Match each patient's acquired acid-base and electrolyte derangement profile with the pharmacological agent most likely responsible for these findings.
- A patient with recurrent nephrolithiasis is prescribed a medication that subsequently causes hypokalemia, mild metabolic alkalosis, and a significant decrease in urinary calcium excretion.Thiazide diuretic (e.g., Chlorthalidone)
- A patient undergoing management for an ocular emergency develops a hyperchloremic normal anion gap metabolic acidosis with an inappropriately elevated urine pH of 7.8.Carbonic anhydrase inhibitor (e.g., Acetazolamide)
- A patient being aggressively diuresed for pulmonary edema develops profound hypokalemia, metabolic alkalosis, hypomagnesemia, and increased urinary calcium losses.Loop diuretic (e.g., Furosemide)
- A patient with advanced hepatic cirrhosis and ascites is started on a diuretic regimen that subsequently causes hyperkalemia and a mild normal anion gap metabolic acidosis.Aldosterone antagonist (e.g., Spironolactone)
Cevap
The correct answer links the hypocalciuric alkalosis to thiazide diuretics, the hyperchloremic acidosis with alkaline urine to carbonic anhydrase inhibitors, the hypercalciuric alkalosis to loop diuretics, and the hyperkalemic acidosis to aldosterone antagonists.
Each pharmacological agent acts on a specific segment of the nephron, creating a unique signature of electrolyte and acid-base changes based on the localized transport mechanisms disrupted.
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Anahtar Kavram
Diuretic-induced acid-base and electrolyte derangements can be precisely distinguished by their unique downstream effects on serum potassium, acid-base balance, and urinary calcium handling.
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