NBME 20 Answers : Block 4 : #17 = A previously healthy 55-year-old man has recently ...

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NBME 20 Answers

nbme20/Block 4/Question#17

A previously healthy 55-year-old man has recently ...

Renal artery stenosis

+10 upvote downvote
submitted by monoloco(57),

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.

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. +

+7 upvote downvote
submitted by hayayah(418),

Also, you shouldn't be seeing end-organ damage or increased renin / kidney response with a previously healthy patient that just developed essential HTN. The body doesn't want to increase renin when it has HTN. However, if you have stenosis, the kidneys freak out because they're not getting enough flow and think the whole body isn't either, so they activate the RAAS system. When you give them an ACE-I, the renin is still being produced by the kidney, it just isn't being converted to angiotensin-II.

To eliminate other choices:

He has increased renin activity so you can eliminate primary aldosteronism. That has inc. aldosterone, dec. renin.
No signs or sxs of Cushing's so that's eliminated.
11-B-hydroxylase deficiency would sxs with the genitalia. You'd have dec. renin activity (aldosterone-like effects still present).
Essential HTN: explained above

+0 upvote downvote
submitted by md_caffeiner(2),

FA19 P592: Renovascular disease: Renal impairment due to ischemia from renal artery stenosis or microvascular disease. renal perfusion (one or both kidneys)  INC renin INC angiotensin HTN. Main causes of renal artery stenosis: Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers. Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females. Clinically, patients can have refractory HTN with negative family history of HTN, asymmetric renal size, epigastric/flank bruits. Most common cause of 2° HTN in adults. Other large vessels are often involved

FA19 P 596: Angiotensin- converting enzyme inhibitors Captopril, enalapril, lisinopril, ramipril. mEChANism Inhibit ACE DECR AT II DECR GFR by preventing constriction of efferent arterioles. INCR renin due to loss of negative feedback.