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BrisketAttack

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This question on NBME 3 has me going nuts:

What will increase serum aldosterone concentration in an experimental subject?

-administration of ACE inhibitor
-increased Na intake
-inhibiting ACTH secretion
-IV 0.9% saline
-Water restriction

Any help would be greatly appreciated.
 

Jbienven

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This question on NBME 3 has me going nuts:

What will increase serum aldosterone concentration in an experimental subject?

-administration of ACE inhibitor
-increased Na intake
-inhibiting ACTH secretion
-IV 0.9% saline
-Water restriction

Any help would be greatly appreciated.



I just took the stupid thing. I put water restriction.
 

BrisketAttack

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I put the same answer, but I don't understand the mechanism at all. It just sounded good. That's not gonna cut it on the real exam. i just got lucky.
 

DragonWell

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This question on NBME 3 has me going nuts:

What will increase serum aldosterone concentration in an experimental subject?

-administration of ACE inhibitor
-increased Na intake
-inhibiting ACTH secretion
-IV 0.9% saline
-Water restriction

Any help would be greatly appreciated.

I can see the water restriction-> hypovolemia-> inc aldosterone reasoning, but I also think that technically the answer could be the ACE. I think Goljan even talks about "aldosterone escape" in patients on an ACE...eventually the aldosterone "breaks through", which is why an ACE + spironolactone is better than just an ACE. I don't know if this is specific to CHF or universal w/ ACE therapy, though.

This may be reading into the question, though.

It was long perceived that ACE inhibition would lead to markedly reduced plasma aldosterone concentrations. However, aldosterone levels increase progressively despite ACE inhibition after AMI,[12] and very high aldosterone levels are seen in a proportion of patients with CHF.[13] This phenomenon by which aldosterone levels tend to return towards, and sometimes reach, pre-treatment levels is known as aldosterone-escape. The potential mechanisms involved in this phenomenon are unclear but have been reviewed recently

http://www.medscape.com/viewarticle/521164_3
 

VPDcurt

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It's definitely water restriction and not an ACE. Mineralocorticoid escape generally occurs in the presence of ECF volume expansion - a condition not stated or even remotely suggested by the simple stem of this question. A major stimulus for aldosterone secretion is the RAA via decreased blood volume.
 

Mr. Freeze

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Think I got tripped up because at the time I didn't see much difference between water restriction and increased salt intake. Got some work to do I guess.
 

osli

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Think I got tripped up because at the time I didn't see much difference between water restriction and increased salt intake. Got some work to do I guess.
Aldosterone retains salt... not what you want if you've eaten too much of it. Increased salt intake would decrease aldosterone levels.

The reason it rises in hypovolemia (after water deprivation) is that by retaining salt you also retain water, helping to offset the low-volume situation that triggered the aldosterone release.
 

Mr. Freeze

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I looked at it, incorrectly, like decreasing water would increase relative [Na] and I guess failed to see the volume component of renin regulation. In looking at it now, what I did was confuse the macula densa mechanism with renin regulation. Just giving away points. ****!!!!!!!!:mad:
 

MAO

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Think I got tripped up because at the time I didn't see much difference between water restriction and increased salt intake. Got some work to do I guess.

increased Na+ intake -->cause hypervolemia -->inhibit renin and increase ANP

water restriction -->hypovolemia-->activate renin angiotensin system --> increase aldosterone
 

hippocampus

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what is aldosterone escape?

what MAO wrote, it this all happening in the ECF compartment?
 

DragonWell

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what is aldosterone escape?

what MAO wrote, it this all happening in the ECF compartment?

The way I understand it, there are actually two definitions. In a pt with Conn's Syndrome, aldosterone escape refers to the fact that even with greatly increased aldosterone levels, the BP will stabilize at an elevated level due to natriuresis. This definition is explained here.

The other definition which is the one that I mentioned in the post above has to due with the fact that even though patients are put on an ACE, it is possible for their aldosterone levels to eventually increase in spite of the med.

Nice explanation here.
 

MAO

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what is aldosterone escape?

what MAO wrote, it this all happening in the ECF compartment?

increased Na+ intake--> increased Na+ filtered in the bowmans space (increased Na+ load) -->70% of it is reabsorbed in PCT ( since amount filtered is more ,the AMOUNT reabsorbed is also more, though % reabsorbed is still 70%) -->along with it water is also reabsorbed -->ECF volume increase.

i hope now it makes sense.........................
 
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