Pharmacology: Antidotes Flashcards
Acetaminophen toxicity
What is the MOA?
N-acetylcysteine (replenishes glutathione)
Salicylate toxicity
NaHCO3 (alkalinize urine)
Dialysis
Amphetamines (basic) toxicity
NH4Cl (acidify urine)
Acetylcholinesterase inhibitor toxicity
Atropine (reverse mACh sx, but not nACh effects–muscle paralysis)
Pralidoxime (affects both m- and n-ACh sx)
Organophosphate toxicity
Atropine (anti-ACh; reverse mACh sx, but not nACh effects–muscle paralysis)
Pralidoxime (affects both m- and n-ACh sx)
Antimuscarinic, anticholinergic toxicity
Pysostigmine salicylate
Beta-blocker overdose
Glucagon (increase of cAMP in the myocardium, in effect bypassing the β-adrenergic second messenger system)
Digitalis toxicity - “yellow vision” with yellow/green halos, bradycardia, prolonged PR
Stop dig. Anti-dig Fab fragments (binds dig)
Treat arrythmias: normalize K+, give Lidocaine, Mg2+
Iron
Deferoxamine (Fe chelator)
Lead
CaEDTA
Dimercaprol (BAL)
Succimer (dimercaptosuccinic acid)
Penicillamine
Mercury
CaEDTA
Dimercaprol (BAL)
Succimer (dimercaptosuccinic acid)
Arsenic
Chelators:
Dimercaprol (BAL)
Succimer (dimercaptosuccinic acid)
Penicillamine
Gold
Chelators:
Dimercaprol (BAL)
Succimer (dimercaptosuccinic acid)
Penicillamine
Copper
Penicillamine
Cyanide
Amyl nitrite: oxidant, induces the formation of metHb. mHb in turn can sequester cyanide as cyanomethemoglobin.
Hydroxocobalamin (B12): binds CN-
Sodium thiosulfate: donating additional sulfur to liver rhodanase to enhance metabolism and detox CN- to thioctyanate