NBME 23 Thromboxane A2 (NBME Answers)

Retired NBME 23 Answers

nbme23/Block 4/Question#1 (reveal difficulty score)
A 65-year-old man is brought to the emergency ...
Thromboxane A2 🔍 / 📺 / 🌳 / 📖
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+8 upvote downvote
submitted by ∗jrod77(32)

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I think they might be describing angina...not sure. TXA2 is responsible for platelet aggregation,so it may be contributing to thrombosis, thus ischemia to the cardiac tissue.

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sympathetikey Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +46

he.sanchez14 If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +5

vik hahah, seems like all in same boat like me +

yb_26 thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +8

youssefa Went for PGE2 ... shit +

need_answers I went for leukotriene B4, what the hell was I doing....SHIT +15

hopsalong I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +

bballhandler11 Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +12

ususmle same here I M PISSED PGE2 +3

krewfoo99 Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +3

djtallahassee ditto on the looked at it for 2 seconds and went PGE2 +1

veryhungrycaterpillar My knee jerk reaction was to go with PGE2 for pain was well, but we must not forget that PGE2 is also a direct vasodilator. It also inhibits platelet aggregation. +

kungfupanda I'm on a whole new level. i thought this might be an asthma attack and i choose LTB4 +2

an1 Intermittent chest pain does seem like angina. E2 does cause pain, but it also causes fEvEr. TXA2 inhibits platelets (unstable) AND increases vascular tone (prinzmetal) which makes it a better option. E2 increases uterine tone (check sketchy), not vascular so it can be chosen if they were to mention labor. +

+3 upvote downvote
submitted by wheredidbuzzwordsgo(3)

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Seems like I did what most of you did. I read the "symptom" as pain and went for PGE2.

Turns out if I had just read the 2008 paper Undiscovered role of endogenous thromboxane A2 in activation of cardiac sympathetic afferents during ischaemia I would have known that TXA2 MAY be a cause of MI pain. https://www.ncbi.nlm.nih.gov/pubmed?term=18483073

There are also theories that the pain is from adenosine/bradykinin/acid/ROS/5-HT which you can read about here:

https://www.ncbi.nlm.nih.gov/pubmed?term=10099685 https://www.ncbi.nlm.nih.gov/pubmed?term=10222339 https://www.ncbi.nlm.nih.gov/pubmed?term=11458709 https://www.ncbi.nlm.nih.gov/pubmed?term=12411532

I found these via the UpToDate page Angina pectoris: Chest pain caused by coronary artery obstruction which does say the mechanism is "complex and not entirely understood."

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makinallkindzofgainz this is all irrelevant. the dude is having an MI so the answer is Thromboxane A2 +

drschmoctor Bruh, you gotta read all the 2008 papers. It was a fire year for obscure shit you need to know in 2020. +15

weirdmed51 Substernal chest discomfort = ANGINA (only pain isn’t chest discomfort) Hence TXA2 which mediated platelet aggregation (like ADP). +

+1 upvote downvote
submitted by asteroides(8)

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This is actually describing myocardial infarction I think, from this article: https://www.ncbi.nlm.nih.gov/pubmed/6485997

We conclude that generation of thromboxane A2 occurs during the early stages of AMI and may be an important pathophysiologic phenomenon in AMI.

Damaged endothelial cells cannot produce PGI1 and prostacyclin => platelets begin to aggregate and release TXA2

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+1 upvote downvote
submitted by ∗thotcandy(131)

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LD4 = vasoconstriction + bronchoconstriction - does it have a role in prinzmetal? I picked this thinking vasospasm due to atherosclerosis.

PGE2 = pain + fever. so i suppose because it's ischemia and not an inflammation, that's not the answer?

TXA2 = PLT aggregation --> thrombus --> ischemia? But i figured that would be more relevant to a stroke or a PE. But I guess TXA2 does play a role in atherosclerosis so it's the biggest contributor.

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+0 upvote downvote
submitted by ∗madamestep(17)

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Something key to note is that it's called "THROMB-oxane" for a reason.

"Named after its role in thrombosis, TxA2 has prothrombotic properties, as it stimulates the activation of platelets and platelet aggregation. TxA2 is also a known vasoconstrictor and gets activated during times of tissue injury and inflammation. While the prostaglandin counterbalances its thrombotic and vasoconstrictor properties prostacyclin (PGI2), there are various physiological and pathological situations where this balanced becomes dysregulated. Increased activity of TxA2 may play a role in the pathogenesis of myocardial infarction, stroke, atherosclerosis, and bronchial asthma. Increased action of TxA2 also has implications in pulmonary hypertension, kidney injury, hepatic injury, allergies, angiogenesis, and metastasis of cancer cells."

https://www.statpearls.com/ArticleLibrary/viewarticle/30114

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