Recognition And Management - NAPLEX
Card 1 of 25
What therapy shifts potassium intracellularly in acute hyperkalemia management?
What therapy shifts potassium intracellularly in acute hyperkalemia management?
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Insulin with dextrose. Insulin activates Na/K-ATPase to drive potassium into cells, with glucose preventing hypoglycemia.
Insulin with dextrose. Insulin activates Na/K-ATPase to drive potassium into cells, with glucose preventing hypoglycemia.
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Which toxidrome presents with hyperthermia, mydriasis, dry skin, and urinary retention?
Which toxidrome presents with hyperthermia, mydriasis, dry skin, and urinary retention?
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Anticholinergic toxidrome. Arises from muscarinic blockade causing decreased secretions, hyperthermia, and altered mental status.
Anticholinergic toxidrome. Arises from muscarinic blockade causing decreased secretions, hyperthermia, and altered mental status.
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What is the major contraindication to flumazenil in overdose management?
What is the major contraindication to flumazenil in overdose management?
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Chronic benzodiazepine use or seizure risk. Risks precipitating withdrawal seizures in dependent users or those with seizure predisposition.
Chronic benzodiazepine use or seizure risk. Risks precipitating withdrawal seizures in dependent users or those with seizure predisposition.
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Which antidote is first-line for benzodiazepine overdose in a benzodiazepine-naive patient?
Which antidote is first-line for benzodiazepine overdose in a benzodiazepine-naive patient?
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Flumazenil. Competitively antagonizes benzodiazepine binding at GABA_A receptors to reverse sedation.
Flumazenil. Competitively antagonizes benzodiazepine binding at GABA_A receptors to reverse sedation.
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Which electrolyte abnormality can cause peaked T waves and widened QRS on ECG?
Which electrolyte abnormality can cause peaked T waves and widened QRS on ECG?
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Hyperkalemia. Elevated extracellular potassium alters cardiac repolarization and conduction on ECG.
Hyperkalemia. Elevated extracellular potassium alters cardiac repolarization and conduction on ECG.
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What is the most immediate cardiac membrane-stabilizing treatment for severe hyperkalemia?
What is the most immediate cardiac membrane-stabilizing treatment for severe hyperkalemia?
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IV calcium (gluconate or chloride). Stabilizes cardiac cell membranes by antagonizing potassium's depolarizing effects.
IV calcium (gluconate or chloride). Stabilizes cardiac cell membranes by antagonizing potassium's depolarizing effects.
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What is the immediate first action for severe hypoglycemia with unconsciousness?
What is the immediate first action for severe hypoglycemia with unconsciousness?
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Give glucagon or IV dextrose. Quickly restores blood glucose to prevent neuronal damage and reverse altered consciousness.
Give glucagon or IV dextrose. Quickly restores blood glucose to prevent neuronal damage and reverse altered consciousness.
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What is the preferred initial management for suspected acute stroke symptoms?
What is the preferred initial management for suspected acute stroke symptoms?
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Activate emergency response and urgent imaging. Facilitates rapid diagnosis and time-sensitive interventions like thrombolysis for ischemic stroke.
Activate emergency response and urgent imaging. Facilitates rapid diagnosis and time-sensitive interventions like thrombolysis for ischemic stroke.
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What is the primary management approach for neuroleptic malignant syndrome?
What is the primary management approach for neuroleptic malignant syndrome?
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Stop antipsychotic; supportive care. Discontinues the offending agent while providing cooling, hydration, and monitoring for complications.
Stop antipsychotic; supportive care. Discontinues the offending agent while providing cooling, hydration, and monitoring for complications.
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Identify the syndrome: hyperreflexia, clonus, agitation, and diaphoresis after serotonergic drugs.
Identify the syndrome: hyperreflexia, clonus, agitation, and diaphoresis after serotonergic drugs.
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Serotonin syndrome. Arises from excessive serotonin leading to neuromuscular excitation and autonomic hyperactivity.
Serotonin syndrome. Arises from excessive serotonin leading to neuromuscular excitation and autonomic hyperactivity.
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Which toxidrome presents with miosis, respiratory depression, and CNS depression?
Which toxidrome presents with miosis, respiratory depression, and CNS depression?
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Opioid toxidrome. Results from mu-opioid receptor agonism depressing respiratory drive and CNS function while constricting pupils.
Opioid toxidrome. Results from mu-opioid receptor agonism depressing respiratory drive and CNS function while constricting pupils.
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What antidote is used for opioid overdose with respiratory depression?
What antidote is used for opioid overdose with respiratory depression?
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Naloxone. Acts as a competitive mu-opioid receptor antagonist to restore ventilation.
Naloxone. Acts as a competitive mu-opioid receptor antagonist to restore ventilation.
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Identify the classic triad suggesting anaphylaxis (three findings).
Identify the classic triad suggesting anaphylaxis (three findings).
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Hypotension, bronchospasm, urticaria/angioedema. Represents multisystem involvement in severe IgE-mediated hypersensitivity reaction.
Hypotension, bronchospasm, urticaria/angioedema. Represents multisystem involvement in severe IgE-mediated hypersensitivity reaction.
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What is the antidotal therapy commonly used for moderate to severe serotonin syndrome?
What is the antidotal therapy commonly used for moderate to severe serotonin syndrome?
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Cyproheptadine. Functions as a serotonin 5-HT2A receptor antagonist to mitigate hyperstimulation symptoms.
Cyproheptadine. Functions as a serotonin 5-HT2A receptor antagonist to mitigate hyperstimulation symptoms.
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What is the preferred first-line agent for anaphylaxis treatment?
What is the preferred first-line agent for anaphylaxis treatment?
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IM epinephrine. Rapidly reverses hypotension, bronchospasm, and angioedema via alpha and beta adrenergic receptor stimulation.
IM epinephrine. Rapidly reverses hypotension, bronchospasm, and angioedema via alpha and beta adrenergic receptor stimulation.
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What is the first-line decontamination method for a recent toxic ingestion when appropriate?
What is the first-line decontamination method for a recent toxic ingestion when appropriate?
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Activated charcoal. Adsorbs toxins in the GI tract to limit systemic absorption if given soon after ingestion.
Activated charcoal. Adsorbs toxins in the GI tract to limit systemic absorption if given soon after ingestion.
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What is the preferred initial management for acute asthma exacerbation with wheezing and dyspnea?
What is the preferred initial management for acute asthma exacerbation with wheezing and dyspnea?
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Inhaled SABA plus systemic corticosteroid. SABA induces rapid bronchodilation, while corticosteroids suppress airway inflammation.
Inhaled SABA plus systemic corticosteroid. SABA induces rapid bronchodilation, while corticosteroids suppress airway inflammation.
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Identify the immediate management for suspected sepsis with hypotension and infection signs.
Identify the immediate management for suspected sepsis with hypotension and infection signs.
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IV fluids and broad-spectrum antibiotics. Provides volume resuscitation for shock and empiric coverage against likely pathogens.
IV fluids and broad-spectrum antibiotics. Provides volume resuscitation for shock and empiric coverage against likely pathogens.
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What is the preferred antidote for acetaminophen overdose with hepatotoxicity risk?
What is the preferred antidote for acetaminophen overdose with hepatotoxicity risk?
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N-acetylcysteine. Replenishes glutathione to neutralize the toxic NAPQI metabolite and prevent liver damage.
N-acetylcysteine. Replenishes glutathione to neutralize the toxic NAPQI metabolite and prevent liver damage.
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Which acid-base pattern is most consistent with salicylate toxicity?
Which acid-base pattern is most consistent with salicylate toxicity?
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Respiratory alkalosis plus anion gap metabolic acidosis. Initial respiratory stimulation causes alkalosis, followed by uncoupling-induced metabolic acidosis.
Respiratory alkalosis plus anion gap metabolic acidosis. Initial respiratory stimulation causes alkalosis, followed by uncoupling-induced metabolic acidosis.
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Which ECG finding most strongly suggests torsades de pointes risk?
Which ECG finding most strongly suggests torsades de pointes risk?
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Prolonged QT interval. Reflects delayed ventricular repolarization predisposing to polymorphic ventricular tachycardia.
Prolonged QT interval. Reflects delayed ventricular repolarization predisposing to polymorphic ventricular tachycardia.
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What is the first-line drug treatment for torsades de pointes?
What is the first-line drug treatment for torsades de pointes?
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IV magnesium sulfate. Suppresses early afterdepolarizations and stabilizes potassium channels in prolonged QT states.
IV magnesium sulfate. Suppresses early afterdepolarizations and stabilizes potassium channels in prolonged QT states.
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Identify the syndrome: fever, rigidity, autonomic instability, and elevated CK after antipsychotic use.
Identify the syndrome: fever, rigidity, autonomic instability, and elevated CK after antipsychotic use.
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Neuroleptic malignant syndrome. Occurs as an idiosyncratic reaction to dopamine blockade causing muscle rigidity and rhabdomyolysis.
Neuroleptic malignant syndrome. Occurs as an idiosyncratic reaction to dopamine blockade causing muscle rigidity and rhabdomyolysis.
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What are the two key antidotes for organophosphate poisoning?
What are the two key antidotes for organophosphate poisoning?
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Atropine and pralidoxime. Atropine competitively inhibits muscarinic receptors, while pralidoxime regenerates acetylcholinesterase.
Atropine and pralidoxime. Atropine competitively inhibits muscarinic receptors, while pralidoxime regenerates acetylcholinesterase.
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Which toxidrome presents with diaphoresis, miosis, bronchorrhea, and bradycardia?
Which toxidrome presents with diaphoresis, miosis, bronchorrhea, and bradycardia?
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Cholinergic (organophosphate) toxidrome. Stems from acetylcholinesterase inhibition leading to excessive muscarinic and nicotinic stimulation.
Cholinergic (organophosphate) toxidrome. Stems from acetylcholinesterase inhibition leading to excessive muscarinic and nicotinic stimulation.
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