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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 ...
Adequate patient education and training on correct procedure for self-administration can lower the incidence rate of reactions. [2] Rotating injection sites, proper sterilization, and allowing the medication to reach room temperature before injection can help prevent ISRs. Applying a cold compress after the injection may be helpful. [2]
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
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.
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]
Extravasation is the leakage of intravenously (IV) infused, and potentially damaging, medications into the extravascular tissue around the site of infusion. The leakage can occur through brittle veins in the elderly, through previous venipuncture access, or through direct leakage from wrongly positioned venous access devices.