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Physical agents such as heat or radiation can damage a cell by literally cooking or coagulating their contents. Impaired nutrient supply, such as lack of oxygen or glucose, or impaired production of adenosine triphosphate (ATP) may deprive the cell of essential materials needed to survive. [3] Metabolic: Hypoxia and ischemia; Chemical agents
Furthermore, decreased levels of IL-13, an antagonistic cytokine of IL-6 was found to be closely associated with short-term (90-day) mortality in severe alcoholic hepatitis patients. [8] Some signs and pathological changes in liver histology include: Mallory's hyaline body – a condition where pre-keratin filaments accumulate in hepatocytes ...
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.
This results in tissue damage to the endothelium because of proteases, oxygen radicals, prostanoids and other substances from leukocytes. Kupffer cell activation contributes to pathogenesis of both chronic and acute alcoholic liver disease in response to ethanol-induced liver injury, common in chronic alcoholics. Chronic alcoholism and liver ...
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 ...
Histopathology of a ballooning hepatocyte.png, H&E stain. Ballooning degeneration centre-left and centre-right. H&E stain. A Councilman body can also be seen in the upper-right of the section. In histo pathology, ballooning degeneration, formally ballooning degeneration of hepatocytes, is a form of liver parenchymal cell (i.e. hepatocyte) death.
The increase in intracellular reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection. [25] This increase in reactive oxygen species causes inflammation [25] and more than 20 types of DNA damage. [26]
The hepatocyte is a cell in the body that manufactures serum albumin, fibrinogen, and the prothrombin group of clotting factors (except for Factors 3 and 4). [ citation needed ] It is the main site for the synthesis of lipoproteins , ceruloplasmin , transferrin , complement , and glycoproteins .