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In ALF, hepatic encephalopathy leads to cerebral edema, coma, brain herniation, and eventually death. Detection of encephalopathy is central to the diagnosis of ALF. It may vary from subtle deficit in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV). Patients presenting as acute and hyperacute liver failure ...
[1] More than 40% of people with cirrhosis develop hepatic encephalopathy. [7] More than half of those with cirrhosis and significant HE live less than a year. [1] In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years. [1] The condition has been described since at least 1860. [1]
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
Hepatotoxicity and drug-induced liver injury also account for a substantial number of compound failures, highlighting the need for toxicity prediction models (e.g. DTI), [2] and drug screening assays, such as stem cell-derived hepatocyte-like cells, that are capable of detecting toxicity early in the drug development process. [3]
Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is a condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
Oxidative DNA damage is mutagenic [27] and also causes epigenetic alterations at the sites of DNA repair. [28] Epigenetic alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate or result in the cell avoiding apoptosis , and thus contribute to liver disease. [ 29 ]
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]
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.