UW Question#2013

[CBG23]

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I don't know if we are allowed to discuss U.W. questions. If not, I'll delete the post ASAP.

I am confused about Q#2013 in the QBank - the explanation still didn't clear up that confusion so I was hoping somewhere here might be able to help me understand why I got this question wrong.

The gist of the question is this:

A patient comes in with a BP=200/120, HR=90, Serum K+=3.0, Elevated plasma Renin, Elevated urinary Aldosterone. The question is: what is most likely to have caused this?

I selected "Adrenal medullary tumor". Why?

His K+ is low, which you might expect based on the fact that his aldosterone is elevated. Since BOTH his aldosterone and his renin levels are elevated, the elevated aldosterone must be due to the increased Renin. So an elevated Renin level accoutns for most of the given findings, BUT not the increased HR.

So, now what can cause an increased Renin and an increased HR? Well, the only thing I could think of was the fact that both the JG cells of the kidney and SA node both express Beta1 receptors. Therefore, increased catecholamines could both increase RAAS activation and increase the HR.

It turns out that the answer was "Juxtaglomerular cell tumor". The reason they say that Pheochromocytoma is not correct is that it doesn't really cause hypokalemia (that seems like a BS explanation considering that pheo can increase Renin--> inc. Aldosterone --> hypokalemia).

The only explanation I could reason out is that a BP of 90 is not high, as I thought it was. I know that > 100 is considered tachycardic, BUT given an increase in BP, I would expect a reflex bradycardia and a HR a lower than 90 (if elevated Renin really was the cause) - this is why I didn't choose JG tumor.

Any thoughts?

 

[1badvette]

it's secondary Hyperaldosteronism due to some kind of renal involvment .... Adrenal tumor secreting aldosterone would not have high renin .

 

[CBG23]

I said adrenal MEDULLARY tumor, not Adrenal CORTEX tumor...

 

[pbnj003]

if this is the question about reninoma then i know which question you are talking about.

basic logic....this dude has severe hypertension. you can also see that he has increased aldosterone and renin.

now if you are to think this through, if this was just a case of hypertension then your renin aldosterone would be low in response to the hypertension. However you have increased renin and aldosterone.

Yes pheochromo would lead to hypertension but it would not cause the high levels of renin and aldosterone.

Honestly common knowledge wise, pheo has nothing to do with K. Its MORE likely that the HIGH aldosterone has something to do with the K in this question. The fact that they put K level in the question (considering thats the only specific electrolyte level they gave) then you have to think that K has something to do with the dx. and the most common association is with aldosterone and k.

Basically guy has hypertension and still has high renin aldosterone. the high aldosterone is causing the hypoK.

If you think "common things are common" a reninoma makes more sense! I think there was more in this quesiton that led to the answer I cant remeber though. I hope i sort of helped! I am on a studying OD so sorry if my answer seems a bit jumbled!

I think you went too deep into this one! keep it simple! Gluck 🙂

 

[CuriousGeorge2]

I think you guys didn't read the OP's post carefully. He says that he knows the high aldosterone level is causing the drop in the potassium. He also says that he knows that since Renin is high and not low, it must be that the increase in Renin is causing the increase in aldosterone. So, he knows that the pathology is that something must be causing Renin to be secreted excessively.

I think the OP believes that Pheochromocytoma is a cause of elevated Plasma Renin and, consequently, aldosterone. This actually makes sense if you read his explanation; the problem with pheochromocytoma is that there are too many catecholamines. Since JG cells of the kidney have beta 1 receptors, the excess catecholamines lead to excess Renin release. The excess renin release would then account for the increase in aldosterone and the low potassium level. Based on my knowledge of physiology, this is all sound reasoning.

In support of the OP's argument, here is something I came across in my endo text:

"Levels of plasma renin activity are not typically suppressed in patients with pheochromocytomas because catecholamines stimulate renin release, and some tumors may secrete renin ectopically." - Greenspan's Basic & Clinical Endocrinology, 9e

Based on this sentence, you would expect Pheos to increase Renin, which would increase aldosterone, which would cause potassium to drop.

The only difference you might expect between Pheochromocytoma and JG tumor is that Pheo. can also stimulate the heart to increas HR, which is what the OP was getting at.

My guess is that in reality pheochromocytoma does not significantly increase Renin, at least not to the extent of the increase you would expect to see with a JG tumor. However, this is just speculation on my part...Maybe someone else can explain why pheo isn't an adequate choice?

 

[pbnj003]

ok agreed.

But remember that Pheo causes large amount of NE to be released.....such a large number of NE increase has more effect on alpha 1 receptors rather than B1. Therefore A1 stimulation would cause decreased Renin if it was Pheo.

 

[kaleerkalut]

ok agreed.

But remember that Pheo causes large amount of NE to be released.....such a large number of NE increase has more effect on alpha 1 receptors rather than B1. Therefore A1 stimulation would cause decreased Renin if it was Pheo.

Sorry wouldn't it cause increased renin since vasoconstriction would cause decreased RBF? Thanks 🙂

 

[pbnj003]

thats good point! i wonder if someone can explain that.

because from what i remember from my gen pharm lectures on ANS was that A1 stimulation in the kidney would cause decreased renin. Becuase with pheo the AMOUNT of NE is so great that it stimulates A1 over B1. But as you said you would expect it to also cause vasoconstriction etc. which would by reflex cause increased Renin.

My guess is that it probably doesnt cause THAT much of a renin increase as is the case in this question. but I wonder if someone else can chime in and explain that.

 

[gravitywave]

thats good point! i wonder if someone can explain that.

because from what i remember from my gen pharm lectures on ANS was that A1 stimulation in the kidney would cause decreased renin. Becuase with pheo the AMOUNT of NE is so great that it stimulates A1 over B1. But as you said you would expect it to also cause vasoconstriction etc. which would by reflex cause increased Renin.

My guess is that it probably doesnt cause THAT much of a renin increase as is the case in this question. but I wonder if someone else can chime in and explain that.

huge amount of NE = a1 stimulation > b1, peripheral vasocontriction causes HTN. kidney won't "see" this increased BP because it will autoregulate RPF at the afferent arteriole (higher BP -> more stretch -> juxtaglomerular smooth muscle constricts)

 

[Fuzuli]

All excellent responses above,so I hope I can add a few points:

The gist of the question is this:

A patient comes in with a BP=200/120, HR=90, Serum K+=3.0, Elevated plasma Renin, Elevated urinary Aldosterone. The question is: what is most likely to have caused this?

Hypertension and hypokalemia is typical for hyperaldosternoism. Increased urinary aldosterone supports this and eliminates other causes mineralocorticoid excess (Cushing's syndrome being the most important one).

So the question we have to answer becomes this: Does the main problem lies within the adrenal gland or kidney?

a. Adrenal (Primary hyperaldosteronism): Autonomous production of aldosterone (i.e. elevated aldosterone with low renin). This would be analogous to adrenal neoplasm producing cortisol for Cushing's syndrome.
b. Kidney (Secondary hyperaldosteronism): Elevated aldosterone isedue to increased increased renin production. This is analogous to Cushing's disease (ACTH produching adenoma of pituitary gland) of Cushing's syndrome.

Since plasma renin is elevated, the problem lies within the kidney. Increase of renin is usually due to a pathologic stimulus causing renin to increase (i.e. non-autonomous - secondary reninism): They are usually due to (a) Vascular diseases (like renal artery stenosis) and (b) Decreased effective arterial volume (like CHF and cirrhosis). Rarely, there could be an autonomous renin secretion due to a renin secreting tumor (primary reninism).

The only explanation I could reason out is that a BP of 90 is not high, as I thought it was. I know that > 100 is considered tachycardic, BUT given an increase in BP, I would expect a reflex bradycardia and a HR a lower than 90 (if elevated Renin really was the cause) - this is why I didn't choose JG tumor.

Any thoughts?

Like you've said, 90 is considered to be within normal range. The question would be a little harder to solve with tachycardia, but the answer still could not have been an adrenal tumor. Adrenal causes of hyperaldosteronism would lead to decreased renin, not increased.