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Ischemic hepatitis, also known as shock liver, is a condition defined as an acute liver injury caused by insufficient blood flow (and consequently insufficient oxygen delivery) to the liver. [5]
The liver plays a vital role in many metabolic processes in the body including protein synthesis, detoxification, nutrient storage (such as glycogen), platelet production and clearance of bilirubin. With progressive liver damage; hepatocyte death and replacement of functional liver tissue with fibrosis in cirrhosis, these processes are disrupted.
Wilson's disease, a condition where copper builds up in the body, can be managed with drugs that bind copper, allowing it to be passed from the body in urine. [59] In cholestatic liver disease, (where the flow of bile is affected due to cystic fibrosis [60]) a medication called ursodeoxycholic acid may be given. [61]
A hepatotoxin (Gr., hepato = liver) is a toxic chemical substance that damages the liver.. It can be a side-effect, but hepatotoxins are also found naturally, such as microcystins and pyrrolizidine alkaloids, or in laboratory environments, such as carbon tetrachloride, or far more pervasively in the form of ethanol (drinking alcohol).
Liver regeneration is the process by which the liver is able to replace damaged or lost liver tissue. The liver is the only visceral organ with the capacity to regenerate. [1] [2] The liver can regenerate after partial hepatectomy or injury due to hepatotoxic agents such as certain medications, toxins, or chemicals. [3]
The complications are hepatic encephalopathy and impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood). The 1993 classification defines hyperacute as within 1 week, acute as 8–28 days, and subacute as 4–12 weeks; [ 1 ] both the speed with which the disease develops and the underlying ...
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]
The hepatocyte plates are one cell thick in mammals and two cells thick in the chicken. Sinusoids display a discontinuous, fenestrated endothelial cell lining. The endothelial cells have no basement membrane and are separated from the hepatocytes by the space of Disse, which drains lymph into the portal tract lymphatics. [citation needed]