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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
<10% surface area <1 cm in depth - II: 10–50% surface area: 1–3 cm - III >50% or >10 cm >3 cm Any injury in the presence of a liver vascular injury or active bleeding contained within liver parenchyma IV: 25–75% of a hepatic lobe Active bleeding extending beyond the liver parenchyma into the peritoneum V >75% of a hepatic lobe
Hepatocytes are separated from the sinusoids by the space of Disse. Hepatic stellate cells are present in the space of Disse and are involved in scar formation in response to liver damage. Defenestration happens when LSECs are lost rendering the sinusoid as an ordinary capillary. This process precedes fibrosis. [6]
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.
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.
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]
Simplified control circuit of human thermoregulation. [8]The core temperature of a human is regulated and stabilized primarily by the hypothalamus, a region of the brain linking the endocrine system to the nervous system, [9] and more specifically by the anterior hypothalamic nucleus and the adjacent preoptic area regions of the hypothalamus.
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 ...