4 Git Liver Mcqs

GIT, Liver4

DIRECTIONS: Each of the numbered items or incomplete statements is followed mostlyby four choices. Select the best possible answer to each case. Correct answer is displayedwith a brief explanation � and reference after every question.

1. What is Schatzki ring:

1. Mid-esophageal web2. Hypopharyngeal web3. Lower esophageal mucosal ring4. None of the above

Answer (3)� Lower esophageal mucosal ring (Schatzki ring) is a thin web-like

constriction located in squamocolumnar mucosal junction at or nearborder of LES. When the lumen diameter is less than 1.3 cm, it causesdysphagia to solid foods, and is episodic. Asymptomatic rings may bepresent in 10% of the normal individuals. Low esophageal muscularring (contractile ring) is located proximal to site of mucosal ring. Itrepresents uppermost segment of the lower esophageal sphincter.Schatzki ring responds to dilatation unlike lower esophageal muscularring that does not respond to dilatation.

Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1745.

2. Triple therapy for eradication of H. pylori includes all, except:

1. Omeprazole 20 mg BD2. Clarithromycin 500 mg BD3. Metronidazole 500 mg BD4. Sucralfate

Answer (4)

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� Regimen recommended for eradication of H. pylori infection:

Triple therapy Dosage

1. Bismuth subsalicylate plus 2 tab qidmetronidazole plus 250 mg qidtetracycline 500 mg qid

2. Ranitidine bismuth citrate plus 400 mg bidtetracycline plus clarithromycin 500 mg bidor metronidazole 500 mg bid

3. Omeprazole (lansoprazole) plus 20 mg bid (30 mg bid)Clarithromycin plus 250 or 500 mg bidMetronidazole or 500 mg bidAmoxicillin 1 gm bid


3. Cushing’s ulcers are seen in:

1. Cushing’s disease2. After aspirin therapy3. Acute upper GI ulcers associated with intracra-nial injury or with

increased intracranial pressure4. 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 ofstomach. Mucosal ischemia and breakdown of normal protective barrierplay an important role in pathogenesis of ulcer in addition tohyperchlorhydria. Curling’s ulcer occurs in patients with severe burns.


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

1. Hypoglycemia2. Hyperosmolar gastric content when emptying into small bowel3. Due to post vagotomy4. All of 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 dumpingoccurs in 15–30 minutes after food intake. Crampy abdominaldiscomfort, nausea, diarrhea, belching, tachycardia, palpitation,diaphoresis and rarely syncope occur. The late phase of dumping

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154 MCQs in Medicine for PG Entrance Examination

typically occurs from 90 minutes to 3 hours after meals. It is thoughtto be secondary to hypoglycemia from excessive insulin release.


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

1. Old age2. High dose, protracted use and combination of NSAID and

glucocorticoids3. Severe intercurrent illness4. Intake of hot drinks

Answer (4)� Risk factors for upper gastrointestinal adverse events in patients taking

NSAIDs:

Increasing age History of upper GI bleedingComorbidity AnticoagulationOral glucocorticoids Combination of NSAIDs therapyHistory of peptic ulcer Increasing dose of NSAIDs.


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

1. Head of pancreas2. Tail of pancreas3. Duodenum4. 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.


7. Bile salts and Vitamin B12 are absorbed from:

1. Proximal intestine2. Mid-intestine3. Distal small intestine4. Caecum

Answer (3)� The site of absorption of nutrients in intestine is as follows:1. Duodenum: Iron, calcium, folate.2. Ileum: Vitamin B

12, bile acids.

3. Colon: Water absorption.

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4. Small bowel: Proximal > distal glucose, amino acids, lipids.Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 1764.

8. Absorption of water and electrolytes occurs mainly at:

1. Jejunum2. Caecum3. Rectum4. Duodenum

Answer (2)� Water absorption occurs in caecum and colon. Short chain fatty acids

are absorbed in colon, and stimulate colonic sodium and fluidabsorption. In antibiotic-induced diarrhea, there is decreased SCFA.


9. Monoglycerides and fatty acids are absorbed from:

1. Proximal intestine2. Ileum3. Colon4. 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 entering liver via portal vein are catabolized tourea, except:

1. Leucine2. Isoleucine3. Valine4. Tryptophan

Answer (4)� These amino acids have important role in the glucose alanine cycle.


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

1. Chemical modification of drug by oxidation, reduction,hydroxylation, sulfoxidation, deami-nation, dealkylation andmethylation

2. Involve enzymes like P450, cytochrome P5, oxidase andglutathione S, acyltransferase

3. Leads to inactivation of drugs like benzodiaze-pine, but activationof drug like cortisone to cortisol

4. All of 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. Inphase II, specific endogenous compounds conjugate to the phase 1metabolites. In phase I, there is oxidation accomplished by cytochromeP450 of CYP family. Phase II reaction is accomplished by glucuronyl,acetyl, sulfo and methyltransferase enzymes.


12. Phase II reaction during metabolism in liver involves:

1. Converting lipophilic substances to water soluble substances2. Formation of glucuronides by conjugation3. Both (1) and (2)4. None of the above

Answer (3)� During metabolism, most drugs after absorption reach liver. Phase I

results in more polar metabolites that are more readily excreted. Inphase II, specific endogenous compounds conjugate to the phase 1metabolites. In phase I, there is oxidation accomplished by cytochromeP450 of CYP family. Phase II reaction is accomplished by glucuronyl,acetyl, sulfo and methyltransferase enzymes.


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

1. Recurs during pregnancy in third trimester2. Subsides within 7–14 days after delivery3. There is an increased sensitivity to hepatic effects of estrogen and

progesterone4. Seen often in elderly multipara

Answer (4)� This is precipitated by oral contraceptives. Itching and steatorrhea can

occur. Pregnant women with intrahepatic cholestasis have increased riskof premature delivery, fetal distress during delivery and still birth. 60–70% of the affected individuals develop cholestasis during subsequentpregnancy.

Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition, page 987.

14. Nutmeg liver is seen in:

1. Budd-Chiari syndrome2. Cardiac cirrhosis3. Biliary cirrhosis4. 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 congestionof liver. Prolong congestion leads to centrilobular hepatic necrosis.Gross examination of liver shows alternating red (congested) and palefibrotic areas, a pathological appearance known as nutmeg liver.


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

1. Polycythemia rubra vera2. Myeloproliferative syndrome3. Paroxysmal nocturnal hemoglobinuria4. Arsenical toxicity

Answer (4)� In addition, it can be seen in other hypercoagulable states,

idiopathic membranous obstruction of IVC, invasion of IVC by renalcell or primary hepatocellular carcinoma. It is not seen with chronicarsenical toxicity.

Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th edition,

pages 982, 983.

16. In recurrent spontaneous bacterial peritonitis, prophylactic antibiotictherapy of choice is all, except:

1. Norflox 400 mg/day2. Trimethoprim + sulphamethazole combination 500 mg a week3. Ciprofloxacin 750 mg once a week4. Doxycycline

Answer (4)� Primary (spontaneous) bacterial peritonitis has a high rate of recurrence

(up to 70% experience recurrence in 1 year). Antibiotic prophylaxisreduces relapse rate to 20%. Doxycycline is not the drug of choice.Norflox, ciprofloxacin and bacterium are used. However, long-term useof the antibiotics leads to resistance and severe hospital-acquiredstaphylo-coccal infection.Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 750.

17. Asterixis in hepatic encephalopathy is present in:

1. Grade IV2. Grade I3. Grade II4. All of the above

Answer (3)

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� Asterixis or flapping tremor is seen in uremia, hepatic coma and corpulmonale stage 2 and stage 3. They are seen in hepatic encephalopathy.In deep coma with hepatic encephalopathy, the flapping tremorsdisappear.

Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th edition, page 950.

18. Microvesicular hepatic steatosis is seen in all, except:

1. Rey’s syndrome2. Acute fatty liver of pregnancy3. Valproic acid therapy4. Alcoholic liver disease

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. Macrovesicular hepatic steatosis is seen in all, except:

1. Alcoholic liver disease2. Diabetes mellitus3. Obesity4. Rey’s syndrome

Answer (4)� In addition, drugs like glucocorticoids, amiodarone, estrogen and

methotrexate can cause fatty liver. Total parenteral nutrition, protein-caloric malnutrition and jejunoileal bypass can cause these changes inliver. Rey’s syndrome causes microvascular hepatic steatosis.


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

1. Ascites occurs in all cases2. Jaundice is always present3. Hypoalbuminuria with elevated alkaline phosphatase4. Portal hypertension is common

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. Pleural fluid amylase elevation occurs in all, except:

1. Acute pancreatitis2. Chronic pancreatitis3. Esophageal perforation4. Intestinal obstruction

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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 pleuraleffusion. In such a situation, pleural fluid amylase is increased. Bothchronic pancreatitis and esophageal perforation can also cause left sidedpleural effusion.


22. Ranson/imrie prognostic criterion is used in:

1. Acute pancreatitis2. Acute fulminant ulcerative colitis3. Hepatic encephalopathy4. Acute renal failure

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. Pancreatic ascites is due to all, except:

1. Pseudocyst leaking into peritoneal cavity2. Disruption of pancreatic duct and fistula between duct and

peritoneal cavity3. Acute pancreatitis4. Secondary to tubercular infection

Answer (4)� Pancreatic ascites is due to leaking pseudocyst or fistula between

pancreatic duct and peritoneal cavity. Diagnosis is made in an inpatientwho has ascites with elevated serum amylase, increased albumin (over<5 g) and serum amylase (over 20,000 U/L).


24. Diagnostic features of pancreatic ascites are:

1. Increased albumin >3.0 g/dL and elevated amylase >20,000 IUin ascitic fluid

2. Increase polymorphs in ascites3. Increased LDH level4. All of the above

Answer (1)� Pancreatic ascites is due to leaking pseudocyst or fistula between

pancreatic duct and peritoneal cavity. Diagnosis is made in an inpatientwho has ascites with elevated serum amylase, increased albumin (over<5 g) and serum amylase (over 20,000 U/L).


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25. Complications of chronic pancreatitis include all, except:

1. Vitamin B12

malabsorption2. Impaired GTT3. Pleural effusion4. Folate malabsorption

Answer (4)� Folate malabsorption is not the complication of chronic pancreatitis.


26. In hepatitis E, mortality is maximum in:

1. Pregnant women2. In all women3. Adolescent4. Infant

Answer (1)� Pregnancy with jaundice is due to hepatitis E, and it carries morbidity.

Ref: Anantnarayan, 6th Edition, page 519.

27. Purtscher’s retinopathy is a complication of:

1. Hypertension2. Type-2 DM3. Pancreatitis4. Wilson’s disease

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 spotsand hemorrhages confined to area of optic disc and macula. It is dueto occlusion of posterior retinal artery with aggregated granulocytes.


28. Diloxanide furoate is not useful in:

1. Extraintestinal amoebiasis2. Cyst passers3. Interstitial amoebiasis4. All of 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 oncysts and trophozoites close to the mucosa. Paromomycin andiodoquinol are luminal amoebicidal. Tissue amoebicidal reaches highconcentration in blood and tissues after oral or parenteraladministration, e.g. metronidazole, tinidazole and ornidazole.


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29. All causes unconjugated hyperbilirubinemia, except:

1. Large hematoma2. Hemolytic anemia3. Megaloblastic anemia4. Rotor’s syndrome

Answer (4)� In Rotor’s syndrome, there is conjugated hyperbiliru-binemia. It is

benign autosomal recessive disorder. Liver has no increasedpigmentation. Another cause of congenital hyperbilirubinemia is DubinJohnson syndrome, which can be differentiated as below:

S. No. Dubin Johnson Rotor

1. Liver pigmented Yes No2. GB visualization No Yes3. Urinary coproporphyrin Normal Increased

excretion4. BSP excretion Delayed and Delayed

reflux back to plasmacirculation clearance


30. Prognostic marker of acute liver failure is:

1. AST2. Factor V levels3. Serum bilirubin4. Prothrombin 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. Sclerosant agents used for endoscopic sclerotherapy are all, except:1. Acetic acid2. Alcohol3. Cyanoacrylate4. Podocyanolate

Answer (1)� Acetic acid is not a sclerosing agent.


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

1. Anti-secretory activity2. Promotes intestinal absorption

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3. Both 1 and 24. Mechanism of action is unknown

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 tuberculosis, which one of the test denoteshepatic involvement:

1. Raised ESR2. Exudative ascitic fluid3. Raised serum alkaline phosphatase4. Elevated acid phosphatase

Answer (3)� Alkaline phosphatase is distributed in bone, RBC and placenta. It is

localized in liver in sinusoidal and biliary canaliculi and gastrointestinaltract. In obstructive jaundice, hepatic metastasis and hepatic granuloma,the enzyme is increased. It is also increased in bone disease like Paget’sdisease, osteomalacia, renal osteodystrophy and primaryhyperparathyroidism. In osteoporosis, alkaline phosphatase level is notincreased.


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

Liver disease Test

1. Hematochromatosis a. Serum ceruloplasmin, serum urine and livercopper estimation

2. Primary biliary cirrhosis b. Serum immunoglobulin, serum anti-nuclearfactor and smooth muscle and liver, kidney,microsomal antibodies

3. Autoimmune chronic c. Serum ferritin, serum iron and iron binding

active hepatitis capacity, saturation, PCR for genetic defect

4. Wilson’s disease 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 bepositive in primary biliary cirrhosis. Alkaline phosphatase will bemarkedly increased along with AMA positivity. Wilson’s disease is dueto copper overload and deficient serum ceruloplasmin level.


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35. Match the following:

Classification of portalhypertension Examples of disease

A. Extrahepatic sinusoidal 1. Veno-occlusive disease

B. Intrahepatic sinusoidal 2. Cirrhosis of liver

C. Sinusoidal 3. Budd-Chiari syndrome

D. Extrahepatic presinusoidal 4. 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 veinthrombosis is frequent. Schistosomiasis (intrahepatic presinusoidal) isinfrequent outside endemic areas.

Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,

page 958.

36. Which is not the complication of portal hypertension:

1. Renal failure2. Hypersplenism3. Ascites and hepatic encephalopathy4. Pancreatitis

Answer (4)� UGI bleeding is common. Effect of hypersplenism is seen. Renal failure

and hepatic encephalopathy with ascites can develop. Pancreatitis isnot a complication for portal hypertension.


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

1. Cirrhosis of liver2. Portal vein thrombosis3. Schistosomiasis4. Budd-Chiari syndrome

Answer (1)� Main cause of portal hypertension is cirrhosis developing secondary

to nutritional deficiency leading to fatty liver and cirrhosis. Alcoholand type B hepatitis also contribute to cirrhosis.


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

1. Somatostatin (octreotide)2. Propranolol3. Vasopressin4. Terlipressin

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

hypertension in long-standing cases of cirrhosis with portalhypertension. It is not useful in acute GI bleeding.


39. About TIPS (transjugular intrahepatic portosystemic stent shunt), whichstatement is true:

1. Stent is placed between portal vein and hepatic vein to reduceportal hypertension

2. Hepatic encephalopathy may occur following shunt3. Used for acute UGI bleeding which is not responding to

sclerotherapy or banding or pharmacological treatment4. All of the above

Answer (4)� Emergency portosystemic shunt carries mortality over 50%. Hence, it

is not done. The procedure is done under radiological control via theinternal jugular veins. Prior patency of portal vein must be determinedangiographically. Coagulation deficiency required correction with freshfrozen plasma and antibiotic cover is provided.


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

1. Nephrotic syndrome2. Protein loosing enteropathy3. Malnutrition4. Abdominal tuberculosis

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 can be found in about 10% of the patients havingascites:

1. Seen on right side only2. Seen on left side only3. It is always bilateral4. None of 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 dueto ascites.


42. LeVeen shunt is used in:

1. Resistant ascites2. Hydrocephalous3. ASD4. 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.


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

1. Infection2. Superior vena caval thrombosis3. Pulmonary bleeding4. Paraplegia

Answer (4)� Complications include infection, SVC thrombosis, pulmonary edema,

bleeding varices from esophagus and disseminated intravascularcoagulopathy. Paraplegia is not a complication of LeVeen shunt.


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

1. TIPPS2. LeVeen shunt3. Porta caval anastomosis4. Propranolol therapy

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

help. Other surgical therapies like TIPPS, LeVeen shunt and portocavalanastomosis are to be considered.


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

1. Abdominal pain and fever in a cirrhotic patient2. Absent bowel sound and rebound tenderness and hepatic

encephalopathy

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3. Diagnostic paracentesis, presence of cloudy fluid, neutrophil count>250/mm

4. Response to broad-spectrum antibiotics like cefotaxime 2 g given12 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 ofover 250/mm in ascitic fluid. If multiple organisms are grown in asciticfluid, it indicates bowel perforation.


46. Regarding lactulose in hepatic encephalopathy all are true, except:

1. Orally given and acts on colonic bacteria in colon2. Dose started as 15–30 ml 8 hourly and increased so as to produce

2 bowel movements3. It has osmotic laxative effect that reduces colonic bacteria, limit

colon absorption of ammonia and promotes incorporation ofnitrogenous bacteria

4. Lactose also acts as lactulose in hepatic encephalopathy

Answer (4)� Lactulose will be absorbed and will neither act locally on colonic

bacteria nor it can prevent ammonia absorption. Only in those caseswith lactose intolerance where lactulose will not be absorbed, actionseen with lactulose is possible.


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

1. Hepatopulmonary syndrome2. Hepatorenal syndrome3. Spontaneous bacterial peritonitis4. Ascites

Answer (4)� Complications like hepatorenal syndrome, hepato-pulmonary syndrome

and spontaneous bacterial peritonitis are of poor prognosis in cirrhosisof liver.


pages 949, 950.

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

1. 50% of cases2. 1–2% of cases3. 10% of cases4. None of 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 viralhepatitis.


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

1. Cytomegalovirus2. Influenza virus3. Epstein Barr virus4. Yellow fever virus

Answer (2)� Influenza virus does not cause hepatitis. However, Herpes simplex virus

can cause hepatitis.Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition, page 969.

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

1. Hepatitis B and C2. Hepatitis A and E3. Hepatitis C and D4. Hepatitis B and D

Answer (2)� Chronic stage is not seen with hepatitis A and E.


pages 964–967.

51. Hepatitis B vaccine prevents:

1. Hepatitis B2. All hepatitis from A to E3. Hepatitis B and D4. 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, 20th Edition, page 967.

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

1. Faeces2. Blood3. Sexual4. Vertical

Answer (1)

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� Faecal spread is not seen. Hepatitis B, D and C spread mainly throughblood.


53. Extrahepatic prodromal features of hepatitis B include:

1. Arthralgia2. Skin rash3. Polyarteritis nodosa4. Bleeding per rectum

Answer (4)� These patients may have serum sickness-like syndrome as a prodromal

feature. In children, cervical lymphadenopathy and splenomegaly canoccur.


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

1. Aminotransferase activity over 400 U/L2. Raised serum bilirubin over 5 mg3. Alkaline phosphatase level below 250 U/L4. Prolongation of prothrombin 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, 20th Edition, page 963.

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

1. Debility lasting for 2–3 months2. Prolonged malaise, anorexia, nausea3. Right hypochondrial discomfort4. Raised bilirubin with raised plasma amino-transferase activity

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 relapsing hepatitis, all statements are true, except:

1. During recovery from viral hepatitis, return of symptoms and signsoccur in 5–15%

2. Asymptomatic biochemical relapses with increase in plasmaaminotransferase activity are even more common

3. Relapsing hepatitis resolves spontaneously4. It implies worse prognosis

Answer (4)

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� Prognostically, it carries no risk. It resolves spontaneously and needsno treatment.

Ref: Harrison’s Principles of Internal Medicine, 2005,16th Edition, page 1834.

57. Systemic complications of viral hepatitis include all, except:

1. Aplastic anemia2. Polyarteritis nodosa3. Glomerulonephritis4. 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. Inaddition, Henoch-Schönlein purpura and papular acroder-matitis havebeen reported in children.


58. Unconjugated hyperbilirubinemia sometimes found after acute viralhepatitis indicates:

1. Relapsing hepatitis2. Intrahepatic cholestatic hepatitis3. Pre-existing Gilbert’s syndrome4. Chronic active hepatitis

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, 20th Edition, page 945.

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

1. Sedative and hypnotics2. Alcohol3. Chloromycetin and tetracycline4. Amoxipen

Answer (4)� All drugs are metabolized in liver except amoxipen. Hence, they are

avoided.Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition, page 973.

60. All of the following factors are contributory to mortality and poorprognosis in viral hepatitis, except:

1. Pre-existing chronic liver disease2. Old age3. Other co-existing diseases like carcinoma or lymphoma4. Level of serum alkaline phosphatase

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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, 20th Edition, page 986.


1. Anti-HAV antibodies a. Incubation period of hepatitis B

2. Anti-Hbs only positive b. Established viral hepatitis

3. HBsAg, IgM, IgG positive c. Immunization without infection

4. HBsAg+IgM positive d. Hepatitis and transient present.Titres fall within 3 months ofrecovery

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 nojaundice but shows HbS antibodies implies that he has been vaccinatedwith 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 who needs hepatitis B vaccination includes all, except:

1. Patient on chronic hemodialysis2. Newborn of infected mother3. Homosexual male4. Patient on anti-TB drugs

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.


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

1. 20% develop cirrhosis within 20 years2. 50% develop cirrhosis after 30 years3. Once cirrhosis develops on chronic HCV infection, rate of

hepatocellular carcinoma is 2–5% per year4. All of 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, 20th Edition, page 968.

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1. Hepatitis D a. Post-transfusional hepatitiscause of chronic hepatitis

2. Hepatitis C b. Spread by faeco-oral route

3. Hepatitis A c. Dane particle contain virus

4. Hepatitis B d. Is an RNA defective virus whichrequires HBV for replication

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-oralroute of trans-mission is seen in hepatitis A. There is no chronic carrierstate with hepatitis A. Dane particle is virus of hepatitis B. It has chroniccarrier state.

Ref: Davidson’s Principles & Practice of Medicine, 2006, 20th Edition,pages 963–968.

65. Anti-HBS implies in viral hepatitis:

1. Previous infection – convalescence 3–9 months2. Previous vaccination3. Both 1 and 24. None of 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, 20th Edition, page 965.

66. In serological diagnosis of hepatitis B virus infection, which test is notuseful:

1. HBsAg2. Anti-HBC3. Anti-HBS4. 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, 20th Edition, page 965.

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

1. HBeAg2. Anti-HBe3. HBcAg4. All of the above

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Answer (1)� HBC active replication of virus in liver is indicated by HBeAg levels.


68. Pregnant women with HEV infection are particularly liable to:

1. Acute hepatic failure2. Cirrhosis of liver3. Chronic active hepatitis4. Recurrent gallstones

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.


69. Mallory’s hyaline is seen in:

1. Alcoholic hepatitis2. Primary biliary cirrhosis3. Viral hepatitis B4. None of the above

Answer (1)� It is an eosinophilic material present in the cytoplasm of hepatocytes.


70. Acute viral hepatitis type of histological picture is seen with all of thedrugs, except:

1. Halothane2. Rifampicin3. Isoniazid4. Chlorpromazine

Answer (4)� Chlorpromazine produces cholestatic hepatitis.


71. Macrovesicular steatosis is seen in all, except:

1. Alcohol2. Obesity3. Fatty liver of pregnancy4. Diabetes mellitus

Answer (3)� In fatty liver of pregnancy microvesicular steatosis is present.


pages 971–973.

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173GIT, Liver

72. Rabeprazole has all the following advantages, except:

1. Least activation time2. Fast H+-K+ ATPase inhibition3. After first dose, intragastric pH becomes 3–44. Often it has many drug interactions

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, 20th Edition, page 889.

73. Rabeprazole 20 cc sodium is superior to omeprazole and lansoprazolebecause it:

1. Does not increase somatostatin level2. Maintains baseline motilin level3. Does not cause any delay in gastric emptying4. All of 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 NSAIDs has highest risk for GI bleed and perforation:

1. Piroxicam2. Indomethacin3. Ibuprofen4. Diclofenac

Answer (1)� Highest risk is with piroxicam and lowest risk is with ibuprofen.


75. Risk factors for NSAID-induced ulcers are all, except:1. Age over 60 years2. Past history of peptic ulcer or adverse event with NSAIDs3. Concomitant corticosteroid use4. Female 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 ofgastrointestinal bleeding caused by NSAIDs appears to be dose related.


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

1. 1% of the patients with rheumatoid and osteoarthritis arehospitalized each year because of NSAID-associated GI bleeding

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2. Endoscopic evidence of peptic ulcer is found in 20% of NSAIDulcers

3. Ibuprofen or diclofenac has lower risk of GI complications4. H

2-antagonists are effective in preventing GI complications

Answer (4)� H

2-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 people if NSAIDs are used, there is:

1. Risk of GI complications2. Elderly with cardiovascular comorbidity often get GI bleed

complications with NSAIDs3. Older people with renal or cardiovascular problems get peripheral

edema or CCF4. All of the above

Answer (4)� GI hemorrhage is a risk with NSAID in elderly, those with

cardiovascular and renal disorders. Due to sodium retention, there isperipheral edema.


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

1. Porphyria2. Lead colic3. Uremia and diabetes4. Black Widow Spider bite

Answer (4)� Other conditions cause abdominal pain.


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

1. Acute polyarticular gout2. When NSAIDs and colchicines are contraindicated3. All of the above4. None of 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 nottolerated.


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175GIT, Liver

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

1. Occurs after partial gastric resection2. Bacterial overgrowth in afferent limb occurs secondary to stasis

and leads to abdominal pain, bloating and diarrhea3. Less common afferent loop syndrome is with severe abdominal

pain and bloating after 20–60 minutes after meal due to incompletedrainage of bile and pancreatic secretions

4. Needs no treatment as it subsides with time

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

1. There is extremely forceful peristaltic activity leading to episodesof chest pain and dysphagia

2. There is no medical treatment available3. Type of esophageal malignancy4. None of 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 andnifedipine are useful in such conditions. It needs to be differentiatedfrom esophageal malignancy.


82. Earliest phenotypic manifestation of idiopathic hereditaryhemochromatosis includes:

1. Post-prandial rise in serum iron levels2. Elevated serum ferritin3. Slate grey pigmentation of skin4. Increase transferrin saturation

Answer (3)� Excessive skin pigmentation is seen in 90% of the symptomatic

patients. Options 1, 2 and 4 are biochemical changes.Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 2301.

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

1. Anti-endomysial antibody2. Anti-histone antibody3. Anti-smooth muscle antibody4. Anti-mitochondrial antibodies

Answer (1)

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� In drug-induced SLE, anti-histone antibody is positive. In primarybiliary cirrhosis, mitochondrial antibody is positive and in autoimmunehepatitis, smooth muscle antibody is positive.


pages 1986, 1961.

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

1. Non-alcoholic steatohepatitis (NASH)2. Alcoholic cirrhosis3. Wilson’s disease4. All of the above

Answer (2)� In NASH, ALT > AST.


pages 16, 1815, 1857.

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

1. There is multiple cystic dilatation of intrahepatic biliary tree2. There is iron overload in liver3. Leads to portal hypertension with hematemesis4. All of the above

Answer (1)� In Caroli’s disease, multiple cystic dilatation of intrahepatic biliary tree

occurs. Eventually, infection and fibrosis occur. Liver transplantationis indicated in end-stage disease.


86. Absence of Helicobacter pylori and obesity both contribute to:

1. Increased damage with gastro-esophageal reflux2. Higher incidence of Barrett’s esophagus3. Esophageal adenocarcinoma4. All of 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. Uncommon causes of mass in left iliac fossa include all, except:

1. Mobile ovarian cyst2. Retroperitoneal tumour3. Malignant undescended testes4. Carcinoma caecum

Answer (4)

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177GIT, Liver

� Carcinoma caecum will cause a mass in right iliac fossa and caecumis a fixed structure.

Ref: Peter J. Toghil, Examining Patient, Introduction to Clinical Medicine,

2nd Edition, ECBS, page 96.

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

1. Contain inflammation or H. pylori2. Elevated gastric acid secretion observed3. Cushing’s ulcer is a name given to gastric ulcer developing after

head trauma4. Curling’s ulcer is seen after severe 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 Hermansky Pudlak syndrome, which statement is incorrect:

1. Autosomal recessive disorder2. There is granulomatous colitis with interstitial lung disease3. There is oculocutaneous albinism4. Usually, there is tendency for recurrent thrombosis

Answer (4)� There is platelet dysfunction which leads to bleeding diathesis.


90. Hypergastrinemia with hypochlorhydria is seen in:

1. Zollinger Ellison’s syndrome2. Vipoma3. Pernicious anemia4. Glucagonoma

Answer (3)� Due to atrophic gastritis, there is hyperchlorhydria, which is

pentagastrin achlorhydria. In other options, there is hyperchlorhydriawith hypergastrinemia.Ref: Harrison’s Principles of Internal Medicine, 2005, 16th Edition, page 604.

91. Anti-LKM antibodies are seen in all, except:

1. Hepatitis C and D2. Drug-induced hepatitis3. Type-2 autoimmune hepatitis4. Primary biliary cirrhosis

Answer (4)

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� Antibodies against liver-kidney microsomes are seen in hepatitis C, D,drug-induced hepatitis and type-2 autoimmune hepatitis. However, theyare absent in primary biliary cirrhosis.


92. In hemochromatosis, daily mucosal absorption of iron is:

1. 1 mg/dL2. 1–5 mg/dL3. 4 mg/dL4. None of the above

Answer (3)� It is 4 mg or more.


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

1. 3–4 g2. 20 g3. 5 g4. None of 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. Principle causes of death in hemochromatosis include all, except:

1. CCF2. Portal hypertension3. Hepatocellular carcinoma4. Malabsorption

Answer (4)� Malabsorption does not occur, and is not a cause of mortality.


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

1. CCF2. Pigmentation3. Diabetes mellitus4. Hypogonadism and arthropathy

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 malabsorption by sequestrating or precipitating bilesalts are all, except:

1. Neomycin2. Calcium carbonate3. Cholestyramine4. 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 cause of diarrhea in AIDS patient is:

1. Kaposi sarcoma affecting intestine2. Amoebic colitis3. Ulcerative colitis4. Tubercular abdomen

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 withmalabsorption:

1. Psoriasis2. Eczematoid dermatitis3. Dermatitis herpetiform4. 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 disorder is protein-loosing enteropathy:

1. Ménétrier’s disease2. Irritable bowel syndrome3. Amoebic colitis4. All of the above

Answer (1)� Hypoproteinemia occurs in Ménétrier’s disease.


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100. Pseudomembranous colitis is due to:

1. Clostridium difficile2. Shigella infection3. Campylobacter infection4. 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 of colon in ulcerative colitis is:

1. 0.5–1% per year after 10 years of diagnosis of disease2. 0.5% per year from the time of diagnosis3. 2% risk from the time of diagnosis4. None of the above

Answer (1)� The risk is 0.5–1% per year after 10 years of diagnosis.


102. Hepatic manifestations of ulcerative colitis include all, except:

1. Cholangiocarcinoma2. Autoimmune chronic active hepatitis3. Pericholangitis4. Hepatoma

Answer (4)� Hepatoma is not a complication of ulcerative colitis.


103. Megacolon is due to all, except:

1. Toxic megacolon in ulcerative colitis2. Hirschsprung’s disease3. Chagas disease4. Amoebic colitis

Answer (4)� Amoebic colitis is not a usual cause of toxic megacolon.


pages 1216, 1217.

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

1. Severe lower abdominal pain2. Rectal bleeding

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3. Hypotension4. Thumb 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-mitochondrial antibody is positive in:

1. Primary biliary cirrhosis2. Autoimmune hepatitis3. Primary sclerosing hepatitis4. Portal cirrhosis

Answer (1)� In primary biliary cirrhosis, AMA is positive.


pages 1860, 1861.

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

1. Brown or black pigmentation of colonic mucosa occurs2. It occurs in patients who chronically take anthracene cathartics

and APGAR after 4–6 months3. Pigment distribution is seen in caecum and proximal colon4. It is a premalignant condition

Answer (4)� Melanosis coli is not a premalignant condition.

Ref: JAPI, Vol. 54, July 2006, page 548.

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