NBME 24 Adenosine (NBME Answers)

NBME 24 Answers

nbme24/Block 3/Question#2 (reveal difficulty score)
A 28-year-old man has a blood pressure cuff ...
Adenosine 🔍 / 📺 / 🌳 / 📖
tags: biochem metabolism acid_base blood_physiology

+95 upvote downvote
submitted by ∗drdoom(1206)

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After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts.

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lispectedwumbologist You're a good man. Thank you. +1

drdoom So glad it helped! +1

seagull very well put, thank you +2

eosinophil_council Great! +

aisel1787 gold. thank you! +

pediculushumanus beautiful explanation! +2

rockodude this explanation was on par with Dr. Sattar IMO +3

flvent2120 Just to add on to this: FA2020 pg. 297. CHALK (Calcium, H+, Adenosine, Lactate, K+) is known to vasodilate muscles during exercise as well as regulate sympathetic tone of arteries at rest +3

omarjenny Dr Sattar and pathoma failed alot people don't recommend them. +

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submitted by newrose(10)

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Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator

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cassdawg My best answer for this is that the best answer is adenosine because it is asking for which is involved in the mechanism of reactive hyperemia (which involves similar mechanisms to autoregulation) of blood flow, which involves CHALK. While vasodilators like PGI2 (protacyclin) are vasodilators it is released at a base level by the lungs and endothelium, and releasedat higher levels in instances such as inflammation. Prostacyclin is not released in reactive hyperemia. If you want a refresher about active v reactive hyperemia: https://slideplayer.com/slide/2541224/9/images/3/Arteriole+Resistance%3A+Control+of+Local+Blood+Flow.jpg. They are both mediated by metabolic intermediates. as mentioned above. +4

cbreland I picked prostacyclin for the same reason. Adensine and the other CHALK metabolites makes sense though. I guess that's why your arteries/veins dilate when working out +2

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submitted by ∗madojo(212)

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I don't know if this was the right way i thought about it but i remembered C.H.A.L.K the things that cause vasodilation in skeletal muscle

C - Co2, H - H+, A- adenosine, L - lactate K- K+

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drdoom This is great; these are all proxies of catabolism, i.e., "net" ATP consumption! (ATP->ADP) +1

drdoom Potassium might be the one that doesn't seem to fit but recall that cells have an H+/K+ antiporter: cells can act as a "sink" for high blood H+; they "take up" H+ (from blood, into cell) but "in exchange" they have to put out a K+ (to maintain a normal electro-gradient). So, as blood acid starts to creep up, cells actually "attempt" to bring it back to equilibrium by sucking up H+ (and putting out K+, which, as you surely recall ;), is the predominant cation within cells). +3

misterdoctor69 @drdoom, would you also venture to say that there is increased Na+/K+ ATPase activity in an increased metabolic state which might also contribute to greater K+ efflux into the blood? +

drdoom @misterdoctor69, no. Potassium flow is driven by its chemical gradient (from inside cell, where its concentration is high, to outside). If K+ efflux is increased, the best culprit would be the H+/K+ antiporter (which “takes up” a proton, but has to “surrender” a potassium, in an attempt to remove acid from the blood — acidic blood, of course, being an inevitable outcome of revved metabolic state: net ATP consumption & high CO2 production). +

+2 upvote downvote
submitted by pmnbp(2)

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could someone please explain why adenosine is correct?

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drdoom After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts. +1

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