Step I Huh Primary Hyperaldolsteronism

[ReidSternberg]

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Why oh why is in Primary Hyperaldosteronism we get no edema when aldosterone pulls in Na and result in increase volume load? Hmmm. Any thoughts??

Thanks.

 

[agranulocytosis]

Why oh why is in Primary Hyperaldosteronism we get no edema when aldosterone pulls in Na and result in increase volume load? Hmmm. Any thoughts??

Thanks.

My guess has to do with the fact that aldosterone does not affect plasma osmolarity. As Na is being reabsorbed, it takes H20 along with it, so the result is increased plasma volume with no decrease in plasma osmolarity. Decreased plasma osmolarity is a factor involved in the formation of edema.

 

[ReidSternberg]

My guess has to do with the fact that aldosterone does not affect plasma osmolarity. As Na is being reabsorbed, it takes H20 along with it, so the result is increased plasma volume with no decrease in plasma osmolarity. Decreased plasma osmolarity is a factor involved in the formation of edema.

Then why do you have edema in secondary hyperaldosteronism then if that was the case? Hmmm. my brain isn't made for all of this thinking ughh.

 

[agranulocytosis]

Then why do you have edema in secondary hyperaldosteronism then if that was the case? Hmmm. my brain isn't made for all of this thinking ughh.

I don't think that it's the hyperaldosteronism that causes the edema...I think it has to do with edema being part of the features which result in 2ndary hyperaldosteronism. A case like CHF would result the formation of edema and the lower plasma volume would signal the RAA system to turn on. It's like the chicken versus the egg, which one comes first?

 

[DragonWell]

I think it's because in Conn's you have aldosterone escape - once the arterial volume increases 15% or so, you have pressure induced natriuresis that causes loss of water and sodium and stabilizes the BP at a somewhat elevated level, but it is stabilized, so the system will adapt to the new higher set point - ie. the HR or TPR will decrease to try to normalize the BP as much as possible.

In a secondary hyperaldosteronism, I think you're seeing the heart or some part of the system fail and that's what's leading to the edema, and as mentioned above the aldosterone is just a maladaptive compensation.

Just hypothesizing...

 

[ROBINHO]

Becos of the Aldosteron escape explained above. Saw that somewhere in USMLEworld and RR

 

[PrussianBlue1]

The context in which I had heard about aldosterone escape was in relation to therapy with ACE inhibitors.

""Aldosterone Escape," in which the body maintains Aldosterone production through mechanisms not involving ATII (though pathways not involved with ACE), has been noted to occur and is not well-understood. In fact, studies have shown that CHF patients treated with ACEI's initially show a decrease in Aldosterone production, but they show a huge increase in Aldosterone production long-term. This "Aldosterone Escape" is the rationale for combining an Aldosterone Antagonist with the ACEI for the most effective therapy."

So it seems here like it is being used to explain an opposite phenomenon? Aldosteron escape in order to prevent a further increase in volume retention? mmm... 😕😕😕

 

[DragonWell]

The context in which I had heard about aldosterone escape was in relation to therapy with ACE inhibitors.

""Aldosterone Escape," in which the body maintains Aldosterone production through mechanisms not involving ATII (though pathways not involved with ACE), has been noted to occur and is not well-understood. In fact, studies have shown that CHF patients treated with ACEI's initially show a decrease in Aldosterone production, but they show a huge increase in Aldosterone production long-term. This "Aldosterone Escape" is the rationale for combining an Aldosterone Antagonist with the ACEI for the most effective therapy."

So it seems here like it is being used to explain an opposite phenomenon? Aldosteron escape in order to prevent a further increase in volume retention? mmm... 😕😕😕

Apparently same term; very different concept. I dont think this has anything to do with the breakthrough of aldosterone on pt's given an ACE. The mechanisms I've read about for aldosterone escape in the context of Conn's relate to either the inability of the PCT to absorb the large amount of Na and water it is receiving or to increased ANP secretion.

 

[ReidSternberg]

I think it's because in Conn's you have aldosterone escape - once the arterial volume increases 15% or so, you have pressure induced natriuresis that causes loss of water and sodium and stabilizes the BP at a somewhat elevated level, but it is stabilized, so the system will adapt to the new higher set point - ie. the HR or TPR will decrease to try to normalize the BP as much as possible.

In a secondary hyperaldosteronism, I think you're seeing the heart or some part of the system fail and that's what's leading to the edema, and as mentioned above the aldosterone is just a maladaptive compensation.

Just hypothesizing...

Boy oh boy. I liking it. Just too cool... thanks👍

 

[agranulocytosis]

I think it's because in Conn's you have aldosterone escape - once the arterial volume increases 15% or so, you have pressure induced natriuresis that causes loss of water and sodium and stabilizes the BP at a somewhat elevated level, but it is stabilized, so the system will adapt to the new higher set point - ie. the HR or TPR will decrease to try to normalize the BP as much as possible.

In a secondary hyperaldosteronism, I think you're seeing the heart or some part of the system fail and that's what's leading to the edema, and as mentioned above the aldosterone is just a maladaptive compensation.

Just hypothesizing...

You're right. I'm going through my 2nd reading of Kaplan right now, and it states the reason for no edema in Conn syndrome is due to Na+ escape and that ANP plays a role (although the mechanism is not entirely understood).