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Histopathology of shock liver, showing its hallmark [1] pathologic finding centrilobular necrosis but viable periportal hepatocytes. H&E stain. The necrotic hepatocytes have barely discernible nuclei. Symptoms: Mental confusion [2] Causes: Heart failure, Infection [3] Diagnostic method: Doppler ultrasound, Blood test [3] Treatment
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.
The typical hepatocyte is cubical with sides of 20-30 μm, (in comparison, a human hair has a diameter of 17 to 180 μm). [1] The typical volume of a hepatocyte is 3.4 x 10 −9 cm 3 . [ 2 ] Smooth endoplasmic reticulum is abundant in hepatocytes, in contrast to most other cell types.
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.
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.
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]
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.
This manifests as lipid peroxidation, mitochondrial damage, and glutathione (an endogenous antioxidant) depletion. [7] Damaged hepatocytes release Danger associated molecular patterns (DAMPs) which are molecules that lead to further activation of the immune system's inflammatory response and further hepatocyte damage. [7]