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lee280
For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks
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notyasupreme
I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it.
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topgunber
sildenafil does make sense, especially since hes on 2 vasodilators. I picked diltiazem because the pt has systolic heart failure. thought it was contra indicated to give CCB to systolic heart failure because you could further decrease contractility. Either way never give NTG and viagra
+1
sexymexican888
Yeah @topgunber I also picked diltiazem.... I guess they were looking for "COMBINATION" rather than a specific contraindication
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pakimd
@lee280 you are right in saying that beta blockers are only contraindicated in acute decompensated heart failure. this is because beta blockers, which would normally prevent the deleterious effects of neurohormones like norepinephrine on cardiac remodeling that occurs in HFrEF, will further impair cardiac output in decompensation. hope this helps :)
+1
leap1608
The answer to all your queries lies in the fact that a combination of Metoprolol and vasodilators would actually be beneficial in dampening the REFLEX TACHYCARDIC effect of nitrates, hydralazines etc. Hence, decreasing the work load on the heart.
+1
lee280
I agree, at the start, I got a bit confused because I felt like the question was probably less specific than it would have been, but NBME being NBME this is really expected. When you think about it more closely, once you consume the meal then ghrelin will peak and start dropping.
+21
notyasupreme
I agree, I had B at first but then thought too deep into it. I thought if she ATE a meal, she'd be full and low ghrelin. Annoying to get a question wrong on something so simple.
+2
radzio1
Also got this question wrong. A really bad explanation what they want from the curve...
+1
shieldmaiden
Basically she is eating at peak ghrelin (B) its drops, then she likely eats a snack on E
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bboucher
They ask what point ''represent the consumption of a meal'' by mean there is no reason you're ghrelin would start dropping before you even started eating (point C which is I guess the other you might have guess) in contrast to B where it follows a natural physiologic cycle where it increase because you get hungry --> You eat because you're hungry --> Abdominal distention due to the food start decreasing ghrelin.
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ali_hassan
I get it now, but when I was doing the test it made absolutely no sense, I was stuck between B - C - D. Word your questions better NBME!
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chaosawaits
I'm reading the question now and I still think "the consumption of a meal" means that the meal has been consumed. I feel like this is really a black & blue dress and once again, I'm not in on the joke.
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chaosawaits
I think the question is actually worded properly because of the lag before ghrelin is released. As you consume the meal, ghrelin release slows down, such that the peak arises by the end of the meal. Therefore B is the right choice because at the end of consumption of the meal is the peak of amount of ghrelin. It's not like as soon as you take a bite of cream of wheat, the ghrelin levels immediately shoot down. Maybe?
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Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]
Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.