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Centrilobular necrosis (CN) is a nonspecific histopathological observation brought on by hepatotoxins like acetaminophen (paracetamol), [1] thioacetamide, tetrachloride, [2] cardiac hepatopathy due to acute right sided cardiac failure, and congestive hepatic injury in veno-occlusive disease, [3] or hypoxic injury due to ischemia. [2]
Congestive hepatopathy, is liver dysfunction due to venous congestion, usually due to congestive heart failure. The gross pathological appearance of a liver affected by chronic passive congestion is "speckled" like a grated nutmeg kernel; the dark spots represent the dilated and congested hepatic venules and small hepatic veins. The paler areas ...
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
Obstruction also causes centrilobular necrosis and peripheral lobule fatty change due to ischemia. If this condition persists chronically what is known as nutmeg liver will develop. Kidney failure may occur, perhaps due to the body sensing an "underfill" state and subsequent activation of the renin - angiotensin pathways and excess sodium ...
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 prevailing theory for the development of autoimmune hepatitis is thought to be the interplay of genetic predisposition, an environmental trigger (virus, drugs, herbs, immunizations), and failure of the native immune system resulting in chronic inflammation of hepatocytes and subsequent fibrosis of the liver. [7] [8] [9]
The degree of parenchymal inflammation is variable and is proportional to duration of disease. [7] [20] [21] Zone 1 (periportal) occurs in phosphorus poisoning or eclampsia. Zone 2 (mid-zonal), although rare, is seen in yellow fever. Zone 3 (centrilobular) occurs with ischemic injury, toxic effects, carbon tetrachloride exposure, or chloroform ...
Necrosis begins after 20 minutes of an infarction. Under 4 hours of ischemia, there are no gross or microscopic changes noted. [2] From 4-24 hours coagulative necrosis begins to be seen, which is characterized by the removal of dead cardiomyocytes through heterolysis and the nucleus through karyorrhexis, karyolysis, and pyknosis. [3]