Hepatic encephalopathy pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Revision as of 17:21, 7 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Pathophysiology
Due to the presence of scarring within the liver, cirrhosis leads to obstruction of the passage of blood through the liver causing portal hypertension. This means it is difficult for blood from the intestines to go through the liver to get back to the heart. Portal-systemic anastamoses ("shunts") develop, and portal blood (from the intestinal veins) will bypass the liver and return to the heart via another route without undergoing first-pass detoxification by the liver.
Furthermore, in cirrhosis and other forms of liver disease, the damaged liver will not be functioning as well as it should be, so even blood that does travel through the liver may not be as detoxified as it otherwise would be. In fact, if the degree of liver damage and malfunction is severe, then, even in the absence of portal hypertension and the consequent bypassing of the liver by blood coming in from the intestines, hepatic encephalopathy will still occur. Such may well be the case, for example, following severe injury due to acetaminophen poisoning or acute viral infection (e.g. hepatitis A).
The toxic substances which accumulate in the setting of liver failure and affect the brain are still not well understood. They have been thought to include ammonia (NH3) and mercaptans. Ammonia is normally converted to urea by the liver and, as with mercaptans, is produced by the bacterial breakdown of protein in the intestines.
Ammonia can cross the blood-brain barrier, where it causes the support cells of the brain (astrocytes) to swell. The swelling of the brain tissue increases intracranial pressure, and can lead to coma or death via herniation of the brainstem.