4
stylohyoid muscle posteriorly, and the anterior belly of the ABPA is a hypersensitivity reaction to Aspergillus species,
contralateral digastric muscle anteriorly. The revised commonly found fungi in soil. It occurs almost exclusively
classification uses the posterior margin of the in patients with asthma or cystic fibrosis. The disease is
submandibular gland as the boundary between levels I and the result of immunologic response to the endoluminal
II as it is clearly identified on ultrasound CT or MRI. Level I growth of species.
is subdivided into level Ia, (submental triangle) which is The diagnosis of ABPA is based on clinical, laboratory and
bound by the anterior bellies of the digastric muscles and radiologic criteria. Primary criteria include asthma,
the hyoid bone, and level Ib (submandibular triangle). radiologic evidence of pulmonary infiltration, positive skin
test to A. fumigatus, eosinophilic precipitating Ab to A.
95. Smoking causes which of the following fumigatus, elevated IgE, elevated A.fumigatus- specific IgE
transformation and IgG and central bronchiectasis. A diagnosis of ABPA is
1. Transitional metaplasia nearly certain when six of these eight criteria are fulfilled.
2. Squamous metaplasia But, many of these findings are nonspecific. Only central
3. Neuroendocrine metaplasia bronchiectasis is nearly pathognomomic and essential to
4. Mucinous metaplasia diagnosis to most cases.
The symptoms include cough, hemoptysis, fever, pleuritic
Ans. 2 pain, wheezing and dyspnea.
Original tissue Stimulus Metaplasstic
tissue 98. A 60 year old male is brought to the Emergency
Ciliated columnar Cigaret smoke Squamous ward with cyanosis, mottling, altered mental status,
epithelium of epithelium tachycardia, and hypotension. Chest X-ray is given
bronchial tree below what could be the diagnosis
Transition Trauma of Squamous
epithelium of calculus epithelium
bladder
Fibrocolagenous Chronic trauma Bone (osseous)
tissue tissue
Esophageal Gastric acid Columnar
squamous epithelium
epithelium
Columnar Vitamin A Squamous
glandular deficiency epithelium
epithelium

96. 40-year-old male present with ascites varies

varicose vain with caput medusa in abdomen along
1. Lead Poisoning
with pedal edema. Occlusion most probably occurs in
2. Ruptured Pericardium
1. IVC
3. Rupture of Aortic Aneurysm
2. Portal vain
4. Duodenal Bleed
3. Hepatic artery
4. Interstitial vain
Ans. 3. Acute aneurysm:
Ruptured Aortic Aneurysm On A Chest X Ray
Ans. 2
There are 3 categories of portal hypertension:
99. Which fistula is most likely to close with
 Prehepatic (thrombosis in splenic or portal vein). conservative management?
 Intrahepatic (postsinusoidal-veno-occlusive disease, 1. Gastric
sinusoidal-cirrhosis, presinusoidal-schistosomiasis) 2. Duodenal
 Posthepatic (heart failure, constrictive pericarditis cor 3. Esophageal
pulmonale also known as RV enlargement from 4. Ileal
pulmonary disease)
Ans. 3
97. Not a major criteria fro ABPA  Reported incidence of esophageal anastomotic leak is
1. High IgE 13-16%.
38
 Most leaks are clinically insignificant and can be
managed with adequate drainage and nutritional
support.
 If retropleural approach is undertaken for primary
esophageal anastomosis with a patent mediastinal
drain is in place, upto 95% of anastomotic leaks close
spontaneously.
 Even when transthoracic repair is followed by
disruption and pleural space contamination, adequate
drainage can usually allow spontaneous closure of
leak.
100. In TIPS, shunt done between:
1. Hepatic artery and splenic vein
2. Hepatic artery and portal vein
3. Bile duct and portal vein
4. Hepatic vein and portal vein
Ans. 4
 What does TIPS mean?
 TIPS stands for transjugular intrahepatic
portosystemic shunt:
o Transjugular—through the jugular vein in
the neck.
o Intrahepatic—within the liver.
o Portosystemic—from the portal vein to
the hepatic vein (The portal vein carries
blood into the liver. The hepatic vein
drains blood from the liver).
o Shunt—a metal tube covered with fabric
that allows flow from one blood system
to another.
 Indications
 Variceal bleeding (preventive in recurrent cases)
 Variceal bleeding (for treatment in acute setting)
 Refractory ascites and hepatic hydrothorax
 Portal hypertensive gastropathy
 Hepatorenal syndrome
 Lower gastrointestinal and stomal varices
101. Comby's sign is seen in?
1. Measles
2. Lichen planus
3. Moniliasis
4. Pemphigus
Ans. 1. The Comby sign is a clinical sign of early measles in
which thin, whitish patches are seen on
the gums and buccal mucosa due
to desquamation of epithelial cell
102. Trimetazidine is an antianginal agent which acts
by inhibition of:
1. Beta oxidation of fatty acids
2. Anaerobic metabolism of glucose
3. Calicum channels
4. Beta adrenergic receptors
39
Ans. 1. Beta oxidation of fatty acids
Normal myocardium utilises more of fatty acids than
glucose for energy production. Oxidation of fatty acids
requires more of oxygen per ATP molecule generated. If
beta oxidation of fatty acids is inhibited, the metabolism
shifts to glucose utilisation which uses less oxygen per
molecule of ATP generated, hence it is useful to the
ischemic myocardium.
103. Prolotherapy is used for the treatment of
1. Osteoarthritis
2. Thrombocytopenia
3. Rickets
4. Leucopenia
Ans. 1
Prolotherapy involves the injection of an irritant solution
into the area where connective tissue has been weakened
or damaged through injury or strain. Many solutions are
used, including dextrose, lidocaine (a commonly used local
anesthetic), phenol, glycerine, or cod liver oil extract. The
injection is given into joint capsules or
where tendon connects to bone. Many points may require
injection. The Injected solution causes the body to heal
itself through the process of inflammation and repair. In
the case of weakened or torn connective tissue, induced
inflammation and release of growth factor at the site of
injury may result in a 30-40% strengthening of the
attachment points, although strong scientific evidence
supporting this is lacking. It is now used in osteoarthritis
and tennis elbow.
104. A 4-month-old child had silvery gray hair, light-
colored skin, recurrent chest infections,
hepatosplenomegaly. Light microscopy of hair showed
characteristic large aggregates of pigment granules
distributed irregularly along the hair shaft. Peripheral
blood smear examination did not show giant granules
in granulocytes. Enlarged hyperpigmented basal
melanocytes with sparsely pigmented adjacent
keratinocytes were seen on the skin biopsy specimen.
What is this syndrome
1. Gricelli Syndrome
2. Apert’s Syndrome
3. Cat eye Syndrome
4. Wegener’s Granulomatosis
Ans 1 Griscelli syndrome - is a rare autosomal recessive
disorder characterized by albinism (hypopigmentation)
with immunodeficiency. Cat Eye Syndrome is a rare
condition caused by The short arm (p) and a small section
of the long arm (q) of humanChromosome 22 being
trisomic) or tetrasomic . The term "Cat Eye" syndrome was
coined due to the particular appearance of the
vertical colobomas in the eyes of some patients.
105. Nicorandil is a:
1. Calcium channel blocker
2. Potassium channel blocker
3. Sodium channel blocker
4. Potassium channel activator
Ans. 4. Potassium channel activator
Nicorandil is an anti anginal agent without any significant
hemodynamic effect.
106. A 36 year old moderate drinker presents with
diabetic ketoacidosis and acute pancreatitis. What is
the likely findings on examination. Serum Triglyceride
level 1800 mg/dl
1. Tendon xanthomas
2. Lipemia retinalis
3. Eruptive tuberous xanthomas
4. Milky Serum
Ans. 3 Eruptive xanthomas are associated with
hypertriglyceridemia, particularly that associated with
types I, IV, and V (high concentrations of VLDL and
chylomicrons). They appear in secondaryhyperlipidemias,
particularly in diabetes.
Acute Pancreatitis : triglyceride levels higher than 500
mg/dL
Eruptive Xanthomas triglyceride count above 1000 mg/dL
Lipaemia Retinalis above 2000 mg /dl
Milky Serum above 2500 mg/dl
107. A 30 year old patient presents with elevated
plasma levels of LDL cholesterol. Patients develop
tendon xanthomas as well as premature
atherosclerosis and Episodes of hemolysis are present.
The hypercholesterolemia does not respond to HMG-
CoA reductase inhibitors; however, aezetimibe, is
effective in reducing plasma sterol levels in these
patients. What is the diagnosis
1. Familial Hypercholesterolemia
2. Polygenic Hypercholesterolemia
3. Sitosterolemia
4. ApoA-V Deficiency
Ans. 3.
Most Probable in Question
Sitosterolemia is inherited as a rare autosomal recessive
condition. It has been shown to result from mutations in
either of two adjacent and oppositely oriented genes
(ABCG5 and ABCG8) located in chromosome 2
It is characterized by hyperabsorption and decreased
biliary excretion of dietary sterols leading
to hypercholesterolemia, tendon and tuberous xanthomas,
premature development of atherosclerosis, and abnormal
hematologic and liver function test results.
Patients with sitosterolemia usually have elevated plasma
levels of LDL cholesterol. Patients develop tendon
xanthomas as well as premature atherosclerosis and can
be mistaken for FH patients. Episodes of hemolysis,
presumably secondary to the incorporation of plant sterols
into the red blood cell membrane, are a distinctive clinical
feature of this disease.
40
Sitosterolemia is confirmed by demonstrating an increase
in the plasma level of sitosterol using gas chromatography.
The hypercholesterolemia does not respond to HMG-CoA
reductase inhibitors; however, bile acid sequestrates and
cholesterol-absorption inhibitors, such as ezetimibe, are
effective in reducing plasma sterol levels in these patients.
108. A 25-year-old man presents to the ER with a 3-
month history of intermittent pounding headaches,
sweating, and palpitations. He denies any symptoms of
depression or anxiety. On examination, he is a thin
gentleman, BP 240/120, heart rate 110/minute,
thyroid not enlarged. There is no prior history of
hypertension.The most likely diagnosis is which of the
following?
1. Carcinoid syndrome
2. Pheochromocytoma
3. Aldosteronoma
4. Renal artery stenosis
Ans. 2The classic triad of pheochromocytoma is sweating,
headache, and palpitations. When these are associated
with hypertension, they have a sensitivity and specificity of
>90% for the diagnosis. Paroxysms are not a component of
aldosterone secreting tumors or renal artery stenosis.
Hyperthyroidism and panic attacks would be in the
differential diagnosis, but thyroid cancer is not associated
with hypertension.
109. A 74-year-old female with a history of
hypertension and hypothyroidism is admitted with
easy bruising, guaiac positive stools, and anemia (Hgb
8.1 g/dL). Screening coagulation tests reveal a
prolonged activated partial thromboplastin time
(aPTT) with a normal prothrombin time (PT) and
platelet count. What is the next step in the diagnosis of
this woman’s problem?
1. Perform upper and lower endoscopy with biopsies.
2. Check factors II, VII, IX, and X levels.
3. Check factors XI, VII, IX, and VIII levels
4. Check an aPTT 1:1 mix with normal plasma and 1-
hour incubation
Ans. 4.A 1:1 mixing study is done when the PT or PTT is
prolonged. The patient’s plasma is mixed with normal
plasma and the abnormal test is repeated. If the mixing of
normal plasma corrects the abnormal test (PT or PTT),
then a factor deficiency is suggested; otherwise, an
inhibitor is suspected. Similarly, an incubated mixing study
is done 1 hour (and occasionally 2 hours)
after mixing of the patient plasma with normal plasma. It is
used to differentiate a lupus anticoagulant from factor
inhibitors.
110. A 61-year-old female is diagnosed with
steoporosis by a screening dual-energy x-ray
absorptiometry (DEXA) scan. Which of these is a risk
factor for postmenopausal osteoporosis?
1. Lack of exercise
2. Obesity
3. Multiparity
4. Late menopause
Ans. 1Risk factors for postmenopausal osteoporosis
include cigarette smoking, thinness, early menopause
(natural or surgical), nulliparity, northern European
heritage, some medications (e.g., glucocorticoids), high
alcohol or caffeine intake, low dietary calcium
consumption, and a family history of osteoporosis. Dietary
calcium and vitamin D supplementation and exercise
(preferably weight bearing) are the classic lifestyle
changes recommended to prevent or treat osteoporosis.
111. A 5-year-old girl presents for evaluation of breast
development, history of multiple bone fractures, and
vaginal bleeding. Physical examination is notable for
“cafe au lait” spots on her skin, tanner stage 2 breasts,
and she appears tall for her age. What is the most
likely cause of precocious puberty in this child?
1. Acromegaly
2. McCune-Albright syndrome
3. Ovarian cyst
4. Ingestion of her mother’s oral contraceptives
Ans. 2. The McCune-Albright syndrome is due to a G-
protein mutation in the alpha-subunit that causes
constitutive stimulatory activity of the tissues. Affected
tissues are autonomously active. McCune-Albright
syndrome classically consists of a triad of cafe au lait skin
spots, cystic bone lesions (polyostotic fibrous dysplasia),
and autonomous endocrine hyperfunction resultingin
sexual precocity. Adominant ovarian cyst develops
independent of stimulation by gonadotropins and it
secretes estradiol, resulting in sexual precocity and
skeletal maturity.
Therefore, the finding of elevated estradiol levels and
suppressed or undetectable gonadotropins is diagnostic.
Affected individualsalso may have hyperthyroidism,
hypercortisolism, pituitary gigantism, or acromegaly.
112. A39-year-old obese female presents with
irregular menstrual periods, mild acne and hirsutism,
and acanthosis nigricans on the nuchal fold, axilla, and
intertriginous areas (inner upper thighs). You suspect
PCOS. Which of the following laboratory tests would be
most important to perform to rule out a likely
confounding diagnosis?
1. 2-hour oral glucose tolerance test
2. Testosterone
3. Prolactin
4. Dehydroepiandrosterone sulfate
Ans. 1PCOS is the most common endocrine disorder of
reproductive age women. Common symptoms include
oligo- or amenorrhea, acne, hirsutism, infertility, and
weight gain. Common tests used to support the diagnosis
of PCOS include LH to FSH ratio, testosterone, DHEAS, and
pelvic ultrasound.
41
Acanthosis nigricans is a raised, velvety, tan skin lesion
commonly seen on the back of the neck, in the axilla, and
the intertriginous areas. Acanthosis nigricans isassociated
with hyperinsulinemia and is a sign that the patient is at
significant risk for prediabetes and frank diabetes. Up to
30% of patients with suspected PCOS have prediabetes,
and 8% are frank type II diabetics.
113. A19-year-old college student is found to have an
elevated serum calcium on routine physical
examination. She has a family history of hypercalcemia
that has not resulted in any known symptoms. Further
workup reveals a slightly elevated serum parathyroid
hormone with depressed levels of serum phosphate. A
24- hour urine calcium excretion is obtained and is
low. Which of the following is the correct diagnosis?
1. Familial hypocalciuric hypercalcemia (FHH)
2. Primary hyperparathyroidism
3. Secondary hyperparathyroidism
4. Tertiary hyperparathyroidism
Ans. 1. FHH, or familial benign hypercalcemia, is a rare
condition characterized by asymptomatic or mildly
symptomatic hypercalcemia. It is inherited as anautosomal
dominant trait and the parathyroid glands are usually
normal in size. The basis for the development of FHH
appears to be mutations in the calcium-sensing receptor
gene which regulates the parathyroid gland setpoint and
modulates the extracellular calcium concentration. The
condition may be mistaken for primary
hyperparathyroidism because, in both conditions, the
serum calcium and parathyroidhormone levels are
elevated with a concomitant low serum phosphate. The
distinction is made by obtaining a 24-hour urine calcium
excretion level. In patients with FHH, the urine calcium
level is low, whereas in primary hyperparathyroidism the
level is high. The distinction is important, as patients with
primary hyperparathyroidism benefit from surgery and
those with FHH do not.
114. A42-year-old male with extensive Crohn’s disease
undergoes a near complete resection of the ileum.
Adeficiency of which of the following vitamin is likely
to result?
1. Niacin
2. Thiamine
3. Vitamin B12
4. Vitamin C
Ans. 3. The distal small bowel (ileum) is the site of
absorption of fat-soluble vitamins (vitamins A, D, E, and K)
as well as vitamin B12. Vitamin B12 binds with intrinsic
factor, a glycoprote insecreted from parietal cells of the
gastric fundus and body. Specific receptors in the terminal
ileum take up the B12 intrinsic factor complex. Vitamin
B12 deficiency leads to megaloblasticanemia. The patient
will require monthly vitamin B12 injections.
115. A young child is brought into the hospital
emergency room because he has episodes of vomiting,
headaches, problems in acquisition of motor skills,
cranial nerve dysfunction, and problems in breathing.
This combination of syndromes most closely relates to
which of the following disorders?
1. Cleft palate
2. Hydrocephalus
3. Anencephaly
4. Syringomyelia
Ans. 2.
The symptoms described arecharacteristic of
hydrocephalus. Hydrocephalus may come about as a result
of defects such as the failure of formation of the cerebellar
vermis, foramensof Magendie and Luschka, or of the
corpus callosum. There is an enlarged cranium as a result
of the buildup of cerebrospinal fluid (CSF), causing brain
damage. Several of the symptoms may also be caused by a
compression of the posterior fossa and the absence of a
cerebellar vermis. Cleft palate is a fissure of the medial
aspect of the lip and would not result in the symptoms
described previously. Anencephaly is the complete or
partial absence of the brain and is not compatible with life.
Syringomyelia is associatedwith bilateral segmental loss of
pain and temperature. Acongenital aneurysm can occur in
a variety of places within the CNS and is typically
associated with stroke in the adult.
116. You are following up in your office with a patient
who had a magnetic resonance imaging (MRI) of his
head for evaluation of persistent headaches. The MRI
report reveals a mass suspicious for malignancy.
While explaining the need for ongoing testing to
determine the etiology, the patient’s spouse asks you,
“What is the most common tumor in the brain?” Which
of the following would be the correct response to this
question?
1. Glioblastoma multiforme
2. Metastatic tumors
3. Meduloblastoma
4. Oligodendroglioma
Ans. 2. Metastatic tumors reach the intracranial
compartment through the blood stream, generally in
patients with advanced cancer. Tumors of different organs
vary in their incidences of intracranial metastasis. For
example, a patient with disseminated melanoma has a
greater than 50% likelihood of acquiring intracranial
metastasis, whereas the incidences of such metastasis in
carcinoma of the breast and lungs is 35%. Certain
carcinomas such as those of the prostate, liver, and
adrenals and sarcomas of all types rarely establish
intracranial metastasis. A metastasis contrast with
theprimary glioma in its discrete appearance, globoid
shape, and prominent halo of edema.
117. A 60-year-old male presents to the office with a
growth on the inside of his lower lip. It has been
42
present for several months and is slowly growing. He
is a nonsmoker but has a long history of chewing
tobacco. Which of the following is the most likely to be
found on biopsy of the lesion?
1. Adenocarcinoma
2. Lymphoma
3. Basal cell carcinoma
4. Squamous cell carcinoma
Ans. 4. Squamous cell carcinoma is the most common
malignant tumor of the oral mucosa and may occur at any
site. It most frequently involves the tongue, followed in
descending order by the floor of the mouth, alveolar
mucosa, palate, and buccal mucosa. The male to female
ratio is 2:1 for the gum, but 10:1 for the lip. There are
substantial variations in the geographical distribution of
the oral cancer. For example, it is the single most common
cancer of men in India.
118. A 25-year-old female presents for evaluation of a
breast mass and tenderness. She describes the breast
soreness as varying with her menstrual cycles. On
examination, you feel a firm, movable, irregular 2 cm
mass. Her breast tissue is diffusely dense bilaterally.
Of the options listed, which is the most likely?
1. Lipoma
2. Fibroadenoma
3. Hemangioma
4. Intraductal papilloma
Ans. 2. Fibroadenoma is the most common benign
neoplasm of the breast and is composed of two types of
tissues. A mesenchymal element most commonly
composed of edematous or collagenized fibrous tissue and
an epithelial component, which consists of compressed,
and sometimes hyperplastic, irregular ductal lumens. They
are usually found in young women and may be hormonally
reactive during pregnancy or menopause.
119. Skeletal Muscle relaxant which is most
cardiostable
1. Vecuronium
2. Atracuronium
3. Cisatracurium
4. Pancuronium
Ans 1. Vecuronium
SMR used in Asthmatics : Atracurium, Vecuronium.
* SMR used to reduce BP : d-TC.
* SMR used to maintain BP : Pancuronium.
* SMR which is cardiostable (commonly used) :
Vecuronium.
* SMR safe in Hepatic Failure & Renal Failure : Atracurium,
Cisatracurium.
* SMR contraindicated in Pregnancy and Renal failure :
Gallamine.
* Pancuronium is Vagolytic and thus it can produce
tachycardiardia.
120. Which of the following is a commonly used trigeminal nerve is typical of orbital apex syndrome.
mechanism for reducing medical errors in hospitals? Proptosis and chemosis are useful signs to distinguish
1. Confidential peer review orbital apex syndrome from cavernous sinus pathology.
2. National hospital accreditation
3. Departmental grand rounds
4. Longer work shifts for employees to promote 122. A 72 year old male is being treated for
continuity of patient care hypertension, gout, Gastro-oesophageal reflux and has
a three year history of type 2 diabetes. He takes a
Ans. 1 variety of medications. His general practitioner is
Medical errors are responsible for more than 98,000 concerned after requesting U+Es on this patient which
excessive patient deaths per year. In order for medical reveal:
errors to be reduced, there need to be mechanisms for Serum Sodium 138 mmol/l
accountability which occur within a supportive Serum Potassium 4.4 mmol/l
environment. Peer review, morbidity and mortality Serum Urea 12.8 mmol/l
rounds, shorter work weeks, and root cause analysis are Serum Creatinine 162 micromol/l
all mechanisms to prevent future errors from fatigue, Of the following drugs that he takes, which one's dose
impaired system processes, and inadequate knowledge. does NOT need to be reduced for this patient?
Frequently when medical errors occur, the families want 1. Allopurinol
to know what is being done to prevent this from 2. Gliclazide
happening again. Although the peer review process is 3. Lansoprazole
confidential and not subject to subpoena, it provides an
effective mechanism to honestly evaluate our colleagues 4. Lisinopril
and enforce necessary discipline to improve patient safety.
Random drug testing is not a systemic solution. Ans. 3

121. 60-year-old woman presented with 3 months
history of diplopia and blurred vision of left eye. She
denied any pain or other neurological symptoms. Her
previous medical history is unremarkable. She smokes
20 cigarettes per day and drinks alcohol in
moderation. Her general medical examination is
normal. Her visual acuity on the right is 6/6 and on the
left 6/36.
There is left partial ptosis and mild proptosis with
conjunctival injection. The left pupil is smaller than
the right but reacting normally to light. There is some
limitation of abduction of the left eye. Fundoscopy
showed a pale left optic disk. The left corneal reflex is
reduced.
Allopurinol is useful in renal impairment, but the dose
should be reduced from 300mg/day to 100mg/day in
moderate to severe renal impairment, as toxicity may
occur, leading to hypersensitivity rashes or hepatitis.
Gliclazide dosage should be reduced in mild renal failure,
and should be stopped in severe renal disease.
Lansoprazole is safe to use in renal impairment (caution in
liver impairment), at a dose of 15-30mg/day.
Lisinopril should be used with caution in renal
impairment. It may potentiate hyperkalaemia and
hypotension, therefore the dose should be reduced to 10-
20mg/day, rather than 20-40mg/day.
Metformin predisposes to lactic acidosis, therefore should
be stopped even with mild renal impairment and general
advice suggests stopping with a creatinine above 150.

The remaining of the neurological examination is 123. A 15-year-old girl is referred to clinic
normal. Routine blood tests including FBC, U+Es, LFTs, complaining of generalised muscle weakness, fatigue
TFTs, Ca, Creatine kinase, autoantibody screen were and polyuria. Her blood pressure in clinic is measured
normal. ECG, CXR were unremarkable. Slit lamp at 90/74 mmHg. Investigations:
examination was normal. Intra-ocular pressures were Serum sodium 127 mmol/l
within normal range. Where is the most likely cause of Serum potassium 3.0 mmol/l
her symptoms? Serum urea 7.2 mmol/l
Serum creatinine 110 umol/l
1. Cavernous sinus Serum chloride 92 mmol/l (NR 97-108 mmol/l)
2. Superior orbital fissure Serum bicarbonate 34 mmol/l (NR 22-28 mmol/l)
3. Orbital apex syndrome Serum magnesium 0.82 mmol/l (NR 0.8-1.1 mmol/l)
4. Optic chiasm Urine sodium 160 mmol/l (NR 40-130 mmol/l)

Ans. 3 Urine calcium 8.0 mmol/24hr (NR 2.5-8.0

mmol/24hr)
The combination of optic neuropathy, proptosis, chemosis, Which of the following is the most likely diagnosis?
horner's syndrome, ophthlmoplegia (in this case due to
6th nerve palsy), and involvement of the first branch of the
43
1. Addison's disease
2. Bartter's syndrome
3. Laxative abuse
4. Liddle's syndrome
Ans. 2
A difficult question! This patient has a hypochloraemic
alkalosis, with high urinary sodium and potassium loss.
Laxative abuse tends to cause low urinary sodium and
potassium, with low serum bicarbonate, due to GI losses.
Thiazide diuretic abuse would fit with the serum findings,
but the urinary sodium and potassium is normal (as water
will follow the electrolytes).
Liddle's syndrome is a congenital form of salt-sensitive
hypertension characterised by a very high rate of renal
sodium uptake, despite low levels of aldosterone,
secondary hypokalaemia and metabolic acidosis. It is
caused by a congenital mutation, which causes a
constitutive hyper reactivity in the epithelial sodium
channel (ENaC).
The increased sodium uptake is accompanied by an
increased water uptake, leading to an increase in blood
volume, and secondary hypertension.
Addison's disease is primary adrenal insufficiency. The
most common cause in the western world is autoimmune
adrenalitis, and worldwide causes include TB, fungal
infections (histoplasmosis, cryptococcus) and
cytomegalovirus. Patients with Addison's disease have
glucocorticoid and mineralocorticoid deficiency. This leads
to hypotension, hyponatraemia (in 90%) and
hyperkalaemia (in 65%).
Bartter's syndrome is a rare, autosomal recessive disorder,
caused by one of three mutations of the ion transporter or
ion channel present in the thick ascending limb of the
distal nephron. Type I and II mutations present in infancy
(often following premature birth and polyhydramnios)
with severe dehydration, hypokalaemic alkalosis,
hypercalciuria and nephrocalcinosis.
Mortality is high. Type III mutations present with a more
varied clinical picture to type I and II, ranging in severity
from near fatal volume depletion with hypokalaemic
alkalosis and respiratory arrest, to mild disease presenting
in teenagers with weakness and polyuria.
Nephrocalcinosis has not been described in type III
mutations, therefore it can differentiate between type I
and II disease, and type III disease. Management is with
long term potassium supplementation and care to avoid
dehydration. The long term prognosis is uncertain.
124. A 32 year-old man presented to hospital with a
four week history of progressively worsening
dyspnoea on exertion. He also complained of a non-
productive cough. Over the two days preceeding
44
admission the patient had become breathless at rest
and was started on oral co-amoxiclav by his general
practitioner.
On examination he was febrile 38°C and looked
unwell. Candida was noted on the tonsilar pillars. No
wheeze or crackles were heard in his chest. His chest
radiograph is shown. Oxygen saturation was 95% on
room air, but fell to 85% following about of coughing.
Arterial blood gases show pO2 of 59 mmHg.
What treatment should be given?
1. Co-amoxiclav + clarithromycin
2. Co-trimoxazole + prednisolone
3. Vancomycin + ceftazidime
4. Cefuroxime + metronidazole
Ans. 2
Oral candidiasis is never normal and should always raise
the possibility of AIDS and the history in this case is
characteristic of Pneumocystis carinii pneumonia. There
are several agents that can be used to treat PCP, though co-
triomoxazole is clearly the most effective and is the
treatment of first choice. Patients often deteriorate after
starting therapy for PCP as the pneumonitis worsens due
to the inflammation associated with dying pneumocysts. In
patients with a pO2<60 mmHg, oral prednisolone is added
to reduce the inflammatory effect.
125. A 26 year old female presents with a six weeks
history of galactorrhea. She has no other symptoms
but takes medication for contraception, dyspepsia and
migraine. Examination reveals slight galactorrhea
with expression from both breasts but is otherwise
normal.
Investigations show:
Prolactin 915 mU/L (<450)
Which one of the following drugs may be responsible?
1. Codeine phosphate
2. Metoclopramide
3. Omeprazole
4. Oral contraceptive pill
Ans. 2
Metoclopramide acts as a dopamine antagonist. Dopamine
inhibits the release of Prolactin from the anterior Pituitary
gland. Therefore ,metoclopramide can predispose to
hyperprolactinemia and consequent galactorrhea.
126. A 70 year old female is admitted acutely unwell. 6
weeks prior to admission she had presented to the GP
with tiredness and weight loss and had been
diagnosed with hypothyroidism based on results
which show a T4 of 7.8 nmol/l (9-22) and a TSH of 4
mu/l (0.5-4.5). She was treated with thyroxine 100
micrograms daily and has since deteriorated. She has
no other past medical history of note, does not smoke
and drinks modest quantities of alcohol. She is a
widow and is self caring. Her mother had
hypothyroidism.
On examination, she is drowsy, thin, has a temperature
of 37.5oC, a pulse of 98 beats per minute and a blood
pressure of 84/50 mmHg. Cardiovascular, respiratory
and abdominal examination are otherwise normal.
There are no neurological abnormalities. The house
officer has sent some emergency bloods on this
patient. Whilst awaiting the results, what is the most
appropriate immediate treatment for this patient?
1. IV 50% Dextrose
2. IV Cefotaxime
3. IV Hydrocortisone
4. IV Thyronine (T3)
Ans. 3
The specific features in this case are the past history of
weight loss associated with a low T4 but normal TSH. The
latter would suggest either sick euthyroidism which can be
associated with hypoadrenalism or secondary
hypothyroidism. In hypoadrenalism which is either
primary or secondary, the addition of thyroxine can
precipitate acute hypoadrenalim which appears to be the
case here. The use of IV steroids is therefore life saving and
should be given without hesitation.
127. A 73-year-old woman presented with thirst and
polyuria of six months duration. She had suffered
several episodes of lower back pain. She was on no
medication. On examination she looked well, had a
dorsal kyphosis and a blood pressure of 170/95
mmHg. Investigations revealed:
erythrocyte sedimentation rate 15 mm/1st hour (0-
30)
serum urea 11.9 mmol/L (2.5-7.5)
serum creatinine 175 umol/L (60-
110)
serum albumin 40 g/L (37-49)
serum total calcium 2.98 mmol/L (2.2-2.6)
What is the most likely cause of the Hypercalcaemia?
1. Metastatic breast cancer
2. Myeloma
3. Osteoporosis
4. Primary hyperparathyroidism
Ans. 4
Comments: The prevalence of hyperparathyroidism is
said to be 4 per 1000 in women over 60, and is 2-3 times
more common in women than men. The lower back pain
may be loin pain due to renal colic caused by renal calculi.
The renal impairment may be associated with renal calculi,
perhaps due to calculi-induced hydronephrosis in extreme
cases. Renal impairment in hyperparathyroidism is not
uncommon. Chronic hypercalcaemia can compromise the
renal concentrating ability, leading to polydipsia and
polyuria. The kyphosis may be due to osteoporosis, which
is commonly seen in conjunction with
hyperparathyroidism. Classically, hypertension has been
45
associated with hyperparathyroidism, but more recent
evidence questions this observation.
128. A 28 year old woman without any past medical
history presents with a 3 month history of arthralgia.
She had no past medical history of note. Examination
reveals swelling of the distal interphalangeal joints of
the middle and ring fingers of the hand and wrist on
the right plus a swollen left ankle. Investigations show:
ESR 40 mm/hr (0-10)
Which of the following is the most likely diagnosis?
1. Acute exacerbation of osteoarthritis
2. Psoriatic arthropathy
3. Rheumatoid arthritis
4. Reactive arthritis
Ans. 2
This woman has psoriatic arthritis. Synovitis is indicative
of an inflammatory arthritis. Rheumatoid arthritis typically
effects the metacarpophalangeal and proximal
interphalangeal joints symmetrically. Psoriatic arthritis
effects the distal interphalangeal joints and tends to be
asymmetrical. Joint involvement in SLEoccurs in the form
of a polyarticular arthralgia, frequently symmetrical and
episodic. Intense tendonitis is more common than
synovitis and can lead to deforming reversible subluxation
of joints without erosive disease (Jaccoud's arthropathy). A
short, striking history of marked, acute polyarticular
symptoms occurs with systemic (viral) infection.
129. A 32-year-old man is referred to the general
medical outpatient clinic. He and his wife had been
referred by his GP to the infertility clinic for
consideration for assisted conception. He is generally
fit and well and works as a central heating engineer.
He has been referred because he has a chronic
productive cough and a history of recurrent chest
infections since childhood in addition to recurrent
sinusitis. Investigations show: Sodium sweat test:
Normal Immunoglobulins (IgG, IgM, IgA): Normal What
is the most likely diagnosis?
1. Bronchiectasis
2. Chediak-Higashi syndrome
3. Cystic fibrosis
4. Primary ciliary dyskinesia
Ans. 4
Primary ciliary dyskinesia is inherited as an autosomal
recessive disorder characterized by abnormal ciliary
motion and impaired mucociliary clearance. The lack of
effective ciliary motility, causes abnormal mucociliary
clearance. This leads to recurrent or persistent respiratory
infections (which may lead to bronchiectasis), sinusitis,
otitis media, and male infertility.
In 50% of the patients, PCD is associated with situs
inversus (Kartagener's syndrome). The principal
differential diagnoses to consider in this case are cystic
fibrosis and primary ciliary dyskinesia. The diagnosis of CF
is based on typical pulmonary and/or gastrointestinal
tract manifestations and positive results on sweat test
(pilocarpine iontophoresis). A negative sweat test is
sufficient evidence to exclude CF as a diagnostic
possibility. While the patient may have bronchiectasis, this
alone is not sufficient to account for his other symptoms.
130. A 80 year old female presents to A+E acutely
unwell after being found unresponsive on the floor of
her house by her son. She had a past history of
hypothyroidism and taking thyroxine daily. However,
her compliance with treatment is questionable. On
examination she was unrouseable with a Glasgow
Coma Scale of 6/15, had a central temperature of 34oC,
Oxygen saturations of 95% on air, a pulse of 44 beats
per minute and a blood pressure of 100/80 mmHg.
There were no specific localizing signs on neurological
examination but both plantars were extensor. Prior to
results of her emergency blood tests being available,
what is the most appropriate immediate treatment for
this patient?
1. Intravenous 50% Glucose
2. Intravenous Hydrocortisone
3. Intravenous Normal Saline
4. Intravenous Thyronine (T3)
Ans. 4
This patient has typical features of Myxoedema coma
which usually occurs in the elderly who are typically non-
compliant. It carries a high mortality and should initially
be treated with IV thyroid hormone – either T4 or T3 –
even before results are obtained. Steroids are often
employed, in case of associated hypoadrenalism but in this
case would probably not be the most immediate choice.
Other treatment includes rewarming. IV fluids should be
used cautiously as these patients are typically fluid
overloaded.
131. Infant circuit for anaesthesia -
1. Bains circuit
2. Magill circuit
3. Ayres t piece
4. Water's circuit
Ans. is ‘3’ i.e., Ayres t piece
Circuit of choice for spontaneous ventilation in
adultMapleson A
Circuit of choice for controlled ventilation in
adultMapleson D (Bain circuit)
Circuit of choice for childrenType F, i.e. Jackson-Rees
(first choice) and
TypeE, i.e. Ayres Tpiece (secondchoice)
132. A 33 year old nurse is admitted for prolonged
fasting. She originally presented to clinic with a
history of episodic sweating and light-headedness
46
which had developed over a six month period with
symptoms being entirely relieved by eating. She had
developed one of these episodes whilst on the ward
and a BM monitor showed a value of 2 mmol/l. She
took some glucose tablets and had quickly recovered.
On examination no specific abnormalities were found
with a blood pressure of 118/74 mmHg, a pulse of 72
beats per minute and a BMI of 22 kg/m2.
She was admitted for a 72 hour fast and at 3 am, 16
hours into the fast she develops typical symptoms. Her
BM is measured at 2.2 mmol/l, the fast is stopped and
bloods taken. The following reveal her results:
Plasma Glucose 1.8 mmol/l (3 – 6)
Plasma 3Beta-HydroxyButyrate 0.5 mmol/l (greater than
1 mmol/l)
Plasma Insulin 450 pmol/l (less than
21)
C-peptide 0.2 nmol/l (less than 0.5)
What is the most likely diagnosis?
1. Adult Glycogen storage disease
2. Factitious hypoglycemia due to Insulin treatment
3. Factitious hypoglycemia due to Sulphonyl urea
treatment
4. Insulinoma
Ans. 2
This patient has developed hypoglycaemia with
suppression of her 3betaHydroxybutyrate (a ketone),
elevated insulin yet suppressed C-peptide. This would
suggest that there is insulin induced hypoglycaemia and as
C-peptide is suppressed indicates exogenous
administration of insulin. Sulphonylureas would produce
raised insulin and C-peptides and could be assessed in
suspicious cases by measuring a sulphonylurea
concentration. Again insulinoma would be associated with
proportionately elevated insulin and C-peptide.
133. A 55 year old female presents with episodic
sweats and tremors which are relieved by glucose. She
has gained approximately 6 kg in weight of late and
drinks approximately 10 units of alcohol weekly. Her
investigations show normal Full Blood Count, Normal
Urea and electrolytes and a fasting plasma glucose
concentration of 4 mmol/l (3-6). What is the most
appropriate investigation for this patient?
1. 72 hour fast
2. CT scan of pancreas
3. EEG
4. Insulin and C-peptide concentration
Ans. 1
This patient describes symptoms suggestive of
hypoglycaemia which are relieved by carbohydrate. The
likely cause is an insulinoma which is producing the
weight gain. The diagnosis is made by demonstration of
inappropriately high insulin and C peptide during
spontaneous hypoglycaemia.
134. A 62-year-old male attends A+E with a severe
nose bleed. He is known to have alcoholic cirrhosis.
His investigations reveal:
haemoglobin 10.9 g/dL (13.0-18.0)
white cell count 5 x 109/L (4-11)
platelet count 60 x 109/L ( 150-400)
prothrombin time 17.5s (11.5-15.5)
APPT 42s (30-40)
fibrinogen 0.7 g/L (1.8-5.4)
What is the most appropriate blood product for this
patient?
1. Cryoprecipitate
2. Factor VIII
3. Platelets
4. Prothrombin complex concentrate
Ans. 1
The most significant abnormality is the low Fibrinogen.
Therefore the best product to correct the fibrinogen out of
those given is cryoprecipitate. To correct a coagulopathy
you need to aim for Fibrinogen > 1.0g/l, Platelets >50 x
109/L, PT and APTT < 1.5 upper range of normal- so from
the results you can see the most significant abnormality is
the low fibrinogen, the platelets are low and APTT/PT
prolonged but not really sufficient to cause bleeding.
135. A 40-year-old farmer presented to Casualty with a
24-hour history of fever and increasing confusion. On
examination he was febrile 39.5‫؛‬C. A generalized
erythematous rash, covering most of his body, was
observed. He also had a paronychial infection of his
right index finger, with lymphangitis extending
caudally and with axillary lymphadenopathy. His heart
rate was measured at 120 beats per minute with a
blood pressure of 80/60 mmHg. What is the most
likely diagnosis?
1. Hantavirus infection
2. Leptospirosis
3. Orf
4. Staphylococcal toxic shock syndrome
Ans. 4
The history is typical of staphylococcal toxic shock
syndrome (TSS) – shock, fever, confusion and rash. The
primary source of infection in this case is the paronychia of
his right index finger. Hantavirus infections (viral
zoonoses transmitted via rodents) typically have two
distinct presentations: either as a haemorrhagic fever with
renal failure or as an acute pulmonary syndrome. The
former manifestation is commonest in the far east and
eastern Europe, while the latter is the predominat form in
the southwestern United States and South America.
Leptospirosis does not typically cause a rash and is often
associated with jaundice; leptospirosis would not explain
the lesion on his finger. Orf, a zoonotic infection caused by
a pox virus, presents with painless ulcerated lesions on the
47
hands of farmers, but does not fully explain this clinical
picture. Stevens-Johnson syndrome typically starts with an
erythema multiforme-type rash that spreads widely and
involves the buccal mucosa and conjunctivae; often caused
by antibiotic therapy, but does not fit the clinical picture
presented here.
136. A 42-year-old HIV-seropositive man presents to
Casualty with a two-week history global headache. His
partner says that he has become increasingly confused
and disorientated. The patient's latest CD4 count,
taken three weeks ago, was 50 cells/mm3. He had
chosen not to take antiretroviral therapy, but was
taking co-trimoxazole as prophylaxis against
Pneumocystis carinii pneumonia. On examination he
had mild weakness of his left arm and leg in all muscle
groups and a right homonymous hemianopia.
Fundoscopy was normal with no evidence of
papilloedema. A CT scan of his brain showed several
areas of low attenuation in both cerebral hemispheres,
but there was no enhancement with contrast and no
mass effect. What is the most likely diagnosis?
1. Cerebral lymphoma
2. Cerebral toxoplasmosis
3. HIV encephalopathy
4. Progressive multifocal leukoencephalopathy
Ans. 4
The most likely diagnosis is Progressive multifocal
leukoencephalopathy (PML), a demyelinating disease seen
in advanced HIV/AIDS and caused by the JC virus. Cerebral
lymphoma and cerebral toxoplasmosis are often
associated with mass effect on CT brain scanning. In CNS
lymphoma there is usually a solitary lesion. Cerebral
toxoplasmosis is frequently associated with multiple
lesions that show ring enhancement with iv contrast. HIV
encephalopathy may be associated with confusion, but is
not associated with this CT appearance. This is not a
typical presentation of neurosyphilis in any of its forms.
137. A 54 year-old male presents with progressive
pins and needles and numbness in both feet which
have deteriorated over the last six months. He has a 10
year history of Type 2 diabetes mellitus and had
cervical spondylosis for which he underwent surgery 8
years ago. He also confessed to drinking
approximately 40 units of alcohol weekly.
On examination he had a mild bilateral weakness of
foot dorsiflexion, both ankle reflexes were absent and
plantar responses were flexor. There was absent
sensation to light touch to mid-shin level with loss of
joint position sensation in the toes and absent
vibration sensation below the hips. He had a marked
sensory ataxia and pseudoathetosis of upper limbs. He
had no evidence of a retinopathy and urinalysis was
normal. What is the most likely diagnosis?
1. Alcohol-induced neuropathy
2. Central lumbar disc prolapse
3. Cervical cord compression
4. Vitamin B12 deficiency
Ans. 4
Diabetic peripheral neuropathy usually goes in parallel
with retinopathy and nephropathy. It is also slowly
progressive and affects mainly spinothalamic pathway.
Alcohol induced peripheral neuropathy is also slowly
progressive and affects mainly spinothalamic pathway.
Vitamin B12 deficiency usually causes a more rapidly
progressive neuropathy with dorsal column involvement
(joint position and vibration involvement with sensory
ataxia and pseudoathetosis of upper limbs).
138. A 44 year old male attends for a health check at a
mobile cardiovascular risk assessment clinic. He takes
no medication but leads a sedentary lifestyle. He is a
non-smoker and family history reveals that his father
had an MI at 60 years old. The results of his lipid
investigations reveal:
Total Cholesterol 5.0 mmol/l (less than 5.5)
Triglycerides 4.0 mmol/l (1- 2.2)
Which of the following is the commonest cause of an
isolated hypertiglycerdemia?
1. Alcohol
2. Diabetes Mellitus
3. Drug Therapy
4. Obesity
Ans. 4
Comments:
The commonest cause of a mild hypertriglyceridaemia is
obesity secondary to a reduced efficacy of lipoprotein
lipase activity and overproduction of VLDL. Obesity
(defined as a BMI above 30) is present in approximately
20% of subjects in the UK and rising and hence this is why
it is the commonest cause of hyperlipidaemia. Alcohol is
probably a close second. Other secondary causes of
hypertriglyceridaemia include pregnancy, hypothyroidism,
diuretics and pancreatitis.
139. A 42 year old female presented with acute back
pain after lifting a chair. The pain is intense, increases
on movement, and radiates bilaterally to the
hypochondriacal region. Upon questioning she denied
previous fractures, but admitted to a gradual loss of
height (5cm from her young adult height) and
occasional self-limiting back pain.
Past medical history included spontaneous
menopause at the age of 37. She had never taken any
regular medications in the past, calcium or Vitamin D
supplements.
Examination revealed a thin woman who had a dorsal
hyperkyphosis. Severe back pain was ellicited on
movement and local percussion.
48
Investigations: Bone mineral density (BMD) was
assessed by dual-energy x'ray absorptionmetry at the
hip and the lumber spine (L1-L4).
BMD T-score at lumber spine: -3.0
BMD T-score at total hip: -2.8
What is the diagnosis?
1. Osteopaenia
2. Osteomalacia secondary to Vitamin D or calcium
deficiency
3. Post menopausal osteoporotic vertebral fractures
4. Senile osteoporosis
Ans. 3
This lady has several risk factors for post-menopausal
osteoporosis, including early onset (<45 years)
menopause, absence of hormone replacement therapy,
calcium and Vitamin D supplemention and low body
weight. Patients with osteoporosis may have no warning
signs until the first fracture occurs. Gradual height loss and
dorsal kyphosis may result from microfractures or
complete fractures of vertebral bodies.
A T-score refers to the difference in standard deviation
(SD) from the mean bone mass. The World Health
Organisation (WHO) criteria for the diagnosis of
osteoporosis is as follows:
Diagnosis
T-Score Normal, > or = to -1.0
Osteopaenia -1.0 to -2.5
Osteoporosis < or = to -2.5
Causes of secondary osteoporosis such as osteomalacia,
bone metastasis, myeloma must be excluded when a
vertebral fracture is found.
140. A 65 year old male is admitted to the coronary
care unit with an acute inferior myocardial infarction.
There are no contra-indications to thrombolysis and
he receives streptokinase with good resolution of ECG
changes. Three days later examination is normal, with
a blood pressure of 134/76 mmHg. Results reveal a
total cholesterol of 4.8 mmol/L (normal <5.2).Which
one of the following drugs does not have good
evidence for reducing future morbidity and mortality?
1. Aspirin
2. Atenolol
3. Simvastatin
4. Nifedipine
Ans. 4
Aspirin leads to a 12% reduced risk of death and 31%
reduced risk of reinfarction in evidence reviewed by the
Antiplatelet therapy trialists and also GISSI studies. Several
trials have demonstrated benefit from long term treatment
with beta blockers, by reducing the incidence of recurrent
MI, and death from all causes.
Numerous trials have shown benefit from ACE inhibitor
therapy post MI in those with and without evidence of left
ventricular impairment.
The 4S (Scandinavian Simvastatin Survival Study)
demonstrated a benefit from lowering cholesterol with
Simvastatin in patients with coronary disease. There is no
evidence to support a beneficial effect of nifedipine post
MI.
141. A 50 year old woman complains of arthritis and
swelling of approximately 4 months duration. On
examination, she has a symmetrical inflammation with
painful movements of the hands and feet and also
swelling of both knees, suggesting a diagnosis of
rheumatoid arthritis. Regarding her joint disease,
which of the following suggest an adverse prognosis?
1. Metastatic disease
2. Polymyalgia rheumatica
3. Spinal stenosis
4. Spondylosis of the lumbar spine
Ans. 4
Articular erosions in rheumatoid arthritis occuring early
on in the course of the disease, especially within the first 6
months of presentation, indicate a poor prognosis. Over
time joint damage will relate to disability. A positive
rheumatoid factor is associated with more severe erosive
disease, extra-articular manifestations including
subcutaneous nodules and increased mortality. An acute
onset of presentation is not a poor prognostic factor.
Raised inflammatory markers (CRP, ESR) and the duration
of the early morning stiffness both correlate with disease
activity.
non invasive and will give a diagnosis. The patient may
have lymphadenopathy, splenmegaly- which would show
on CT, but no diagnosis can be made from this. A bone
marrow is invasive, and the BM is sometimes not involved
in low grade lymphoproliferative disorders and similarly
there may be no cytogenetic abnormality. The FBC is not
suggestive of TB or malignancy, therefore sputum
examination would not be useful.
143. A 45 year old male diabetic is seen in clinic at the
diabetic clinic for annual review. He has been a
diabetic for 8 years and attends clinic regularly. He is
also being treated for hypertension and takes
metformin 500mg tds, gliclazide 80mg daily,
atorvastatin 10mg/d, ramipril 10mg/d and
bendrofluazide 2.5 mg/d. The registrar notes that he
has central obesity and some thin skin and arranges
tests for Cushing's syndrome. He is seen three months
later in clinic, is seen by another registrar who does
not think that he has any features to suggest Cushing's
syndrome and has the results of the previously
requested investigations:
HbA1c 8.1% (<6.5)
Fasting glucose 9 mmol/l (3.5-6)
24hr Urine free cortisol 354 mmol/d (<250)
9am Plasma ACTH concentration 12 ng/dl (10 –50)
CT abdomen 3cm right sided adrenal
mass
What is the adrenal mass?
1. Aldosterone secreting adenoma
2. Cortisol secreting adenoma

142. A 72 year old male presents with a five day 3. Ectopi CRF producing Phaeochromocytoma
history of cough, dyspnoea and fever. His chest X-ray 4. Incidentaloma
shows a left basal consolidation. His Full Blood Count
shows: Ans. 2
Haemoglobin 11 g/dL (13.0-16.5) The patient is likely to have Cushing's syndrome as
White cell count 30 x 109/L (4-11) suggested by the elevated UFC and the lowish ACTH plus
Neutrophils 10 x 109/L (2-7) adrenal mass on CT would suggest that this is due to a
Lymphocytes 20 x 109/L (1-4) functional adrenal adenoma. The absence of physical signs
Monocytes 1 x 109/L (0-0.8) of Cushing's syndrome
Eosinophils 0.4 x 109/L (0.04-0.4)
Basophils 0.1 x 109/L (0-0.1) 144. A 50 year old woman with a long history of
Which one of the following is the most appropriate test alcohol abuse is prescribed Phenytoin for epilepsy.
to establish the diagnosis? Examination was normal except for a liver edge. Her
1. Bone marrow aspirate full blood count reveals
2. Bone marrow cytogenetics hemoglobin 10.0 g/dL (13-18)
3. CT abdomen MCV 122 fL (80-96)
4. Immunophenotyping of white cells White cell count 2.2 x 109/L ( 4-11)
Platelet count 85 x 109/L ( 150-400)
What is the most likely explanation for these results?
Ans. 4 1. Alcoholic liver disease
Apart from the mild neutrophilia, which could be 2. Aplastic anaemia
explained by the infection, the significant abnormality on 3. Folic acid deficiency
the FBC is the lymphocyte count. Such a high lymphocyte
count could be suggestive of a lymphoproliferative 4. Hypothyroidism
disorder such as chronic lymphocytic leukaemia. The best
way to diagnose these is immunophenotyping of the blood- Ans. 3
49

Folic acid deficiency would give all these results. In
addition she has good reason to be folate deficient- drinks
a considerable amount and is on anticonvulsants.
Alcoholic liver disease, on its own would not make you
leucopenic. Hypothyroidism, would cause a raised MCV,
but not the other parameters. Scurvy does not cause this
picture. Aplastic anaemia could cause this haematological
picture, but the clinical scenario leads you towards folic
acid deficiency.
145. A 38 year old man presented with intermittent
severe headaches. He was prescribed Spironolactone
50mg and Bendrofluazide 2.5mg daily for
hypertension. On examination his pulse was 112 beats
per minute, with regular rhythm, and blood pressure
was 190/110 mmHg. Investigations revealed:
serum sodium 132 mmol/L (137-144)
serum potassium 3.4 mmol/L (3.5-4.9)
serum urea 7.0 mmol/L (2.5-7.5)
Which one of the following is the most useful
investigation in establishing the diagnosis?
1. A 24 hour urinary 5-hydroxyindoleacetic acid
concentration
2. A 24 hour urinary catecholamine concentration
3. A 24 hour urinary free cortisol concentration
4. A radionuclide hippuran renogram
Ans. 2
This question is typical of an MRCP question which may be
used as a "good discriminatory question"! It seems
nebulous at first, but on further investigation it is
extremely complex. One can imagine the smirks of the old
gentlemen in the college at the post-exam port soiree.
The answer is unlikely to be carcinoid given the lack of
symptoms of carcinoid syndrome. The flushing attacks of
the carcinoid syndrome are accompanied by hypotension.
Renal anatomy and function is studied with sequential
images using radionuclides that are indexes of tubular
function (131-I Hippuran). The clinical history here is not
suggestive of renal artery stenosis. Given the patients'
young age, and markedly raised BP on treatment, we
should consider an endocrine cause.
The electrolyte disturbance is mild, and is of dubious
relevance in this question. Diuretic use may be causing the
hyponatremia and hypokalemia, indeed the commonest
cause of hypokalemia in hypertension is diuretic therapy.
However, spironolactone use could, theoretically, mask a
more significant hypokalemia. There is no clinical history
to suggest Cushing's, and primary aldosteronism is not
associated with a tachycardia. An aldosterone;rennin ratio
would not be appropriate at this stage given that the
patient is receiving spironolactone.
50
The history of episodic headaches is central to this
question, together with the tachycardia. These paroxysmal
headaches suggest the diagnosis of phaeochromocytoma;
often the symptoms are vague, and rarely is the classical
presentation encountered. Patients with
pheochromocytoma may develop a severe vascular
headache (Bridgwater and Starling, 1982). Thomas et al.
(1966) reviewed the histories of 100 patients with proven
pheochromocytoma seen at the Mayo Clinic and found that
episodic headache was present in 80%. It was usually of
rapid onset, bilateral, severe, throbbing, and associated
with nausea in about half of the cases.
146. A 30-year-old man presented with a painless
visual loss of his left eye over 24 hours. In two weeks
he lost the vision of his right eye. There has not been
any improvement of his visual acuity over the next 2
months. He denied any other symptoms. His previous
medical history is unremarkable. He smokes 10
cigarettes per day and drinks 20 units of alcohol per
week. There is no relevant family history. He does not
take any drugs. General medical examination is
normal. His visual acuity is 6/60 on the right and
finger counting on the left. His colour vision is
impaired in both eyes. He has bilateral optic atrophy.
The remaining of his neurological examination is
normal. Blood tests including FBC, U+Es, LFTs, TFTs,
Ca, glucose, autoantibody screen, VDRL, Vit B12 are
normal. CXR is normal. MRI brain and orbits are
normal. CSF analysis is unremarkable. What is the
most likely diagnosis?
1. Multiple sclerosis
2. Alcohol/tobacco induced optic neuropathies
3. Leber's optic atrophy
4. Giant cell arteritis
Ans. 3
Leber's optic atrophy usually affects young men. It causes
sequential optic neuropathies in days to weeks. It is typical
painless and severe. Visual acuity fails to improve. Optic
neuritis is usually painful, and visual acuity improves over
a matter of weeks. Giant cell arteritis affects elderly
patients. Alcohol/Tobacco optic neuropathies are usually
chronic.
147. A 69 year-old man is admitted with pain and
numbness in his right foot, following a right hip
replacement. In his past medical history he had been
treated for lower backache by his GP. On examination,
there was weakness of all movements at the right
ankle, with absent right ankle jerk, and sensory
impairment on the lateral aspect and sole of the foot.
Where is the most likely site of the lesion?
1. Femoral nerve
2. Lumbosacral plexus
3. Obturator nerve
4. Sciatic nerve
Ans. 4
Sciatic nerve palsy is a known complication of a total hip
replacement (as femoral nerve palsy). It causes global
weakness of the ankle due to the involvement of both of its
branches: tibial nerve (plantaflexion and inversion) and
common peroneal nerve (dorsiflexion and eversion). The
left ankle jerk is absent due to tibial nerve involvement
148. An 18 year old female presents with an acute
exacerbation of asthma associated with a chest
infection. She is unable to complete a sentence and her
peak flow rate was 35% of her normal level. She is
treated with high flow oxygen, nebulized
bronchodilators and oral steroids but this is
associated with little change in her condition. Which of
the following treatments, given intravenously, would
be the most appropriate for this patient?
1. Aminophylline
2. Augmentin
3. Hydrocortisone
4. Magnesium
Ans. 4
This patient has acute severe asthma (PEFR 33-50%
predicted/best, unable to complete sentences in one
breath, respiratory rate > 25 breaths/min, pulse rate > 110
beats/minute). She has not responded to initial treatment
and the treatment of choice now is intravenous
magnesium 1.2 – 2g over 20 minutes.
149. A 22-year-old nursery school teacher is referred
to clinic by her GP. She gives several weeks' history of
swollen, tender finger joints. She has no past history of
note and has been entirely well apart from a recent
viral infection. She had no significant travel history.
The only sick contacts she could recall were several of
the children in her class who had recently been off sick
with a mild self-limiting illness consisting of a fever,
rhinorrhoea and a rash. On examination the
metocarpo-phalangeal joints and proximal
interphalangeal joints of both hands are swollen and
tender. What is the most likely diagnosis?
1. Adult Still's disease
2. Lyme disease
3. Parvovirus B19 infection
4. Rheumatoid arthritis
Ans. 3
Parvovirus B19 is a single-strand DNA virus. The most
widely known clinical manifestation of parvovirus B19 is
erythema infectiosum ('slapped cheek syndrome'), a mild
viral illness of childhood characterized by a classic
exanthem in which both cheeks appear bright red as
though they had been slapped. Although usually a benign
51
self-limiting viral illness, parvovirus B19 infection may
have more serious sequelae. The virus has a tropism for
rapidly dividing erythrocyte precursors which they infect
and destroy. Thus, no reticulocytes (immature
erythrocytes) are available to replace aging or damaged
erythrocytes as they are cleared by the reticuloendothelial
system. This may not have any significant impact on
otherwise healthy individuals, but can trigger an aplastic
crisis – particularly in patients with haemoglobinopathies.
Parvovirus B19 infection may also be associated with a
symmetrical post infectious arthritis, affecting the small
joints of the hands and feet.
The knees or elbows are rarely involved. The arthritis is
much more common in adults, particularly in women, and
may persist for weeks to months (even years in a small
number of patients). The arthritis may mimic rheumatoid
arthritis. Unlike rheumatoid arthritis, the post infectious
arthritis associated with parvovirus B19 does not cause
permanent damage to bones or joints.
150. A 17 year old girl is admitted with a 2 day history
of rigors due to a urinary tract infection. On
examination she appears unwell, has a Body Mass
Index of 31kg/m2, a temperature of 39°C; examination
is otherwise normal. Initial biochemistry revealed:
Potassium 4 mmol/L (3.5-5)
Urea 7 mmol/L (2.5-7)
Glucose 33 mmol/L (3.0-6.0)arterial
blood gases
pH 7.3 (7.36-7.44)
Standard bicarbonate 14 mmol/l
Base deficit -10
urinalysis negative for ketones Which one of the
following is the best initial treatment for her
hyperglycaemia?
1. Metformin
2. Metformin plus Gliclazide
3. Rosiglitazone
4. Sliding scale IV insulin infusion
Ans. 4
Comments: This patient has a metabolic acidosis with pH
of 7.3 and low bicarbonate likely due to sepsis. She is a
type 2 diabetic with uncontrolled hyper glycaemia but is
unlikely to have diabetic ketoacidosis because the urine is
negative for ketones. It is important that her glycaemia is
controlled to promote recovery from the sepsis this is best
achieved with intravenous insulin initially.