For acetaminophen toxicity

Figure 18.9. Proposed scheme for acetaminophen toxicity and the role of mitochondria and peroxnitrite. [Adapted from Jaeschke and Bajt (2006).]...

Indications Emphysema, bronchitis, tuberculosis, bronchiectasis, tracheostomy care, antidote for acetaminophen toxicity... 

Acetaminophen may worsen kidney function and increase blood pressure.1516 Nevertheless, acetaminophen remains the preferred analgesic for mild to moderate pain in patients with hypertension or kidney disease owing to the greater risks associated with NSAID use.17 Monitoring specifically for these toxicities generally is unnecessary. 

The answer is c. (Hardman, pp 632-633.) Nausea, vomiting, abdominal pain, and diarrhea are early signs of the severe liver toxicity caused by high levels of acetaminophen other symptoms of acetaminophen toxicity include dizziness, excitement, and disorientation. N-acetyl-L-cysteine is the appropriate treatment for acetaminophen overdose. 

Oral 5 mg oxycodone plus 325 or 500 mg acetaminophen tablets. Note High-dose acetaminophen has potential for hepatic toxicity with repeated use. 

Acetaminophen [a seat a MIN oh fen] and phenacetin [fe NASS e tin] act by inhibiting prostaglandin synthesis in the CNS. This explains their antipyretic and analgesic properties. They have less effect on cyclooxygenase in peripheral tissues, which accounts for their weak anti-inflammatory activity. Acetaminophen and phenacetin do not affect platelet function or increase blood clotting time, and they lack many of the side-effects of aspirin. [Note Phenacetin can no longer be prescribed in the United States because of its potential for renal toxicity. However, it is present in some proprietary preparations.]... 

FIGURE 37.2. Metabolism and mechanism of acetaminophen toxicity. Bioactivation of acetaminophen by P450 enzymes results in the formation of the reactive intermediate (NAPQI) which forms covalent protein adducts with glutathione which is then converted to mercapturic acid. When the amount of the reactive metabolite formed exceeds the glutathione available for binding, the excess metabolite binds to tissue molecules resulting in centrilobular hepatic necrosis. 

The packaging of the kava products was unavailable for identification purposes. Liver biopsy revealed active fulminant hepatitis with extensive necrosis and tests for viral hepatitis were negative. She underwent a successful liver transplantation and was able to return to normal activity upon recovery (34). Unfortunately, no information was provided indicating that acetaminophen toxicity had been ruled out, and the observed toxic effect could also have been associated with a large, undiagnosed acetaminophen ingestion. 

C. M-acetyl benzoquinoneimine is toxic, whereas acetaminophen glu-curonide, acetaminophen sulfate, and acetaminophen glutathionate are nontoxic acetaminophen conjugates. A -acetyl-p-aminophenol is another name for acetaminophen. 

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