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Old 05-26-2013
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Liver Gastroenterology Q22

A 58 year-old man is evaluated for a new diagnosis of cirrhosis. The patient has a medical history of diabetes mellitus, hypertriglyceridemia, and hypertension. He takes pioglitazone, rosuvastatin, lisinopril, and atenolol. He is a lifetime nonsmoker and has never used IV drugs. He drinks about one glass of wine weekly. For about 4–8 years in his 20s, he admits to binge drinking as much as 12–18 beers on the weekends, but has not drunk more than two glasses of wine weekly for many years. He has never had a blood transfusion and has been in a monogamous sexual relationship for 30 years. He has no family history of liver disease. He works as a machinist in a factory mak-ing airplane engines. He denies chemical exposures. His physical examination is notable for a body mass index of 45.9 kg/m 2 . He has stigmata of chronic liver disease including spider angiomata and caput medusa. Moderate ascites is present. Workup has shown no evidence of viral hepatitis, hemochromatosis, Wilson’s disease, autoimmune hepatitis, or α 1 antitrypsin deficiency. He undergoes liver biopsy, which shows fibrosis in a perivenular and perisinusoidal distribution. Which of the following state-ments is TRUE regarding the cause of the patient’s cirrhosis?
A. As opposed to individuals with metabolic syndrome alone, these individuals do not show significant insu-lin resistance.
B. The aspartate aminotransferase is commonly ele-vated to more than twice the alanine aminotrans-ferase level.
C. The lack of steatohepatitis on liver biopsy rules out nonalcoholic fatty liver disease as a cause of the patient’s cirrhosis.
D. The prevalence of the milder form of this disorder is between 10 and 20% in the United States and Europe, with as much as 10–15% of affected individuals developing cirrhosis in some series.
E. Treatment with ursodeoxycholic acid and HMG-CoA reductase inhibitors has been demonstrated to improve outcomes in this disorder
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Old 05-26-2013
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I think this guy is in the cirrhotic stage of ALCOHOLIC STEATOHEPATITIS.. that the physicians just happen to find when it is in the cirrhotic stage (therefore C is wrong)

A is wrong because metabolic syndrome causes diabetes secondary to fatty acid deposition and pancreatic increased workload and insulin resistance.
I dont know anything about D
E is the tx for PBC and PSC
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Old 05-27-2013
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The answer is D. . The prevalence of the milder form of this disorder is between 10 and 20% in the United States and Europe, with as much as 10–15% of affected individuals developing cirrhosis in some series.

This patient presents with nonalcoholic fatty liver disease (NAFLD) that has progressed to cirrhosis. It is now commonly thought that many indi-viduals previously identified as having cryptogenic cirrhosis had NAFLD as a cause of end-stage liver disease. With the rising prevalence of obesity in the United States and Europe, NAFLD is expected to continue to rise. At present, the prevalence of NAFLD is estimated between to be 14–20%. Of these individuals, 30–40% with nonalcoholic steato-hepatitis will develop advanced fibrosis and 10–15% will develop outright cirrhosis. Most patients diagnosed with NAFLD are asymptomatic with incident note of elevated liver enzymes found on testing for other reasons. The ALT is typically slightly higher than the AST, and both enzymes are only mildly elevated. In most instances the ALT and AST are only 1.5–2 times the upper limit of normal. NAFLD often accompanies other components of the metabolic syndrome, with insulin resistance being a common link between these disorders. The diagnosis of NAFLD requires a careful history and examination to rule out other disorders. Alcohol intake should be less than 20 g/d. Comprehensive testing should include serologies for viral hepatitis, iron studies, ceruloplasmin, α 1 antitrypsin levels, and autoimmune serologies. Liver biopsy most commonly shows macrovesicular steatosis with a mixed inflammatory infiltrate in a lobular distribution. The fibrosis that occurs has a characteristic perivenular and perisinusoidal distribution. In cirrhotic patients, steatosis may not be seen, but can recur following transplant. The only known effective treatment for NAFLD is weight loss and exercise. Thiazolidinediones are currently being studied given their effects on insulin resistance. In addition, ongoing research into statins and ursodeoxycholic acid is being undertaken, but no specific medication can be recom-mended at this point for patients with NAFLD.
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