Abstract
Chronic hepatic injury from alcohol, viral hepatitis, fatty liver disease, or other causes can result in cirrhosis of the liver. At the cellular level, repeated injury and healing causes activation of resident hepatic fibroblasts, known as stellate cells, which produce extracellular matrix components that result in fibrosis of the liver and architectural distortion. As a result, blood flow through the liver is slowed and leads to increased pressure in the mesenteric venous system known as portal hypertension. The complications of portal hypertension are numerous and include ascites, spontaneous bacterial peritonitis, varices, volume overload, hepatorenal syndrome, hepatic encephalopathy, portopulmonary hypertension, hepatopulmonary syndrome, and cirrhotic cardiomyopathy. This chapter shall characterize the pathophysiology of portal hypertension and how patients with portal hypertension present to clinical attention. The approach to treatment for ascites, varices, and hepatic encephalopathy will be discussed as the main clinically encountered complications of portal hypertension.
Published Version
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