TUM Library

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Contents: Portal hypertension causes regional circulatory derangements that result in extra- and intra-vascular volume overload and organ dysfunction -- Vascular tone is mediated by autonomic input and chemical mediators many of which are released by local vascular endothelium -- Intrahepatic portal hypertension develops as a result of anatomic changes in the cirrhotic liver that cause sinusoidal narrowing and loss of compliance -- Reflex SMA vasoconstriction and portosystemic shunting up-regulate VEGF eNOS and iNOS with resultant vasodilation -- There is secondary: ADH secretion with retention of free water; renal salt retention; renal afferent arteriolar vasoconstriction -- Affected individuals develop progressive volume overload with associated afterload reduction and increases in cardiac output (hyperdynamic circulation) -- Fluid is forced off the surface of the liver and accumulates in the abdominal cavity as ascites -- Blood is shunted around the liver through latent venous connections that become varices -- Renal function is impaired (hepatorenal syndrome) -- Volume overload may cause secondary pulmonary hypertension -- Affected individuals may also develop primary pulmonary hypertension due to anatomic alterations of pulmonary microvasculature (porto-pulmonary hypertension) -- The ability of the heart to respond to stress is impaired -- Patients develop intrapulmonary shunts that cause hypoxemia (hepatopulmonary syndrome) -- The only real remedy for these problems is orthotopic liver transplantation.

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