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NAFLD comprises two histological categories: NAFL, and the more aggressive form NASH. The presence of at least 5% fatty liver is common to both NAFL and NASH, but the features of substantial lobular inflammation and hepatocyte injuries such as ballooning or Mallory hyaline only occur in NASH.
In histology (microscopic anatomy), the lobules of liver, or hepatic lobules, are small divisions of the liver defined at the microscopic scale. The hepatic lobule is a building block of the liver tissue, consisting of portal triads, hepatocytes arranged in linear cords between a capillary network, and a central vein.
The intercellular surfaces are the ones that are between two adjacent hepatocytes and they are not in contact with sinusoids or canaliculi. These are simple surfaces specialized in the cellular adherence and in the communication between hepatocytes through gap junctions. [6] Hepatocytes measure between 20 and 30 μm in each dimension
The priming phase of liver regeneration following partial hepatectomy occurs outside of hepatocytes in the ECM and it prepares the liver for regeneration and hepatocyte proliferation. [5] During proliferation phase of liver regeneration, there is a communication between β-catenin, the Notch signaling pathway, and two growth factors, EGF and HGF.
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]
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.
Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver cells surrounding the central venule of the liver) to become deoxygenated compared to the relatively better-oxygenated periportal hepatocytes adjacent to the hepatic arterioles.
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 ...