A 23-year-old woman with a 2-year history of progressive hirsutism, moderate inflammatory acne, and irregular menstrual cycles occurring every 45–60 days presents to her gynecologist for follow-up. Laboratory workup confirms hyperandrogenism with an elevated free testosterone of 42 pg/mL (normal 1–8.5 pg/mL) and a normal DHEA-sulfate level, consistent with ovarian rather than adrenal origin. She is started on spironolactone 100 mg daily for symptom management. Her baseline vital signs are stable (BP 118/76 mmHg, HR 82/min, RR 16/min, temperature 98.6°F), and her baseline serum potassium is 4.1 mEq/L with normal renal function. Three weeks later, repeat laboratory testing reveals a serum potassium of 5.8 mEq/L (normal 3.5–5.0 mEq/L), while free testosterone has appropriately decreased to 9 pg/mL. She reports no nausea, palpitations, muscle weakness, or dietary changes. Her BMI is 26 kg/m² and she takes no other medications. Which mechanism best explains her laboratory abnormality?
- A)Flutamide
- B)Finasteride
- C)Eplerenone
- D)Clomiphene
- E)SpironolactoneGABARITO
Explicação
Spironolactone antagonizes aldosterone receptors and also has antiandrogen effects, making it useful in hirsutism and hyperaldosteronism. Hyperkalemia is a predictable consequence of its potassium sparing mineralocorticoid receptor blockade. Ver explicação completa e trilha adaptativa →