humpf!!
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9) A 52-year-old man is found to have hypertension during a routine examination A systolic bruit is heard over the left renal artery Angiography shows a discrete 95% obstructive lesion within the left renal artery; the right renal artery is normal The right kidney is 11 ern, and the left kidney is 8.5 cm Which of the following describes the most likely response to treatment?
A) Decreased plasma renin activity and decreased serum angiotensin I concentration following administration of a loop diuretic
B) Decreased plasma renin activity following administration of an angiotensin-converting enzyme inhibitor (ACEI)
C) Increased plasma renin activity and decreased serum angiotensin I concentrations following administration of a loop diuretic
D) Increased plasma renin activity following administration of an ACEI
I think it's D
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| Bartek
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I agree with D:
In patient with decreased renal perfussion I would expect RAA system activation (BRS Costanzo 100-101).
If I successfully control BP in this patient, BP decrease further stimulates RAA -> significant increase of plasma renin (and big increase of angiotensin I, due to renin catalyzing action).
A,B - not OK, as renin will definitely increase
C - not OK: loop diuretic -> blood volume down -> RAA activation = renin up, but also angiotensin-1 UP
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| robin082006
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ACE--> decreased angiotensin II--> decreased Aldosterone---> increased Renin
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| Musuq
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The RAA renin-angiotensin-aldosterone system is a series of reactions designed to help regulate blood pressure.
When blood pressure falls (for systolic, to 100 mm Hg or lower), the kidneys release the enzyme renin into the bloodstream. Renin splits angiotensinogen, a large protein that circulates in the bloodstream, into pieces. One piece is angiotensin I. Angiotensin I, which is relatively inactive, is split into pieces by angiotensin-converting enzyme (ACE). One piece is angiotensin II, which is very active. Angiotensin II, a hormone, causes the muscular walls of small arteries (arterioles) to constrict, increasing blood pressure. Angiotensin II also triggers the release of the hormone aldosterone from the adrenal glands. Aldosterone causes the kidneys to retain salt (sodium) and excrete potassium. The sodium causes water to be retained, thus increasing blood volume and blood pressure.
Giving ACEI to this patient will lower the blood pressure (even more dramatically in the left kidney) and thus the yuxtaglomerular cells (in aa) will detect this decreased pressure which promotes Renin release thus increasing BP.
RENIN release is the normal response only to a drop in BP (yuxtaglom cells) in affer art.
in fact, patients that are taking antihypertensive drugs always show the following: decrease TPR, decr CO, decr body fluid volume, decr BP may result in homeostatic regulation [reflex tachycardia (increase sympathetic activ) & Edema (Incr RENIN activity) ]
thus RENIN is only produced as the BP decreases in the afferent arteriole
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| rm
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i pick C --- a patient who has renal artery should not be given ACEI because you need the angiotensin2 to protect the stenotic kidney, since thats they onyl good kidney. the other is damaged by the increased velocity of blood coming towards it (flea bitten or glodblatts kindney).
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| rm
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i pick C --- a patient who has renal artery should not be given ACEI because you need the angiotensin2 to protect the stenotic kidney, since thats they onyl good kidney. the other is damaged by the increased velocity of blood coming towards it (flea bitten or glodblatts kindney).
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| vamsi2004
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its true that ACEIs should not be used in renal artery stenosis bcos it causes ARF. but then wats the answer for this question????
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| docswapna
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i also think C. but is it right?
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| young_doc
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vamsi2004 wrote:
its true that ACEIs should not be used in renal artery stenosis bcos it causes ARF. but then wats the answer for this question????
hmm..how would using ACEI in renal artery stenosis cause ARF? Please explain.
We have to treat the source of the HT. In this case it's due to the increased Renin. Hence the use of an ACEI.
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| docswapna
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youngdoc, its mentioned in kaplan that ACEI cause ARF when used in renal artery stenosis. dunno the actual mechanism. what do u think is the ans for this q?
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| klimt
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ACEI are indeed contraindicated in patients with renal artery stenosis...
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| ManuNastai
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I would have picked D, but C is correct too. the question remains "which one is the treatment?"
you're right guys, ACE inh. are contraindicated in stenosis. here's the mechanism:
by inhibiting ACE you decrease the AT II and you don't want that because AT II produces constriction of the eferent arteriole mainly and by doing this produces a increase in the hidrostatic pressure in the glomerulus and increases an otherwhise decreased glomerular filtration rate. so, you don't want do inhibit the synthesis of that dude!
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| tran6996
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ACE-i is contraindicated in BILATERAL renal artery stenosis. In this case, it's only the L side
I would go for D
how can C be correct ? increase renin would incrase Ang1 (not dec)
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| Musuq
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D!!!
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| sjain4
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The reason they are ever contraindicated, is that ACEI can cause dilatation of efferents, reducing GFR. GFR is maintained in those w/ Stenotic R.A. by way of Angiotensin II constricting the efferent arterioles.
But the right renal artery is fine, so I believe ACEI's aren't contraindicated. Even if they were, thats not what the question's asking. THE ANSWER IS D.
There is no way C is correct, even if loops would increase renin activity, how would that result in a decrease in angiotensin I????
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