injuries poisoning
Acetaminophen Poisoning
Pathophysiology of Acetaminophen Poisoning
The principal toxic metabolite of acetaminophen, N-acetyl-p-benzoquinone imine (NAPQI), is produced by the hepatic cytochrome P-450 enzyme system; glutathione stores in the liver detoxify this metabolite. An acute overdose depletes glutathione stores in the liver. As a result, NAPQI accumulates, causing hepatocellular necrosis and possibly damage to other organs (eg, kidneys, pancreas). Theoretically, alcoholic liver disease Alcohol-Related Liver Disease Alcohol consumption is high in most Western countries. According to a survey using the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) definition of alcohol... read more or undernutrition Overview of Undernutrition Undernutrition is a form of malnutrition. (Malnutrition also includes overnutrition.) Undernutrition can result from inadequate ingestion of nutrients, malabsorption, impaired metabolism, loss... read more could increase risk of toxicity because hepatic enzyme preconditioning may increase formation of NAPQI and because undernutrition (also common among alcoholics) reduces hepatic glutathione stores. However, therapeutic doses of acetaminophen in alcoholic patients are not associated with hepatic injury.