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DIRECTIONS: Each of the numbered items or incomplete statements is followed mostly 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. What is Schatzki ring:

1. Mid-esophageal web 2. Hypopharyngeal web 3. Lower esophageal mucosal ring 4. 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 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1745.

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

1. Omeprazole 20 mg BD 2. Clarithromycin 500 mg BD 3. Metronidazole 500 mg BD 4. Sucralfate Answer (4)

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Regimen recommended for eradication of H. pylori infection:


Triple therapy 1. Bismuth subsalicylate plus metronidazole plus tetracycline Ranitidine bismuth citrate plus tetracycline plus clarithromycin or metronidazole Omeprazole (lansoprazole) plus Clarithromycin plus Metronidazole or Amoxicillin Dosage 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

2.

3.

Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1754.

3. Cushings ulcers are seen in:

1. Cushings disease 2. After aspirin therapy 3. Acute upper GI ulcers associated with intracra-nial injury 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. Curlings ulcer occurs in patients with severe burns.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1760.

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

1. Hypoglycemia 2. Hyperosmolar gastric content when emptying into small bowel 3. Due to post vagotomy 4. 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 dumping occurs in 1530 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1757.

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

1. Old age 2. High dose, protracted use and combination of NSAID and glucocorticoids 3. Severe intercurrent illness 4. Intake of hot drinks 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2042.

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

1. Head of pancreas 2. Tail of pancreas 3. Duodenum 4. Stomach Answer (4) Site of gastrinoma are as follows: Duodenum: 5070% Pancreas: 2040% Other intraabdominal sites, mesentery, lymph node, biliary tract, liver, stomach and ovary.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2227.

7. Bile salts and Vitamin B12 are absorbed from:

1. Proximal intestine 2. Mid-intestine 3. Distal small intestine 4. Caecum Answer (3) The site of absorption of nutrients in intestine is as follows: 1. Duodenum: Iron, calcium, folate. 2. Ileum: Vitamin B12, bile acids. 3. Colon: Water absorption.

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4.

Small bowel: Proximal > distal glucose, amino acids, lipids.


Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1764.

8. Absorption of water and electrolytes occurs mainly at:

1. Jejunum 2. Caecum 3. Rectum 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1763.

9. Monoglycerides and fatty acids are absorbed from:

1. Proximal intestine 2. Ileum 3. Colon 4. Mid-intestine Answer (1) See above two answers.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 1765, 1766.

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

1. Leucine 2. Isoleucine 3. Valine 4. Tryptophan Answer (4) These amino acids have important role in the glucose alanine cycle.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1667.

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 and methylation 2. Involve enzymes like P450, cytochrome P5, oxidase and glutathione S, acyltransferase 3. Leads to inactivation of drugs like benzodiaze-pine, but activation of 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. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 13.

12. Phase II reaction during metabolism in liver involves:

1. Converting lipophilic substances to water soluble substances 2. Formation of glucuronides by conjugation 3. 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. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 13.

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

1. Recurs during pregnancy in third trimester 2. Subsides within 714 days after delivery 3. There is an increased sensitivity to hepatic effects of estrogen and progesterone 4. 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 risk of premature delivery, fetal distress during delivery and still birth. 60 70% of the affected individuals develop cholestasis during subsequent pregnancy.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 987.

14. Nutmeg liver is seen in:

1. 2. 3. 4.

Budd-Chiari syndrome Cardiac cirrhosis Biliary cirrhosis 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1862.

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

1. Polycythemia rubra vera 2. Myeloproliferative syndrome 3. Paroxysmal nocturnal hemoglobinuria 4. Arsenical toxicity 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: Davidsons Principles & Practice of Medicine, 2006, 20th edition, pages 982, 983.

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

1. Norflox 400 mg/day 2. Trimethoprim + sulphamethazole combination 500 mg a week 3. Ciprofloxacin 750 mg once a week 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 750.

17. Asterixis in hepatic encephalopathy is present in:

1. Grade IV 2. Grade I 3. Grade II 4. All of the above Answer (3)

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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: Davidsons Principles & Practice of Medicine, 2006, 20th edition, page 950.

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

1. Reys syndrome 2. Acute fatty liver of pregnancy 3. Valproic acid therapy 4. Alcoholic liver disease Answer (4) Alcoholic liver disease and tetracycline lead to microvesicular hepatic steatosis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1718.

19. Macrovesicular hepatic steatosis is seen in all, except:

1. Alcoholic liver disease 2. Diabetes mellitus 3. Obesity 4. Reys 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. Reys syndrome causes microvascular hepatic steatosis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1718.

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

1. Ascites occurs in all cases 2. Jaundice is always present 3. Hypoalbuminuria with elevated alkaline phosphatase 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1872.

21. Pleural fluid amylase elevation occurs in all, except:

1. 2. 3. 4.

Acute pancreatitis Chronic pancreatitis Esophageal perforation 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 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1902.

22. Ranson/imrie prognostic criterion is used in:

1. Acute pancreatitis 2. Acute fulminant ulcerative colitis 3. Hepatic encephalopathy 4. Acute renal failure Answer (1) Ranson, imrie, apache II prognostic criteria have multiple factor scoring system which assess patients increased risk of dying.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1898.

23. Pancreatic ascites is due to all, except:

1. Pseudocyst leaking into peritoneal cavity 2. Disruption of pancreatic duct and fistula between duct and peritoneal cavity 3. Acute pancreatitis 4. 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 inpatient who has ascites with elevated serum amylase, increased albumin (over <5 g) and serum amylase (over 20,000 U/L).
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1902.

24. Diagnostic features of pancreatic ascites are:

1. Increased albumin >3.0 g/dL and elevated amylase >20,000 IU in ascitic fluid 2. Increase polymorphs in ascites 3. Increased LDH level 4. 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 inpatient who has ascites with elevated serum amylase, increased albumin (over <5 g) and serum amylase (over 20,000 U/L).
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1902.

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160 MCQs in Medicine for PG Entrance Examination 25. Complications of chronic pancreatitis include all, except:

1. Vitamin B12 malabsorption 2. Impaired GTT 3. Pleural effusion 4. Folate malabsorption Answer (4) Folate malabsorption is not the complication of chronic pancreatitis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1903.

26. In hepatitis E, mortality is maximum in:

1. Pregnant women 2. In all women 3. Adolescent 4. Infant Answer (1) Pregnancy with jaundice is due to hepatitis E, and it carries morbidity.
Ref: Anantnarayan, 6th Edition, page 519.

27. Purtschers retinopathy is a complication of:

1. Hypertension 2. Type-2 DM 3. Pancreatitis 4. Wilsons 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 spots and hemorrhages confined to area of optic disc and macula. It is due to occlusion of posterior retinal artery with aggregated granulocytes.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1898.

28. Diloxanide furoate is not useful in:

1. Extraintestinal amoebiasis 2. Cyst passers 3. Interstitial amoebiasis 4. 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 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1217.

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GIT, Liver 29. All causes unconjugated hyperbilirubinemia, except:

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1. Large hematoma 2. Hemolytic anemia 3. Megaloblastic anemia 4. Rotors syndrome Answer (4) In Rotors 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 Yes No Normal Delayed and reflux back to circulation Rotor No Yes Increased Delayed plasma clearance

Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1821.

30. Prognostic marker of acute liver failure is:

1. AST 2. Factor V levels 3. Serum bilirubin 4. Prothrombin time Answer (4) In acute hepatic encephalopathy, prolongation of prothrombin time is a poor prognostic sign.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1811.

31. Sclerosant agents used for endoscopic sclerotherapy are all, except:

1. Acetic acid 2. Alcohol 3. Cyanoacrylate 4. Podocyanolate Answer (1) Acetic acid is not a sclerosing agent.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1860.

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

1. Anti-secretory activity 2. Promotes intestinal absorption

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3. Both 1 and 2 4. 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 denotes hepatic involvement:

1. Raised ESR 2. Exudative ascitic fluid 3. Raised serum alkaline phosphatase 4. 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 gastrointestinal tract. In obstructive jaundice, hepatic metastasis and hepatic granuloma, the enzyme is increased. It is also increased in bone disease like Pagets disease, osteomalacia, renal osteodystrophy and primary hyperparathyroidism. In osteoporosis, alkaline phosphatase level is not increased.
Ref: Harrisons 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
1. Hematochromatosis 2. Primary biliary cirrhosis

Test
a. Serum ceruloplasmin, serum urine and liver copper estimation b. Serum immunoglobulin, serum anti-nuclear factor and smooth muscle and liver, kidney, microsomal antibodies c. Serum ferritin, serum iron and iron binding capacity, saturation, PCR for genetic defect d. Serum immunoglobulins, serum antimitochondrial antibodies

3. Autoimmune chronic active hepatitis 4. Wilsons disease

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 along with AMA positivity. Wilsons disease is due to copper overload and deficient serum ceruloplasmin level.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1813.

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GIT, Liver 35. Match the following:

163

Classification of portalhypertension A. B. C. D. Extrahepatic sinusoidal Intrahepatic sinusoidal Sinusoidal Extrahepatic presinusoidal

Examples of disease 1. 2. 3. 4. Veno-occlusive disease Cirrhosis of liver 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 958.

36. Which is not the complication of portal hypertension:

1. Renal failure 2. Hypersplenism 3. Ascites and hepatic encephalopathy 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 959.

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

1. Cirrhosis of liver 2. Portal vein thrombosis 3. Schistosomiasis 4. Budd-Chiari syndrome 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 957.

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

1. 2. 3. 4.

Somatostatin (octreotide) 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1859.

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

1. Stent is placed between portal vein and hepatic vein to reduce portal hypertension 2. Hepatic encephalopathy may occur following shunt 3. Used for acute UGI bleeding which is not responding to sclerotherapy or banding or pharmacological treatment 4. 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 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 960.

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

1. Nephrotic syndrome 2. Protein loosing enteropathy 3. Malnutrition 4. Abdominal tuberculosis Answer (4) Ascitic collection is due to infection. It consists of inflammatory exudates.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1867.

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

1. Seen on right side only 2. Seen on left side only 3. It is always bilateral 4. 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 due to ascites.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 948.

42. LeVeen shunt is used in:

1. Resistant ascites 2. Hydrocephalous 3. ASD 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 949.

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

1. Infection 2. Superior vena caval thrombosis 3. Pulmonary bleeding 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 949.

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

1. TIPPS 2. LeVeen shunt 3. Porta caval anastomosis 4. Propranolol 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1867.

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

1. Abdominal pain and fever in a cirrhotic patient 2. 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 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 950.

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

1. Orally given and acts on colonic bacteria in colon 2. Dose started as 1530 ml 8 hourly and increased so as to produce 2 bowel movements 3. It has osmotic laxative effect that reduces colonic bacteria, limit colon absorption of ammonia and promotes incorporation of nitrogenous 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 cases with lactose intolerance where lactulose will not be absorbed, action seen with lactulose is possible.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 951.

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

1. Hepatopulmonary syndrome 2. Hepatorenal syndrome 3. Spontaneous bacterial peritonitis 4. Ascites Answer (4) Complications like hepatorenal syndrome, hepato-pulmonary syndrome and spontaneous bacterial peritonitis are of poor prognosis in cirrhosis of liver.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, pages 949, 950.

48. Non-AE viral hepatitis accounts for:

1. 2. 3. 4.

50% of cases 12% of cases 10% of cases None of the above

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Answer (2) Viral hepatitis is mainly due to hepatitis A, B, C, D, E viruses. Only 12% of jaundice with hepatitis are due to other non-AE viral hepatitis.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 969.

49. Causes of non-AE viral hepatitis include all, except:

1. Cytomegalovirus 2. Influenza virus 3. Epstein Barr virus 4. Yellow fever virus Answer (2) Influenza virus does not cause hepatitis. However, Herpes simplex virus can cause hepatitis.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 969.

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

1. Hepatitis B and C 2. Hepatitis A and E 3. Hepatitis C and D 4. Hepatitis B and D Answer (2) Chronic stage is not seen with hepatitis A and E.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, pages 964967.

51. Hepatitis B vaccine prevents:

1. Hepatitis B 2. All hepatitis from A to E 3. Hepatitis B and D 4. Hepatitis C Answer (3) Hepatitis virus B vaccine can prevent both hepatitis B and D viral infections.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 967.

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

1. Faeces 2. Blood 3. Sexual 4. Vertical Answer (1)

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Faecal spread is not seen. Hepatitis B, D and C spread mainly through blood.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 962.

53. Extrahepatic prodromal features of hepatitis B include:

1. Arthralgia 2. Skin rash 3. Polyarteritis nodosa 4. Bleeding per rectum Answer (4) These patients may have serum sickness-like syndrome as a prodromal feature. In children, cervical lymphadenopathy and splenomegaly can occur.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 963.

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

1. Aminotransferase activity over 400 U/L 2. Raised serum bilirubin over 5 mg 3. Alkaline phosphatase level below 250 U/L 4. 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: Davidsons 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 23 months 2. Prolonged malaise, anorexia, nausea 3. Right hypochondrial discomfort 4. 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: Harrisons 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 signs occur in 515% 2. Asymptomatic biochemical relapses with increase in plasma aminotransferase activity are even more common 3. Relapsing hepatitis resolves spontaneously 4. It implies worse prognosis Answer (4)

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


Ref: Harrisons Principles of Internal Medicine, 2005,16th Edition, page 1834.

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

1. Aplastic anemia 2. Polyarteritis nodosa 3. Glomerulonephritis 4. Polycythemia Answer (4) Polycythemia is not a chronic complication of viral hepatitis. Other systemic complication mentioned are seen in non-AE hepatitis. Aplastic anemia develops after 1 year from the onset of jaundice. In addition, Henoch-Schnlein purpura and papular acroder-matitis have been reported in children.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 963.

58. Unconjugated hyperbilirubinemia sometimes found after acute viral hepatitis indicates:

1. Relapsing hepatitis 2. Intrahepatic cholestatic hepatitis 3. Pre-existing Gilberts syndrome 4. Chronic active hepatitis Answer (3) Unconjugated hyperbilirubinemia or increase in hemoglobinemia with normal liver enzymes is a feature of Gilberts syndrome.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 945.

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

1. Sedative and hypnotics 2. Alcohol 3. Chloromycetin and tetracycline 4. Amoxipen Answer (4) All drugs are metabolized in liver except amoxipen. Hence, they are avoided.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 973.

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

1. 2. 3. 4.

Pre-existing chronic liver disease Old age Other co-existing diseases like carcinoma or lymphoma 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 986.

61. Match the following:

1. 2. 3. 4.

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

a. b. c. d.

Incubation period of hepatitis B Established viral hepatitis Immunization without 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 its 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 965.

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

1. Patient on chronic hemodialysis 2. Newborn of infected mother 3. Homosexual male 4. 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.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 967.

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

1. 20% develop cirrhosis within 20 years 2. 50% develop cirrhosis after 30 years 3. Once cirrhosis develops on chronic HCV infection, rate of hepatocellular carcinoma is 25% per year 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 968.

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

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

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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, pages 963968.

65. Anti-HBS implies in viral hepatitis:

1. Previous infection convalescence 39 months 2. Previous vaccination 3. Both 1 and 2 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 965.

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

1. HBsAg 2. Anti-HBC 3. Anti-HBS 4. 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: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 965.

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

1. 2. 3. 4.

HBeAg Anti-HBe HBcAg All of the above

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

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

1. Acute hepatic failure 2. Cirrhosis of liver 3. Chronic active hepatitis 4. Recurrent gallstones Answer (1) Pregnant woman with HEV has a risk for developing hepatic encephalopathy which is associated with high mortality (1525%). However, chronic infection does not occur.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 968.

69. Mallorys hyaline is seen in:

1. Alcoholic hepatitis 2. Primary biliary cirrhosis 3. Viral hepatitis B 4. None of the above Answer (1) It is an eosinophilic material present in the cytoplasm of hepatocytes.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 970.

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

1. Halothane 2. Rifampicin 3. Isoniazid 4. Chlorpromazine Answer (4) Chlorpromazine produces cholestatic hepatitis.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 973.

71. Macrovesicular steatosis is seen in all, except:

1. Alcohol 2. Obesity 3. Fatty liver of pregnancy 4. Diabetes mellitus Answer (3) In fatty liver of pregnancy microvesicular steatosis is present.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, pages 971973.

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GIT, Liver 72. Rabeprazole has all the following advantages, except:

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1. Least activation time 2. Fast H+-K+ ATPase inhibition 3. After first dose, intragastric pH becomes 34 4. Often it has many drug interactions Answer (4) Rabeprazole has all these advantages over other proton pump inhibitors. Drug interaction is not present.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 889.

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

1. Does not increase somatostatin level 2. Maintains baseline motilin level 3. Does not cause any delay in gastric emptying 4. 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. Piroxicam 2. Indomethacin 3. Ibuprofen 4. Diclofenac Answer (1) Highest risk is with piroxicam and lowest risk is with ibuprofen.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 1091.

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

1. Age over 60 years 2. Past history of peptic ulcer or adverse event with NSAIDs 3. Concomitant corticosteroid use 4. 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 of gastrointestinal bleeding caused by NSAIDs appears to be dose related.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1755.

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

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

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2. Endoscopic evidence of peptic ulcer is found in 20% of NSAID ulcers 3. Ibuprofen or diclofenac has lower risk of GI complications 4. H2-antagonists are effective in preventing GI complications Answer (4) H2-antagonists are ineffective, and omeprazole or misoprostol can reduce NSAID-induced peptic ulceration.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, pages 1090, 1091.

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

1. Risk of GI complications 2. Elderly with cardiovascular comorbidity often get GI bleed complications with NSAIDs 3. Older people with renal or cardiovascular problems get peripheral edema or CCF 4. 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 is peripheral edema.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 1092.

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

1. Porphyria 2. Lead colic 3. Uremia and diabetes 4. Black Widow Spider bite Answer (4) Other conditions cause abdominal pain.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 83.

79. ACTH IM injection 4080 IU in a single dose 12 hourly 2 days is effective in:

1. Acute polyarticular gout 2. When NSAIDs and colchicines are contraindicated 3. All of the above 4. None of the above Answer (3) Short course oral steroid 3050 mg x 57 days or IM ACTH 4080 IU BD 2 days can be used when colchicine or NSAID is not tolerated.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2046.

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

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1. Occurs after partial gastric resection 2. Bacterial overgrowth in afferent limb occurs secondary to stasis and leads to abdominal pain, bloating and diarrhea 3. Less common afferent loop syndrome is with severe abdominal pain and bloating after 2060 minutes after meal due to incomplete drainage 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: Harrisons 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 episodes of chest pain and dysphagia 2. There is no medical treatment available 3. Type of esophageal malignancy 4. 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 and nifedipine are useful in such conditions. It needs to be differentiated from esophageal malignancy.
Ref: Davidsons Principles & Practice of Medicine, 2006, 20th Edition, page 882.

82. Earliest phenotypic manifestation of idiopathic hereditary hemochromatosis includes:

1. Post-prandial rise in serum iron levels 2. Elevated serum ferritin 3. Slate grey pigmentation of skin 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2301.

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

1. Anti-endomysial antibody 2. Anti-histone antibody 3. Anti-smooth muscle antibody 4. Anti-mitochondrial antibodies Answer (1)

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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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 1986, 1961.

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

1. Non-alcoholic steatohepatitis (NASH) 2. Alcoholic cirrhosis 3. Wilsons disease 4. All of the above Answer (2) In NASH, ALT > AST.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 16, 1815, 1857.

85. Carolis disease has which of these features:

1. There is multiple cystic dilatation of intrahepatic biliary tree 2. There is iron overload in liver 3. Leads to portal hypertension with hematemesis 4. All of the above Answer (1) In Carolis disease, multiple cystic dilatation of intrahepatic biliary tree occurs. Eventually, infection and fibrosis occur. Liver transplantation is indicated in end-stage disease.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1873.

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

1. Increased damage with gastro-esophageal reflux 2. Higher incidence of Barretts esophagus 3. Esophageal adenocarcinoma 4. All of the above Answer (4) In Barretts 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 cyst 2. Retroperitoneal tumour 3. Malignant undescended testes 4. Carcinoma 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. Regarding stress-related mucosal injury, which statement is incorrect:

1. Contain inflammation or H. pylori 2. Elevated gastric acid secretion observed 3. Cushings ulcer is a name given to gastric ulcer developing after head trauma 4. Curlings ulcer is seen after severe burns Answer (1) Both Curlings ulcer and Cushings ulcer are stress related. There is no inflammation or mucosal injury.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1760.

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

1. Autosomal recessive disorder 2. There is granulomatous colitis with interstitial lung disease 3. There is oculocutaneous albinism 4. Usually, there is tendency for recurrent thrombosis Answer (4) There is platelet dysfunction which leads to bleeding diathesis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1560.

90. Hypergastrinemia with hypochlorhydria is seen in:

1. Zollinger Ellisons syndrome 2. Vipoma 3. Pernicious anemia 4. Glucagonoma Answer (3) Due to atrophic gastritis, there is hyperchlorhydria, which is pentagastrin achlorhydria. In other options, there is hyperchlorhydria with hypergastrinemia.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 604.

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

1. Hepatitis C and D 2. Drug-induced hepatitis 3. Type-2 autoimmune hepatitis 4. 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, they are absent in primary biliary cirrhosis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1828.

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

1. 1 mg/dL 2. 15 mg/dL 3. 4 mg/dL 4. None of the above Answer (3) It is 4 mg or more.


Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2298.

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

1. 34 g 2. 20 g 3. 5 g 4. None of the above Answer (1) Iron absorption by mucosal block occurs as per the need, and body iron content remains around 34 g.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2298.

94. Principle causes of death in hemochromatosis include all, except:

1. CCF 2. Portal hypertension 3. Hepatocellular carcinoma 4. Malabsorption Answer (4) Malabsorption does not occur, and is not a cause of mortality.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2298.

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

1. CCF 2. Pigmentation 3. Diabetes mellitus 4. Hypogonadism and arthropathy Answer (4) Complications like hypogonadism and arthropathy do not improve even after phlebotomies and chelating agent therapy.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 2298.

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

1. Neomycin 2. Calcium carbonate 3. Cholestyramine 4. Penicillamine Answer (4) Penicillamine does not cause bile salt deficiency-induced malabsorption.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1965.

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

1. Kaposi sarcoma affecting intestine 2. Amoebic colitis 3. Ulcerative colitis 4. Tubercular abdomen Answer (1) Intestinal lesion due to Kaposi sarcoma is the most common cause of AIDS diarrhea.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1110.

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

1. Psoriasis 2. Eczematoid dermatitis 3. Dermatitis herpetiform 4. Lupus vulgaris Answer (4) Lupus vulgaris is a skin lesion that occurs due to TB and is not associated with malabsorption.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 1770, 1771.

99. Which one of the disorder is protein-loosing enteropathy:

1. Mntriers disease 2. Irritable bowel syndrome 3. Amoebic colitis 4. All of the above Answer (1) Hypoproteinemia occurs in Mntriers disease.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1775.

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180 MCQs in Medicine for PG Entrance Examination 100. Pseudomembranous colitis is due to:

1. Clostridium difficile 2. Shigella infection 3. Campylobacter infection 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 760.

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

1. 0.51% per year after 10 years of diagnosis of disease 2. 0.5% per year from the time of diagnosis 3. 2% risk from the time of diagnosis 4. None of the above Answer (1) The risk is 0.51% per year after 10 years of diagnosis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1731.

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

1. Cholangiocarcinoma 2. Autoimmune chronic active hepatitis 3. Pericholangitis 4. Hepatoma Answer (4) Hepatoma is not a complication of ulcerative colitis.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, page 1784.

103. Megacolon is due to all, except:

1. Toxic megacolon in ulcerative colitis 2. Hirschsprungs disease 3. Chagas disease 4. Amoebic colitis Answer (4) Amoebic colitis is not a usual cause of toxic megacolon.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 1216, 1217.

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

1. Severe lower abdominal pain 2. Rectal bleeding

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3. Hypotension 4. 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: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 226, 227.

105. Anti-mitochondrial antibody is positive in:

1. Primary biliary cirrhosis 2. Autoimmune hepatitis 3. Primary sclerosing hepatitis 4. Portal cirrhosis Answer (1) In primary biliary cirrhosis, AMA is positive.
Ref: Harrisons Principles of Internal Medicine, 2005, 16th Edition, pages 1860, 1861.

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

1. Brown or black pigmentation of colonic mucosa occurs 2. It occurs in patients who chronically take anthracene cathartics and APGAR after 46 months 3. Pigment distribution is seen in caecum and proximal colon 4. 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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