The cytochrome P450 system oxidizes acetaminophen to produce a highly reactive intermediary metabolite, N-acetyl-p-benzo-quinone imine (NAPQI).
Ipecac has no role in acetaminophen overdose because the vomiting it induces delays the effective administration of activated charcoal and (oral) NAC.
Previously there was reluctance to give activated charcoal in acetaminophen overdose, because of concern that it may also absorb NAC.
After acetaminophen overdose, when AST and ALT exceed 1000 IU/L, acetaminophen-induced hepatotoxicity can be diagnosed.
Acetaminophen is metabolized primarily in the liver, where most of it is converted to inactive compounds by conjugation with sulfate and glucuronide, and then excreted by the kidneys.
The toxic dose of acetaminophen is highly variable.
Use of a pain-killing drug like acetaminophen is just one approach, which may be used alone or in cooperation with other treatments.
Like NSAIDs and unlike opioid analgesics, acetaminophen does not cause euphoria or alter mood.
In 1899, acetaminophen was found to be a metabolite of acetanilide.
Gastric lavage is helpful within the first two to four hours of acetaminophen ingestion.
Without timely treatment, acetaminophen overdoses can lead to liver failure and death within days.
That is, it has been assumed that acetaminophen acts by reducing production of prostaglandins, which are involved in the pain and fever processes, by inhibiting the cyclooxygenase (COX) enzyme.
NAC is most effective if given early, but still has beneficial effects if given as late as 48 hours after acetaminophen ingestion.
The toxic effects of acetaminophen are due to a minor alkylating metabolite (N-acetyl-p-benzo-quinone imine), not acetaminophen itself or any of the major metabolites.
Individuals who have overdosed on acetaminophen generally have no specific symptoms for the first 24 hours.
Acetaminophen absorption from the gastrointestinal tract is complete within two hours under normal circumstances.
The mortality rate from acetaminophen overdose starts to climb two days after the ingestion, reaches a maximum on day four, and then gradually decreases.
The prognosis of acetaminophen varies depending on the dose and the appropriate treatment.
Acetaminophen and NSAIDs have the benefit of being free of problems with physiological addiction, chemical dependency, physiological tolerance, and withdrawal.
Drug nomograms are available that will estimate a risk of toxicity based on the serum concentration of acetaminophen at a given number of hours after ingestion.
By this time, acetaminophen had already been synthesized by Harmon Northrop Morse via the reduction of p-nitrophenol with tin in glacial acetic acid.
Prostaglandins participate in the inflammatory response, but acetaminophen has no appreciable anti-inflammatory action.
Acetaminophen should not be taken after alcohol consumption, because the liver, when engaged in alcohol breakdown, cannot properly dispose of acetaminophen, thus increasing the risk of hepatotoxicity.
One gram of acetaminophen three times a day is equivalent to analgesia provided by NSAIDs in osteoarthritis, for example.
Acetaminophen is also combined with oxycodone and marketed in the U.S. as "Percocet."
An acetaminophen level drawn in the first four hours after ingestion may underestimate the amount in the system because acetaminophen may still be in the process of being absorbed from the gastrointestinal tract.
When co-administered with amitriptyline, 50 mg twice a day, the combination is as effective as acetaminophen with codeine, but does not lose effectiveness as an analgesic over time as does chronic administration of narcotics.
To determine the risk of potential hepatotoxicity, the acetaminophen level should be traced along the standard nomogram.
Excessive consumption of alcohol can impair liver function and increase the potential toxicity of acetaminophen.
Acetaminophen is an organic compound that inhibits synthesis of prostagladins in the central nervous system, thus raising the body's pain threshold, and further impacts the temperature-regulating center of the brain, thus reducing fever.
Oral NAC (available in the United States under the name "Mucomyst®") is a safe drug, is indicated in acetaminophen overdose during pregnancy, and life-threatening adverse reactions do not occur.
Acetaminophen is extremely toxic to cats and should not be given to them under any circumstances.
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Acetaminophen has long been suspected of having a similar mechanism of action to aspirin because of the similarity in structure.
Chronic alcoholism, which also induces CYP2E1, is also well known to increase the risk of acetaminophen-induced hepatotoxicity (Zimmerman & Maddrey 1995).
When used responsibly, acetaminophen is one of the safest medications available for analgesia.
U.S. patent 6,126,967 filed September 3, 1998, was granted for "Extended release acetaminophen particles."
The treatment for uncomplicated acetaminophen overdose, similar to any other overdose, is gastrointestinal decontamination.
In 1963, acetaminophen was added to the British Pharmacopoeia, and has gained popularity since then as an analgesic agent with few side effects and little interaction with other pharmaceutical agents.
Activated charcoal absorbs acetaminophen well and therefore reduces its gastrointestinal absorption.
In 1893, acetaminophen was discovered in the urine of individuals who had taken phenacetin, and was concentrated into a white, crystalline compound with a bitter taste.
Damage generally occurs in hepatocytes as they metabolize the acetaminophen.