Acute liver failure pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
== Pathophysiology== | == Pathophysiology== | ||
In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the [[hepatic lobule|centrizonal distribution]] and progressing towards portal tracts. The degree of [[parenchyma]]l inflammation is variable and is proportional to duration of [[disease]]<ref>{{cite journal |author=Boyer JL, Klatskin G |title=Pattern of necrosis in acute viral hepatitis. Prognostic value of bridging (subacute hepatic necrosis) |journal=N. Engl. J. Med. |volume=283 |issue=20 |pages=1063-71 |year=1970 |pmid=4319402 |doi=}}</ref | In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the [[hepatic lobule|centrizonal distribution]] and progressing towards portal tracts. The degree of [[parenchyma]]l inflammation is variable and is proportional to duration of [[disease]]<ref>{{cite journal |author=Boyer JL, Klatskin G |title=Pattern of necrosis in acute viral hepatitis. Prognostic value of bridging (subacute hepatic necrosis) |journal=N. Engl. J. Med. |volume=283 |issue=20 |pages=1063-71 |year=1970 |pmid=4319402 |doi=}}</ref>. | ||
==References== | ==References== |
Revision as of 20:11, 28 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the centrizonal distribution and progressing towards portal tracts. The degree of parenchymal inflammation is variable and is proportional to duration of disease[1].