Hepatitis In hemochromatosis, excess amounts of iron accumulate in multiple body sites, including the liver, which can lead to cirrhosis. In Wilson's disease, excess amounts of copper accumulate in the liver and brain, causing cirrhosis and dementia. When the liver is involved, alpha-1-antitrypsin deficiency and Wilson's disease tend to present as hepatitis in the neonatal period or in childhood. Hemochromatosis typically presents in adulthood, with the onset of clinical disease usually after age 50. Ischemic hepatitis (also known as shock liver) results from reduced blood flow to the liver as in shock, heart failure, or vascular insufficiency. The condition is most
Mechanism of anoxic depolarization in the brain infarction, the release of glutamate and aspartate into the extracellular space causes an uncontrollable intracellular mobilization of Ca, mainly through the NMDA receptors. This is a critical stage in the development of neuronal damage, because it is the Ca overload that gives rise to several downstream cascades of events that lead to necrotic neuronal death, or to apoptosis, including free radical and nitric oxide productions that cause damage to the membrane. Another cytotoxic event that follows anoxic depolarization is lactate accumulation and acidosis as a result of glycolysis, which causes damage to the mitochondria. Ischemic insult also causes blood-brain barrier