Cirrhosis

Cirrhosis is the late stage of chronic liver disease characterized by extensive fibrosis and regenerative nodules that distort liver architecture and impair function. It results from prolonged hepatocellular injury and can progress to liver failure and portal hypertension.

Common causes include chronic alcohol use, hepatitis B and C infections, and nonalcoholic fatty liver disease. Other causes are autoimmune hepatitis, biliary diseases such as primary biliary cholangitis and primary sclerosing cholangitis, and metabolic disorders like hemochromatosis and Wilson's disease.

Pathophysiology involves increased intrahepatic resistance to blood flow and loss of functional liver mass. This leads to portal hypertension, ascites, and impaired synthesis of proteins such as albumin and clotting factors, as well as impaired detoxification.

Clinical features range from fatigue and weight loss to jaundice. Complications include ascites, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatocellular carcinoma risk.

Diagnosis combines history, examination, laboratory tests showing chronic liver injury, and imaging. Ultrasound, CT, or MRI assess nodularity and signs of portal hypertension; elastography can measure liver stiffness. Liver biopsy is not always required; staging uses Child-Pugh and MELD scores.

Management targets the underlying cause and complications. This includes abstinence or treatment for alcohol and viral hepatitis, weight management for NAFLD, vaccination, and avoidance of hepatotoxins. For complications, diuretics and sodium restriction for ascites, paracentesis, endoscopic therapy or beta-blockers for varices, antibiotics for infections, lactulose and rifaximin for encephalopathy, and consideration of liver transplantation for advanced disease.

Prognosis depends on stage and complications, with scores such as Child-Pugh and MELD guiding prognosis and transplant decisions.