question about aldosterone

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aldowaldo

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hello all.

question about aldosterone: if a patient is hypovolemic, aldosterone would become activated to cause sodium resorption, right? then there'd be K+ excretion and H+ excretion into the urine. this patient i'm assuming would be hypokalemic with metabolic alkalosis.

so than why is volume depletion a causes of hyperkalemia?
 
hello all.

question about aldosterone: if a patient is hypovolemic, aldosterone would become activated to cause sodium resorption, right? then there'd be K+ excretion and H+ excretion into the urine. this patient i'm assuming would be hypokalemic with metabolic alkalosis.

so than why is volume depletion a causes of hyperkalemia?

Potassium secretion in the cortical collecting tubules is dependent on the negative intraluminal gradient established by the sodium channel (ENaC). With decreased renal perfusion (from VOLUME DEPLETION), less sodium gets to the CCT, and no negative gradient is established. Bingo, decreased ability of sodium to be excreted.

However, there will be a neurohormonal response (decreased renal perfusion -> renin -> angiotensin system -> increased aldosterone release). The aldosterone will stimulate sodium reabsorption in the CCT, leading to hypokalemia.

So: acute: hyperkalemia
Chronic: hypokalemia
 
Are you sure there's hyperkalemia in contraction alkalosis? I'm pretty sure there is hypokalemia...

Unless you're in a hypoperfusive metabolic acidosis (shock) which would cause K+ movement out of cells and a hyperkalemia.
 
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