Addison's disease. Hyperaldosteronism

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anbuitachi

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In first aid, it says Addison's involves all 3 layers of adrenal cortex. yet pts don't show lack of sex characteristics like in 17 hydroxylase deficiency. Why is that?

Also First aid mentions secondary hyperaldosteronism can be caused by Cirrhosis, nephrotic syndrome, CHF. How do these mechanisms work? Especially for nephrotic syndrome and cirrhosis.. Thanks!!

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In first aid, it says Addison's involves all 3 layers of adrenal cortex. yet pts don't show lack of sex characteristics like in 17 hydroxylase deficiency. Why is that?

Also First aid mentions secondary hyperaldosteronism can be caused by Cirrhosis, nephrotic syndrome, CHF. How do these mechanisms work? Especially for nephrotic syndrome and cirrhosis.. Thanks!!

If addison's disease was present at birth it would show a lack of characteristics. Most cases of addison's, though, are autoimmune and develop well after puberty. After puberty DHEA (from the reticularis) is only a minor portion of androgens, most are through ovaries/testes.

Hyperaldosteronism from cirrhosis/nephrotic/CHF is through the RAA system.
 
If addison's disease was present at birth it would show a lack of characteristics. Most cases of addison's, though, are autoimmune and develop well after puberty. After puberty DHEA (from the reticularis) is only a minor portion of androgens, most are through ovaries/testes.

Hyperaldosteronism from cirrhosis/nephrotic/CHF is through the RAA system.

Thanks, though how does cirrhosis/nephrotic/CHF activate RAA system? first aid says it has something to do wiht low intravascular volume, but im not sure how those 3 are involved w/ low intravascular volume..?
 
Thanks, though how does cirrhosis/nephrotic/CHF activate RAA system? first aid says it has something to do wiht low intravascular volume, but im not sure how those 3 are involved w/ low intravascular volume..?

Well I know CHF increases ACE in the lungs. Outside of knowing that the other two cause an upregulation in the RAAS I can't tell you why, maybe someone smarter can chime in.
 
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Thanks, though how does cirrhosis/nephrotic/CHF activate RAA system? first aid says it has something to do wiht low intravascular volume, but im not sure how those 3 are involved w/ low intravascular volume..?

In liver failure there is decreased synthesis of albumin. In nephrotic syndrome you lose albumin in the urine. In either case, there is decreased capillary oncotic pressure, fluid leaves the vessel, you get your low intravascular volume.

The kidney picks this up as low volume and stimulates RAAS to bring the volume back up to normal.

In CHF the idea is two things: low blood going forward, and again the kidney sees this as low volume, triggering RAAS -> fluid retention -> edema. There is also backup of blood, contributing to edema also.
 
In liver failure there is decreased synthesis of albumin. In nephrotic syndrome you lose albumin in the urine. In either case, there is decreased capillary oncotic pressure, fluid leaves the vessel, you get your low intravascular volume.

The kidney picks this up as low volume and stimulates RAAS to bring the volume back up to normal.

In CHF the idea is two things: low blood going forward, and again the kidney sees this as low volume, triggering RAAS -> fluid retention -> edema. There is also backup of blood, contributing to edema also.

thanks!
 
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