Liver
Core concepts
Organize by injury pattern: hepatocellular versus cholestatic. Viral hepatitis serologies are heavily tested: acute hepatitis B shows HBsAg and anti-HBc IgM; resolved infection shows anti-HBs and anti-HBc IgG; isolated anti-HBc can reflect window period or remote infection. Hepatitis C is now curable with direct-acting antivirals. Autoimmune hepatitis shows elevated IgG and positive ANA or anti-smooth muscle antibody; primary biliary cholangitis shows antimitochondrial antibody with cholestatic enzymes.
Cirrhosis complications include varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatorenal syndrome. Ascitic fluid analysis: a polymorphonuclear count of 250 or more defines SBP. Model for End-stage Liver Disease score guides transplant priority. Drug-induced liver injury, Wilson disease in young patients, and hemochromatosis (ferritin plus transferrin saturation) round out the differential.
Traps
Do not diagnose SBP on culture alone; the cell count drives treatment. Distinguish hepatorenal syndrome from prerenal azotemia by lack of response to volume. Isolated anti-HBc needs further testing before concluding immunity. Transaminase levels do not correlate with severity in acute liver failure; encephalopathy and coagulopathy define it.
Rule of thumb
In any patient with cirrhosis and ascites, perform diagnostic paracentesis on admission; a PMN count of 250 or more means start antibiotics even before cultures return.