A nurse is reviewing a patient’s medications before administration. Which drug-to-drug interactions will most concern the nurse in a patient with a history of heart failure and a potassium level of 5.5 mEq/L?
Metoprolol [Lopressor] and furosemide [Lasix]
Furosemide [Lasix] and enalapril [Vasotec]
Captopril [Capoten] and spironolactone [Aldactone]
Amlodipine [Norvasc] and propranolol [Inderal]
The Correct Answer is C
Choice A reason: Metoprolol (beta-blocker) and furosemide (loop diuretic) are commonly used in heart failure. Furosemide may lower potassium, counteracting hyperkalemia (5.5 mEq/L), and metoprolol doesn’t significantly affect potassium. This combination poses less risk for hyperkalemia exacerbation, making it less concerning than potassium-sparing combinations.
Choice B reason: Furosemide promotes potassium excretion, potentially reducing hyperkalemia (5.5 mEq/L), while enalapril (ACE inhibitor) may increase potassium. However, furosemide’s effect often offsets enalapril’s, making this combination less likely to worsen hyperkalemia significantly compared to two potassium-sparing drugs, so this choice is less critical.
Choice C reason: Captopril (ACE inhibitor) and spironolactone (potassium-sparing diuretic) both increase potassium levels by reducing aldosterone activity, exacerbating hyperkalemia (5.5 mEq/L). In heart failure, this combination risks severe hyperkalemia, causing arrhythmias, making it the most concerning interaction requiring close monitoring or adjustment.
Choice D reason: Amlodipine (calcium channel blocker) and propranolol (beta-blocker) primarily affect blood pressure and heart rate, not potassium levels. Their interaction may cause bradycardia or hypotension but doesn’t worsen hyperkalemia (5.5 mEq/L), making this combination less concerning for the patient’s current electrolyte status.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: Beta 1-adrenergic drugs, like dobutamine, stimulate beta-1 receptors in the heart, increasing cyclic AMP and calcium influx, enhancing myocardial contractility. This increases stroke volume by strengthening heart contractions, directly improving cardiac output, making this the correct choice for the drug’s mechanism of action.
Choice B reason: Cardiac afterload is the resistance the heart pumps against. Beta 1-adrenergic drugs don’t directly reduce afterload; they increase contractility. Increasing afterload would decrease stroke volume, opposing the drug’s purpose, making this choice incorrect for the drug’s effect on stroke volume.
Choice C reason: Venous return affects preload, not directly influenced by beta 1-adrenergic drugs. These drugs enhance contractility, increasing stroke volume independently of venous return. While preload impacts output, it’s not the primary mechanism of beta-1 stimulation, making this choice incorrect.
Choice D reason: Cardiac preload is the initial stretch of the heart, influenced by venous return. Beta 1-adrenergic drugs increase contractility, not preload, to boost stroke volume. Preload changes are secondary and not the primary action of these drugs, making this choice incorrect.
Correct Answer is C
Explanation
Choice A reason: Synthesis of more receptor sites (upregulation) typically occurs with receptor antagonists, not agonists, as the body compensates for blocked receptors. This would increase drug sensitivity, not decrease effectiveness. For most medications, continuous exposure leads to desensitization, not receptor proliferation, making this choice incorrect for explaining tolerance.
Choice B reason: Decreased receptor selectivity implies a drug binding to unintended receptors, causing varied effects, not reduced efficacy. Tolerance results from receptor desensitization, not altered selectivity. This mechanism doesn’t explain the patient’s “immunity” to the drug’s therapeutic effects, making this choice scientifically inaccurate for the scenario.
Choice C reason: Desensitization occurs when continuous drug exposure reduces receptor responsiveness, leading to tolerance. For example, opioid receptors downregulate or internalize with prolonged agonist exposure, decreasing drug efficacy. This explains the patient’s perception of “immunity” as the drug’s effect diminishes over time, making this the correct choice.
Choice D reason: The body does not produce antagonists to compete with drugs for receptor sites. Tolerance arises from receptor desensitization or metabolic changes (e.g., enzyme induction), not endogenous antagonist production. This mechanism is not a recognized pharmacological process for reduced drug effectiveness, making this choice incorrect.
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