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This deck focuses on Adverse Effects And Drug Interactions, giving you a quick way to review the definitions, rules, and examples that matter most for Nclexrn.
Study Adverse Effects And Drug Interactions in Nclexrn 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 medication interaction causes disulfiram-like reaction: metronidazole plus what?
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Alcohol. Metronidazole inhibits aldehyde dehydrogenase, causing acetaldehyde buildup from alcohol metabolism, resulting in nausea, flushing, and hypotension similar to disulfiram.
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This deck focuses on Adverse Effects And Drug Interactions, giving you a quick way to review the definitions, rules, and examples that matter most for Nclexrn.
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: Alcohol. Metronidazole inhibits aldehyde dehydrogenase, causing acetaldehyde buildup from alcohol metabolism, resulting in nausea, flushing, and hypotension similar to disulfiram.
Answer: Grapefruit juice. Grapefruit juice inhibits CYP3A4 enzymes, reducing statin metabolism and elevating blood levels, which heightens the risk of muscle toxicity and other adverse effects.
Answer: Tyramine-rich foods (aged cheese, cured meats, draft beer). MAOIs inhibit tyramine metabolism, allowing its accumulation to displace norepinephrine and trigger a sympathomimetic crisis with severe hypertension.
Answer: Hypokalemia. Loop diuretics inhibit sodium-potassium-chloride cotransport in the loop of Henle, causing excessive potassium loss in urine and subsequent hypokalemia.
Answer: Clopidogrel (or other antiplatelet agents). Aspirin and clopidogrel both inhibit platelet aggregation through different mechanisms, resulting in amplified anticoagulant effects and heightened hemorrhage potential.
Answer: Hypokalemia. Hypokalemia enhances digoxin's binding to sodium-potassium ATPase, amplifying its cardiac effects and increasing susceptibility to toxic arrhythmias.
Answer: Angioedema (face, lips, tongue swelling). ACE inhibitors can cause bradykinin accumulation, leading to angioedema with potential airway obstruction, demanding immediate discontinuation to prevent fatal complications.
Answer: Naloxone. Naloxone competitively antagonizes opioid receptors in the central nervous system, rapidly reversing respiratory depression by restoring normal ventilatory drive.
Answer: PDE-5 inhibitors (sildenafil, tadalafil, vardenafil). Both nitrates and PDE-5 inhibitors promote vasodilation via nitric oxide pathways, causing synergistic blood pressure drops that can result in hypotensive crisis.
Answer: MAO inhibitors (or other serotonergic drugs). SSRIs increase serotonin levels, and combining with MAOIs prevents serotonin breakdown, leading to excessive accumulation and syndrome manifestation.
Answer: Dysrhythmias (bradycardia, heart block, ventricular ectopy). Digoxin toxicity disrupts cardiac ion channels, precipitating arrhythmias that can lead to hemodynamic instability or sudden cardiac death if not addressed promptly.
Answer: Macrolides (e.g., erythromycin, clarithromycin). Macrolides inhibit cytochrome P450 enzymes, decreasing warfarin metabolism and increasing its plasma concentration, thereby enhancing anticoagulation and bleeding susceptibility.
Answer: Myopathy/rhabdomyolysis (muscle pain with dark urine). Statins can impair muscle cell integrity, leading to breakdown and release of myoglobin, which may cause acute kidney injury if not reported early.
Answer: Neuroleptic malignant syndrome (fever, rigidity, autonomic instability). Antipsychotics block dopamine receptors, potentially causing a hyperthermic catabolic state with muscle rigidity and vital sign instability, requiring urgent intervention.
Answer: Do not exceed recommended daily dose; risk of hepatotoxicity. Acetaminophen overdose overwhelms hepatic glutathione, leading to metabolite accumulation and liver cell necrosis, making dose adherence critical for safety.
Answer: Major bleeding (e.g., intracranial or GI hemorrhage). Warfarin inhibits vitamin K-dependent clotting factors, and excessive anticoagulation can lead to life-threatening hemorrhages in critical areas like the brain or gastrointestinal tract.
Answer: Heparin-induced thrombocytopenia (HIT). Heparin can trigger an immune-mediated platelet destruction, leading to thrombocytopenia and paradoxical thrombosis, mandating regular platelet count surveillance during therapy.
Answer: ACE inhibitors/ARBs (especially with diuretics: "triple whammy"). ACE inhibitors/ARBs reduce glomerular filtration pressure, and NSAIDs further impair renal blood flow via prostaglandin inhibition, especially with diuretics causing volume depletion.
Answer: Hyperthermia, agitation, diaphoresis, tremor, hyperreflexia, diarrhea. These symptoms reflect serotonin excess affecting neuromuscular, autonomic, and gastrointestinal systems, signaling a medical emergency to prevent seizures or coma.
Answer: Leafy green vegetables (e.g., spinach, kale, broccoli). High vitamin K content in these vegetables promotes synthesis of clotting factors, antagonizing warfarin's anticoagulant mechanism and reducing its therapeutic efficacy.
Answer: Broad-spectrum antibiotics (especially clindamycin). Broad-spectrum antibiotics disrupt normal gut flora, allowing overgrowth of Clostridium difficile, which produces toxins leading to severe diarrhea and colitis.