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NBME 24 Answers

nbme24/Block 3/Question#2 (46.0 difficulty score)
A 28-year-old man has a blood pressure cuff ...

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 +68  upvote downvote
submitted by drdoom(615),
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teArf eht uffc is e,tid the lelcs dan utisse talisd ot teh ufcf ilwl ueoncint nuiogsmcn PTA (t&;PgPTA-AD), tbu on shefr bldoo will be vrdlediee to “lre”ac hawt illw be an anuaglmuccti ounmta of APD dna treho iobemett.als ADP e)d(Ao=enins is fielts a rpyox of omuconintps adn vredsi vaniasdtiool fo erai!trse i(oovtnuEl is sta)rm! isgcneranI nDi/AsedoPeAn ni a cal“ol rmenein”tnov is a nsigla ot the yodb ahtt a tlo of ipcunnosmto is gurrcocni ee;hrt tush, setraeri dan oatsieelrr arunaltyl ldieat to erecaisn ldoob owlf aster dna p“ewes yaw”a olbaictme ucobpst.ryd

lispectedwumbologist  You're a good man. Thank you. +  
drdoom  So glad it helped! +1  
seagull  very well put, thank you +1  
eosinophil_council  Great! +  
aisel1787  gold. thank you! +  
pediculushumanus  beautiful explanation! +1  

 +8  upvote downvote
submitted by newrose(8),

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

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: They are both mediated by metabolic intermediates. as mentioned above. +  

 +4  upvote downvote
submitted by madojo(121),

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+

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). +2  
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? +  

 +1  upvote downvote
submitted by pmnbp(1),
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udclo somnoee elpaes pnxeali yhw eondsniae is or?tercc

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