Cirrhosis results from fibrosis and nodular regeneration after hepatic necrosis. The two most common causes of cirrhosis in the United States are alcoholic cirrhosis and posthepatic cirrhosis. The end result of cirrhosis is liver failure and portal hypertension. Portal hypertension leads to hepatic vascular resistance causing va-riceal hemorrhage while liver failure leads to encephalopathy and ascites (Table 13.1).

Cirrhosis is categorized as:

1. prehepatic

2. intrahepatic

3. post-hepatic

Intrahepatic portal hypertension may be further classified as presinusoidal, sinusoidal, or postsinusoidal. Portal vein thrombosis is the most common cause of pre-hepatic portal hypertension. Schistosomiasis is the most common cause of presinusoidal intrahepatic portal hypertension, while alcoholic cirrhosis is the most common cause of sinusoidal hypertension. Budd-Chiari syndrome is one cause of postsinusoidal hypertension.

Patients with cirrhosis often have elevated liver enzymes. These can include as-partate aminotransferase (AST) and alanine aminotransferase (ALT) as well as alkaline phosphatase, and gamma-glutamyl transpeptidase (GGT).

Elevation of the hepatocellular enzymes to more than three times their normal level is indicative of significant, ongoing hepatocellular necrosis, which is often present

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