Includes Tylenol and numerous brands and products including<unk> 
Now the most common cause of acute liver failure in the US
Adults: 4 g/day
Peds: 75 mg/kg/day
>10 g or >200 mg/kg as single ingestion or over 24hr period OR
>6 g or >150 mg/kg per 24hr period x 2days
200 mg/kg in healthy children 1-6 years of age
Toxic dose is 150 mg/kg
Give NAC if level is >150 mcg/mL four hours post-ingestion
Initial loading dose of NAC is 150 mg/kg IV (140 mg/kg PO)
Poorly understood
Possibly through inhibition of Cyclooxygenase-3 (COX-3)
Decreases synthesis of prostaglandins
Antipyresis through inhibition of hypothalamic heat center
Decreases synthesis of prostaglandins
A - Rapid and near complete absorption
D - Vd = 0.95 L/kg
M - T 1/2 = 1.5-2 hrs
40-60% - Glucuronidation
20-40% - Sulfuronidation
5-10% - Metabolism through CYP450/CYP2E1 (Forms NAPQI)
Metabolized by first-order kinetics
E - Conjugated and unconjugated excreted through kidneys
40-60% - Glucuronidation
20-40% - Sulfuronidation
5-10% - Metabolism through CYP450/CYP2E1 (Forms NAPQI)
Metabolized by first-order kinetics<unk>  is metabolized by sulfation and glucuronide conjugation. This process becomes overwhelmed in overdose and metabolism is shifted to the CYP 450 pathway generating toxic NAPQI.
APAP toxic metabolite NAPQI usually quickly detoxified by glutathione stores in liver
In overdose, glutathione runs out, NAPQI accumulates → liver injury
NAC increases availability of glutathione
NAC is a precursor
In overdose, glutathione runs out, NAPQI accumulates → liver injury
NAC is a precursor
Acetaminophen toxicity
Acetaminophen toxicity 
Mescaline toxicity
Viral hepatitis
Cocaine toxicity
Hepatitis A
Carbamate toxicity
Hepatitis B