Search results
Results from the WOW.Com Content Network
This process is impaired in all subtypes of hepatic encephalopathy, either because the hepatocytes (liver cells) are incapable of metabolising the waste products or because portal venous blood bypasses the liver through collateral circulation or a medically constructed shunt.
Small vacuoles of fat accumulate and become dispersed within cytoplasm. Mild fatty change may have no effect on cell function; however, more severe fatty change can impair cellular function. In the liver, the enlargement of hepatocytes due to fatty change may compress adjacent bile canaliculi, leading to cholestasis. Depending on the cause and ...
In ALF, hepatic encephalopathy leads to cerebral edema, coma, brain herniation, and eventually death. Detection of encephalopathy is central to the diagnosis of ALF. It may vary from subtle deficit in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV). Patients presenting as acute and hyperacute liver failure ...
Late complications of cirrhosis or liver failure include portal hypertension (high blood pressure in the portal vein due to the increased flow resistance through the damaged liver), coagulation disorders (due to impaired production of coagulation factors), ascites (heavy abdominal swelling due to buildup of fluids in the tissues) and other ...
The decreased blood flow to the liver is usually due to shock or low blood pressure. However, local causes involving the hepatic artery that supplies oxygen to the liver, such as a blood clot in the hepatic artery, can also cause ischemic hepatitis. [medical citation needed]
This impaired compensatory liver regenerative response further leads to a ductular reaction; a type of abnormal liver cell architecture. [7] Due to the release of DAMPs and PAMPs, an acute systemic inflammatory state can develop after extensive alcohol intake that dominates the clinical landscape of acute severe alcoholic hepatitis.
Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency [11] and glycogen storage disease type II. [ 12 ] In transthyretin-related hereditary amyloidosis , the liver produces a mutated transthyretin protein which has severe neurodegenerative or cardiopathic effects.
Hepatotoxicity and drug-induced liver injury also account for a substantial number of compound failures, highlighting the need for toxicity prediction models (e.g. DTI), [2] and drug screening assays, such as stem cell-derived hepatocyte-like cells, that are capable of detecting toxicity early in the drug development process. [3]