Which patient below is at greatest risk for developing gout?

Choice A reason: Furosemide, a loop diuretic, inhibits the sodium-potassium-chloride cotransporter in the thick ascending limb of the loop of Henle, preventing sodium and water reabsorption. This increases urine output significantly, often within minutes, making it highly effective for conditions like edema or heart failure, producing a rapid diuresis of up to 20% of filtered sodium.

Choice B reason: Spironolactone, a potassium-sparing diuretic, inhibits aldosterone in the distal tubule, reducing sodium reabsorption and increasing urine output. However, its diuretic effect is weaker than furosemide, as it affects only 2-3% of filtered sodium. It is primarily used for managing hyperaldosteronism or potassium retention, not rapid urine flow increase.

Choice C reason: Hydrochlorothiazide, a thiazide diuretic, inhibits sodium-chloride reabsorption in the distal convoluted tubule, increasing urine output. Its effect is milder than furosemide, impacting about 5-10% of filtered sodium. It is commonly used for hypertension but is less potent for rapid diuresis in conditions requiring significant urine flow.

Choice D reason: Mannitol, an osmotic diuretic, increases urine flow by preventing water reabsorption in the proximal tubule and loop of Henle. It is effective in acute settings like cerebral edema but less commonly used for routine diuresis compared to furosemide, which has a broader and more rapid effect on urine output.

Choice A reason: Ascites results from increased permeability of peritoneal capillaries, often due to inflammatory molecules like cytokines in conditions such as liver cirrhosis or portal hypertension. This allows plasma proteins and fluid to leak into the peritoneal cavity, causing fluid accumulation. This statement accurately describes the pathophysiology of ascites in liver-related disorders.

Choice B reason: Low aldosterone levels do not cause ascites; instead, high aldosterone in liver disease (e.g., cirrhosis) promotes sodium and water retention, exacerbating fluid accumulation. This statement is inaccurate, as secondary hyperaldosteronism due to reduced liver metabolism of aldosterone is a key factor in ascites development.

Choice C reason: The liver’s failure to produce clotting factors can lead to bleeding tendencies, like variceal hemorrhage, but this does not directly cause ascites. Ascites is driven by fluid leakage from capillaries, not bleeding. This statement is inaccurate, as clotting factor deficiency is unrelated to peritoneal fluid accumulation.

Choice D reason: While fluid imbalance contributes to ascites, the primary mechanism involves portal hypertension and capillary permeability, not just osmotic pressure changes. This statement is overly vague and less accurate than the specific role of inflammatory molecules increasing capillary leakage in the peritoneal cavity.