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This deck focuses on Overdose And Exposure Management, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Study Overdose And Exposure Management in NAPLEX with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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Which antidote is used for acetaminophen overdose to prevent hepatic injury?
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N-acetylcysteine (NAC). Replenishes glutathione to neutralize the hepatotoxic metabolite NAPQI in acetaminophen overdose.
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This deck focuses on Overdose And Exposure Management, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: N-acetylcysteine (NAC). Replenishes glutathione to neutralize the hepatotoxic metabolite NAPQI in acetaminophen overdose.
Answer: Digoxin immune Fab. Binds free digoxin to form complexes that are rapidly excreted, reversing cardiac toxicity.
Answer: Idarucizumab. Specifically binds dabigatran as a monoclonal antibody to neutralize its anticoagulant activity.
Answer: Acute opioid withdrawal. Rapid opioid receptor displacement in dependent individuals precipitates symptoms like agitation and vomiting.
Answer: Naloxone. Competitively antagonizes mu-opioid receptors to rapidly reverse respiratory depression in opioid toxicity.
Answer: Restore adequate ventilation, not full arousal. Prioritizes reversing life-threatening respiratory depression while avoiding precipitation of severe withdrawal.
Answer: Hydroxocobalamin. Chelates cyanide ions to form nontoxic cyanocobalamin for urinary excretion.
Answer: Intranasal naloxone. Offers rapid absorption and user-friendly administration without needles, ideal for non-professionals.
Answer: Deferoxamine. Chelates excess serum iron to form ferrioxamine, facilitating renal elimination and reducing toxicity.
Answer: Flumazenil. Acts as a competitive antagonist at GABA_A receptors to reverse benzodiazepine-induced sedation.
Answer: Glucagon. Stimulates cardiac adenylate cyclase independently of beta-receptors to improve hemodynamics.
Answer: Octreotide. Suppresses insulin release from beta cells to mitigate prolonged hypoglycemic effects of sulfonylureas.
Answer: Adsorb drug in GI tract to reduce absorption. Binds toxins in the gastrointestinal lumen to limit systemic absorption and enhance fecal excretion.
Answer: 4-factor PCC plus vitamin K. PCC rapidly replenishes clotting factors, while vitamin K sustains long-term reversal of warfarin.
Answer: Atropine. Blocks muscarinic receptors to counteract excessive cholinergic activity from cholinesterase inhibition.
Answer: Dextrose. Provides immediate glucose to correct severe hypoglycemia from excessive insulin or sulfonylurea action.
Answer: Seizures. Precipitates withdrawal in dependent users or unmasks convulsant effects in polydrug overdoses.
Answer: Calcium salts (calcium chloride or calcium gluconate). Overcomes channel blockade by increasing extracellular calcium to stabilize cardiac membranes.
Answer: Serum acetaminophen concentration with time since ingestion. Plotted on the Rumack-Matthew nomogram to predict hepatotoxicity risk and determine treatment necessity.
Answer: High-dose insulin euglycemia therapy (HIE). Enhances myocardial carbohydrate metabolism to provide inotropic support in refractory poisoning.
Answer: No GI decontamination; supportive care and urgent evaluation. Prevents further tissue injury by avoiding emesis or lavage that could exacerbate corrosive damage.
Answer: Methylene blue. Accelerates methemoglobin reduction to hemoglobin via the NADPH-methemoglobin reductase pathway.
Answer: Protamine sulfate. Forms stable complexes with heparin to neutralize its anticoagulant effects and stop bleeding.
Answer: Pralidoxime (2-PAM). Regenerates inhibited acetylcholinesterase by cleaving the organophosphate-enzyme bond.
Answer: Andexanet alfa. Serves as a decoy target for factor Xa inhibitors to restore normal hemostasis.