A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 72-year-old anthropologist with long-standing hypertension visits your office for a routine exam. You notice an abnormality on his laboratory results caused by his regimen of captopril and triamterene. What abnormality did you most likely find?
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A
HyperkalemiaCorrect. ACE inhibitors (decreased aldosterone) and potassium-sparing diuretics (ENaC blockade) both retain potassium; their combination is the classic cause of iatrogenic hyperkalemia.
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B
HypernatremiaIncorrect. Hypernatremia is not a characteristic effect of either captopril or triamterene; both tend to promote natriuresis, if anything causing mild hyponatremia.
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C
ThrombocytopeniaIncorrect. Thrombocytopenia is not a typical adverse effect of either drug; rarely captopril can cause cytopenias but it's not the most likely lab abnormality.
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D
AnemiaIncorrect. Anemia is not a characteristic finding of this drug combination; ACE inhibitors can rarely cause anemia by lowering erythropoietin in some settings, but hyperkalemia is the expected lab abnormality.
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E
Metabolic acidosisIncorrect. Metabolic acidosis can occur with ACE inhibitors via type 4 RTA from hypoaldosteronism, but it is a secondary consequence rather than the primary, most likely lab abnormality with this combination; hyperkalemia is the classic finding.
↑ Tap an answer to reveal the reasoning
Answer: A. Captopril is an ACE inhibitor and triamterene is a potassium-sparing diuretic that blocks the epithelial sodium channel (ENaC) in the cortical collecting duct. Both drug classes independently raise serum potassium, and combining them dramatically increases the risk of hyperkalemia.
ACE inhibitors block conversion of angiotensin I to angiotensin II, which decreases aldosterone secretion from the adrenal cortex. Lower aldosterone reduces Na+ reabsorption and K+ secretion in the distal nephron, retaining potassium. Triamterene (and amiloride) directly block ENaC, decreasing the favorable electrochemical gradient for K+ secretion through ROMK channels, again retaining potassium. The combined effect is additive.
This is a high-yield drug interaction tested on Step 1: any combination of ACE-I/ARB, aldosterone antagonist (spironolactone, eplerenone), or ENaC blocker (amiloride, triamterene) significantly raises hyperkalemia risk, especially in patients with CKD, diabetes (type IV RTA), or those on NSAIDs/heparin/digoxin. ACE inhibitors do not cause hypernatremia (they actually slightly lower Na+), thrombocytopenia, or anemia as expected adverse effects in this combination.
**Why each option:**
**A.** Correct. ACE inhibitors (decreased aldosterone) and potassium-sparing diuretics (ENaC blockade) both retain potassium; their combination is the classic cause of iatrogenic hyperkalemia.
**B.** Hypernatremia is not a characteristic effect of either captopril or triamterene; both tend to promote natriuresis, if anything causing mild hyponatremia.
**C.** Thrombocytopenia is not a typical adverse effect of either drug; rarely captopril can cause cytopenias but it's not the most likely lab abnormality.
**D.** Anemia is not a characteristic finding of this drug combination; ACE inhibitors can rarely cause anemia by lowering erythropoietin in some settings, but hyperkalemia is the expected lab abnormality.