Which physiologic change most commonly contributes to edema in a patient with cirrhosis?

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Multiple Choice

Which physiologic change most commonly contributes to edema in a patient with cirrhosis?

Explanation:
Edema in cirrhosis is driven mainly by activation of the renin-angiotensin-aldosterone system in response to a perceived drop in effective circulating volume from portal hypertension and splanchnic vasodilation. When aldosterone levels rise, the kidneys increase sodium reabsorption in the distal tubules, and water follows sodium, expanding the extracellular fluid and producing edema. While hypoalbuminemia from liver dysfunction can contribute by lowering plasma oncotic pressure, the most influential and common mechanism is the sodium-retaining effect of aldosterone. The idea that portal pressure would decrease or that the RAAS would be reduced doesn’t fit the cirrhotic physiology, since portal hypertension promotes fluid shifts and triggers increased RAAS activity rather than suppression.

Edema in cirrhosis is driven mainly by activation of the renin-angiotensin-aldosterone system in response to a perceived drop in effective circulating volume from portal hypertension and splanchnic vasodilation. When aldosterone levels rise, the kidneys increase sodium reabsorption in the distal tubules, and water follows sodium, expanding the extracellular fluid and producing edema.

While hypoalbuminemia from liver dysfunction can contribute by lowering plasma oncotic pressure, the most influential and common mechanism is the sodium-retaining effect of aldosterone. The idea that portal pressure would decrease or that the RAAS would be reduced doesn’t fit the cirrhotic physiology, since portal hypertension promotes fluid shifts and triggers increased RAAS activity rather than suppression.

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