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This deck focuses on Toxicology And Overdose Management, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
Study Toxicology And Overdose Management in NREMT Paramedic Level 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 methemoglobinemia with hypoxia and chocolate-brown blood?
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Methylene blue. Methylene blue acts as an electron donor, accelerating methemoglobin reduction to functional hemoglobin via enzymatic pathways.
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This deck focuses on Toxicology And Overdose Management, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
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: Methylene blue. Methylene blue acts as an electron donor, accelerating methemoglobin reduction to functional hemoglobin via enzymatic pathways.
Answer: Pralidoxime (2-PAM). Pralidoxime regenerates acetylcholinesterase by removing the bound organophosphate, restoring normal enzyme function when given timely.
Answer: Restore adequate ventilation, not full arousal. Naloxone competitively antagonizes opioid receptors to reverse life-threatening respiratory depression without needing complete consciousness.
Answer: No antidote; give 100% oxygen and consider hyperbaric oxygen. High-flow oxygen displaces CO from hemoglobin, accelerating elimination; hyperbaric therapy enhances this in severe cases, as no specific antidote exists.
Answer: Widened QRS complex. TCAs block sodium channels, delaying ventricular depolarization and prolonging the QRS duration on ECG.
Answer: Fomepizole. Fomepizole inhibits alcohol dehydrogenase, preventing conversion of these alcohols into their toxic acidic metabolites.
Answer: Cholinergic toxidrome (organophosphates/carbamates). Inhibition of acetylcholinesterase leads to acetylcholine excess, causing parasympathetic overstimulation with these hallmark symptoms.
Answer: Glucagon. Glucagon stimulates cardiac adenylate cyclase independently of beta receptors, increasing heart rate and contractility.
Answer: Dissociative (PCP/ketamine) toxidrome. Dissociative agents disrupt glutamate signaling, inducing perceptual dissociation with sympathetic activation and specific nystagmus patterns.
Answer: Scene safety/BSI, ABCs, oxygen/ventilation, circulation, then tox-specific care. This protocol prioritizes provider protection and stabilization of vital functions before addressing the specific toxic exposure.
Answer: N-acetylcysteine (NAC). NAC replenishes glutathione, enabling detoxification of the hepatotoxic metabolite NAPQI produced in acetaminophen overdose.
Answer: Inducing vomiting or neutralization attempts. These actions risk re-exposure of tissues to corrosives or generate heat/exothermic reactions, potentially worsening mucosal injury.
Answer: Benzodiazepines. Benzodiazepines enhance GABAergic transmission, effectively managing sympathetic overstimulation and associated complications.
Answer: Anticholinergic toxidrome. Muscarinic receptor blockade inhibits parasympathetic responses, leading to sympathetic dominance and altered mental status.
Answer: CNS depression, respiratory depression, and miosis. Opioid receptor activation suppresses central nervous system activity, reduces respiratory drive, and constricts pupils via parasympathetic effects.
Answer: Carboxyhemoglobin level by CO-oximetry (not standard pulse oximetry). CO-oximetry specifically quantifies carboxyhemoglobin, providing accurate severity assessment unlike standard oximetry which is unreliable in CO poisoning.
Answer: Rapid active cooling plus benzodiazepines and supportive airway/ventilation. Active cooling mitigates heat-induced organ damage, while benzodiazepines control contributing factors like agitation, with ventilatory support as required.
Answer: Sedative-hypnotic toxidrome. Sedative-hypnotics potentiate GABA-mediated inhibition, causing central depression without marked autonomic instability, often with ocular signs.
Answer: Sodium bicarbonate. Bicarbonate alkalinizes serum and provides sodium, reducing TCA affinity for sodium channels and stabilizing cardiac membranes.
Answer: Remove clothing and irrigate skin with copious water. Immediate removal of contaminants and dilution with water minimize chemical absorption and tissue damage in prehospital settings.
Answer: Ventilate with BVM and oxygen; support airway before or with naloxone. Respiratory failure is the primary life threat in opioid overdose, requiring immediate ventilatory support to maintain oxygenation.
Answer: Hydroxocobalamin. Hydroxocobalamin binds cyanide to form non-toxic cyanocobalamin, rapidly restoring cellular respiration in acute poisoning.
Answer: Calcium (e.g., calcium chloride or calcium gluconate). Administering calcium overcomes channel blockade by increasing extracellular calcium gradient, improving cardiac conduction and contraction.
Answer: Atropine. Atropine competitively blocks muscarinic receptors, counteracting the excessive cholinergic activity from organophosphate exposure.
Answer: Sympathomimetic toxidrome. Sympathomimetic agents enhance catecholamine effects, resulting in hyperstimulation of the sympathetic nervous system.