![]() ![]() However, successful implementation of a national childhood HBV immunization program can lead to a low prevalence of HBsAg among children and adolescents. α1-Antitrypsin deficiency with the PAS-positive periportal globules is associated with development of cirrhosis, but this is far less common than alcoholic cirrhosis.ġ4 E In regions where HBV is endemic, vertical transmission produces a carrier rate of 90% to 95%. Massive hepatocellular necrosis may occur rarely as a complication of HAV infection or ingestion of massive amounts of acetaminophen. Interface hepatitis is a characteristic of chronic active HBV or HCV infection. Budd-Chiari syndrome in hepatic venous thrombosis leads to hepatic enlargement, and it is rare. Concentric bile duct fibrosis is seen in primary sclerosing cholangitis, which may be idiopathic or may appear in association with inflammatory bowel disease. The architectural changes of cirrhosis persist for decades after cirrhosis develops. If the patient is currently not drinking alcohol, no fatty change (steatosis) would be present. The massive upper gastrointestinal bleeding suggests esophageal varices as a consequence of portal hypertension from cirrhosis. If liver stem cells support hepatocyte regeneration, and ductular reactions are minimal, then cirrhosis may be less progressive, and thin septae suggest some degree of regression. Portosystemic shunts give rise to esophageal varices that bleed to cause hematemesis.Ĩ F Portal bridging fibrosis and nodular hepatocyte regeneration are features of cirrhosis. In hepatopulmonary syndrome there are pulmonary intravascular dilations due to NO synthesis in the lung, not liver. Hyperbilirubinemia in this case is due to hepatic failure. ![]() This patient has no signs and symptoms of congestive heart failure-notice the normal JVP. The splanchnic arterial vasodilation is caused by increased nitric oxide (NO) production in the splanchnic arterial bed. The latter is an important factor in the pathogenesis of portal hypertension and consequent ascites. The ascites is caused by portal hypertension which results from two major changes: (1) mechanical obstruction to blood flow in the liver due to scarring and compression of sinusoids by regenerating nodules, and (2) splanchnic arterial vasodilation giving rise to hyperdynamic circulation which leads to increased portal venous blood flow. 6 E This patient most likely has alcoholic cirrhosis with hepatic failure and portal hypertension. ![]()
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