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Hepatobiliary1. Regarding pancreatitisa. The second most common cause is infectious agentsb. Trypsin is implicated as an activator of the kinin system <= correct, prekallikrein -> kallikrein w/ activation of kininsc. The chronic form is usually due to gallstones - EtOHd. Duct obstruction is not the mechanism in alcoholic pancreatitis - although there is direct acinar injury, functional obstruction is caused by Ampulla of Vater sphincter contraction and increased pancreatice protein production -> blockagee. Elastase is the only pancreatic enzyme that acts to limit pancreatitis2. In acute pancreatitisa. Fat necrosis occurs in other intra-abdominal fatty deposits <= correct, regional fatb. Trauma is the precipitating cause in 30% of cases – 80% are associated with biliary tract disease gallstones > EtOHc. Alcohol is directly toxic to the Islets of Langerhansd. Kallikrein converts trypsin to activate the complement systeme. Erythromycin has been implicated in severe cases3. With regards to jaundicea. Conjugated bilirubin causes kernicterus in adultsb. Unconjugated bilirubin does not colour sclerac. Unconjugated bilirubin is tightly bound to albumin <= correctd. Unconjugated bilirubin produces bilirubin in urinee. Conjugated bilirubin is tightly bound to albumin4. In cirrhosisa. Fibrosis is confined to the delicate bands around central veins – bridging between veins and portal tractsb. Nodularity is uncommon - parenchymal nodules are characteristicc. Vascular architecture is preservedd. The Ito cell is a major source of excess collagen <= types I and IIIe. The left lobe of the liver is most affected5. Cirrhosis is associated witha. ?b. reorganized liver vasculature with scarringc. ?d. ?e. ?6. oesophageal varicesa. occur in one third of all cirrhosis patients – 90% of cirrhotic patients develop theseb. account for more than 50% of episodes of haematemesis – only one of the many cuasesc. are most often associated with hepatitis C cirrhosis – most commonly with EtOHd. have a 40% mortality during the first episode of rupture <= “as many as half”e. lie primarily in the middle portion of the oesophagus – distal/lower7. Acute pancreatitisa. Occurs in approximately 5% of patients with gallstones <=b. Is idiopathic in 50% - in 10-20%c. Interstitial form is characterized by necrosis of acinar and ductal tissue – only fat necrosis, this is seen in necrotisin (note also haemorrhagic also)d. May result from trypsin, which is secreted in active form, converting prolipase in acinar tissuee. Has a 25% acute (first week) mortality rate – mortality rate 5%8. The least frequent cause of cirrhosis is:a. Hepatitis Bb. Alcoholic liver diseasec. Hepatitis Cd. Alpha-1 antitrypsin deficiency <=e. Primary haemochromatosis9. Regarding chronic pancreatitisa. Pancreatic abscess formation is a feature – acute, but pseudocysts form in bothb. Alcohol is the most implicated aetiological agent <= correctc. Manifestations include duct obstruction, secondary diabetes and duodenal obstruction – not duodenald. Does not involve fibrosis of parynchymal tissuee. Is not associated with an increased risk of pancreatic cancer10. In hepatitis Ba. Acute infection causes subclinical disease in 65% of cases <= ‘70%’b. The majority of cases of persistent infection result in cirrhosis – 30% carrier, 12-20% cirrhoticc. Surface antigen (HbsAg) appears soon after overt disease – before symptoms, peaks withd. Infection does not play a role in development of hepatocellular carcinomae. Anti HBs appears soon after HbsAg - ? Nb chronic carrier HbsAg >6months11. Hepatitis Ca. Is acquired by faecal-oral transmissionb. Has its highest seroprevalence in haemodialysis patientsc. Transmission by sexual contact is at a high rated. Causes chronic hepatitis at a higher rate than does hepatitis B <= chronic disease in 80-85% (c.f. <5%) and cirrhosis in 20-30%e. Exposure confers effective immunity to subsequent infection12. Fatty change/steatosis, which is false?a. Unmasking of normal fat content <=b. Caused by decreased protein (protein malnutrition)c. In the heart is caused by severe anaemia - correctd. Diabetese. Alcohol13. Cholelithiasisa. Gallstones always produce symptomsb. Rapid weight loss reduces the risk of gallstones – risk forc. Cholesterol stones are the predominant type of gallstone <= correct 90%d. Brown stones are usually visible on xray <= are ‘radio-opaque’ 50-75% (brown w/ infection, balck if just bile salts)e. Crohn’s disease is associated with the development of gallstones - ?14. A young baby with jaundice, dark urine and pale stools is most likely to havea. Physiologic jaundice of the newborn – immature liver -> unconjugatedb. Breast milk jaundice - unconjugatedc. Gilbert’s syndrome – metabolic issue leads to unconjugated formd. Biliary atresia <= causes a third of neonatal cholestasis and conjugatede. None of the above15. Conjugated hyperbilirubinaemia occurs ina. Gilbert’s syndromeb. Physiologic jaundicec. Excess production of bilirubind. Decreased hepatic uptakee. Cholestasis <=16. Cirrhosisa. Is a reversible disorder of the liverb. Is developed by most alcoholics – no 10-15% (women more b/c cant tolerate EtOH and estrogen make gut more permeable to endotoxin -> Kupffer cell inflammation)c. It is rarely preceded by steatosisd. It may have no clinical manifestation <= correct, is often silent until advance (40% of patients)e. It is characterized by fatty change and perivenular fibrosis – bridging fibrosis, parenchymal nodules, parenchymal architecture disruption17. Cirrhosisa. Reversible if cryptogenicb. Left lobe is most often affectedc. ?d. results in changes of the vascular channels (disruption of vascular architecture) <=e. ?18. Cirrhosisa. Chronic inflammation is the causeb. ?c. ?d. ?e. ?19. Regarding hepatic failurea. Occurs with loss of functional liver capacity of 60% - 80-90%b. Encephalopathy is a result of increased ammonia formation – decreased metabolism -> ureac. The liver is the predominant site of synthesis of albumin <=d. ?e. ?20. Liver failurea. Has a 20-40% mortality – 80%b. Can be caused by tetracycline’s <=c. Rarely results in cirrhosis- chronic liver failure (most common form) w/ end-point = cirrhosisd. Not associated with ascitese. ?21. Hepatitis Aa. Dane particlesb. Vertical transmissionc. 20% carrier rated. ?e. ?22. Hepatitis B infectiona. HbeAg is associated with viral replication <=b. Surface antigen occurs after symptomsc. Anti Hbe occurs during disappearance of HbeAgd. IgG represents recent infectione. ?23. Hepatitis Ba. Anti-HBs appears soon after HbsAgb. Infection does not play a role in hepatocellular carcinomac. HbsAg appears soon after overt diseased. The majority of cases of persistent infection result in cirrhosise. Acute infection causes subclinical disease in 65% of cases <=24. Hepatitis Ca. Has a high association with sexual transmission – parenteral (but high risk group includes multiple sex partners)b. Transmission increases with pregnancyc. 50% get cirrhosis – 20-30%d. greater than 50% of infections become chronic <= 80%e. ?25. Hepatitis Ea. Mortality of 20% in pregnant females <=b. Incubation of 5 days – 4-5 weeksc. Faecal-oral transmission <= true!d. ?e. ?26. In viral hepatitisa. The majority of cases of acute hepatitis B infection result in a carrier stateb. Hepatitis A virus has an outer surface envelope of protein, lipid and carbohydratec. Anti HBs appears in the first week of infectiond. The major cause of death from Hep B is hepatocellular carcinoma - ? cirrhosis (6-15% of cirrhotics develop HCC)e. Anti HCV IgG does not confer immunity to hepatitis C <= 90% of chronic Hep C have this27. An infectious complication of transfusiona. Is most commonly hep C – most commonly a non-A non-B (i.e. don’t know)b. Is most commonly hep Bc. Is rarely transmission of HIV since screening was instituted <=d. Never includes gonorrhoea or malariae. Can be clinically apparent mononucleosis in 7% of cases28. Acute pancreatitisa. May be caused by infection with E colib. Often causes diabetesc. Is most commonly associated with ischaemiad. May cause hypocalcaemia <=e. Is associated with type III hyperlipoproteinaemia29. Acute pancreatitisa. May be caused by helminth infection <= causes cholecystis, cholangitis and abscessesb. Causes hypercalcaemiac. Develops in 50% of patients with gallstones – 5% (but 80% is from gallstones and EtOH)d. Leads to inhibition of elastasee. Involves acinar cell injury as a late event – be the cause (mumps, drugs, trauma, ischaemia)Note gallstone disease M:F 3:1, EtOH disease M:F 6:130. acute pancreatitisa. is associated with increased levels of serum amylase with normal lipaseb. occurs most often in later life – define ‘later’…c. occurs in about 5% of patients with gallstones <=d. when associated with alcohol is not usually preceded by chronic pancreatitise. is often associated with hypercalcaemia31. In acute pancreatitisa. Less than 5% are idiopathic – 10-20%b. 35% of patients with gallstones develop pancreatitis – 5%c. gallstones are present in 80% of patients – gallstones AND EtOH account for 80%d. trypsin plays a central role in the activation of the bradykinin system <=e. ?32. Which of the following may occur in acute pancreatitisa. Hypercalcaemiab. Glycosuria <=c. ?d. ?e. ?33. all are effects of acute pancreatitis excepta. diabetes mellitus <= this is from chronicb. pseudocystc. ARDSd. Low platelts - DICe. ?34. acute pancreatitisa. intraductal activation of proteolytic enzymes <=b. affects intraperitoneal fat onlyc. alcohol and gallstones cause 60%d. backflow of bile is a significant risk factore. proteases, trypsin etc are released from alpha islet cells35. All are true about chronic pancreatitis excepta. 10% develop pseudocysts - trueb. diabetes may develop - truec. associated with pancreatic carcinoma – in those with hereditary cause 40% risk (unclear for others)d. alcohol is the main aetiologic factor - truee. ? <=? 36. Chronic pancreatitis causesa. Hypercalcaemiab. Hypermagnesaemiac. Steatorrhoea <=d. Hypoglycaemiae. ?37. In acute pancreatitisa. Less than 5% are idiopathic – 10-20%b. 35% of patients with gallstones develop pancreatitis – 5%c. gallstones are present in 80% of cases - d. trypsin plays a central role in the activation of the kinin system <=e. ?38. The characteristic fetor of hepatic failure is caused by formation ofa. Methionineb. Ethanolc. Mercaptans <= “My captain has bad breath”d. Sulfurse. Mercaptopurines39. The following apply to cirrhosis EXCEPT:a. It is among the top 10 leading causes of death in the western world – actually it is number 12 in the USb. The central pathogenic process is progressive fibrosisc. It may be clinically silentd. Alcoholic liver disease is the aetiology in 30% of cases – ? Together EtOH and viral hepatitis account for the majoritye. Collagen type I and III are deposited in all parts of the lobule40. Ascitesa. Is due to lymphatic obstructionb. Involves percolation of hepatic lymph into the peritoneal cavity <=c. Does not involve renal retention of sodium and waterd. Incolves increased vascular permeabilitye. Is not associated with hepatic sinusoidal hypertension41. unconjugated bilirubina. is soluble in aqueous solutionb. is not protein boundc. when present in excess is readily excreted in urined. can cause kernicterus if present inexcess in neonates <=e. is the major form of bilirubin elevated in gallstone obstruction of the biliary tree42. The complications of chronic pancreatitis include all of the following EXCEPT:a. Duct obstructionb. Disseminated intravascular coagulation <=c. Pseudocystd. Malabsorptione. Secondary diabetes43. Chronic pancreatitisa. Has equal prevalence between the sexesb. Is predisposed to by hyperlipoproteinaemia <=c. Does not commence until adulthoodd. Always has an identifiable precipitating factore. Always can be diagnosed by elevated serum amylase44. Acute pancreatitisa. Is a recognised sequelae in about 15% of patients with gallstonesb. Can be caused by the use of sulphonamides <=c. Is an idiopathic condition in 40%d. Can lead to symptomatic hypercalcaemiae. Is a common cause of secondary diabetes mellitus45. bilirubina. is excreted in urine as urobilinogenb. levels are decreased in pernicious anaemiac. conjugation is impaired in Dubin Johnson Syndromed. is formed from globin moleculese. is elevated in Gilbert Syndrome in predominantly the unconjugated form <=46. In regards to gallstonesa. Cholesterol stones arise exclusively in the gallbladder and consist of 50-100% cholesterol <=b. About 1% of black stones are radio-opaquec. There are no hereditary factors involvedd. In the west, about 80% are crystalline cholesterol monohydrase and 50% are cholesterol stonese. Rapid weight reduction is not a risk factor for gallstone formation47. regarding cirrhosis of the liver, which of the following is FALSE?a. It is an important cause of death in the Western sorldb. The most important cause is alcoholic liver diseasec. It is often complicated by hepatocellular carcinomad. It causes osteoporosise. It causes reversible fibrosis of the liver <= ................
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