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In pharmaceutical and veterinary applications, propionic acid and its saltsespecially sodium propionateare used as auxiliary and therapeutic substances

Some patients experience a brief head rush immediately after injecting, which resolves in minutes

Introduction Mechanism of action central reversible inhibition of cyclooxygenase (COX) inactivated peripherally Clinical use used as an antipyretic and analgesic especially useful in the pediatric population to avoid a risk of Reye syndrome in children with viral infection not used for inflammation Toxicity massive hepatic necrosis pathogenesis cytochrome P450 in the liver metabolizes acetaminophen into N-acetyl-p-benzoquinoneimine (NAPQI) NAPQI depletes glutathione, which forms toxic byproducts that result in hepatic necrosis chronic alcoholism induces cytochrome P450, thus exacerbating the toxicity clinical manifestations immediately after ingestion, nausea, vomiting, malaise, and lethargy are common early manifestations of overdose are nonspecific and are not reliable predictors of hepatotoxicity, so serum acetaminophen levels should be determined liver enzymes may rise at 8-12 hours if patients severely overdose 48-72 hours later, hepatitis progresses rapidly and patients may die from multi-organ failure, including acute renal failure treatment N-acetylcysteine (NAC) is the antidote for acetaminophen toxicity useful for up to 24 hours after ingestion activated charcoal if ingested within 4 hours acetaminophen levels should be drawn 4 hours after ingestion or immediately if ingestion occurred more than 4 hours prior to evaluation minimal gastrointestinal irritation Create a free account or log in to see the cards.

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