Budd-Chiari syndrome pathophysiology: Difference between revisions
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== Overview== | == Overview== | ||
Any obstruction of the [[vein|venous]] vasculature of the liver is referred to as Budd-Chiari syndrome, from the [[venule]]s to the[[right atrium]]. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes hepatic necrosis and eventual centrilobular fibrosis due to ischemia. Renal failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin-angiotensin pathways and excess sodium retention. | |||
==Pathophysiology== | |||
==References== | ==References== | ||
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[[Category:Needs content]] | [[Category:Needs content]] | ||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
[[category:Hepatology]] | [[category:Hepatology]] | ||
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{{WH}} | |||
Revision as of 17:29, 18 July 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to theright atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes hepatic necrosis and eventual centrilobular fibrosis due to ischemia. Renal failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin-angiotensin pathways and excess sodium retention.