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?

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.

Choice A reason: Antidotes counteract specific toxins or drugs (e.g., naloxone for opioids). Antihistamines don’t neutralize allergens but block histamine receptors to reduce allergic symptoms like itching or sneezing. They target H1 or H2 receptors, not a toxin, making this choice incorrect for describing antihistamine mechanism of action.

Choice B reason: Antihistamines are antagonists, binding to histamine receptors (H1 or H2) without activating them, preventing histamine from triggering allergic responses like vasodilation or bronchoconstriction. This competitive inhibition reduces symptoms such as itching, sneezing, or gastric acid secretion, making this the correct choice for their pharmacological action.

Choice C reason: Agonists activate receptors to produce a response. Antihistamines block histamine receptors, not activate them, preventing allergic effects. Acting as agonists would mimic histamine, worsening symptoms like swelling or itching, which is opposite to their therapeutic role, making this choice incorrect.

Choice D reason: Activators is a vague term not used in pharmacology to describe drug action. Antihistamines specifically act as receptor antagonists, not general activators. They inhibit histamine effects without stimulating other pathways, making this choice inaccurate for explaining the mechanism of antihistamines in allergy management.