​Pathology - Liver Cirrhosis

​Pathology - Liver Cirrhosis
Micronodular cirrhosis can be caused by alcoholism, hemochromatosis, or Wilson disease.
Macronodular liver cirrhosis can be caused by hepatitis B virus (HBV), hepatitis C virus (HCV), drug-induced hepatitis, or biliary cirrhosis. Wilson's disease: lack of alpha-1-antitrypsin; advanced cirrhosis caused by alcohol consumption.

Pathology 
In micronodular cirrhosis, nodules are homogenous and smaller than 3 mm. In macronodular cirrhosis, fibrous bands divide the liver into irregular nodules larger than 3 mm.
Microscopic findings show widespread liver fibrosis followed by nodular regeneration without typical hepatic structure, along with reconfiguration of vascular patterns.
Pathophysiology: Liver damage causes elevated portal venous pressures, leading to redirected blood flow to portosystemic anastomoses such as gastroesophageal collaterals, resulting in esophageal varices. Reduced plasma oncotic pressure caused by decreased albumin production in the failing liver, along with impaired breakdown of aldosterone, leads to peripheral edema and ascites.
Encephalopathy occurs due to the liver's inability to metabolize ammonia, which is a neurotoxic.
Weakness: weight loss; ascites; jaundice; spider nevi; gynecomastia; testicular atrophy; asterixis; coarse hand tremor; ankle edema.

Complications may involve gastrointestinal hemorrhage from esophageal or gastric varices. Hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, and heightened susceptibility to hepatocellular cancer.


Laboratory results include macrocytic anemia, thrombocytopenia, delayed prothrombin time due to coagulation-factor insufficiency, hypoalbuminemia, hyperbilirubinemia, elevated ALT, AST, and ALP values, and high blood ammonia levels.

Treatment includes alcohol abstinence, low-salt diet, diuretic therapy, lactulose for encephalopathy, and liver transplant.