Disease Information for Acetaminophen (Tylenol) overdose

Clinical Manifestations
Signs & Symptoms
Diaphoresis profuse/active sweating/acute
Yellow skin discoloration
Relentless vomiting/retching/purging
Right Upper Quadrant Pain/Tenderness
Upper Abdominal Pain
Stupor/poor reponse to stimulus
Rumack-Matthew Nomogram abnormal
Disease Progression
Course/Slow curve fast break/over hours
Course/Slow curve/fast break over 24 hrs
Demographics & Risk Factors
Established Disease Population
Patient/Alcoholism/chronic alcoholic
Patient/Drug overdose
Patient/Depression, chronic
Population Group
Status/College student/campus living
Young Adult
Sex & Age Groups
Population/Young adult
Laboratory Tests
Abnormal Lab Findings (Non Measured)
AST/SGOT above 1000 units/very high
Transaminase elevation (Lab)
Transaminase Levels Extreme
Abnormal Lab Findings - Decreased
Glucose, blood (Lab)
Neutrophiles (Lab)
Abnormal Lab Findings - Increased
ALT (SGPT) (Alanine transferase) (Lab)
Ammonia blood (Lab)
Anion gap (Lab)
Aspartamine aminotransferase (SGOT, AST) (Lab)
AST (SGOT) (aspartamine transferase) (Lab)
Bilirubin, serum (Lab)
Glucose, blood (Lab)
URINE 5-Hyroxyindole acetic acid
Diagnostic Test Results
BX/Liver biopsy/Centrilobular necrosis/hepatic congestion
BX/Liver biopsy/Hepatocyte necrosis
Associated Diseases & Rule outs
Associated Disease & Complications
Acetamenophen (Tylenol) effect/toxicity
Acidosis, metabolic
Acute hepatic necrosis/yellow atrophy
Acute Renal Failure
Drug induced Hepatic toxicity
Erythema multiforme
Fetal cardiotoxicity/overdose
Fetal wastage
Fulminant hepatic failure
Hepatic encephalopathy
Hepatic necrosis, subacute
Metabolic Acidosis with High Anion Gap
Renal papillary necrosis
Toxic hepatitis
Disease Synergy - Causes
Risk factor/Alcohol ingestion
Risk factor/Alcoholism
Synergy/G6PD deficiency
Synergy/Grapefruit juice intake
Disease Mechanism & Classification
DRUG/Antiphlogistic/NSAIDS drug (category)
DRUG/Maternal medication/fetal effect
DRUG/P450 metabolic pathway/competitor
DRUG/Toxic metabolite (NAPQI) benzoquinoneimine
DRUG/Toxic metabolites (example)
DRUG/P450 cytochrome system/toxic metabolite
Pathophysiology/Glutathione (reduced) depleted stores
Pathophysiology/Liver cell necrosis
Pathophysiology/Renal concentration capacity defect
TOXIN/Increases Respiratory Rate
TOXIN/Latency after exposure/ingestion
TOXIN/Poison Toxic metabolites/effect
TOXIN/Slow curve fast break 24 hrs
4 hydroxyacetanilide, Acetamide N (4 hydroxyphenyl), Acetamidophenol, Acetaminophen, Acetaminophen (product), Acetaminophen (substance), ACETAMINOPHEN PREPARATION, Acetaminophen product, Acetominophen, ACMP, APAP, Hydroxyacetanilide, N (4 Hydroxyphenyl)acetamide, N (4 Hydroxyphenyl)acetanilide, N Acetyl p aminophenol, Overdose effect, p Acetamidophenol, p Hydroxyacetanilide, Paracetamol, Paracetamol chemical, Paracetamol (substance), Paracetamol product, Brand name/Datril (Acetomenophen), Brand name/Tylenol (Acetaminophen), Brand name/Tylox (Oxycodone) combination, Synonym/Paracetamol (APAP/Para-aminophenol)
Drug Therapy - Indication
RX/Acetylcysteine (Mucomist/NAC) (oral)
RX/Charcoal/Activated charcoal
RX/Cimetidine (Tagamet)
RX/Ethanol (Eythyl alcohol) infusion
RX/N-Acetylcysteine (NAC) IV ?
Other Treatments
TX/Gastric lavage.

Acetaminophen is widely used for its analgesic and antipyretic properties

It is now the most common drug for self poisoning, probably owing to its widespread use and its over-the-counter (OTC) availability

The toxic dose is approx. 140mg/kg

In the adult, hepatic toxicity is possible following a dose of only 7g; in patients taking enzyme-inducing drugs this "threshold" dose is lower

Fatalities can occur after a dose of 10-15g

Acetaminophen toxicity involves a primary centrilobular hepatic necrosis, but may also produce renal and pancreatic damage, cardiovascular collapse, and coma

Measurement of the acetaminophen blood level in overdose allows estimation of likely outcome, and so can be used to guide treatment

Acetaminophen toxicity is increased where there is enzyme induction

Hepatotoxicity is caused by a metabolite of acetaminophen, and not by the parent drug

Only 10% of patients develop a significant rise in hepatic enzymes

Acetaminophen is rapidly absorbed from the gut, and is metabolized by the liver where the metabolites are conjugated with glutathione and are then excreted in the urine. In acetaminophen poisoning, the conjugation pathways become saturated either by an overwhelming availability of the substrate or through a reduction in glutathione, and the toxic metabolite N-acetyl-p-benzoquinoneimine is available to bind to hepatocytes, causing a centrilobular hepatic necrosis

Patients with reduced glutathione stores (malnutrition, AIDS, and anorexia nervosa), or those taking hepatic enzyme-inducing drugs (phenobarbital, phenytoin, carbamazepine, rifampin, isoniazid, and chronic alcohol), are at a greater risk from acetaminophen toxicity

Treatment with N-acetylcysteine increases the availability of glutathione and is lifesaving

In the small number of fatalities, death usually occurs between days 3 and 5 postingestion from multiorgan failure

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External Links Related to Acetaminophen (Tylenol) overdose
PubMed (National Library of Medicine)
NGC (National Guideline Clearinghouse)
Medscape (eMedicine)
Harrison's Online (accessmedicine)
NEJM (The New England Journal of Medicine)