4 Git Liver Mcqs

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GIT, Liver

follow ed mostly DIRECTIONS: Each of the numbered items or incomplete statements is followed by four choices. Select the best possible answer to each case. Correct answer is displayed with a brief explanation  and reference after every question.

1. Wha Whatt is Scha Schatzk tzkii ring: ring:

1. 2. 3. 4.

Mid id--esop opha haggeal web web Hypop oph haryng ngeeal web web Lowe Lo werr eso esoph phag agea eall muc mucos osal al ri ring ng None of th the above

Answer (3)  Lower esophageal mucosal ring (Schatzki ring) is a thin web-like constriction located in squamocolumnar mucosal junction at or near border of LES. When the lumen diameter is less than 1.3 cm, it causes dysphagia to solid foods, and is episodic. Asymptomatic rings may be present in 10% of the normal individuals. Low esophageal muscular ring (contractile ring) is located proximal to site of mucosal ring. It represents uppermost segment of the lower esophageal sphincter. Schatzki ring responds to dilatation unlike lower esophageal muscular ring that does not respond to dilatation.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1745.

2. Triple therap therapy y for for eradicatio eradication n of H. pylori  includes all, except :

1. 2. 3. 4.

Ome mep pra razzole 20 mg mg BD Clar Cl arit ithr hrom omyc ycin in 50 500 0 mg mg BD BD Metr Me tron onid idaz azol olee 500 500 mg BD Sucralfate

Answer (4)

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 Regimen recommended for eradication of  H. pylori infection:

1.

2.

3.

Triple therapy

Dosage

Bismuth subsalicylate plus metronidazole plus tetracycline Ranitidine bismuth citrate plus tetracycline plus clarithromycin or metronidazole Omeprazole (lansoprazole) plus Clarithromycin plus Metronidazole or Amoxicillin

2 tab qid 250 mg qid 500 mg qid 400 mg bid 500 mg bid 500 mg bid 20 mg bid (30 mg bid) 250 or 500 mg bid 500 mg bid 1 gm bid

 Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1754.

3. Cus Cushin hing’s g’s ulcer ulcers s are seen seen in:

1. Cus ush hin ingg’s dis diseease 2. Af Afte terr as aspi piri rin n th ther erap apyy 3. Acut Acutee up upper per GI GI ulcers ulcers ass associa ociated ted with with intra intracracra-nial nial injur injuryy or with increased intracranial pressure 4. In severe burns Answer (3)  Cushing ulcers are stress-related ulcer. They show acute erosive gastric mucosal changes or frank ulceration and bleeding. Ulcer is commonly observed in acid-producing fundus and body of  stomach. Mucosal ischemia and breakdown of normal protective barrier play an important role in pathogenesis of ulcer in addition to hyperchlorhydria. Curling’s ulcer occurs in patients with severe burns.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1760.

4. Symptoms Symptoms of late dumping dumping syndrome syndrome occur 3 hours hours after eating, eating, and is due to:

1. 2. 3. 4.

Hypoglycemia Hyperosm Hype rosmolar olar gas gastric tric cont content ent when empt emptying ying into smal smalll bowel bowel Due to po post vagot oto omy All of of th the above

Answer (1)  Hyperosmolar gastric content causes dumping syndrome in early phase. It occurs after vagotomy and drainage, especially in Billroth procedure. Two phases of dumping – early and late – can occur. Early dumping occurs in 15–30 minutes after food intake. Crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia, palpitation, diaphoresis and rarely syncope occur. The late phase of dumping

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typically occurs from 90 minutes to 3 hours after meals. It is thought to be secondary to hypoglycemia from excessive insulin release.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1757.

5. Risk factors factors for NSAID NSAID induced induced mucosal mucosal injury includes includes all, all, except :

1. Old age 2. Hig High h dose, dose, protr protract acted ed use use and and combina combination tion of NSAID NSAID and and glucocorticoids 3. Se Seve vere re in inte terrcu curr rren entt ill illne ness ss 4. Int ntaake of of hot hot dr drin inkks Answer (4)  Risk factors for upper gastrointestinal adverse events in patients taking NSAIDs: Increasing age Comorbidity Oral glucocorticoids History of peptic ulcer

History of upper GI bleeding Anticoagulation Combination of NSAIDs therapy Increasing dose of NSAIDs.

 Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2042.

6. ZE syndrome syndrome or gastrino gastrinoma ma tumors tumors are most seen seen in:

1. 2. 3. 4.

Head of of pa pancreas Tail of pa pan ncr creeas Duodenum Stomach

Answer (4)  Site of gastrinoma are as follows: Duodenum: 50–70% Pancreas: 20–40% Other intraabdominal sites, mesentery, lymph node, biliary tract, liver, stomach and ovary.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2227.

7. Bil Bile e salts salts and and Vitami Vitamin n B12 are absorbed from:

1. 2. 3. 4.

Pro roxxima mall int inteesti tine ne Mid-intestine Dist Di stal al sm smal alll in inte test stin inee Caecum

Answer (3)  The site of absorption of nutrients in intestine is as follows: 1. Du Duod oden enum um:: Iron Iron,, calc calciu ium, m, fol folat ate. e. 2. Ileum: Vi Vitamin B12, bile acids. 3. Co Colo lon: n: Wat ater er ab abso sorp rpti tion on..

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4.

155

Smalll bowel: Smal bowel: Prox Proximal imal > distal distal gluc glucose, ose, amin amino o acids, acids, lip lipids ids..  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1764.

8. Absor Absorption ption of water water and electrolyte electrolytes s occurs mainly mainly at:

1. 2. 3. 4.

Jejunum Caecum Rectum Duodenum

Answer (2)  Water absorption occurs in caecum and colon. Short chain fatty acids are absorbed in colon, and stimulate colonic sodium and fluid absorption. In antibiotic-induced diarrhea, there is decreased SCFA.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1763.

9. Monog Monoglyceri lycerides des and fatty fatty acids are are absorbed absorbed from: from:

1. 2. 3. 4.

Pro roxxima mall int inteesti tine ne Ileum Colon Mid-intestine

Answer (1)  See above two answers.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 1765, 1766.

10. All of the amino acids acids entering entering liver via portal portal vein are catabolized catabolized to urea, except :

1. 2. 3. 4.

Leucine Isoleucine Valine Tryptophan

Answer (4)  These amino acids have important role in the glucose alanine cycle.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1667.

11. In phase I reaction in liver, which detoxification detoxification mechanism mechanism is involved:

1. Chemical Chemical modi modifica fication tion of drug drug by by oxidat oxidation, ion, redu reductio ction, n, hydroxylation, sulfoxidation, deami-nation, dealkylation and methylation 2. Invo Involve lve enzy enzymes mes like P450 P450,, cytochr cytochrome ome P5, P5, oxidas oxidasee and glutathione S, acyltransferase 3. Lea Leads ds to inac inactiva tivation tion of drugs drugs like benz benzodia odiaze-p ze-pine, ine, but activ activation ation of drug like cortisone to cortisol 4. All of of th the above

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Answer (4)  During metabolism, most drugs after absorption reach liver. Phase I results in more polar metabolites that are more readily excreted. In phase II, specific endogenous compounds conjugate to the phase 1 metabolites. In phase I, there is oxidation accomplished by cytochrome P450 of CYP family. Phase II reaction is accomplished by glucuronyl, acetyl, sulfo and methyltransferase enzymes.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 13.

12. Phase II reaction reaction during during metabolism metabolism in liver liver involves: involves:

1. 2. 3. 4.

Converting Converti ng lipop lipophilic hilic subs substanc tances es to water water solu soluble ble subs substanc tances es Forma Fo rmatio tion n of of gluc glucuro uronid nides es by con conjug jugat ation ion Both (1 (1) an and (2 (2) None of th the above

Answer (3)  During metabolism, most drugs after absorption reach liver. Phase I results in more polar metabolites that are more readily excreted. In phase II, specific endogenous compounds conjugate to the phase 1 metabolites. In phase I, there is oxidation accomplished by cytochrome P450 of CYP family. Phase II reaction is accomplished by glucuronyl, acetyl, sulfo and methyltransferase enzymes.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 13.

13. Regarding Regarding intrahepatic intrahepatic cholestasis cholestasis of pregnancy, pregnancy, all statements statements are true true except :

1. Recur Recurss durin duringg preg pregnan nancy cy in thir third d trime trimeste sterr 2. Su Subsi bsides des wit within hin 7–1 7–14 4 days days aft after er del delive ivery ry 3. Ther Theree is an an increase increased d sensitiv sensitivity ity to hepa hepatic tic effec effects ts of estr estrogen ogen and progesterone 4. Se Seen en of ofte ten n in in eld elder erly ly mu mult ltip ipar araa Answer (4)  This is precipitated by oral contraceptives. Itching and steatorrhea can occur.. Pregnant women with intrahepatic cholestasis have increased risk  occur of premature delivery, fetal distress during delivery and still birth. 60– 70% of the affected individuals develop cholestasis during subsequent pregnancy.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 987.

14. Nut Nutmeg meg live liverr is seen seen in: in:

1. 2. 3. 4.

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Budd-C Budd -Chi hiar arii sy synd ndro rome me Card rdiiac cir irrh rhos osis is Bil ilia iary ry cir irrrho hossis Hemochromatosis

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Answer (2)  In right-sided failure, retrograde transmission of elevated venous pressure via inferior vena cava and hepatic veins leads to congestion of liver. Prolong congestion leads to centrilobular hepatic necrosis. Gross examination of liver shows alternating red (congested) and pale fibrotic areas, a pathological appearance known as nutmeg liver.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1862.

15. Budd-Chiari syndrome syndrome resulting in occlusion of hepatic vein or IVC can occur in all, except :

1. 2. 3. 4.

Polycy Poly cyth them emia ia ru rubr braa ver veraa Myel My elop opro roli life fera rati tive ve sy synd ndro rome me Parox Pa roxys ysmal mal noc noctur turnal nal hem hemog oglob lobinu inuria ria Ars rseeni niccal tox toxic icit ityy

Answer (4) In addition, it can be seen in other hypercoagulable states,  idiopathic membranous obstruction of IVC, invasion of IVC by renal cell or primary hepatocellular carcinoma. It is not seen with chronic arsenical toxicity.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th edition,  pages 982, 983.

16. In recurrent spontaneou spontaneous s bacterial peritonitis, peritonitis, prophylact prophylactic ic antibiotic therapy of choice is all, except :

1. 2. 3. 4.

Nor orfl flo ox 400 mg mg/d /daay Trime rimethop thoprim rim + sulph sulphamet amethazo hazole le combin combinatio ation n 500 mg a wee weekk Cipr Ci prof oflo loxa xaci cin n 750 750 mg on once ce a wee weekk Doxycycline

Answer (4)  Primary (spontaneous) bacterial peritonitis has a high rate of recurrence (up to 70% experience recurrence in 1 year). Antibiotic prophylaxis reduces relapse rate to 20%. Doxycycline is not the drug of choice. Norflox, ciprofloxacin and bacterium are used. However, long-term use of the antibiotics leads to resistance and severe hospital-acquired staphylo-coccal infection.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 750.

17. Asteri Asterixis xis in hepatic hepatic encephalopa encephalopathy thy is present present in:

1. 2. 3. 4.

Grade IV Grade I Grade II All of of th the above

Answer (3)

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MCQs in Medicine for PG Entrance Examination  Asterixis or flapping tremor is seen in uremia, hepatic coma and cor

pulmonale stage 2 and stage 3. They are seen in hepatic encephalopathy. In deep coma with hepatic encephalopathy, the flapping tremors disappear.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th edition, page 950.

18. Microv Microvesicul esicular ar hepatic hepatic steatosis steatosis is seen seen in all, except :

1. 2. 3. 4.

Rey’s sy syndrome Acut Ac utee fat fatty ty li live verr of of pre pregn gnan ancy cy Val alpr proi oicc aci acid d the thera rapy py Alco Al coho holi licc liv liver er di dise seas asee

Answer (4)  Alcoholic liver disease and tetracycline lead to microvesicular hepatic steatosis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1718.

19. Macro Macrovesicu vesicular lar hepatic hepatic steatosis steatosis is seen seen in all, except :

1. 2. 3. 4.

Alcoho Alco holi licc liv liver er di dise seas asee Dia iabe bete tess mel elli litu tuss Obesity Rey’s sy syndrome

Answer (4)  In addition, drugs like glucocorticoids, amiodarone, estrogen and methotrexate can cause fatty liver. Total parenteral nutrition, proteincaloric malnutrition and jejunoileal bypass can cause these changes in liver. Rey’s syndrome causes microvascular hepatic steatosis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1718.

20. In amyloid amyloid liver, liver, which one is commonl commonly y seen:

1. 2. 3. 4.

Ascite Asci tess oc occu curs rs in al alll cas cases es Jaun Ja undi dice ce is al alwa ways ys pr pres esen entt Hypoa Hy poalbu lbumin minuri uriaa with elev elevate ated d alkalin alkalinee phospha phosphata tase se Port Po rtal al hy hype pert rten ensi sion on is co comm mmon on

Answer (3)  Ascites is seen in advanced stage in only 20% of the patients. Jaundice and portal hypertension are usually absent.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1872.

21. Pleura Pleurall fluid amylase amylase elevat elevation ion occurs occurs in all, all, except :

1. 2. 3. 4.

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Acut utee pa pancre reaati titi tiss Chro Ch roni nicc pa panc ncre reat atit itis is Esop Es opha hage geal al per perfo fora rati tion on Inte In test stin inal al ob obst stru ruct ctio ion n

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Answer (4)  In pancreatic duct, disruption is posterior and internal fistula may develop between pancreatic duct and the pleural space producing pleural effusion. In such a situation, pleural fluid amylase is increased. Both chronic pancreatitis and esophageal perforation can also cause left sided pleural effusion.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1902.

22. Ranso Ranson/imrie n/imrie progno prognostic stic criterion criterion is used used in:

1. 2. 3. 4.

Acut utee pa pancre reaati titi tiss Acut Ac utee fulm fulmin inan antt ulcer ulcerat ativ ivee coli coliti tiss Hepa He pati ticc ence enceph phal alop opat athy hy Acut utee ren renaal fa fail ilu ure

Answer (1)  Ranson, imrie, apache II – prognostic criteria have multiple factor scoring system which assess patients’ increased risk of dying.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1898.

23. Pancre Pancreatic atic ascite ascites s is due to to all, all, except :

1. Pseud Pseudocy ocyst st lea leakin kingg into into per perito itone neal al cav cavity ity 2. Dis Disrupt ruption ion of panc pancrea reatic tic duct duct and and fistul fistulaa betwee between n duct duct and peritoneal cavity 3. Acut utee pa pancre reaati titi tiss 4. Se Seco cond ndar aryy to tube tuberc rcul ular ar infe infect ctio ion n Answer (4)  Pancreatic ascites is due to leaking pseudocyst or fistula between pancreatic duct and peritoneal cavity. Diagnosis is made in an inpatient who has ascites with elevated serum amylase, increased albumin (over <5 g) and serum amylase (over 20,000 U/L).  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1902.

24. Diagno Diagnostic stic features features of pancrea pancreatic tic ascites ascites are:

1. Increa Increased sed albu albumin min >3.0 >3.0 g/dL g/dL and elev elevate ated d amylas amylasee >20,00 >20,000 0 IU in ascitic fluid 2. In Incr crea ease se po poly lymo morp rphs hs in asc ascit ites es 3. Inc ncre reaased LD LDH le level 4. All of of th the above Answer (1)  Pancreatic ascites is due to leaking pseudocyst or fistula between pancreatic duct and peritoneal cavity. Diagnosis is made in an inpatient who has ascites with elevated serum amylase, increased albumin (over <5 g) and serum amylase (over 20,000 U/L).  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1902.

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25. Compl Complication ications s of chronic chronic pancreatitis pancreatitis include include all, all, except :

1. 2. 3. 4.

Vitamin B malabsorption Impaired GT GTT Pleural ef effusion Fola Fo late te ma mala labs bsor orpt ptio ion n 12

Answer (4)  Folate malabsorption is not the complication of chronic pancreatitis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1903.

26. In hepatitis hepatitis E, E, mortality mortality is maximu maximum m in:

1. 2. 3. 4.

Pregnant women In all women Adolescent Infant

Answer (1)  Pregnancy with jaundice is due to hepatitis E, and it carries morbidity.  Ref: Anantnarayan, 6th Edition, page 519.

27. Purtsc Purtscher’s her’s retinopa retinopathy thy is a complica complication tion of:

1. 2. 3. 4.

Hypertension Type-2 DM Pancreatitis Wils lson on’’s di dissease

Answer (3)  It is an unusual complication that leads to sudden and severe loss of  vision in case of acute pancreatitis. Fundus shows cotton wool spots and hemorrhages confined to area of optic disc and macula. It is due to occlusion of posterior retinal artery with aggregated granulocytes.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1898.

28. Diloxa Diloxanide nide furoate furoate is not usefu usefull in:

1. 2. 3. 4.

Extrai Extr aint ntes esti tina nall am amoe oebi bias asis is Cyst passers Inte In ters rsti titi tial al amo amoeb ebia iasi siss All of of th the above

Answer (1)  Diloxanide furoate is used as luminal amoebicidal. It is not useful in extra-intestinal amoebiasis. It is poorly absorbed from gut. It acts on cysts and trophozoites close to the mucosa. Paromomycin and iodoquinol are luminal amoebicidal. Tissue amoebicidal reaches high concentration in blood and tissues after oral or parenteral administration, e.g. metronidazole, tinidazole and ornidazole.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1217.

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29. All causes causes unconjugat unconjugated ed hyperbiliru hyperbilirubinemi binemia, a, except :

1. 2. 3. 4.

Large hematoma Hemolytic an anemia Mega Me galo lobl blas asti ticc an anem emia ia Roto tor’ r’ss syndr dro ome

Answer (4)  In Rotor’s syndrome, there is conjugated hyperbiliru-binemia. It is benign autosomal recessive disorder. Liver has no increased pigmentation. Another cause of congenital hyperbilirubinemia is Dubin Johnson syndrome, which can be differentiated as below: S. No.

1. 2. 3. 4.

Liver pigmented GB visualization Urinary coproporphyrin excretion BSP excretion

Dubin Johnson

Rotor  

Yes No Normal

No Yes Increased

Delayed and reflux back to circulation

Delayed plasma clearance

 Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1821.

30. Progno Prognostic stic marker marker of acute liver liver failure failure is: is:

1. 2. 3. 4.

AST Factor V levels Serum bilirubin Prothrombin ti time

Answer (4)  In acute hepatic encephalopathy, prolongation of prothrombin time is a poor prognostic sign.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1811.

31. Sclero Sclerosant sant agents agents used for endoscopic endoscopic sclerothe sclerotherapy rapy are all, except :

1. 2. 3. 4.

Acetic acid Alcohol Cyanoacrylate Podocyanolate

Answer (1)  Acetic acid is not a sclerosing agent.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1860.

32. What is the mechanism mechanism of action of racecadotril (enkephalin’s inhibitor) in the management of diarrhea:

1. Anti Anti-s -sec ecre reto tory ry act activ ivit ityy 2. Pr Prom omot otes es in inte test stin inal al abs absor orpt ptio ion n

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3. Both 1 and 2 4. Me Mech chan anis ism m of of act actio ion n is is unk unkno nown wn Answer (3)  Encephalin inhibitor is used in diarrhea. It controls diarrhea by promoting intestinal absorption, and has anti-secretory effects.  Ref: Medicine Update, Vol. 13, No. 11, 2006.

33. In a patient with abdominal abdominal tuberculo tuberculosis, sis, which one one of the test denotes hepatic involvement:

1. 2. 3. 4.

Raised ESR Exud Ex udat ativ ivee asc ascit itic ic fl flui uid d Rais Ra ised ed ser serum um alk alkal alin inee phos phosph phat atas asee Elev El evat ated ed ac acid id ph phos osph phat atas asee

Answer (3)  Alkaline phosphatase is distributed in bone, RBC and placenta. It is localized in liver in sinusoidal and biliary canaliculi and gastrointestinal tract. In obstructive jaundice, hepatic metastasis and hepatic granuloma, the enzyme is increased. It is also increased in bone disease like Paget’s disease, osteomalacia, renal osteodystrophy and primary hyperparathyroidism. In osteoporosis, alkaline phosphatase level is not increased.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1816.

34. Match the liver diseases with specific investigations to be done for diagnosing the diseases:

Liver disease

Test  

1. Hematochromatosis 2. Pr Prim imar aryy bil bilia iary ry ci cirr rrho hosi siss

3. Autoimm mmu une ch chronic active hepatitis 4. Wilson’s disease

a. Serum ceruloplasmin, serum urine and liver copper estimation b. Se Seru rum m imm immun unog oglo lobu buli lin, n, se seru rum m ant antii-nu nucl clea earr factor and smooth muscle and liver, kidney, microsomal antibodies c. Serum fe ferrri rittin, serum iron and iron binding capacity, saturation, PCR for genetic defect d. Serum immunoglobulins, serum antimitochondrial antibodies

Answer 1 → c, 2 → d, 3 → b, 4 → a  Hemochromatosis is due to iron overload. Hence, serum ferritin and TIBC will be useful in autoimmune hepatitis. ANA and SMA will be positive in primary biliary cirrhosis. Alkaline phosphatase will be markedly increased incre ased along with AMA positivity. positivity. Wilson’s Wilson’s disease is due to copper overload and deficient serum ceruloplasmin level.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1813.

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35. Mat Match ch the the foll followi owing: ng:

Classification of portalhypertension

Examples of disease 

A. B. C. D.

1. 2. 3. 4.

Extrahepatic sinusoidal Intrahepatic sinusoidal Sinusoidal Extrahepatic presinuso soiidal

Veno-occlusive disease Cirrhosis of liver Ci Budd-Chiari syndrome Portal vein thrombosis

Answer A → 3, B → 1, C → 2, D → 4  Commonest cause of portal hypertension is cirrhosis of liver (sinusoidal). In children and adolescents, extrahepatic portal vein thrombosis is frequent. Schistosomiasis (intrahepatic presinusoidal) is infrequent outside endemic areas.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,  page 958.

36. Which is not not the complicati complication on of portal portal hypertensio hypertension: n:

1. 2. 3. 4.

Renal failure Hypersplenism Ascit As cites es an and d he hepat patic ic enc enceph ephalo alopa pathy thy Pancreatitis

Answer (4)  UGI bleeding is common. Effect of hypersplenism is seen. Renal failure and hepatic encephalopathy with ascites can develop. Pancreatitis is not a complication for portal hypertension.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 959.

37. Commo Commonest nest cause cause of portal hypertension hypertension in adults adults in our country country is:

1. 2. 3. 4.

Cir irrrho hossis of li livver Port Po rtal al ve vein in th thro romb mbos osis is Schistosomia iassis Budd Bu dd-C -Chi hiar arii sy synd ndro rome me

Answer (1)  Main cause of portal hypertension is cirrhosis developing secondary to nutritional deficiency leading to fatty liver and cirrhosis. Alcohol and type B hepatitis also contribute to cirrhosis.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 957.

38. Reduction in portal venous pressure during during the acute bleed is achieved achieved by all drugs, except :

1. 2. 3. 4.

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Somato Soma tost stat atin in (o (oct ctre reot otid ide) e) Propranolol Vasopressin Terlipressin

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Answer (2)  Propranolol is used as prophylactic agent in reducing portal

hypertension in long-standing cases of cirrhosis with portal hypertension. It is not useful in acute GI bleeding.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1859.

39. About TIPS (transjugu (transjugular lar intrahepatic intrahepatic portosystemic portosystemic stent stent shunt), which which statement is true:

1. Stent Stent is plac placed ed betwe between en porta portall vein vein and hepa hepatic tic vein vein to to reduce reduce portal hypertension 2. He Hepat patic ic ence encepha phalop lopath athyy may occu occurr followi following ng shunt shunt 3. Use Used d for acu acute te UGI UGI bleedin bleedingg which which is not resp respondin ondingg to sclerotherapy or banding or pharmacological treatment 4. All of of th the above Answer (4)  Emergency portosystemic shunt carries mortality over 50%. Hence, it

is not done. The procedure is done under radiological control via the internal jugular veins. Prior patency of portal vein must be determined angiographically. Coagulation deficiency required correction with fresh frozen plasma and antibiotic cover is provided.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 960.

40. In all these conditions, conditions, ascites develops develops due to hypoproteine hypoproteinemia, mia, except  in:

1. 2. 3. 4.

Nephr hrot otiic sy synd ndro rome me Prot Pr otei ein n lo loos osin ingg en ente tero ropa path thyy Malnutrition Abdo Ab domi mina nall tube tuberrcu culo losi siss

Answer (4)  Ascitic collection is due to infection. It consists of inflammatory exudates.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1867.

41. Pleural effusion effusion can be found in about about 10% of of the patients patients having ascites:

1. 2. 3. 4.

Seen on ri Seen righ ghtt si side de on only ly Seen on on lef leftt si side on only ly It is al alwa ways ys bi bila late tera rall None of th the above

Answer (1)  Most pleural effusion seen in association with ascites are small in size and are are present on right side. Occasionally, massive hydrothorax

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occurs. Pleural effusion on left side should not be assumed to be due to ascites.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 948.

42. LeV LeVeen een shun shuntt is used used in: in:

1. 2. 3. 4.

Resis ista tan nt ascit itees Hydr dro ocepha halo lou us ASD CCF

Answer (1)  The LeVeen shunt is a long tube with non-return valve running subcutaneously from peritoneum to internal jugular vein in the neck. It allows ascitic fluid to pass directly into systemic circulation.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 949.

43. All of them them are the the complicatio complications ns of LeVeen LeVeen shunt, shunt, except :

1. 2. 3. 4.

Infection Supe Su peri rior or ve vena na ca cava vall thro thromb mbos osis is Pul ulm mon onaary bl bleedi din ng Paraplegia

Answer (4)  Complications include infection, SVC thrombosis, pulmonary edema, bleeding varices from esophagus and disseminated intravascular coagulopathy. Paraplegia is not a complication of LeVeen shunt.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 949.

44. In resistant resistant ascites, ascites, following following modes of therapy therapy are available available,, except :

1. 2. 3. 4.

TIPPS LeVeen sh shunt Port Po rtaa cav caval al an anas asto tomo mosi siss Pro ropr praano nolo loll the therapy

Answer (4)  Medical treatment to reduce portal hypertension will not be of much

help. Other surgical therapies like TIPPS, LeVeen shunt and portocaval anastomosis are to be considered.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1867.

45. Definitive Definitive diagnosis diagnosis of spontaneous spontaneous bacterial bacterial peritonitis peritonitis (SBP) (SBP) is made by:

1. Abdomi Abdominal nal pa pain in and and fev fever er in in a cirr cirrhot hotic ic pati patient ent 2. Abs Absent ent bowe bowell sound sound and rebou rebound nd tender tendernes nesss and hepat hepatic ic encephalopathy

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3. Diagno Diagnostic stic parac paracent entesi esis, s, presen presence ce of cloudy cloudy fluid, fluid, neutro neutrophil phil count count >250/mm 4. Res Respons ponsee to broa broad-sp d-spectr ectrum um antibi antibiotics otics like cefo cefotaxi taxime me 2 g given given 12 hourly for 5 days Answer (3)  All features described above are seen in SBP, but definitive diagnosis is made by ascitic fluid examination which shows neutrophil count of  over 250/mm in ascitic fluid. If multiple organisms are grown in ascitic fluid, it indicates bowel perforation.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 950.

46. Regard Regarding ing lactulose lactulose in hepatic hepatic encephalopath encephalopathy y all are true, except :

1. Orally Orally giv given en and and acts acts on colo colonic nic bact bacteri eriaa in colo colon n 2. Dose started started as as 15–30 15–30 ml 8 hourly hourly and and increas increased ed so so as to produc producee 2 bowel movements 3. It has has osmotic osmotic laxa laxative tive effe effect ct that that reduc reduces es coloni colonicc bacter bacteria, ia, limit limit colon absorption of ammonia and promotes incorporation of  nitrogenous bacteria 4. Lac Lactose tose also acts as lactu lactulose lose in hepat hepatic ic encep encephalo halopath pathyy Answer (4)  Lactulose will be absorbed and will neither act locally on colonic bacteria nor it can prevent ammonia absorption. Only in those cases with lactose intolerance where lactulose will not be absorbed, action seen with lactulose is possible.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 951.

47. Prognosis in cirrhosis with hepatic encephalopathy becomes poor with the onset of all, except :

1. 2. 3. 4.

Hepato Hepa topu pulm lmon onar aryy sy synd ndro rome me Hepa He pato tore rena nall sy synd ndro rome me Spon Sp onta tane neou ouss bacte bacteri rial al peri perito toni niti tiss Ascites

Answer (4)  Complications like hepatorenal syndrome, hepato-pulmonary syndrome and spontaneous bacterial peritonitis are of poor prognosis in cirrhosis of liver.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,  pages 949, 950.

48. Non-A– Non-A–E E viral viral hepatitis hepatitis accoun accounts ts for: for:

1. 2. 3. 4.

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50% of cases 1–2% of cases 10% of cases None of th the above

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Answer (2)  Viral hepatitis is mainly due to hepatitis A, B, C, D, E viruses. Only 1–2% of jaundice with hepatitis are due to other non-A–E viral hepatitis.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 969.

49. Causes of non-A–E non-A–E viral viral hepatitis hepatitis include include all, all, except :

1. 2. 3. 4.

Cyto tom megalo lovvir irus us Influenza virus Eps psttei ein n Barr vir irus us Yell llo ow fe fever vir virus us

Answer (2)  Influenza virus does not cause hepatitis. However, Herpes simplex virus can cause hepatitis.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 969.

50. Chronic infection infection leading leading to chronic active hepatitis hepatitis is not a feature feature of:

1. 2. 3. 4.

Hepatitis B and C Hepatitis A an and E Hepatitis C and D Hepatitis B and D

Answer (2)  Chronic stage is not seen with hepatitis A and E.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,   pages 964–967.

51. Hep Hepati atitis tis B vaccine vaccine preven prevents: ts:

1. 2. 3. 4.

Hepatitis B Alll hep Al hepat atit itis is fr from om A to to E Hepatitis B and D Hepatitis C

Answer (3)  Hepatitis virus B vaccine can prevent both hepatitis B and D viral infections.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 967.

52. Follow Following ing modes modes of spreading spreading are seen seen in hepatitis hepatitis B, except :

1. 2. 3. 4.

Faeces Blood Sexual Vertical

Answer (1)

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MCQs in Medicine for PG Entrance Examination  Faecal spread is not seen. Hepatitis B, D and C spread mainly through

blood.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 962.

53. Extrah Extrahepatic epatic prodrom prodromal al features features of hepatitis hepatitis B include: include:

1. 2. 3. 4.

Arthralgia Skin rash Poly Po lyar arte teri riti tiss no nodo dosa sa Bleed edin ingg pe per re rectu tum m

Answer (4)  These patients may have serum sickness-like syndrome as a prodromal feature. In children, cervical lymphadenopathy and splenomegaly can occur.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 963.

54. Severe liver liver damage damage in viral hepatitis hepatitis is indicate indicated d by:

1. 2. 3. 4.

Aminotran Aminot ransfe sferas rasee acti activit vityy over over 400 U/L Rais Ra ised ed se seru rum m bil bilir irub ubin in ove overr 5 mg mg Alkali Alk aline ne pho phosph sphata atase se le leve vell below below 250 U/L Prol Pr olon onga gati tion on of of prot prothr hrom ombi bin n time time

Answer (4)  Prolongation of prothrombin time is a feature of diffuse liver damage. It is bad prognostic sign, heralding hepatic encephalopathy.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 963.

55. All of the following following are the features features of post-hepatit post-hepatitis is syndrome, syndrome, except :

1. 2. 3. 4.

Debili Debi lity ty la last stin ingg for for 2– 2–3 3 mon month thss Prolon Pro longe ged d mal malais aise, e, an anore orexia xia,, naus nausea ea Righ Ri ghtt hypo hypoch chon ondr dria iall disc discom omfo fort rt Raised Rais ed biliru bilirubin bin with with raise raised d plasma plasma amino amino-tra -transfe nsferase rase acti activity vity

Answer (4)  There is no clinical or biochemical evidence of liver disease. There is past history of jaundice.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1834.

56. About relapsin relapsing g hepatitis, hepatitis, all statement statements s are true, except :

1. During During recove recovery ry from from viral viral hepat hepatitis, itis, retu return rn of symp symptoms toms and signs signs occur in 5–15% 2. Asy Asymptom mptomatic atic bioch biochemic emical al relap relapses ses with incr increas easee in plas plasma ma aminotransferase activity are even more common 3. Re Relap lapsin singg hepat hepatiti itiss resol resolve vess spont spontane aneous ously ly 4. It imp impli lies es wo wors rsee pro progn gnos osis is Answer (4)

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 Prognostically, it carries no risk. It resolves spontaneously and needs

no treatment.  Ref: Harrison’s Principles of Internal Medicine, 2005,16th Edition, page 1834.

57. System Systemic ic complication complications s of viral hepatitis hepatitis include include all, except :

1. 2. 3. 4.

Aplastic anemia Poly Po lyar arte teri riti tiss no nodo dosa sa Glom Gl omer erul ulon onep ephr hrit itis is Polycythemia

Answer (4)  Polycythemia is not a chronic complication of viral hepatitis. Other systemic complication mentioned are seen in non-A–E hepatitis. Aplastic anemia develops after 1 year from the onset of jaundice. In addition, Henoch-Schönlein purpura and papular acroder-matitis have been reported in children.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 963.

58. Unconjugated Unconjugated hyperbilir hyperbilirubinem ubinemia ia sometimes sometimes found after acute viral hepatitis indicates:

1. 2. 3. 4.

Rela lap psin ingg hep hepati titi tiss Intrah Int rahep epati aticc cho choles lestat tatic ic hep hepati atitis tis PrePr e-ex exis isti ting ng Gilb Gilber ert’ t’ss syndr syndrom omee Chro Ch roni nicc act activ ivee hepa hepati titi tiss

Answer (3)  Unconjugated hyperbilirubinemia or increase in hemoglobinemia with normal liver enzymes is a feature of Gilbert’s syndrome.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 945.

59. All the drugs drugs are to be avoided avoided in viral viral hepatitis, hepatitis, except :

1. 2. 3. 4.

Sedati Seda tive ve an and d hyp hypno noti tics cs Alcohol Chlo Ch loro romy myce ceti tin n and and tetr tetrac acyc ycli line ne Amoxipen

Answer (4)  All drugs are metabolized in liver except amoxipen. Hence, they are avoided.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 973.

60. All of the following following factors are contributo contributory ry to mortality and and poor prognosis in viral hepatitis, except :

1. 2. 3. 4.

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Pre-exist Pre-ex isting ing chr chroni onicc liv liver er dis disea ease se Old age Otherr co-ex Othe co-existin istingg dise disease asess like like car carcinom cinomaa or or lymph lymphoma oma Leve Le vell of of seru serum m alka alkalin linee pho phosph sphat atase ase

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Answer (4)  Extreme age, other chronic debilitating illness and chronic liver disease contribute to higher mortality rate in viral hepatitis.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 986.

61. Mat Match ch the the follo followin wing: g:

1. 2. 3. 4.

Anti-HAV antibodies Anti-Hbs only positive HBsAg, Ig IgM, Ig IgG positive HBsAg+IgM positive

a. b. c. d.

Incubation period of hepatitis B Established viral hepatitis Immunization wi without in infection Hepatitis and transient present. Titres fall within 3 months of  recovery

Answer 1 → d, 2 → c, 3 → b, 4 → a  In hepatitis A, anti-HAV antibody which is IgG type is positive, but it’s level decreases with recovery in 3 months’ time. If a person has no  jaundice but shows HbS antibodies implies that he has been vaccinated with HBsAg vaccine (hepatitis B) in established hepatitis B. HBsAg, IgM and IgG are positive.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,  page 965.

62. Risk group group who needs hepatitis hepatitis B vaccinat vaccination ion includes includes all, except :

1. 2. 3. 4.

Patien Pati entt on ch chro roni nicc hemo hemodi dial alys ysis is Newb Ne wbor orn n of inf infec ecte ted d moth mother er Homosexual ma male Pati Pa tien entt on on ant antii-TB TB dr drug ugss

Answer (4)  In addition to the above risk group, medical/nursing personnel like dentists, surgeons and obstetricians will also need hepatitis B vaccine. In general, all laboratory staff handling blood needs protection.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 967.

63. Regarding Regarding cirrhosis cirrhosis developing developing in chronic chronic hepatitis hepatitis C patients, which which statement is true:

1. 20% dev develo elop p cirr cirrhos hosis is wit within hin 20 ye year arss 2. 50% devel develop op cir cirrho rhosis sis aft after er 30 ye year arss 3. Once cirr cirrhosis hosis deve develops lops on chronic chronic HCV infec infection, tion, rate of  hepatocellular carcinoma is 2–5% per year 4. All of of th the above Answer (4)  All the above statements are true. Further, misuse of alcohol increases the chances of development of cirrhosis and hepatocellular carcinoma.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 968.

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64. Mat Match ch the the foll followi owing: ng:

1. Hepatitis D

a. Post-transfusional hepatitis cause of chronic hepatitis b. Spread by faeco-oral route c. Dane particle contain virus d. Is an RNA defective virus which requires HBV for replication

2. Hepatitis C 3. Hepatitis A 4. Hepatitis B

Answer 1 → d, 2 → a, 3 → b, 4 → c  Hepatitis D has no independent existence. It coexists with hepatitis B. 90% of post-transfusional hepatitis are due to hepatitis C. Faeco-oral route of trans-mission is seen in hepatitis A. There is no chronic carrier state with hepatitis A. Dane particle is virus of hepatitis B. It has chronic carrier state.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,   pages 963–968.

65. Anti-H Anti-HBS BS implies implies in viral viral hepatitis: hepatitis:

1. 2. 3. 4.

Previous Previo us infec infectio tion n – conva convales lesce cenc ncee 3–9 mont months hs Prev Pr evio ious us va vacc ccin inat atio ion n Both 1 and 2 None of th the above

Answer (3)  With previous infection along with anti-HBS, anti-HBC is also present. If anti-HBC is absent, it means previous vaccination.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 965.

66. In serological serological diagnosis diagnosis of hepatitis hepatitis B virus infectio infection, n, which test is not useful:

1. 2. 3. 4.

HBsAg Anti-HBC Anti-HBS HBcAg

Answer (4)  Hepatitis core antigen is not present in blood. It is found in liver. Antibodies to HBcAg is found in blood (anti-HBC).  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 965.

67. In chronic HBV HBV infection, infection, continued continued active replication replication of virus virus in liver is indicated by:

1. 2. 3. 4.

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HBeAg Anti-HBe HBcAg All of of th the above

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Answer (1)  HBC active replication of virus in liver is indicated by HBeAg levels.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 965.

68. Pregna Pregnant nt women with with HEV infection infection are particular particularly ly liable to:

1. 2. 3. 4.

Acutee he Acut hepa pati ticc fa fail ilur uree Cir irrrho hossis of li livver Chro Ch roni nicc act activ ivee hepa hepati titi tiss Recu Re curr rren entt ga gall llst ston ones es

Answer (1)  Pregnant woman with HEV has a risk for developing hepatic encephalopathy which is associated with high mortality (15–25%). However, chronic infection does not occur.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 968.

69. Mal Mallor lory’s y’s hyalin hyaline e is seen in:

1. 2. 3. 4.

Alc lcoh ohol olic ic he hepa pati titi tiss Prim Pr imar aryy bili biliar aryy cirr cirrho hosi siss Vir iraal hep epat atit itis is B None of th the above

Answer (1)  It is an eosinophilic material present in the cytoplasm of hepatocytes.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 970.

70. Acute viral viral hepatitis hepatitis type of histologic histological al picture is seen seen with all of the drugs, except :

1. 2. 3. 4.

Halothane Rifampicin Isoniazid Chlo lorrproma mazzine

Answer (4)  Chlorpromazine produces cholestatic hepatitis.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 973.

71. Macrov Macrovesicul esicular ar steatosis steatosis is seen seen in all, all, except :

1. 2. 3. 4.

Alcohol Obesity Fatt Fa ttyy liv liver er of pr preg egna nanc ncyy Dia iabe bete tess mel elli litu tuss

Answer (3)  In fatty liver of pregnancy microvesicular steatosis is present.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,   pages 971–973.

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72. Rabep Rabeprazole razole has has all the followi following ng advantages advantages,, except :

1. 2. 3. 4.

Leastt ac Leas acti tiva vati tion on ti time me Fast H -K ATPase inhibition After Aft er firs firstt dose, dose, int intrag ragas astri tricc pH beco becomes mes 3–4 Ofte Of ten n it has has man manyy drug drug int inter erac acti tion onss +

+

Answer (4)  Rabeprazole has all these advantages over other proton pump inhibitors. Drug interaction is not present.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 889.

73. Rabeprazole Rabeprazole 20 cc sodium sodium is superior to omeprazole omeprazole and lansopraz lansoprazole ole because it:

1. 2. 3. 4.

Does not Does not inc increa rease se som somato atosta statin tin lev level el Main Ma inta tain inss base baseli line ne mot motil ilin in lev level el Doess not Doe not cause cause any del delay ay in in gastr gastric ic empt emptyin yingg All of of th the above

Answer (4)  It is superior to omeprazole and lansoprazole because of its above effects.  Ref: Journal of Health Sciences, Vol. 51, No. 4, 2005, pages 504, 507.

74. Which of these these NSAIDs has has highest risk risk for GI bleed and perforatio perforation: n:

1. 2. 3. 4.

Piroxicam Indomethacin Ibuprofen Diclofenac

Answer (1)  Highest risk is with piroxicam and lowest risk is with ibuprofen.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition, page 1091.

75. Risk factors factors for for NSAID-indu NSAID-induced ced ulcers ulcers are all, except :

1. 2. 3. 4.

Age ov over 60 60 ye years Past histo history ry of peptic peptic ulce ulcerr or adve adverse rse eve event nt with with NSAI NSAIDs Ds Conc Co ncom omit itan antt cort cortic icos oste tero roid id use use Female ge gender

Answer (4)  There is no gender bias in NSAID-induced side effects. High dose or multiple NSAIDs use can also get ulcer complications. Risk of  gastrointestinal bleeding caused by NSAIDs appears to be dose related.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1755.

76. About NSAID-in NSAID-induced duced GI bleed, bleed, which which statement statement is not true:

1. 1% of of the patie patients nts with rheu rheumatoi matoid d and and osteoa osteoarthri rthritis tis are hospitalized each year because of NSAID-associated GI bleeding

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2. Endoscop Endoscopic ic evide evidence nce of peptic peptic ulce ulcerr is found in 20% 20% of of NSAID NSAID ulcers 3. Ibupr Ibuprofen ofen or diclo diclofena fenacc has has lowe lowerr risk risk of GI GI compli complicati cations ons 4. H -antagonist -antagonistss are effective in preventing GI complications 2

Answer (4)  H2-antagonists are ineffective, and omeprazole or misoprostol can reduce NSAID-induced peptic ulceration.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,  pages 1090, 1091.

77. In elderly elderly people people if NSAIDs NSAIDs are are used, there there is: is:

1. Risk Risk of GI co comp mpli lica cati tion onss 2. Elde Elderly rly with card cardiova iovascul scular ar comorb comorbidity idity often get GI bleed bleed complications with NSAIDs 3. Olde Olderr people people with rena renall or cardi cardiova ovascul scular ar proble problems ms get get periph peripheral eral edema or CCF 4. All of of th the above Answer (4)  GI hemorrhage is a risk with NSAID in elderly, those with cardiovascular and renal disorders. Due to sodium retention, there is peripheral edema.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition, page 1092.

78. Abdom Abdominal inal pain with with rigidity rigidity of abdominal abdominal muscle muscle and back is seen seen in:

1. 2. 3. 4.

Porphyria Lead colic Uremi miaa and and di diaabe bettes Blac Bl ackk Wid Widow ow Sp Spid ider er bi bite te

Answer (4)  Other conditions cause abdominal pain.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 83.

79. ACTH IM injection injection 40–80 40–80 IU in a single single dose 12 hourly × 2 days is effective in:

1. 2. 3. 4.

Acutee pol Acut polya yart rtic icul ular ar go gout ut When Whe n NSAIDs NSAIDs and and colch colchic icine iness are cont contrai raindi ndica cated ted All of of th the above None of th the above

Answer (3)  Short course oral steroid 30–50 mg x 5–7 days or IM ACTH 40–80 IU × BD × 2 days can be used when colchicine or NSAID is not tolerated.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2046.

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80. About afferent afferent loop loop syndrome, syndrome, which which statement statement is not true: true:

1. Occurs Occurs aft after er par partia tiall gas gastri tricc rese resecti ction on 2. Bact Bacterial erial over overgrowt growth h in affer afferent ent limb occur occurss second secondary ary to stasis stasis and leads to abdominal pain, bloating and diarrhea 3. Les Lesss common common affe afferen rentt loop loop syndro syndrome me is with with seve severe re abdomi abdominal nal pain and bloating after 20–60 minutes after meal due to incomplete drainage of bile and pancreatic secretions 4. Ne Needs eds no trea treatme tment nt as it subs subside idess with with tim timee Answer (4)  Antibiotic therapy in bacterial overgrowth, induction of emesis in afferent loop syndrome and surgical revision are needed.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1757.

81. Regard Regarding ing ‘nutcracker’ ‘nutcracker’ esophagus esophagus,, which statement statement is true:

1. There There is extre extremely mely for forcefu cefull peristal peristaltic tic activ activity ity leadin leadingg to episod episodes es of chest pain and dysphagia 2. The There re is no med medica icall trea treatme tment nt av avail ailabl ablee 3. Typ ypee of eso esoph phag agea eall mali malign gnan ancy cy 4. None of th the above Answer (1)  ‘Nutcracker’ esophagus is a term given to diffuse esophagus spasms. It is seen in elderly and leads to dysphagia and chest pain. Nitrates and nifedipine are useful in such conditions. It needs to be differentiated from esophageal malignancy.  Ref: Davidson’s Principles & Practice of Medicine, 2006, 20 th Edition, page 882.

82. Earliest Earliest phenotypic manifestation manifestation of idiopathic hereditary hereditary hemochromatosis includes:

1. 2. 3. 4.

Post-pran Post-p randia diall rise rise in ser serum um iro iron n lev levels els Elev El evat ated ed se seru rum m fer ferri riti tin n Slat Sl atee gre greyy pig pigme ment ntat atio ion n of of ski skin n Incr In crea ease se tra trans nsfe ferr rrin in sat satur urat atio ion n

Answer (3) pigmentation is is seen in in 90% of the symptomatic  Excessive skin pigmentation patients. Options 1, 2 and 4 are biochemical changes.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2301.

83. Gluten sensitive sensitive enteropathy enteropathy (coeliac (coeliac sprue) sprue) is associated associated with positive: positive:

1. 2. 3. 4.

Anti-e Anti -end ndom omys ysia iall an anti tibo body dy Anti An ti-h -his isto tone ne an anti tibo body dy Anti An ti-s -smo moot oth h mu musc scle le an anti tibo body dy Anti An ti-m -mit itoc ocho hond ndri rial al an anti tibo bodi dies es

Answer (1)

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MCQs in Medicine for PG Entrance Examination  In drug-induced SLE, anti-histone antibody is positive. In primary

biliary cirrhosis, mitochondrial antibody is positive and in autoimmune hepatitis, smooth muscle antibody is positive.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 1986, 1961.

84. Ratio of AST/ALT AST/ALT > 1 is presen presentt in:

1. 2. 3. 4.

Non-alcoh Non-al coholi olicc ste steato atohep hepat atiti itiss (NA (NASH SH)) Alc lcoh ohol olic ic cir cirrrho hossis Wils lson on’’s di dissease All of of th the above

Answer (2)  In NASH, ALT > AST.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 16, 1815, 1857.

85. Caroli Caroli’s ’s disease disease has which which of these these features: features:

1. 2. 3. 4.

There is multi There multiple ple cys cystic tic dilat dilatatio ation n of intra intrahepa hepatic tic bilia biliary ry tree tree Ther Th eree is is iro iron n ove overl rloa oad d in in liv liver er Leads Le ads to porta portall hyper hyperte tensi nsion on with with hemat hemateme emesis sis All of of th the above

Answer (1)  In Caroli’s disease, multiple cystic dilatation of intrahepatic biliary tree occurs. Eventually, infection and fibrosis occur. Liver transplantation is indicated in end-stage disease.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1873.

86.. Ab 86 Abse senc nce e of Helicobacter pylori  and obesity both contribute to:

1. 2. 3. 4.

Increase Increa sed d damag damagee with with gastro gastro-es -esoph ophag agea eall reflux reflux Higher Hig her inc incide idence nce of Barr Barrett ett’’s esop esophag hagus us Esop Es opha hage geal al ad aden enoc ocar arci cino noma ma All of of th the above

Answer (4)  In Barrett’s esophagus, esophageal adenocarcinoma and GERD,  H.  pylori absence and obesity have contributory roles.  Ref: JAPI, Vol. 55, June 2007, page 435.

87. Uncom Uncommon mon causes causes of mass in left left iliac fossa fossa include include all, except :

1. 2. 3. 4.

Mob obil ilee ov ovari riaan cy cyst Retr Re trop oper erit iton onea eall tum tumou ourr Mali Ma lign gnan antt und undes esce cend nded ed te test stes es Carcino noma ma caecum

Answer (4)

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 Carcinoma caecum will cause a mass in right iliac fossa and caecum

is a fixed structure.  Ref: Peter J. Toghil, Examining Patient, Introduction to Clinical Medicine,  2nd Edition, ECBS, page 96.

88. Regard Regarding ing stress-related stress-related mucosal mucosal injury, which statement statement is incorrect: incorrect:

1. Cont Contai ain n inf infla lamm mmat atio ion n or or H. pylori  2. Ele Eleva vated ted ga gastr stric ic acid acid se secr creti etion on obs observ erved ed 3. Cush Cushing’ ing’ss ulcer ulcer is a name name given given to to gastric gastric ulce ulcerr developi developing ng after after head trauma 4. Cur Curlin ling’ g’ss ulcer ulcer is see seen n after after se sever veree burns burns Answer (1)  Both Curling’s ulcer and Cushing’s ulcer are stress related. There is no inflammation or mucosal injury.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1760.

89. About Hermansk Hermansky y Pudlak syndrome, syndrome, which which statement statement is incorrect: incorrect:

1. 2. 3. 4.

Autoso Auto soma mall rec reces essi sive ve di diso sord rder er Theree is Ther is granu granulomat lomatous ous coli colitis tis with inte interstit rstitial ial lung dise disease ase Ther Th eree is ocu oculo locu cuta tane neou ouss albi albini nism sm Usually Usua lly,, there there is tend tendency ency for rec recurre urrent nt throm thrombosi bosiss

Answer (4)  There is platelet dysfunction which leads to bleeding diathesis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1560.

90. Hyperg Hypergastrine astrinemia mia with hypoch hypochlorhyd lorhydria ria is seen in: in:

1. 2. 3. 4.

Zollin Zoll inge gerr Ell Ellis ison on’’s syn syndr drom omee Vipoma Pern rnic icio iou us ane nem mia Glucagonoma

Answer (3)  Due to atrophic gastritis, there is hyperchlorhydria, which is pentagastrin achlorhydria. In other options, there is hyperchlorhydria with hypergastrinemia.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 604.

91. Anti-L Anti-LKM KM antibodi antibodies es are seen in in all, except :

1. 2. 3. 4.

Hepatitis C and D Drug Dr ug-i -ind nduc uced ed he hepa pati titi tiss Typ ypee-2 2 auto autoim immu mune ne hep hepat atit itis is Prim Pr imar aryy bili biliar aryy cirr cirrho hosi siss

Answer (4)

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MCQs in Medicine for PG Entrance Examination  Antibodies against liver-kidney microsomes are seen in hepatitis C, D,

drug-induced hepatitis and type-2 autoimmune hepatitis. However, they are absent in primary biliary cirrhosis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1828.

92. In hemochromat hemochromatosis, osis, daily daily mucosal absorpti absorption on of iron is:

1. 2. 3. 4.

1 mg/dL 1–5 mg/dL 4 mg/dL None of th the above

Answer (3)  It is 4 mg or more.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2298.

93. Body iron iron content content of a healthy adult adult is maintaine maintained d around: around:

1. 2. 3. 4.

3–4 g 20 g 5g None of th the above

Answer (1)  Iron absorption by mucosal block occurs as per the need, and body iron content remains around 3–4 g.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2298.

94. Princi Principle ple causes causes of death in hemochroma hemochromatosis tosis include include all, except :

1. 2. 3. 4.

CCF Por orta tall hyp hypert rteens nsio ion n Hepa He pato toce cell llul ular ar ca carc rcin inom omaa Malabsorption

Answer (4)  Malabsorption does not occur, and is not a cause of mortality.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2298.

95. Removal of excessive iron by by therapeutic modalities modalities hemochromatosis improves all complications, except :

1. 2. 3. 4.

in

CCF Pigmentation Dia iabe bete tess mel elli litu tuss Hypo Hy pogo gona nadi dism sm an and d art arthr hrop opat athy hy

Answer (4)  Complications like hypogonadism and arthropathy do not improve even after phlebotomies and chelating agent therapy.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2298.

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96. Drugs causing causing malabsorptio malabsorption n by sequestrating sequestrating or precipitating precipitating bile salts are all, except :

1. 2. 3. 4.

Neomycin Calc lciu ium m carb rbon onaate Chole lesstyramin inee Penicillamine

Answer (4)  Penicillamine does not cause bile salt deficiency-induced malabsorption.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1965.

97. Most common common cause cause of diarrhea diarrhea in AIDS patient patient is:

1. 2. 3. 4.

Kaposii sa Kapos sarc rcoma oma aff affec ectin tingg int intest estine ine Amoebic colitis Ulc lceera rati tivve col colit itis is Tub ubeercu cula larr abd abdom omen en

Answer (1)  Intestinal lesion due to Kaposi sarcoma is the most common cause of  AIDS diarrhea.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1110.

98. Which of the dermatological disorder is not associated with malabsorption:

1. 2. 3. 4.

Psoriasis Ecze Ec zema mato toid id de derm rmat atit itis is Derm De rmat atit itis is he herp rpet etif ifor orm m Lupus vulgaris

Answer (4)  Lupus vulgaris is a skin lesion that occurs due to TB and is not

associated with malabsorption.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 1770, 1771.

99. Which one of the the disorder is protein-l protein-loosing oosing enteropa enteropathy: thy:

1. 2. 3. 4.

Ménétr Méné trie ier’ r’ss di dise seas asee Irri Ir rita tabl blee bow bowel el syn syndr drom omee Amoebic colitis All of of th the above

Answer (1)  Hypoproteinemia occurs in Ménétrier’s disease.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1775.

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100. Pseud Pseudomemb omembranou ranous s colitis colitis is due to: to:

1. 2. 3. 4.

Clostridium difficile  Shigella infection Campylobacter  infection E. coli 

Answer (1)  Cl. difficile is an obligatory Gram-positive and spore-forming anaerobe.

The most common antibiotics associated with diarrhea are clindamycin, ampicillin and cephalosporin.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 760.

101. Risk of carcinoma carcinoma of of colon in ulcerativ ulcerative e colitis colitis is:

1. 2. 3. 4.

0.5–1% per 0.5–1% per year year afte afterr 10 years years of diag diagnos nosis is of dise diseas asee 0.5% 0.5 % per per ye year ar fro from m the the tim timee of of dia diagno gnosis sis 2% ri risk sk fr from om the the ti time me of dia diagn gnos osis is None of th the above

Answer (1)  The risk is 0.5–1% per year after 10 years of diagnosis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1731.

102. Hepati Hepatic c manifestation manifestations s of ulcerative ulcerative colitis colitis include all, all, except :

1. 2. 3. 4.

Cholan Chol anggio ioca carc rcin inom omaa Autoim Aut oimmun munee ch chron ronic ic act active ive he hepat patiti itiss Peric ich hola lan ngitis Hepatoma

Answer (4)  Hepatoma is not a complication of ulcerative colitis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1784.

103.. Meg 103 Megaco acolon lon is due to to all, all, except :

1. 2. 3. 4.

Tox oxic ic meg megac acolo olon n in ulc ulcera erativ tivee coli colitis tis Hirs Hi rsch chsp spru rung ng’’s di dise seas asee Chagas disease Amoebic colitis

Answer (4)  Amoebic colitis is not a usual cause of toxic megacolon.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 1216, 1217.

104. Acute fulminant fulminant ischemic ischemic colitis colitis clinically clinically presents presents with all, except :

1. Seve Severe re lo lowe werr abd abdom omin inal al pa pain in 2. Rectal bl bleeding

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3. Hypotension 4. Thumb pr printing Answer (4)  This is a radiological sign that occurs due to submucosal hemorrhage and edema. It is seen in KUB in chronic ischemic colitis.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 226, 227.

105. Anti-m Anti-mitocho itochondrial ndrial antibod antibody y is positive positive in:

1. 2. 3. 4.

Primar Prim aryy bili biliar aryy cirr cirrho hosi siss Auto Au toim immu mune ne he hepa pati titi tiss Prim Pr imar aryy scl scler eros osin ingg hep hepat atit itis is Portal ci cirrhosis

Answer (1)  In primary biliary cirrhosis, AMA is positive.  Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition,  pages 1860, 1861.

106. In melanosis melanosis coli, coli, which stateme statement nt is not true: true:

1. Brown Brown or or black black pigm pigment entati ation on of colon colonic ic mucos mucosaa occurs occurs 2. It o occurs ccurs in patien patients ts who chron chronically ically take anthra anthracene cene catha cathartics rtics and APGAR after 4–6 months 3. Pigm Pigment ent dist distribut ribution ion is see seen n in cae caecum cum and prox proximal imal colo colon n 4. It is a pre prema mali lign gnan antt con condi diti tion on Answer (4)  Melanosis coli is not a premalignant condition.  Ref: JAPI, Vol. 54, July 2006, page 548.

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