nbme 4;2;21 - dmaha

[ArchivalUser]

the clue here is that is a HTN difficult to treat (max doses and still uncontrolled), so when that happens is usually a secondary cause, being renovascular HTN the second MCC , and the other clue is that she's a 62 yr old who has been a smoker w/ claudication = atherosclerosis. fibromuscular dysplasia usually occurs in pts

[ArchivalUser]

Its not B) I put that and it was incorrect.

[ArchivalUser]

Unequal versus delayed pulses.

PLEASE AND PLEASE, lets not confuse differential amplitude with radio-femoral delay!!! I made this silly mistake reading the question until I saw this options.

This patient has unequal amplitude of the peripheral pulses which may result from:

1. Obstructive arterial diseases, most commonly atherosclerosis but can also be due to arterial thrombosis from prior catheterization

2. Aortic dissection

3. Aortic aneurysm

4. Takayasu disease

5. Coarctation of the aorta (here amplitude is not just diminished, but there will be a delay in the onset of femoral pulse picked up as radio-femoral delay)

6. Prior surgical ligation (eg, history of classic Blalock-Taussig shunt)

7. Supravalvular aortic stenosis in which the right carotid, brachial, and radial pulses are larger in amplitude and volume than those on the left side because of the preferential streaming of the jet toward the innominate artery.

Extra:
On the normal K, she is on maximum dose of ACE-I or ARB which may offset hypokalemia. Infact, even if she had a stenosis of a single solitary kidney or had bilateral renal artery stenosis, ACE-I or ARB + diuretic therapy is still the preferred agent to treat since it blunts the raved-up RAS system that occurs in this setting. The concern is in the few (about 10%) who have serious decline in their GFR following or whose elevation in creatine exceeds 30% after administering ACEI or ARB. This means that almost 80% of these patients can tolerate ACE-I or ARB.

If GFR worsens, cut down on diuretic therapy first (to optimize volume as a strategy to enhance kidney persuasion), if that fails back-off on ACEI/ARB.

[ArchivalUser]

@spartanike wow awesome explanation.

[ArchivalUser]

Thanks @prettymuch!

[ArchivalUser]

great explanation

[ArchivalUser]

Hi. Could anyone correct me if I am wrong. I read that Mcc for secondary HTN is Renovascular disease. Thanks.