Medicine 2003

1) Heptoglobin: This is ONE of those MCQs which don’t make any sense but still
you have to select this option. Heptoglobin actually binds to Hb (NOT
Heme) in INTRA-Vascular Hemolysis and is marker of Intra-vascular
hemolysis (will be LOW)

2) Trop-T: After 1 hour NONE of the given marker will be positive (raised). ALL
Cardiac markers tends to be positive AFTER 6-12 hours (some books
say 3-12 h) but Trop-I and Trop-I is somehow superior to others as it
is Cardiac Specific. The value of CK-MB in M.I is that it reaches to Peak
level on 3rd day & then its level decline, so if there is RE-Infarction then it will
help us to diagnose this New Re-infarct.

3) 07mmol/l: The logic is simple= The 7mmol/l is border-line and you should
not be confuse if you have very Low level (Normal Person) OR very High
level (Diabetic) . Confusion is being in b/w.

4) ONLY 2 types of Anemia will give you HYPER-segmented Neutrophil. (1) B12
deficiency (2) Folic Acid deficiency. Only one will give you Neurological
symptoms (Vit B12 deficiency). HYPER Segmented means more than 3-
5 Lobes in more than 5% of Neutrophils OR ONLY one Neutrophil
with 7 lobes.

5) This is too easy! Retro-Strenal will give you shortness of breath on lying
down.

6) Acute Hepatitis B infection = HBsAg +ve, HBeAg HBV DNA +ve and Anti-
HBc-IgM. Carrier (infective) stage of Hepatitis B =HBsAg +ve, HBeAg HBV
DNA +ve, Anti-HBc-IgG. On the other hand Healthy Career = HBsAg +ve,
Anti-HBc-IgG & IgM +ve. Immunized pt serology will be Anti-HBs. Resolving
Hepatitis serology = Anti-HBc-IgG +ve & Anti-HBs +ve.

Remember these pearls: (1) HBsAg is the FIRST MARKER of infection. (2)
HBeAg and HBV DNA are INECTIVE particles (If these are positive then pt is
Highly Infective). (3) Marker of RECENT infection is Anti-HBc-IgM. (4) ONLY
marker that will be present in WINDOW PERIOD is Anti-HBc-IgM.

Now this pt has HBsAg +ve, HBeAg –ve & anti-HBc +ve, which means he has
in RECOVERED (Transient resolving stage of Hepatitis B). It is strongly
recommended that you should understand these serology concepts. For that,
Check First aid for USMLE Step 1 (Microbiology portion) or Goljan Pathology
(Hepato-Biliary and Pancreatic Diseases Chapter).
7) Councilman bodies are characteristic of Apoptosis. Just memorize it. No
Concept

8) In Huntington Disease (HD) the area of BRAIN involved is Caudate Nucleus.

You already know what is the main symptom of HD? Yes you’re right it is
chorea. Just remember C for Caudate and C for Chorea.

9) Papilledema is pathogmnonic sign of INCREASE Intra-Cranial Pressure and

you know Hydrocephalus is also another way of saying “Raised
Intracranial pressure”.

10) ACE inhibitors (Captopril): You know that Diabetics are at risk of
Nephropathy because of Micro-Albumineuria. The only way to prevent this
Micro-Albuminuria is to give ACEi to Diabetic patient. So Captopril is the right
choice.

11) Post-Ductal Coarctation of Aorta: If it was Pre-ductal then we will have

LOW B.P in both upper as well as in lower limb. Low B.P in Lower limb and
Normal B.P in Upper limb mean that the problem is AFTER emergence of
Artial supply to Upper Limb.

12) Auriculotemporal Nerve is the branch of Mandibular division of

Trigeminal Nerve (5th cranial nerve) that carry pain fibers from Parotid gland.
Along with Masseteric nerve it also supplies the TemporoMandibular Joint.

13) The general rule is: Almost ALL Blood related Hyper-Sensitivity
Reactions are TYPE-II.

14) This is what we have in Polyarteritis Nudosa (Fibrinoid necrosis). PAN is

type of vasculitis involving small and medium size arteries and with this type
Vasculitis we have Fibrinoid Necrosis. Question repeated in Feb 2014
Medicine Paper

15) FEV1/FVC which will be LOW in ALL Obstructive diseases. Asthma is

one of them and the patient will have LOW FEV1, FVC and FEV1/FVC.

16) No concept in this Question. Just remember Mucor for Diabetes (the
same question was given in Feb 2014 Medicine B)

17) Injury in the left 4th intercostals space just lateral to sternum will cause
damage to Intercostals Membrane.
18) To be honest I search out Harrison’s Internal Medicine for Typhoid Lab
Investigations: From there what I got was MASS Confusion. General rule is: In
1st week: Blood Culture. 2nd week Stool Culture BUT according to CPSP it is
Blood Culture + Widal test. In 3rd week: Bone Marrow Culture. Point to
remember is If patient use antibiotic within 5 days prior to Blood culture then
there is good chance that sensitivity of test will be reduced but this is NOT
TRUE for Bone Marrow Culture.

19) General concept is That HYPERGlycemia must be the cause but it is

NOT true. In Normal person excessive sugar intake can cause Hyper-
glycemia but they will not have Ketone Bodies in urine. Ketone bodies are
DUE TO Insulin deficiency.

20) Calcium Channel Blockers are the drugs of choice in ASTHMA so

Verapamil is the correct answer. Beta-blockers are generally contra-
indicated in Asthmatic pts. [Contrary to common belief (1/3) Asthmatic
Patient can also tolerate Beta-Blockers. So if there is morality benefit in
some diseases (like CHF, MI) and you have no other choice then you can use
beta-blockers but under general conditions For Asthmatic patients use
Calcium Channel Blockers]. We avoid ACE inhibitors in these pts because
ONE of the main side-effect of ACEi is dry cough and you will not want to
burden Asthmatic pts with Cough.

21) General rule is: TSH is the most sensitive test for Thyroid related
diseases (for both Hypo and Hyper).

22) You remember DEXTRO-Cardia? Yes! Heart on RIGHT side. Dextro is for
Right. So D-sugar (Dextro-Sugar) means OH on RIGHT.

23) Middle cerebral artery is the large terminal branch of Internal Carotid
artery. It supplies entire lateral surface of cerebral hemispheres except
superolateral surfaces which is supplied by anterior cerebral artery. (Middle
Cerebral Artery supplies all motor area of cerebral cortex the leg area).
Occlusion of left middle cerebral artery can cause An Aphasia (as in this pt).

24) Posterior auricular artery supplies the Auricle & the scalp.

25) HLA stands for Human Leukocytes Antigen. If we were not wrong and
our teachers didn’t misguide us then Leukocytes is the another name of
White Blood Cells (WBCs). [Question was repeated in Feb 2014 Surgery
paper]
26) This is again a type of MCQs which has info that you’re suppose to
memorize. No concept. DR4 is associated with Rheumatoid Arthritis. HLA-
B27 is for Sero-negative diseases (Like Aknylosing Sponitilitis) etc

27) This is the very definition of Osmotic Diarrhea (gets better with
Fasting).
Osmotic diarrhea: Loss of Hypotonic fluids, No inflammation in mucosa, high-
volume, due to disaccharidase deficiency, “Stunned gut” in Giardiasis.
Secretary diarrhea: Loss of Isotonic fluids, No inflammation in bowel mucosa,
high volume, due to production of Enterotoxicins (in Vibrio Chlera –
stimulates Cl- channels regulated by cAMP & cGMP).

28) RF is for Rheumatoid Arthritis, X-Ray is too non-specific (will not help
you in terms of Pulmonary Embolus) CPK is for muscles related diseases (no
role in P.E) same is true for Ultrasound. The ONLY modality that helps in
terms of pulmonary Embolism is Gallium Scan.

29) Low Testosterone Level is ONE of the causes of Male Infertility. No

Concept in this MCQ, Just remember the relationship b/w Testosterone and
Infertility.

30) A typical presentation of GOUT and Diagnosis is established by finding

Negative biferinges on polarized light (on synovial Fluid). Remember that:
Uric Acid Level may be NORMAL or even Low in Acute episode so it
doesn’t help in term of Diagnosis. Similar situation do occur in G6PD
deficiency, If you check G6PD level during (or short after) acute attack the
Level will be NORMAL or Even HIGHER (because after hemolysis there will be
excess of Reticulocytes and level of combined reticulocytes G6PD will be
HIGH – despite the deficiency of G6PD) that’s the reason why Bite cells and
Heinz bodies on peripheral smear is the best INITIAL test and to Confirm
G6PD deficiency we check the level AFTER 2, 3 months of acute attack –
when things move back to normal (Retic count become Normal). R.F & ESR
will help in Rheumatoid Arthritis, Culture of Synovial fluid will be best option
if we suspect Septic Arthritis, X-Ray of involved joint will be helpful in R.A
and Osteoarthritis.

31) When you have Immuno-compromised patient (HIV positive, Immuno-

suppressant user or Lymphoma) then there will be good chances of
opportunistic infections and the presentation given in this question is of
typical Meningitis and the most common pathogen (fungal) in these group of
patients is Cryptococcus.

32) This MCQ was also repeated in Feb 2014 Medicine test.
Regarding Transplant Rejection Remember: Both HYPER-acute & Chronic is
 Irreversible & ONLY Acute is reversible. Immuno-suppressive therapy will
ONLY effect on T-Cells (will reduce it) and immunity related to T-cells is
CELLULAR. Humoral means Antibodies mediated and it will NOT response to
Immuno-suppressant. So the correct answer is Acute Cellular Rejection.

33) ECG changes with negative Cardiac marker exclude M.I, although
typical question of Pericarditis will be like “patient chest pain relieved on
leaning forward and worsen with bending backward. Pleurisy pain will be
Pleuritic (intensity changes with respiration) and Dissecting Aortic Aneurysm
pain will radiate to back (area b/w scapulae)

34) Winged Scapula is due to the paralysis of Long Thoracic Nerve (that
supplies seratus anterior muscle). Axilllary nerve damage (fracture of
surgical neck of humerus)) will lead to paralysis of Deltoid muscle and loss of
cutaneous sensation over the lower half of deltoid muscle. Accessory nerve
paralysis will leads to Nonfunctional Sternocledonastoid & Trapezius
muscles. The primary clinical manifestation of spinal accessory nerve palsy
is a marked ipsilateral weakness when the shoulders are elevated
(shrugged) against resistance. Median nerve paralysis would lead to Ape’s
Hands deformity. Upper Limb Nerve Injuries (MOST, MOST, MOST important)
If you’re going to study just ONE topic from whole Upper Limb, then that
ONE topic should be Upper Limb Nerve Injuries.

35) Simple solution for this kind of questions: Remember that ONLY TWO
cranial nerves arise from Midbrain (3rd & 4th). FOUR (5th, 6th, 7th & 8th) cranial
nerves arise from Pons. Now this pt has facial paralysis so his Facial nerve
would be damaged. And facial nerve (7th CN) arises from PONS.

36) Pain from epigastric region is mediated by Greater Splanchnic Nerve.

37) Difficulty in extension of metacarpophalyngeal joints means that

Extensor compartment is compromised. Radial nerve supplies this
compartment. In this pt sensation is intact which means that superficial
(cutaneous) branch is intact. Muscular compartment is deep so it must be
the Deep branch of Radial nerve that would be damaged in given pt. There
may be a better way of explanation for this question but mine method was
like this. To fabricate logic.

38) The same MCQ was also repeated in Feb 2014 Medicine Test. Here
is ONE point you should remember if the question says that patient is on
Gluten FREE diet from 7, 10 days and still have Diarrhea don’t Jump
to Giardiasis (it is still Celiac Disease. Intestinal Mucosa/Villi takes time
to regenerate so even in Celiac disease the Gluten Free Diet will NOT
improve the patient conditions till 2, 3 weeks) BUT if a question didn’t
 mentioned the time (like this one) then they are telling you that it is
not Celiac. Whipple’s will also presents with chronic malabsorption
(50%) but along with Diarrhea there will be Neurological symptoms
(30%) as well as Joint pain (80%). Correct answer is Giardiasis.

39) Thiazide Diuretics are one of the minor cause of Acute Pancreatitis is
and once you pick the diagnosis (in this question) then it seem easy to select
Serum Amylase. Epigastric Pain radiating to back and Epigastric tenderness
are the KEY to diagnosis of Acute Pancreatitis. Of NOTE: You know that
Serum Lipase is MORE SPECIFIC than AMYLASE in Pancreatitis. (Just to
refresh your memory)

40) The Key differentiating point b/w Leukemia and Aplastic Anemia is that
In Leukemia Bone Marrow will be HYPER-plastic while in Aplastic Anemia it
will be HYPO-plastic.

41) The Optic nerve fibers terminate in Lateral Geniculate Body (LGB).
Auditory nerve (8th) is related to Medial Geniculate Body while Optic nerve is
to LGB.

42) Remember this Pearl: Until proven otherwise female patient

presented with Jaundice, Pruritis & Xanthoma, diagnosis is Primary
Biliary Cirrhosis. Once you pick the diagnosis then it easy to select Anti-
Mitochondrial antibodies.

43) This is the very definition of X-lined Recessive disease. Before going to
exam hall make sure you know these all definition because CPSP loves to
give 1 or 2 MCQs from these diseases.

44) High urine osmolarity and Low Plasma osmolarity signifies the EXCESS
of ADH which another way of saying SIADH. In Dehydrated patients the Urine
as well as Blood osmolarity (BOTH) will be High. In Diabetes Inspidus and
Mellitus Urine Osmolarity will be Low and Plasma osmolarity will be High.

45) Hyper-pigmentation, Hypotension and Hypoglycemia is equal to

Addison disease or Adrenal insufficiency (Decrease glucocorticoids).

46) You may select 5% Dextrose but you know what, The FASTEST way to
INCrease blood glucose level is Glucagon. If you don’t have Glucagon in
options then select Dextrose but when Glucagon is there then it will be the
best choice.

47) Small cell carcinoma is related to HIGH number of ectopic hormone

production (paraneoplastic syndrome) like ACTH, ADH etc. Squamous cell
 carcinoma is related to Parathyroid hormone like protein production but NOT
ACTH.

48) That’s why we sometimes object on CPSP questions. The given

presentation is too non-specific. HYPOtension and Diaphoresis (sweating)
with chest pain is most likely M.I. Pleurisy related chest pain will change with
Respiration (Increase with Inspiration and Decrease with Expiration),
P.Embolism will presents with Dyspnea (main symptom), Myocarditis pain
will change with position and Angina pain will be excersional and will NOT
related with Hypotension & sweating (in many cases).

49) The Patient is 1 month old and empiric therapy will depend upon
causative organisms (most common pathogen). For below 1 month of age
CDC (Centre of Disease Control) recommendations for Pyogenic Meningitis
are Cefoxitime PLUS Vancomycin PLUS Ampicillin. We avoid Ceftraixone in
infants (till 2months) as there is theoretical risk of Kernicterus. General Rule
is: Above 2 months (and below 60 years) Empiric therapy with Ceftriaxone +
Vancomycin. Below 1 months or above 60 years add Ampicilin as L.
Monocytegenes (one of 4, 5 most common etiological agent in these age
population) intrinsically resistant to ALL Cephalosporins and in below 2
months of age patient replace Ceftraixone with Cefoxitime. I know things are
messed up for you now so let’s clear it with examples.
23 days old patient with meningitis: Treat him with Cefoxitime +
Vancomycin + Ampicillin.
36 days old patient with meningitis: treat him with Cefoxitime +
Vancomycin.
3 months old patient with meningitis: Treat him with Ceftriaxone +
Vancomycin.
40 years old patient with meningitis: treat him Ceftriaxone +
Vancomycin.
67 years old patient with meningitis: Treat him Ceftriaxone +
Vancomycin + Ampicillin.
Remember that above given therapy is empiric you have to change it
according to culture & sensitivity (C&S) once you got the C & S report. This is
what you would do on any exam in the whole world but as you can see there
is no such option so what will you select? Well Pencillin is best option among
them. Empiric therapy means that it will cover maximum suspected
pathogens. Aminoglycosides will cover ONLY gram negative but the S.
pneumonae (gram positive cocci) is leading cause (NOT number ONE) in
neonatal meningitis (most common cause is Streptococcus
agalactiae – group B streptococcus). As we said earlier you can’t use
Ceftriaxone in patient who is less than 2 months of age. Ampicillin is essential
along with Penicillin in this patient but ONLY Ampicillin will not cover most of
 the organisms. Cephadrin also has very narrow spectrum. Penicillin is the
best choice in given options.

50) Atrophy of Thenar Eminence is due to Paralysis of Median Nerve and

Wasting (atrophy) of Hypothenar Eminence is because of Ulnar nerve palsy.
So the correct answer is Ulnar nerve damage. Radial nerve will gives you
Wrist drop.

51) Atrial Fibrillation (A. Fib) means Atria is beating so fast that there is
literally no relaxation phase. When Atria beats that much fast you will NOT
find any P wave on ECG tracing. For P wave to be there on ECG there must
depolarization (contraction) and then repolarization (relaxation) but this
distinction is lost in A Fib.
Bradycardia: well if the question asks what will NOT be related to A. Fib then
select Bradycardia (slow heart rate). In A. Fib heart beats FAST not
SLOW.
P-R prolongation is characteristic of AV block (Heart Block).
Q-wave means OLD Infarct.
S-T segment elevation means Ischemia (related to M.I)

52) Na+ channel blockage means NO ACTION POTENTIAL. Opsonin makes

bugs as Target for Neutrophil in Acute Inflammation and has No role in
Membrane conduction (No relation with Na+ channel). Calmodulin binds
to Ca++ (in smooth muscles) and has no relationship with Na+ channel.
Troponin is related to Ca++ in skeletal muscles and no relationship with
Na+ channel. Tretadotoxin is the ONE which blocks Na+ channel. If you read
the word Tretadotoxin carefully you notice “TOXIN” in it. So it is Toxic and it
must block something? Yes it blocks Sodium channel.

53) Nerve Gas contains Acetylchoinesterase inhibitors which leads increase

synaptic acetylcholine at muscarinic & nicotinic receptor sites.

54) Stomach carcinoma has many risk factors like H. Pylori infection,
Smoking, Alcohol & Nitrosamines etc but there is NO evidence that it has
any association with hydrocarbons. In given options ONLY bronchogenic
carcinoma has strong associations with hyrdocarbons.

55) Same MCQ was repeated in Feb 2014 Medicine paper but with
little modification. If question asks (like this one) that GFR is measured
by? Then Select INULIN. If question says “GRF is clinically measured or GFR
in clinical setting measured by? Then select CREATININE. PAH is used for
measurement of Renal Plasma Flow. Inulin is neither reabsorbed nor
secreted in nephron (lumen) so it is ideal for GFR measurement. PAH doesn’t
 reabsorbed but secret in some amount inside nephron lumen and ideal for
renal plasma flow measurement. Creatinine is mainly use for measurement
of GRF in clinical setting.

56) Great thing about Great Sephanous vein is that it can be used for
Venesection in states where IV cannulation is a problem (can’t pass IV line).
It is superficial & comparatively big vein. What else I should add to that?

57) M.I pain is severe and patients are anxious so you need to give kind of
pain killer that not only relieve their pain but also reduce their anxiety.
Morphine will do that and additionally it has some VasoDilator effect.
Nitrates and Streptokinase are good in management of M.I but it doesn’t
have any Analgesic effect. Remember question asked about Pain
medication. NSAIDs & Aspirin will reduce pain (additionally aspirin is best in
terms of mortality benefit but again question is about Pain NOT mortality
benefit and aspirin is weak analgesic in regular doses).

58) Parathyroid hormone and Vit D regulate the Ca++ homeostasis.

Normally inside kidney alpha-hydroxylase1 catalyze the reaction and
activate Vit D (1, 25 Dihydroxycholicalciferol). In chronic Renal Failure this
step is compromised (No Active Vit D) the Ca++ level falls and Phosphorus
level goes up. That’s the reason why we give Calcium and Vit D to CRF
patients along with Phosphorus binders. Try to understand this concept
because CPSP loves this topic and they give 1 or 2 MCQs in every test. Just
to repeat: Low Calcium and High Phosphorus and CRF patient, cause of this
abnormality is “Lack of Active Vit D”. They may change the question and ask
“Known CRF patient presented to you with HIGH PTH level, what will be
his/her Calcium and Phosphorus level?” Answer should be “High Phosphorus
& Low Calcium”. You can see that PTH level is raised in this presumptive
question. It is because whenever Calcium level is below normal and
Parathyroid gland is present (not surgically removed) and working fine then
PTH level will be elevated. As you know High PTH is also called
Hyperparathyroidism and this specific type (secondary to Vit D deficiency in
CRF) is known as Secondary Hyperparathyroidism (contrary to primary
where Ca++ would be high in this type Ca++ will be low)

59) “Lead II, III, AVF are INFERIOR leads.” So changes in these leads
signify INFERIOR wall M.I. Anterior wall leads = V1-V4. AnteroSeptal leads =
V1-V2, Apical leads are V3-V4. AnteroLateral leads = V4-V6, Lateral leads =
I, aVL.

60) The presentations given in this question is typical of Portal Vein

Obstruction (Portal Hypertension).
61) Blood Pressure is Sodium dependent. Sodium will retain water and will
cause Increase Stroke Volume as well as Increase Total Peripheral
Resistance (TPR). K+ has inverse relation with B.P, if you have high B.P then
there are good chances that your K+ level will be low (as in Conn’s disease –
HyperAldosteronism). Ca++ under normal circumstances has little effect on
B.P (in long standing Hyperparathyroidism there will be Diastolic
Hypertension).

62) You know normal mechanics of Skeletal Muscle Contraction &

Relaxation. Normally Ca++ binds to Toponin which in turns binds and slide
Tropomysin out of binding site of Actin and Myosin then binds to Actin. To
unbind actin & Myosin two factors play important role. 1 st : ATP and 2nd : Ca+
+ If there is lack of ATP binding of actin & myosin will persist (as occur in
Roger Mortis) OR if there is low Ca++ the Calcium will not move back to
Sarcoplasm (Normally Ca++ released from Sarcoplasm and Contraction do
occur after that Ca++ re-enter to Sarcoplasm –relaxation phase then Next
phase of contraction – it moves out) for example in HYPOcalcemia then
binding of Actin & Myosin will persist and Muscle will remain in Contraction
phase (No relaxation phase) that’s what we call Tetany.

63) Patent Ductus Arteriosis (PDA) is associated with Congenital Rubella

and Machinery murmur (which is heard during Systole & Diastole). VSD is
associated with Harsh PanSystolic murmur at lower left sternal border, ASD
is associated Mild Systolic murmur at upper sternal border in secundum
type. Mitral stenosis is associated with Diastolic rumbling murmur. Aortic
stenosis is associated with Systolic murmur often with systolic thrill. Forget
above all just remember PDA is associated with Machinery murmur heard in
both Systole & Diastole.

64) As we said earlier Wrist drop is due Radial Nerve.

65) Median nerve has close relation with Supracondyle of Humerus and
fracture of supracondyles can damage median nerve due this close
association.

66) Anatomy: Whenever you have knee injury question and they ask about
ligament that would be expected to injured, Select Anterior cruciate. Anterior
cruciate ligament is WEAKER than posterior cruciate and that’s why injury to
this ligament is more common.

67) ANA: found in 95% to 99% of cases. A negative ANA is extremely

sensitive for lupus, but a positive ANA has little specificity. Many
rheumatologic diseases are associated with a positive ANA.
 Anti-SSA and anti-SSB: Found in 10% to 20% of cases. They add little to
the diagnosis. These tests are most often found in Sjogren syndrome (65%
of cases).

Anti-double-stranded (DS) DNA (60%) and anti-Sm (30%): These are

found only in SLE. They are extremely specific for SLE. Correct answer is
Anti-ds DNA.

68) Long Thoracic nerve supplies Seratus anterior and its action is to Draw
scapula forward around the chest. When this muscle is compromised (injury
to Long thoracic nerve) person will have hard time to raise arm above the
head and the inferior angle of scapula will be prominent. We call such type
of scapula as Winged scapula.

69) Generally speaking the best initial test for evaluation of iron deficiency
is to look for Red blood cells Distribution Width (RDW) that will be increase.
There are some unique pearls about Fe deficiency that you should
memorize. ONLY microcytic anemia with Increased RDW is Fe
deficiency anemia. ONLY microcytic anemia with Increased Total
Iron Binding Capacity (TIBC) is Fe deficiency anemia. The best
indicator of iron deficiency is to look for Ferritin level (will be Decreased). If
question asks what is the most accurate test for Fe deficiency
anemia? Select Bone Marrow Examination BUT normally we don’t do
that. Serum iron will not be helpful as it can also be decreased in anemia of
Chronic disease, Increase Ferritin (Acute phase reactant) is seen with any
acute infection. Correct answer of this MCQ is Decreased Ferritin.

70) General pearl is Hematuria + Hemoptysis = Good pasture

syndrome (try to memorize this). ALL others options will give you
Hematuria upto some extent but none of them will presents with Hemoptysis
except Good Pasture Syndrome.

71) Drug of choice for Mountain Sickness is Acetazolamide.

72) This patient diagnosis is Nephrotic Snydrome in which Albumin is lost

in urine (Albuminuria). Albumin is major contributor to Plasma Osmotic
Pressure. Low Albumin means Low plasma osmotic pressure.

73) Non-selective proteinuria (> 150mg/24 hr but < 3.5 g/24 hr) : Damage
of Glomerular Basement Membrane (GBM) results in Loss of Albumin &
Globulins i.e Post-Streptococcal Glomerulonephritis.
Selective Proteinuria (>3.5 g/24 hr): Loss of negative charge on GBM with
loss of albumin but NOT globulin, for example Minimal change disease (Lipoid
Nephrosis)
74) Non-keratinizing stratified squamous metaplasia can originate in
Bronchi. Risk factors are smoking, loss of cilia, exposure to dust of different
kinds.
75) Histology: In duodenum there are sub-mucosal Branner’s glands while
in Ileum payer patches are found.

76) In Acute Hepatitis there will be many raised markers like elevated
Bilirubin, Alkaline phosphates but most SPECIFIC one is AST & ALT. AST is
mitochondrial enzyme will be raised more in Alcoholic or Drugs induced
Hepatitis while ALT (cytoplasmic enzyme) will be raised more in viraL
hepatitis, Remember BOTH enzyme will be raised in either types but in drugs
or alcohol related AST level will be much higher and in viraL ALT (compare
to AST) will be raised.

77) Lymphoid tissue + Stratified squamous epithelium = Tonsil. Tonsil

slide description is CPSP favorite. It will be very hard to remember histology
of all body system but at least you should memorize Tonsil.

78) BIOPSY is ALWAYS the most accurate test for T.B where on
examination presence of Casaeting Granuloma is Diagnostic of T.B. Many
other granulamatous disease will give you Langerhans cells, Non-caeseting
granuloma.
For ANY Infectious diseases the MOST ACCURATE test will always be the
CULTURE (remember this point)

79) Guillain-Barre Syndrome (GBS) is an autoimmune damage of multiple

peripheral nerves. By definition, there is no CNS involvement. A
circulating antibody attacks the myelin sheaths of the peripheral nerves,
removing their insulation. GBS is associated with Campylobacter jejuni
infection. Look for Weakness in the legs that ascend from the feet and
moves toward the chest.
CSF shows increased protein with a normal cell count.
The most specific diagnostic test is nerve conduction
studies/electromyography.
Question asked about Diagnostic investigation (Most Accurate) and that is
Nerve Conduction Velocity Testing.

80) Same MCQ with little modifications repeated in Feb 2014 Medicine
Paper. Major Opsonin are IgG (Fc fragment) and C3b. In Feb 2014 they
asked the same question but in correct choice ONLY C3b was given (No IgG
was there in any option). Opsonin function is to bind bacteria with
Neutrophil and this job is done by C3b along with IgG.
 Major point is: before entering to exam hall make sure you memorize Major
Opsonin, Chemotactic agents (C5a, LTB4 & IL-8), Anaphylatoxin (C3a & C5a),
Ca5 also activate Neutrophil adhesion molecule.

81) MCV of 116 fL is another way of saying Megaloblastic anemia. You can
easily recall from your Pharmacology concept/knowledge that Methotrexate
causes Folic Acid deficiency so it must be the causative agent in this lady.
Gold, Chloroquine (especially in G6PD deficiency pts), Pencillamine can
cause hemolytic anemia. Doxorubicin is notorious for Cardio-toxicity but
none of them will cause Megaloblastic anemia (with MCV 116) except
Methotrexate.

82) While dealing with such kinds of questions search out two things.
Patient is pregnant? After how much time she died? If time is NOT given (like
this question) then go for Amniotic Fluid Embolism but if time is given
(suppose after 60 hr of accident pregnant patient died) then they are telling
you that DON’T select Amniotic fluid embolism instead go with Fat
embolism.
Remember that in amniotic fluid embolism pt will show symptoms short after
accident (within hours NOT days). Correct answer of this MCQ is Amniotic
fluid embolism.

83) Diabetics are at risk of Oculomotor nerve plasy. Horner syndrome =

Loss of sweating on effected side + drooping of eyelid + Constricted pupil
(Meiosis) NOT with Dilated pupil (Mydriasis).

84) Most common cause of Oxidative stress in G6PD deficiency is

INFECTION. Drugs that can cause hemolysis are Anti-malarial (Chloroquin,
Primaquine) Sulfonamides (Co-trimoxazole etc), Dapsone, Nitrofurantion
(drug of choice in pregnant women with cystitis). Fava beans can also induce
hemolysis in these pts. Auto-immune hemolytic anemias are ExtraVascular
NOT IntraVascular (in given pt hemolysis is IntraVascular) and drugs that
commonly induce hemolysis are Penicillin, alpha-methyldopa, quinidine).
Factor IX deficiency will cause Hemophilia NOT hemolysis. Liver Diease will
mainly presents with Bleeding/Coagulation disorder NOT hemolytic anemia.
Correct answer is G6PD deficiency.

85) FEV1 of 50% with Cyanosis means that pt is NOT getting enough
Oxygenation so the best initial management will be to give him Oxygen.
Giving him Steroids (IV or Inhalational) or bronchodilators will NOT help him.
These 3 modalities are mainly used for Bronchospasm (to relieve it) and
problem with brochospasm pts is NOT getting enough O2 but to get rid of
CO2 (Expiration is problem NOT Inspiration). This pt has Inspiration problem
NOT expiration. Antibiotics will NOT help him as he needs emergency
management and antibiotics will take time to show its action and other thing
is that we don’t know what is the etiology of this pt current problem? If it is
NOT infectious then antibiotics will be of no value EVEN in long run.

86) The presentations of given pt is highly suggestive of Medial Medullary

Syndrome (MMS) which is due to occlusion of vertebral artery or anterior
 spinal artery. MMS presents with a lesion of HypoGlossal nerve (12 th CN) as
the cranial nerve sign & lesions to both medial lemniscus and the
corticospinal tract. Corticospinal tract lesions produce CONTRAlateral spastic
hemiparalysis. Lesions of 12th Cranial nerve in the medulla produce
ipsilateral paralysis of half the tongue with atrophy. Upon protrusion, the
tongue will deviates toward the side of the lesion.

87) Most of inhaled foreign bodies (while in standing/sitting or even in

supine position) will lodge in Right Lower Bronchus. You know the reason.
For better understanding please study Goljan pathology Respiratory unit
(Clinical box 16.1 Aspiration Sites in the Lungs)

88) Posterior part of Posterior limb carries corticospinal fibers and damage
to this portion will cause motor weakness without sensory loss.

89) 3rd & 4th from Mid-Brain and 5th to 8th from Pons.

90) She has A +ve blood group so logically she must receive blood from A
+ve.

91) Hematemesis is the common complication of Cirrhosis (poral

hypertension – Varices). 70-80% pts will respond ONLY to aggressive fluids
replacement, blood, and fresh frozen plasma but on the same time giving
Octreotide (Sandostatin) & sometimes Vit K to these pts is also essential in
terms of their management. So answer to this question will be both Blood
transfusion and Sandostatin.

92) ALL beta-blockers can cause erectile impotence.

93) Chest pain that is NOT pleuratic (Not change with respiration) is most
likely to be Cardiac origin (Myocarditis). ALL others given options pain will
change with respiration.

94) Penicillinase-resistant penicillins (PRPs): oxacillin, cloxacillin,

dicloxacillin, and nafcillin. These agents are very active against S. aureus.
Aminoglycosides are for Gram negative bacilli (rods) like E-Coli etc,
Metronidazole is best for below Diaphragm anaerobes, Many strains of S.
aureus is now resistant to Ampicillin. So the correct answer is Cloxacillin.

95) Hx of PPH + Low K+ Low Na + Low Glucose + Low B.P = Sheehan’s

Syndrome

96) Mid-line mass in young child that moves with swallowing is

Thyroglossal cyst. Those listed in other options are more likely to lie laterally
in the neck (rather than in the midline of the thyroid descent)
97) History of Throat infection and now presented with wrist pain: you
must think about post-streptococcal infection and Rheumatic Fever. To
confirm that you will need ASO titer.
ANA, Rheumatoid Factor, Anti-SS & ANCA will be helpful for Rheumatological
diseases like Rheumatoid Arthritis, SLE, but NOT in this case.

98) History of mishandled labor & Now Fever & prolonged PT + aPTT with
Low TLC is equal to D.I.C. Whenever you have labor in question think of 3
main things (1) Sheehan’s Syndrome (pituitary apoplexy – sudden onset of
neurologic dysfunction due to postpartum necrosis) (2) Amniotic fluid
embolism (there will be Hx of trauma) (3) DIC. In DIC Look for: Elevation of
BOTH PT and aPTT, Low platelet count, Elevated d-dimer and fibrin split
products & Decreased fibrinogen level (it has been consumed).
All others 3 options (Hemorrhagic shock, Septic shock & Uterine rupture) by
itself will NOT give you prolong PT & aPTT but they can lead to DIC. Correct
answer is DIC

99) Young pt with Hx of sore throat and cervical lymphadenopathy and

ATYPICAL lymphocytes (more than 20%) on peripheral smear is Equal to
Infectious Mononucleosis. Causes of Atypical lymphocytosis are CMV, EBV,
viral hepatitis & Phenytoin. You may think of Leukemia but in given options
NO Acute Lymphocytic Leukemia (ALL) - the most common childhood
leukemia. CML & AML are predominantly adult diseases. Hodgkin will NOT
present with Atypical lymphocytosis.

100) Pons [Need explanation]

101) In Liver Billirubin binds Uridyl glucoronyl transferase. No hard concept,

just memorizes it.

102) Ascending from depth (rapidly) causes Caisen diease (also called
bending) and the pathogenesis of this disease is that N2 dissolved in blood
vessels (in deep sea) when a person ascend quickly to the surface the
dissolved N2 produce bubbles in arteries. Main symptom of Caisen disease is
Seizures.

103) The idea behind this question is do you what type of Necrosis does
occur in brain tissue? You know that! Liquefactive Necrosis. Coagulative
type of necrosis occurs in heart, kidney etc etc… Karhyexis & Karyolysis are
the feature of Apoptosis NOT necrosis.

104) Child with recurrent chest infections & malabsorption (chronic

diarrhea) is almost always Equal to Cystic Fibrosis. Once you pick up the
diagnosis then it is logical and easy to go with Sweat Test. Typical question
of Cystic Fibrosis will be like this “a young child presented with repeated
chest infection and greasy, frothy stool which is difficult to flush and one of
his uncle has same symptoms OR a young child presented with recurrent
chest infection, chronic diarrhea and rectal prolapse.” Remember 3 main
 causes of RECTAL PROLAPSE in children of age below 2 years. (1)
Cystic Fibrosis (2) Whooping Cough (3) Trichuriasis.
In June 2013 Surgery paper question was given that young child with
anemia and rectal proplase was operated by surgeon. After surgery the
surgeon told to parents that their child has a parasitic infection. What is the
most probable parasite? And the answer to that question was Trichuriasis.
Complete blood count, Colonoscopy, Liver biopsy (will add NOTHING for Dx
of Cystic Fibrosis), CT scan of chest - will add very little (that may show
Bronchiactasis). So the correct answer to this question is Sweat Test.

105) As we discussed in MCQ 6. Positive HBsAg and Anti-HBc-IgG with

Negative Anti-HBc-IgM = RECOVERED (Suffered in past).

106) This pt most probable diagnosis is Sarcoidosis and it is multi-systemic

disease. Doing Montoux test, Sputum exam would be good for T.B but NOT
in sarcoidosis. Chest X-ray of this pt will show Bi-hillar lymphadenopathy.
Chest CT is much better than X-ray but if you read the question then you will
notice that they asked what should be the NEXT investigation. Ordering
Cardiac enzyme for M.I pt without doing ECG is wrong. Same is the case with
Chest X-ray & CT chest. CT is better than X-ray (as cardiac enzyme are
better than ECG) but you will do investigations in right order (at least on
exam)

107) Read the question carefully: after injury pt can’t move the leg
ANTERIORLY, on exam Tibia is displaced ANTERIORLY. Recall what we said
earlier ANTERIOR ligament is WEAK. So with these three ANTERIOR words
answer to this question must be Anterior cruciate ligament injury. Again if
they give you a question of Knee ligaments injury then more than 90%
chances are that correct answer will be ANTERIOR cruciate ligament.

108) The most common cause of Pelvic Inflammatory Disease is Chlamydia.

Candida infection will presents will Vaginosis, Syphilis will presents with
ulcer/chancres and lymphadenopathy. Gonorrhea can presents with similar
symptoms but the most common pathogen is Chlamydia.

109) Methotrexate is the 2nd line therapy of Rheumatoid Arthritis.

110) Most of fat absorption takes place in ileum and after ileostomy the
absorption area will be compromised. As result there will be loss of fats.

111) Episodic Hypertension + Palpitation & sweating episodes +

Headache = Phaeochromocytoma. It is a tumor of adrenal medulla and
the main pathology in this condition is EXCESS of circulating Catecholamine
(Epinephrine & Nor-epinephrine). Generally the tumor is removed surgically
and before the removal of tumor it is essential to give alpha-blockers (like
Phenoxybenzamine) as well as beta-blockers (1 st ALPHA then Beta blockers)

112) Horner Syndrome = Loss of Sweating on affected side + Meiosis +

Ptosis (drooping of eyelid).
113) Diabetics are at risk of Atypical & Gram negative bacterial Pneumonia
as neutrophils become lazy (poor opsonization, chemotaxis & Phagocytosis)
in Diabetes and systemic effect of these bugs is peripheral Vasodilation and
Increased vascular permeability (Septic Shock). Cardiac pathology will cause
cardiogenic shock NOT septic. Protein loss (Albumin) is the main
pathogenesis of Nephrotic Syndrome pts. Anaphylaxis is due to ALLERGEN.
Hypovaluma will cause vasoconstriction (HypoVolumic shock). Correct
answer is Increased vascular permeability.

114) Dialysis is done to remove excess of waste & harmful substances from
the body and its basic principle is on Osmosis. Chronic Renal Failure Pts will
have High K+ & Urea while Low HCO3. To maintain normal homeostasis you
will need LOW Potassium, Urea & High Bicarbonate in Dialysis fluid.
Generally K, Urea are in LOW concentration (than plasma) and HCO3,
Glucose are in HIGHER concentration. Ca++, Mg+, Na+ are almost equal to
plasma concentration. As result the excess of K+ and Urea will excrete (from
plasma) and HCO3 & glucose will absorb (into plasma).

115) Tracheostomy is done b/w 2nd & 3rd tracheal ring.

116) Night blindness is the first sign of Vit A deficiency and other
manifestations of Vit A deficiency include Keratitis, Metaplasia, Bitot spot
(Keratomalacia, Xerophthalmia) etc. Aphtous ulcer is idiopathic condition
and has NO known association with any nutritional deficiency. Bleeding
gums (scurvy) & Gingivitis is due to Vit C deficiency. Cheliosis is due to
Riboflavin (Vit B2) deficiency.

117) All given options will add to T.B diagnosis but you can see the question
asked about definite diagnostic feature/test that is Casaeous Necrosis. Giant
cells & Epitheloid cells are present in many granulomatous infections.
Montoux test will ONLY helpful in term of screening (will tell us is there any
prior exposure? And positive test is NOT 100% diagnostic of current
infection). X-ray chest and all other Radiological tests would NEVER be the
most accurate test for any infectious disease. As we said earlier the MOST
Accurate test will always be BIOPSY/CULTURE (in this case Caseous
Necrosis).

118) Myasthenia gravis (MG) is a disorder of muscular weakness from the

production of antibodies against acetylcholine receptors at the
neuromuscular junction. MG pts have Thymoma or Thymic Hyperplasia and
that’s why we do X-ray chest/CT chest in these pts.
For Myasthenia Gravis Best initial test: acetylcholine receptor
antibodies (80%- 90% sensitive). Most accurate test: Electromyography
shows decreased strength with repetitive stimulation. This pt muscle
weakness is due Myasthenia Gravis which is by itself secondary to
Thymoma.
119) Increased Indirect Bilirubin level along with High Reticulocytes count is
diagnostic of Hemolytic anemia. Viral hepatitis will presents with high
Alkaline phosphatase level, raised ALT/AST & Direct Bilirubin but
Reticulocytes count will be NORMAL. Obstruction of CBD will not give you
raised reticulocytes count and there will be raised GGT & Alkaline
phosphatase. G6PD deficiency will also produce hemolytic anemia but in that
case hemolysis will be Intravascular which will be manifested as Raised
Direct Bilirubin & Reticulocytes count and Low Heptoglobin. In given pt
Hemolysis is of Extra-vascular type. So the correct answer is Hemolytic
Anemia.

120) This pt has raised Direct Bilirubin & Alkaline phosphatase level. Her
SGPT (AST) level is normal. Viral & Alcohol hepatitis will NOT presents with
normal AST/ALT level (both will be elevated). Given pt labs are telling us that
her problem is outside the liver architecture (normal SGPT) but inside
hepato-billiary system (raised alkaline phosphatase & Direct Bilirubin). So
the correct answer is Extrahepatic Billiary Obstruction.

121) IL-3 is secreted by T-cells and supports the growth & differentiation of
Bone Marrow Stem cells. Functions Like GM-CSF (Granulocytes Monocytes-
Colony Stimulating Factor). [Reference: First Aid for USMLE step 1-
Immunology]

122) Already discussed (MCQ111) that it is essential to give Alpha blockers

(1st) and (then) beta-blockers to Pheochromocytoma pt before surgery.

123) Already discussed (MCQ 42) Primary Biliary Cirrhosis = Anti-

mitochondrial antibodies (>90%).

124) Dysphagia + Iron deficiency anemia = Plummer Wilson’s

Syndrome.
Vit B 12 & Folate deficiency will give you High MCV (megaloblastic anemia)
while Hemolytic anemia & hereditary spherocytosis will give you Normocytic
& Nomrochromic anemia but this pt has Microcytic Hypochromic anemia (Fe
deficiency).

125) This pt has Acute Renal Failure (ARF) and he has HYPOkalemia &
HYPOnatremia. You have to give him something that will NOT ONLY correct
his HYPOnatremia but also his LOW K+ and for that purpose the best option
is to give him 0.9% NaCl + Potassium. Giving him 5% D/W & Insulin is like
shooting him in the skull. Insulin will drive K+ into the cells and will worsen
his HYPOkalemia. Diuretics will NOT help him. In fact it may worsen his
 HYPOkalemia (Except K+ sparing Diuretics). Giving him Fresh Frozen Plasma
is like giving chocolate to a girl who is dying of thirst (Will NOT be helpful).
5% D/W is good for mild to moderate dehydrated pt with Normal K+ & Na+
level but this pt is NOT a good candidate for such kind of luxury fluid. Give
him Normal Saline with Potassium – That’s all!

126) History of sore-throat and now presented with blood in urine. You will
easily diagnose him as case of Post-streptococcal Glomerulonephritis. No Big
Deal!

127) It is simple! Chronic Epigastric pain (Ulcer) now presented with Cervical
Lymphadenopathy (Virchow Node) and biopsy report revealed Lymphoma.
They are telling you that Please select H. Pylori (Nasty bug that causes
Peptic ulcer and 4% of Gastric – NOT DUODENAL ULCER – ulcer can
transform into malignancy and it is strongly associated with Lymphoma –
MALToma)

128) Staging – Hate it. When metastasis do occur from Colorectal carcinoma
to Liver, Kidney = Stage IV. Now we have two options with stage IV (IV-A &
IV-B) so which one is correct? After searching Robbin’s Pathology, Current
Diagnosis and Treatment in Gastroenterology, Hepatology & Endoscopy and
Harrison’s Principles of Internal Medicine I came to know that THERE IS NO
STAGE IV-A or IV-B. ONLY STAGE IV. The correct answer to this question is
Stage IV-A. By the way staging of Colorectal carcinoma is done by DUKE’s
staging system & well-known TNM classification method.

129) Again this is type of MCQ which is directly related to the simple fact
“How much you remembered your pathology” Mallory bodies are the
characteristic of Alcoholic Hepatitis. I remembered Alcoholic related
abnormalities like this “In Liver it will give Mallory bodies while In Brain
Mamalliry Bodies will be effected in Alcohol related Wernicke-Korsakoff’s
Syndrome – secondary to Thiamine (Vit B1) deficiency.

130) Pulse Pressure = Systolic BP – Diastolic BP. Mean Arterial Pressure =

2/3 Diastolic pressure + 1/3 Systolic pressure

131) Apoptosis: These are the characteristic features of apoptosis.

132) Axillary nerve arises from the POSTERIOR CORD of brachial plexus and
supplies deltoid muscle as well as skin over Lower half of deltoid. (Upper half
skin supply is from Supraclavicular nerves).

133) Embryology: Meninges + neural tissue = Meningomyelocele. ONLY

meninges = Meningocele.
134) Lymphocytic Predominant (and Nodular Sclerosing) type has Best
prognosis (Nodular sclerosing type is common in Women. Other types are
more common in men) while Lymphocytic Depleted & Mixed Cellularity types
have poor prognosis.

135) Remember this Pearl: Any pt with age > 50 years, presented
with PR (per rectal) bleeding or constitutional symptoms (weight
loss, fatigue etc) and microcytic (Fe deficiency) anemia = Colorectal
Carcinoma.

136) While reading this question carefully separate: (1) 20 years old (Young)
Female, (2) Fever, (3) Irregular movements of limbs, head & neck (Chorea –
to be specific Syenham’s Chorea) and (4) Subcutaneous nodule. Now you
can diagnosis of this pt (Rheumatic Fever). In given options ONLY ASO titer
will help us in terms of her diagnosis.ASO titer is for beta-hemolytic
Streptococci.

137) Episodes Abdominal pain + Joint pain + Fatigue + Splenomegaly =

Sickle Cell Disease (with Sickle Cell Crisis). Carriers (those who have Hb SC)
will be asymptomatic. Symptom/Crisis means Full blown disease (Hb SS).

138) Pleura are THE MOST SENSIVE to Pain.

139) Klebsiella is non-motile gram negative bacilli. ONLY gram negative

bacteria will produce Endo-toxin. Some Gram negative and Gram positive
bacteria can produce Exo-toxin. Neuro-toxin, Hema-toxin TSST toxin all are
kind of Exo-toxin. Bacteria is NOT necessarily present at the time of toxin
activity while Endo-toxin will work when bacteria is present (as they are
component of bacterial cell wall). Exo-toxin separate/secreted from bacteria
and circulate freely. Correct answer is Endo-toxin

140) Chronic Hepatitis (B & C) is routinely monitored via ALT (SGPT).

Albumin is for hepatic function in chronic liver disease (it tells how efficiently
liver is working - Low albumin means Liver function is declining). GGOT &
Alkaline phosphatase is for acute problem. The Best of ALL (to know
functional status of liver in Cirrhosis) is Prothrombin Time or PT. In
full-blown Cirrhosis you may have NORMAL ALT (SGPT) level as almost all
liver cells will be dead and dead cells don’t produce ALT (or anything). At
that time ONLY ONE test will help you and that will be PT. So the correct
answer is SGPT (ALT).

141) Nasal deformity + Acid Fast Bacilli = Leprosy. If the question says
“granuloma, nasal deformity, hematuria and positive c-ANCA” then they are
 telling you that please select Wegner’s Disease. BUT when question is
crystal clear like this one then select Leprosy with Eye Closed.

142) Hypoxia will lead to activate Erythropoietin which will in turn stimulate
Erythropoiesis. WITHOUT HYPOXIA NO ACTIVATION of Erythropoietin. So
don’t get confuse that which one is the stimulus for Erythropoiesis? It is
Hypoxia. If you don’t have that (Hypoxia) stimulus Erythropoietin (EPO) is
NEVER going to increase RBC production.
For example after living on normal sea level for many decades you shifted to
high altitude then your erythropoiesis will boost up. Don’t tell me that it will
be because of your Erythropoietin (you have these Kidney & EPO for decades
then why now they came into action?). Something is change with your
current journey. Yes Oxygen tension and now you have HYPOXIA and this
hypoxia activated your Kidney (EPO) which then in turn boosts up your
Erythropoiesis.

143) Colon (Large Intestine) is the major site of K+ secretion and after
Colostomy a portion of Colon will not be available for this job (K+ level will
be increased). So normally we advise these pts to utilize minimum amount
of (restrict) K+. If pts don’t follow the instruction (like one in given question)
then they will have HIGH K+ level. The idea behind this question is “Do you
know where in GI tract, maximum amount of Potassium is secreted?” So tell
them “Yes! I know K+ from Kolon (Colon).”

144) Posterior-gray column

145) Position & Vibration sensations enter the spinal cord in the Dorsal gray
column and ascend in Dorsal-Medial Leminiscus System.

146) Hepatitis A has no chronic stage and completely resolved. So

histologically Liver will be normal.

147) Ferritin is Acute phase reactant and is related to Iron Homeostasis. It

has NO role in Thyroid hormone synthesis/regulation etc.

148) Philadelphia Chromosome is present in more than 95% of CML pts.

There are two misconceptions regarding Philadelphia chromosome 1st: It
is CML specific (No it is NOT. It can also be seen in AML – that’s why it is NOT
the most accurate test for CML. Most accurate test is finding of BCR-ABL
fusion gene that is present in 100% cases) and 2nd: It is good prognostic sign
(No it is NOT. It is worse prognostic sign). Now toward our question:
Philadelphia chromosome is present in ALL blood cell lineage including
Erythroblast, Granulocytes, Monocytes, Megakaryocytes, B & T cells
progenitors BUT NOT present in circulating cells/B & T lymphocytes. From
 above discussion it is clear that Philadelphia chromosome can ONLY be seen
in Bone Marrow.

149) Graft versus host disease pathogenesis: Donor Cytotoxic T cell

recognize host tissue as foreign & proliferation in host tissue that will cause
severe organ damage. Correct answer to this question is cytotoxic T cells.
Antigen-Antibody complex is actually Type III hypersensitivity reaction that
has no role in Graft versus host reaction. Natural Killer cell is for viruses.
Marcophages (Antigen Presenting Cell) is related to chronic inflammation.
Histiocytes are specialized skin marcophages.

150) Bluish color red mass one face in young children is Most likely to be
Capillary Hemangioma. These lesions regress spontaneously.

151) Excess of Protein (amino-acids) will be converted into glucose and

Glucagon is well-known for Gluconeogenesis. Increased amino acid is not
correct because normal body will change surplus amino acids into glucose
via Glucagon. Insulin will be Decreased NOT Increased.

152) The right sequence of body fuel is “Carbohydrate 1 st then Fat and lastly
Protein.” In Feb 2014 question was given that after 48 hours fasting what
will be the major fuel for body metabolism? Options were (A) Muscle
Glycogen (B) Liver Glycogen (C) Protein (D) Fatty Acids (E) Triglycerides. It is
recommended that you should carefully read and understand this topic in
USMLE first aid (Biochemistry portion). General sequence is that initially
Liver Glycogen will be utilized in Fasting state after that Muscle Glycogen.
Body stored (Both muscle as well as liver) Glycogen are utilized within 24
hours (and it is almost impossible to stay at Glycogen after 48 hours). After
Glycogen the main fuel for body will be Fat. Protein will be utilized at the
end.

153) This MCQ was repeated in Feb 2014 Medicine Paper B. Oral
anticoagulant therapy is just another way of saying Warfarin. Monitoring of
Warfarin is done by Prothrombin Time (PT) and monitoring of Heparin is done
by activated Partial Thromboplastin Time (aPTT). Kindly memorize these two.
CPSP loves this topic. One way to remember Warfarin PT and Extrinsic
pathway: Ex-PresidenT went for Warfare.
Just to repeat it & clarify ONE minor point: Whether the pt is antigoagulated
with with Heparin or Warfarin, BOTH PT & aPTT are prolonged, because
BOTH inhibit factors in Common Final Pathway. Experience has shown
that PT performs better in monitoring Warfarin, while aPTT performs
better in monitoring Heparin.
154) As we discussed earlier in Amniotic fluid embolism question, the critical
thing in Embolism question is TIMING. This pt has femur fracture and
developed symptoms after 24 hours. They are simply telling you that please
select Fat embolism. Thrombo-embolism symptoms will be sudden in onset
and there will be risk factors in question stem. If answer to this question was
Thrombo-embolism then question would be like this. “Pt was operated for
femur fracture 1 week back, he was not mobilized since operation and now
presented with shortness of breath and chest pain.” CPSP loves Embolism
questions. We will go in further details accordingly. Lets move forward for
the time being.

155) Young pregnant pt in 3rd trimester presented with chief complaint of

Jaundice your presumptive diagnosis must be Obstetric Cholestasis.
Cholestasis means failure normal amount of bile to reach duodenum. Such
pts will present with Jaundice & Itching (Pruritis). Labs of such pts will show
Elevated Alkaline phosphatase & GGT. Oh look at these options (B) SGPT (C)
ALT. we thought these two are the same things. Well! As we said earlier in
other MCQs that ALT & AST will be raised in viraL & drugs and alcohol
induced Hepatitis. Creatine Kinase (CK) is an enzyme involved in metabolic
break down of Creatine to Creatinine. Isomers of creatine or creatinine
kinase originate from Brain & Thyroid (BB), Skeletal Muscles (MM) and
Cardiac Muscle (MB). CK-MB has NOTHING to do with Liver problems. It will
be raised in Cardiac problems (M.I).

156) Carcinoma of Liver (Hepatoma) with Ascites & peripheral Edema are
the signs of Portal Vein Obstruction. Hepatoma, Cirrhosis all mean Liver is
NOT working and when Liver is out of order Portal Vein will have hard time to
do his job that will produce Portal Hypertension. Inferior Vena Cava
Obstruction can give you ascites & peripheral edema but question already
gave us the pt diagnosis (Hepatoma). Budd-Chiari Syndrome is rare
condition of Hepatic Vein occlusion that can presents with classical triad of
Abdominal Pain + Ascites + Hepatomegaly.
Bottom line is this pt Portal vein obstruction (secondary to Liver Carcinoma)
is the main culprit of Ascites and Edema.

157) Smoker lungs: there will be Decreased number of cilia, Increased (NOT
decreased) number of Goblet cells, Mucosal Hypertrophy (NOT atrophy),
Decreased (NOT increased) number of submucosal glands. So the correct
answer is Decreased number of cilia.

158) This MCQ was repeated in Feb 2014 Medicine B paper.

DiphyloBothrium latum is associated with vit B12 deficiency. The
presentations given in this question is consistent with Vit B12 deficiency and
Parasite that usually plays the role of an etiological agent is DiphyloBothrium
 latum. No hard concept, just remember DiphyloBothrium with Vit B12
deficiency.

159) Klebsiella is CATALASE positive bacteria. Chronic granulomatous

diease (CGD) is an X-linked recessive (65%) & Autosomal recessive (35%)
disease. The X-linked type is characterized by deficient Nicotinamide
Adenine Dinucleotide PHosphate (NADPH) oxidase in the cell membrane of
Neutrophil & Monocytes.
Bacterial Killing is done by O2-dependent myeloperoxidase (MPO) system.
“Normally reduced NADPH converts molecular O2 to O2* which
releases energy called the Respiratory burst. There is an enzyme
called Superoxide desmutase which converts O2* to H2O2
(Hydrogen peroxide). Body can combine H2O2 with Cl- in the
presence of MPO system to produce HOCl* (bleach – bactericidal).
So we have these systems inside Neutrophils & Monocytes to deal
with Bacteria.”
Due to deficiency of NADPH oxidase, there is lack of Respiratory burst
(mechanism via which Neutrophil kills the nasty bugs). CTALASE positive
organism (like Klebsiella & S. aureus) are ingested by Neutrophil but NOT
KILLED (as O2 can’t be converted to O2* so bacterial CATALASE will degrade
that H2O2. Bacterial Catalase will utilize H2O2 and there will be NO peroxide
for formation of bleach –HOCl*). On the other hand CATALASE negative bugs
(Streptococcus species) are ingested & KILLED (H2O2 will be utilize for HOCl*
formation as there will be NO Catalase in these bacteria). As CATALASE
positive organisms can’t be KILLED in these (CGD) pts so the Neutrophils are
eventually replaced by Lymphocytes & Macrophages (cells of chronic
inflammation) macrophages fuse together to form multinucleated giant cells.
Bruton’s agammaglobunlinemia is an Opsonization defect. Although not
given in Options there is another disease called MPO (MyeloPerOxidase)
deficiency where body (Neutrophils) can produce Normal respiratory burst
(O2* and H2O2) BUT the absence of MPO prevents synthesis of bleach
(HOCl*). If you’re still confused (I am afraid that you will be right now) that
what does it mean (the whole discussion) then kindly check Goljan Pathology
Chapter 2 3rd Ed, under the discussion of Acute Inflammation. Hopefully you
get a better understanding from there.

160) I think this one is easy! Lymphocytes + NORMAL glucose + High

Protein (on CSF exam) = Viral Meningitis. There are some unique points
regarding VIRAL Meningitis that you should keep in mind.
1st: Contrary to common belief initially (within first 24 hours) the
predominant cells in CSF are NEUTROPHILS not Lymphocytes. Lymphocytes
replace Neutrophils after 24 hours.
 2nd: Contrary to common belief CSF Glucose level will NOT always NORMAL in
Viral Meningitis. Mumps & Herpes Meningitis can give you LOW glucose level
on CSF exam.
Encephalitis pts will presents with CONFUSION and the best initial test is
Head CT (without contrast) and the most ACCURATE test is PCR of the CSF.

161) A lot of confusion regarding this MCQ. Before your first attempt your
seniors will tell you “many CPSP questions don’t make any sense.” Actually it
is NOT correct. All these questions that you have in MCQs books are just
what candidates recall after their test. In reality more than 95% questions
will be crystal clear. You will get it on first read (although you can debate on
quality of question but you can’t say question was confusion in maximum
cases). The ONLY problem with CPSP questions (less than 5%) is that it will
be from that area which will be NOT clear to anyone till that date. Many
other professional examinations around the world avoid such questions
(controversial area). For instance USMLE will never ask this question with
given options. They will clearly test your knowledge NOT how tricky you are.
If this question was given by USMLE then they will go you either Bronchgenic
Carcinoma OR Mesothelioma but NOT BOTH Options for a single question
with such a confusing description. Now lets move to the answer: MOST
COMMON Cancer & MOST COMMON Cancer KILLER is Bronchogenic
Carcinoma. You also know that exposure to Asbestoses can increase the risk
of Bronchogenic Carcinoma 70 times. From this discussion you will say “Ok!
So we should select Bronchogenic carcinoma as an answer”. NO! Don’t do
that. Mesothelioma is also highly associated with Asbestoses. General rule is:
If question stem have smoker as well as Asbestoses then select
Bronchogenic Carcinoma BUT if they simply ask regarding asbestoses
association with type of cancer (Like this question) OR in question where pt
is Non-smoker then select Mesothelioma.

162) You will say “That must be Occulomotor plasy as you said earlier that
Diabetics are at risk of 3rd cranial nerve palsy” yes! They are but kindly read
the question again and extract just two things out of it. (1) Drooping of
eyelid. (2) Small pupil – Meiosis. Now recall what we said about Horner
Syndrome? In Horner Syndrome there will be (1) Ptosis (drooping of eyelid.
(2) Meiosis- small pupil.(3) Anhydrosis (loss of sweating) of that side. BUT we
have ONLY two of them then how come it will be Horner? Seriously! If you
have all the three features in questions then who will NOT diagnose this
case? By the way in that (previous question of Occulomotor plasy) pt Pupils
were dilated NOT constricted. Bottom Line is “Horner Syndrome is the
correct answer to this question.”
163) The most common arteries that involved in Pulmonary Embolism are
Medium sized pulmonary arteries. This is factual question and you can’t
explain it further.

164) ADP + PiATP. If we are not wrong, in this process ATP is synthesized!
So enzyme which catalyzes this reaction must be called something
synthetic. Yes ATP Synthase. I memorized this enzyme the way I explained.
Don’t know what else I should do, to make it simple.

165) Villous Atrophy is mainly associated with Diarrhea (malabsorption).

Mucosal Atrophy occurs in Starvation states (Lack of Enternal nutrition). Skip
lesions in Inflammatory Bowel Disease (Crohn’s)

166) Kawasaki Disease is necrotizing medium-sized vessel vasculitis

involving CORONARY arteries. It is the MOST COMMON acquired heart
disease in children, surpassing Acute Rheumatic Fever. It mainly effects
Asian descent children of age less than 5 years and more common in Boys >
girls. Clinical Features include Fever, Eryhtema, Conjunctivitis, edema of
hands & feet convalescing with DESQUAMATED RASH & CERVICAL
LYMPHADEOPATHY. Treatment is IV immune-globulin, Aspirin. Here is Two
Unique Points about Kawasaki: (1st) Generally Almost ALL types of
Vasculitis are treated with Corticosteroids but it is CONTRAINDICATED in
Kawasaki. (2) Generally Aspirin is avoided in children because of the risk of
developing Reye Syndrome but Kawasaki disease is the ONLY indication
of Aspirin in children. You may say why that much coverage to this
disease? Brother CPSP loves diseases/mechanisms with some unique
characteristics or that has some exceptions and Kawasaki is best for that.
Thromboembolism is VERY Unlikely in children. Poly Arteritis Nudosa (PAN)
can also involve coronary arteries but it will also (and most commonly)
involve Renal & Mesenteric arteries (it will spare Pulmonary arteries). PAN
has strong association with Hepatitis B (upto 30% involvement).
Hepatitis C can also be associated but general rule is: PAN is with HBV
and Cryoglobulinemia is with HCV, Multiple Myeloma [Remember
these associations]. PAN is disease of adults and it will be VERY Unlikely for
children to have it. Correct answer to this question is Kawasaki disease.

167) Amylase is from Sliva & Pancreatic Juices, Lactase is from small
intestine submucosal glands, Trypsin is active form of Trypsinogen which is
secreted by Pancreas and then converted into Trypsin in duodenum by
Enteropeptidase. So the correct answer is Enterokinase.

168) From your basic knowledge of general pathology you will jump into
Coagulative Necrosis because you studied that Coagulative necrosis is seen
 in Kidney, Heart & Liver etc. But just re-read the question. Question says
distorted area, epitheliod cells, lymphocytes & giant cells. If you can recall
these all are the features of what? Yes! Casaeting Necrosis! But it is LIVER
how come in Liver? Well! It is not unusual for Granuloma to be formed inside
Liver. Caseous Necrosis is a variant of Coagulative Necrosis. This question is
repeated many times in past few years. So make sure that you clarify your
concept regarding Liver, Coagulative & Caseous Necrosis. Presence of
Epitheliod cells, lymphocytes and giant cells is equal to Caseous
Necrosis EVEN if they give you that presentation inside Brain, Liver, Kidney
(Irrespective to the site/tissue of granuloma).

169) Normal IgA level Excluded IgA deficiency (B-cell disorder). These pts
are at risk of Anaphylaxis if exposed to blood products that contain IgA.
SCID stands for Severe Combined Immunodeficiency Disease – an
autosomal recessive disorder (Combined B & T cells disorder). Bruton’s
Agammaglobulinemia (Opsonization defect) is a B-cell disorder in which
pts are at risk of SinoPlumonary infections. They will be fine till 6 months (as
maternal antibodies are present up to 6 months) after that these pts start
showing symptoms. Di George syndrome (T-cells disorder) is due to
Failure of 3rd & 4th pharyngeal pouches to develop and as result No Thymus
& parathyroid glands development.. Clinical features of DiGeorge syndrome
are: Hypothyroidism (tetany) absent thymic shadow on X-ray. These pts are
at risk of Graft vs Host reaction. Wiskott-Aldrich syndrome is combined B
& T cells X-linked recessive disorder whose symptom triad is: Eczema,
Thrombocytopenia, SinoPulmonary Infections. These pts have LOW IgM,
HIGH IgA & IgE and NORMAL IgG. So the correct answer to this question is
Wiskott - Aldrich syndrome.
I know you will feel exhausted and for your ease I will suggest please ignore
everything in above explanation and just remember these: While transfusing
blood to IgA deficient pt, use IgA deficient blood. DiGeorge syndrome
is due to failure of 3rd & 4th pouches development & No Thymic
Shadow on X-ray. Wiskott – Aldrich syndrome: pts with present with
Eczema + recurrent chest infection & Thrombocytopenia. That’s all!

170) Kawasaki disease is already discussed along with Poly Arteritis Nodusa
(PAN) in MCQ 166. The correct answer is Kawasaki disease. Now few words
about Buerger’s disease or Thromboangitis Obliteran & Takayasu arteritis Or
Pulseless disease. Buerger’s disease is EXCLUSIVELY a disease of SMOKERS.
It is medium-sized vessel vasculitis with digital thrombosis. Clinical features
include Resting pain on the forefoot with possible ischemic ulcer or gangrene
& Reynaud’s phenomenon. Treatment is SMOKING cessation & IV
prostacyclin analogue (iloprost). Takayasu disease is the granulomatous
large vessel vasculitis involving Aortic arch vessel. It is more common in
Asian women & children. Clinical features include: Absent upper extremities
 pulse, discrepancy in blood pressure b/w arms > 10 mmHg, visual defects
and sometimes stroke. It is generally treated with Corticosteroids. Again you
may think why that much details? Well you can ignore all the above
explanation BUT you have to remember these two points: (1) Buerger’s is
a Disease of Smokers that will ONLY be effectively treated with Smoking
cessation. (2) Young Asian female + Diminished pulses = Takayasu's
arteritis.

171) Remember this; Young woman (20-40 yrs old) with Tight Skin +
Heartburn + Raynaud's phenomenon = Scleroderma.
Scleroderma or Progressive Systemic Sclerosis is disease of Unknown
etiology. Scleroderma is diffuse in 20% of cases and limited in 80%. Limited
scleroderma is also known as CREST syndrome (Calcinosis, Raynaud,
Esophageal dysmotility, Sclerodactyly, Telangiectasia).
Regarding diagnostic testing: There is no single diagnostic test. ANA is
present in 95 percent of cases but is nonspecific. Antitopoisomerase (anti-
Sci 70) is only present in 30 percent of patients. Anticentromere
antibodies are extremely specific for CREST syndrome.
Lungs Fibrosis and pulmonary hypertension (these are the leading cause of
death) in Systemic Sclerosis.
SLE, Poly Arteritis Nodusa & Serum Sickness will NOT presents with Dsyphgia
& Dysarthria. This pt gender and symptoms are consistent with Systemic
Sclerosis. Yes! SLE is common is also common is females but as I said it will
NOT give you Difficulty in swallowing and difficulty in speech. It will classically
presents with Rash (Butterfly rash) Joint pain, Photosensitivity and Oral Ulcer,
Fatigue etc.

172) Effects of Glucagon are: (1) Break down of Glycogen (Glycogenolysis) &
Production of New glucose (Gluconeogenesis). (2) Break-down of Lipids
(Lipolysis) & Ketone production. (3) Inhibition of Insulin. Additionally its
secretion is increased in starvation so that more & more glucose are produce
for energy utilization. In given question all other options are correct except
the one which say “It is Non ketogenic” because Glucagon IS KETOGENIC.

173) An antibody with highest concentration in serum is IgG. Below are the
some unique characteristics of each antibody:
(1) IgG = Smallest (in size) antibody, Highest concentration in serum, One
that crosses placenta and antibody that is known as a Warm antibody.
(2) IgM = Largest in size, antibody that is mainly Intravascular, Earliest
antibody to be synthesized and Cold antibody.
(3) IgE = Reagenic antibody, antibody with Minimum life, Heat labile
antibody.
(4) IgA = Antibody that protect surfaces, antibody that is present in body
fluids like Saliva, Breast Milk
174) Women are Fatty compare to men. Their muscles have larger fat
content than men. In ALL other parameters (Power, Strength, Endurance &
Myoglobin) male muscles are Superior than female muscles.

NOTE: File was uploaded in bit hurry. Explanation to some questions will be
deficient (will improve with time. I.A)

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