Abstract

1.Regarding anti-tubercular therapy (ATT) related hepatotoxicity the following are TRUE:1.Transient asymptomatic rise of transaminases is common and settles spontaneously with continuation of isoniazid.2.Most common pattern of ATT induced hepatotoxicity is cholestatic.3.ATT induced acute liver failure has worse prognosis virus related acute liver failure.4.Combination therapy increases the risk of hepatotoxicity.5.Daily dosing regimen increases risk of hepatotoxicity.2.Regarding the mechanisms of ATT related hepatotoxicity the following are TRUE:1.Slow acetylators have less risk of isoniazid induced hepatotoxicity.2.Rifampicin increases isoniazid induced hepatotoxicity by inducing cytochrome P450 enzymes.3.Rifampicin can cause both conjugated and unconjugated hyperbilirubinemia without hepatocellular damage.4.Pyrazinamide induced hepatotoxicity is dose dependent.5.Women have lower risk of ATT induced hepatotoxicity due to lower cytochrome P450 enzyme activity.3.Regarding model for end stage liver disease (MELD) the following are TRUE EXCEPT:1.MELD was initially developed as a score to predict survival following surgical porto-systemic shunting for refractory ascites or variceal bleeding.2.Upper value of serum creatinine is capped at 4 mg/dl.3.Addition of etiology of liver disease improves the predictive ability of the MELD score.4.MELD scores are also predictive of post transplant morbidity, length of ICU stay and cost of transplantation.5.Addition of other recipient and donor criteria to MELD may be useful in optimizing transplant risk in patients with high MELD scores.4.Regarding use of MELD for applications other than liver transplantation the following are TRUE EXCEPT:1.MELD score does not predict occurrence of infection and mortality in hospitalized patients with cirrhosis.2.MELD score can be used to estimate mortality after surgery in patients with cirrhosis.3.MELD score can be used to estimate hepatic failure after hepatic resection for hepatocellular carcinoma.4.MELD score does not predict mortality after hepatic resection for hepatocellular carcinoma.5.MELD is a predictor of rebleeding and mortality after variceal hemorrhage.5.Regarding development of non-alcoholic fatty liver disease (NAFLD) after liver transplant the following are TRUE:1.Recurrence of NAFLD in patients transplanted for cryptogenic cirrhosis is almost universal.2.De-novo development of NAFLD in patients transplanted for other indications is rare.3.NAFLD post liver transplant is an insidious process requiring months to years to develop.4.Risk factors for recurrent or de-novo NAFLD after transplant are similar to those for NAFLD in native liver.5.Well defined evidence based paradigms are available for treatment of NAFLD after liver transplant.6.Regarding hepatitis C virus (HCV) infection in patients of end stage renal disease (ESRD) on regular hemodialysis the following are TRUE:1.The prevalence of HCV infection is higher in ESRD patients than in the general population.2.Duration of hemodialysis is not a risk factor for HCV positivity.3.Guidelines routinely recommend use dedicated dialysis machines, patient isolation, and a ban on reuse of dialyzer in patients with HCV infection.4.Routine screening for HCV infection should be done in all ESRD patients on hemodialysis.5.HCV positive patients have worse outcome after renal transplant.7.Regarding gastric varices in patients with portal hypertension the following are TRUE EXCEPT:1.Gastric varices account for only 5–10% of all upper digestive bleeds.2.Bleeding from gastric varices is correlated with hepatic venous pressure gradient.3.Patients with extrahepatic portal vein obstruction are more likely to have isolated gastric varices than patients with cirrhosis.4.Transjugular intrahepatic porto-systemic shunt is the first line treatment of gastric varices.5.Balloon occluded retrograde transvenous obliteration is a newer modality for treatment of gastric varices.8.Regarding the mechanisms responsible for progression of steatosis to steatohepatitis in NAFLD the following are TRUE EXCEPT:1.Hepatic triglyceride is directly toxic to the liver and degree of steatosis is correlated with inflammation.2.Free fatty acids cause liver injury directly as well as via lipid peroxidation.3.Patients with steatohepatitis have higher oxidative stress compared with chronic viral hepatitis.4.Levels of inflammatory cytokines are similar in steatohepatitis and simple steatosis.5.Iron overload and hemochromatosis gene mutations are important cause of oxidative stress in Asian patients with steatohepatitis.9.Regarding primary cholestatic liver diseases the following are TRUE:1.Specific anti-nuclear antibodies directed against nuclear body or envelope proteins are useful for diagnosis of primary biliary cirrhosis (PBC).2.The Barcelona and Paris criteria are used to asses response to therapy in primary sclerosing cholangitis (PSC).3.Ursodeoxycholic acid decreases risk of colonic neoplasia in PSC.4.Colectomy prior to liver transplantation decreases risk of recurrence of PSC after transplantation.5.Immunoglobulin G4-associated cholangitis is steroid unresponsive.10.Regarding evaluation of a patient with ascites the following are TRUE EXCEPT:1.Bedside inoculation of ascitic fluid into blood culture bottles increases bacterial detection.2.Yield of malignant cytology improves if multiple samples of fluid are tested.3.CA 125 is a useful investigation in a patient with suspected malignant ascites.4.Serum-ascites albumin gradient (SAAG) ≥ 1.1 is has good accuracy for underlying portal hypertensive ascites even in cases of mixed ascites.5.Pro-brain natriuretic peptide cannot differentiate ascites due to heart failure from ascites due to cirrhosis.

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