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NBME 20 Answers

nbme20/Block 4/Question#17 (32.1 difficulty score)
A previously healthy 55-year-old man has ...
Renal artery stenosis🔍
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 +15 
submitted by hayayah(1056),
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sammyj98  I like you sticking up for the kidneys, thinking they're increasing Renin for the benefit of the whole body, but lets face it, the kidneys are a couple selfish dicks who want the high blood pressure all for themselves. LeftVentricularSolidarity +4  



 +13 
submitted by monoloco(132),
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sA a reul of m,bhtu fi uyo vige oesoemn an ACE rinhbtoii nad etyh gte a m,pebrol ehty hda nlera traery isossent yu(slual etabll,liray ro so we ewer thguta at oru emd o)shl.oc alboPbyr sah ot do tiwh scrddeaee FRG sahtkn to adsdrecee iitgsAnoenn sic–evleteII vnrscsntctaooiio fo the ertneffe lotareeir ;t&g= eddeescra udmsoi lrydveie to calmua nesad g&=t; isercndae eninr esaeel.r

lilyo  Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions. This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback. +2  
drpee  We should always expect GFR to drop a little after adding an ACE-inhibitor due to efferent arterial vasodilation. For this reason we should also expect Renin levels to rise via tubuloglomerular feedback. So it's not really the reaction to the ACE inhibitor that gives this away as RAS (which is why I got it wrong). I think what we are expected to be looking at it are lab values: Hypokalemia, and secondary hyperaldosteronism. https://www.aafp.org/afp/2017/1001/hi-res/afp20171001p453-t5.gif +  
stepwarrior  ACE inhibitors would actually have the opposite effect of AT-II, and result in efferent dilation. But the actual mechanism of increased renin activity per UWorld is lack of systemic vasoconstriction by AT-II leading to blood shunting away from the kidney. +  



 +0 
submitted by medstudent(11),

I struggled with why this couldn’t be essential HTN for a while. I think what it comes down to is this, and someone help me out if I’m incomplete/wrong.

In bilateral RAS, ACE inhibitors will decrease the GFR from dilation of efferent arteriole and they can’t increase the GFR further because they’re already maxed out on afferent dilation to keep up GFR in the first place.

In essential HTN, yes ACE inhibitors decrease GFR from dilation of efferent arterioles, however they’re able to maintain GFR through autoregulation because they haven’t touched their afferent arteriole. So this means that renin won’t actually increase.

TL;DR: Bilateral RAS is unable to use autoregulation to correct the decrease in GFR where essential is able to.




 -2 
submitted by md_caffeiner(45),
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