Tyramine Q

[hartbot]

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So I came across a question which basically described an in vitro experiment where drug x increases the contraction of a blood vessel segment in response to NE. The 2 answer choices which were possible were cocaine and tyramine. I thought both just increase the synaptic conc of norep, and that neither have a direct action on the BV.

Does anyone know how to differentiate the two???

 

[2001bmw330xi]

sure it didn't include "with cheese" somewhere in there? 😉

just teasing - def sounds confusing. hopefully somebody can answer it !!

 

[username456789]

Like the Transformers, I'm thinking this a case of more than meets the eye.

You're likely glossing over a detail in the experiment that you deemed insignificant but provided the definitive clue.

However, Cocaine is a bigtime NE reuptake blocker. Tyramine actually causes release of preformed neurosecretory granules or whatever. Did the experiment involve denervation by any chance?

At least that's how I remember it. I'm too lazy to look it up.

 

[hartbot]

"Diagram shows contraction of a blood vessel segment in response to IN VITRO administration of Norepinephrine (NE) and drug X. Drug X is most likely which of the following?

NE: Increases contraction
NE+X:Greater contraction than NE alone

A) Cocaine
B) Guanethidine
C) Isoproterenol
D) Metoprolol
E) Phenoxybenzamine
F) Reserpine
G) Tyramine

Based on what guy said, I'm leaning toward cocaine

 

[username456789]

Actually, based on that I might think Tyramine. Would NE reuptake be going on with an in vitro experiment? Is it a blood vessel alone, or is there a nerve involved too? I'd expect that by adding Tyramine, you'd cause release of performed NE in the nerve terminal (basically squeeze all the juice out of the neuron, in addition to the NE you added).

Who knows, I'm confusing myself. I never worked in a lab and always hated that stuff, so basic science lab setups aren't my forte.

 

[anumama]

Ah I think I know what question you're talking about (NBME #6). So the answer is cocaine because with the application of the drug and then NE, there was an increase in the blood vessel contraction. Thats due to the cocaine acting as reuptake inhibitor, so there is more NE in the synapse to cause a greater smooth muscle cell contraction. As for tyramine, I believe it causes the release of more NE. If you look at the graph that was provided, the second drug itself did not have any direct effect (ie did not cause BV constriction), but constriction only occurred when NE was introduced. Thus it couldnt be tyramine because that itself would cause BV constriction.

I believe this sort of interplay between the two drugs is called permissive, whereby one drug (drug #2 in this case) potentiates the effect of another drug (NE in this case), with drug 2 not having any DIRECT effect on the parameter being measured.

Hope this helps--I suck at explaining 😛

 

[hartbot]

thanks anumama, that totally makes sense

 

[username456789]

If you look at the graph that was provided, the second drug itself did not have any direct effect (ie did not cause BV constriction), but constriction only occurred when NE was introduced. Thus it couldnt be tyramine because that itself would cause BV constriction.

Yup, that would provide the definitive clue right there!

 

[psychforme]

answer is d. metoprolol

This is in a jar so cocaine has no effect. Norepi is a1, a2 and b1 agonist. Metoprolol blocks b1 ( not b2) which has no direct vasoconstricting effect. However, by blocking b1 more Norepi is available to bind a1 causing vasoconstriction!

Tricky q. Lucky you psychforme was here to clear everything up or you would have gotten this concept wrong on the test.

 

[bergwood]

answer is d. metoprolol

This is in a jar so cocaine has no effect. Norepi is a1, a2 and b1 agonist. Metoprolol blocks b1 ( not b2) which has no direct vasoconstricting effect. However, by blocking b1 more Norepi is available to bind a1 causing vasoconstriction!

I was way too tired when I responded to this...

 

[username456789]

answer is d. metoprolol

This is in a jar so cocaine has no effect. Norepi is a1, a2 and b1 agonist. Metoprolol blocks b1 ( not b2) which has no direct vasoconstricting effect. However, by blocking b1 more Norepi is available to bind a1 causing vasoconstriction!

Tricky q. Lucky you psychforme was here to clear everything up or you would have gotten this concept wrong on the test.

Since when do blood vessels have b1 receptors? (honest question, I've never heard of that before, and I'd assume they'd have to be present on the blood vessel for any of this to be relevant).

 

[psychforme]

Since when do blood vessels have b1 receptors? (honest question, I've never heard of that before, and I'd assume they'd have to be present on the blood vessel for any of this to be relevant).

They always did in the juxtaglomerular apparatus. A pubmed search also brings up a bunch of beta1-receptors in mice vasculature.

 

[username456789]

They always did in the juxtaglomerular apparatus. A pubmed search also brings up a bunch of beta1-receptors in mice vasculature.

No offense but I'm far from sold on your explanation. For all intents and purposes for Step I, I'm pretty sure there would be no b1 receptors present in this milieu.

 

[hartbot]

No offense but I'm far from sold on your explanation. For all intents and purposes for Step I, I'm pretty sure there would be no b1 receptors present in this milieu.

I'm gonna have to side with him, and the original explanation.

I think the question only stated in vitro experiment, not denervated muscle

 

[psychforme]

I'm gonna have to side with him, and the original explanation.

I think the question only stated in vitro experiment, not denervated muscle

Not sure what you're getting at but I am pretty certain (like 100%) nerves do not remain intact when you cut out the vessel and put it in a tube. How do you know the vessel isn't from the JGA?

 

[hartbot]

How do you know the vessel isn't from the JGA?

I dont, and your explanation would make sense if these b1 receptors actually existed on blood vessels.

But what I've learned is that the boards doesnt play tricks. They ask questions which can only have one answer, and they wouldnt ask a question that makes you assume something like this.

 

[psychforme]

I dont, and your explanation would make sense if these b1 receptors actually existed on blood vessels.

But what I've learned is that the boards doesnt play tricks. They ask questions which can only have one answer, and they wouldnt ask a question that makes you assume something like this.

Umm the boards do play tricks. And you think it makes more sense that the innervation stays intact in a tube?

 

[username456789]

Umm the boards do play tricks. And you think it makes more sense that the innervation stays intact in a tube?

Not these kinds of tricks. Please stop being difficult for the sake of saving face. No Step I question would presume that A) a medical student has sifted through pubmed to find random articles about mice blood vessels and how they differ from human blood vessels, B) a medical student having read these articles would assume that "blood vessel placed in a dish" meant "mouse blood vessel placed in a dish", nor C) a medical student would read "blood vessel placed in a dish" and understand that they actually meant JG cells.

You gave it a good effort, and it seems to have fallen short. Like most of the answers here. I get that your gig is "I'm a badass who waltzes in to save the day and kicks ******s in the face", but maybe you should sit this one out.

 

[psychforme]

Not these kinds of tricks. Please stop being difficult for the sake of saving face. No Step I question would presume that A) a medical student has sifted through pubmed to find random articles about mice blood vessels and how they differ from human blood vessels, B) a medical student having read these articles would assume that "blood vessel placed in a dish" meant "mouse blood vessel placed in a dish", nor C) a medical student would read "blood vessel placed in a dish" and understand that they actually meant JG cells.

You gave it a good effort, and it seems to have fallen short. Like most of the answers here. I get that your gig is "I'm a badass who waltzes in to save the day and kicks ******s in the face", but maybe you should sit this one out.

Wow who is pretending to be the badass here? I was helpful and gave a good explanation compared to anything else in this thread. Expecting the vessel to be from a mouse is not far-fetched when we talk lab medicine.

 

[username456789]

Expecting the vessel to be from a mouse is not far-fetched when we talk lab medicine.

It is, in fact, extremely far fetched for this exam when it is not stated as such. Even more far fetched to assume that anyone would know that said mouse blood vessel had b1 receptors.

 

[psychforme]

It is, in fact, extremely far fetched for this exam when it is not stated as such. Even more far fetched to assume that anyone would know that said mouse blood vessel had b1 receptors.

So you are saying reuptake stays intact in denervated tissue?

 

[knuckles]

you two are adorable

 

[username456789]

So you are saying reuptake stays intact in denervated tissue?

Since you've turned this into a 3rd grade playground, I'm ending this with this post. I don't know what the correct answer is because none seem to fit within experimental parameters, but I know that your explanation is faulty and that bothers you immensely, which is understandable given the way in which you delivered it. The utility of this discourse has been lost as you can't seem to even conceive that you may indeed be incorrect. Instead you defend your answer with silly red herrings.

Either way, I'm sure this is all headed for the trash anyway.

 

[psychforme]

Since you've turned this into a 3rd grade playground, I'm ending this with this post. I don't know what the correct answer is because none seem to fit within experimental parameters, but I know that your explanation is faulty and that bothers you immensely, which is understandable given the way in which you delivered it. The utility of this discourse has been lost as you can't seem to even conceive that you may indeed be incorrect. Instead you defend your answer with silly red herrings.

Either way, I'm sure this is all headed for the trash anyway.

No, my explanation is 100% correct and you have in no way disproven it. You are basing your argument on that "the nbme wouldn't do that because it is too difficult for me to understand".

 

[Ableton]

No, my explanation is 100% correct and you have in no way disproven it. You are basing your argument on that "the nbme wouldn't do that because it is too difficult for me to understand".

Actually, your far-fetched explanation is 0% correct and I do have proof - I had the question and got it right by selecting cocaine. 🙄

 

[FutrPharm]

Actually, your far-fetched explanation is 0% correct and I do have proof - I had the question and got it right by selecting cocaine. 🙄

Yeah the correct answer is cocaine. The NBME 6 has extended feedback... I picked cocaine as my answer, and that question wasn't in my feedback section (which only consists of wrong answers).

 

[Phloston]

(Even though this thread is two years old, I'm posting for the sake of future NBME6 test-takers who will inevitably encounter this thread through Google)

I put metoprolol because I would have thought that blocking beta-1 would leave more NE available per unit time to bind alpha-1. Not only that, but I didn't think this question was hard at all, and I don't believe that reasoning is wrong whatsoever.

But by all means, I too purchased the extended feedback, and metoprolol wasn't correct.

My guess would be metoprolol is wrong because Vmax on alpha-1 isn't technically increased by merely blocking beta-1. However, with cocaine, the Vmax is increased because NE re-uptake is inhibited. Cocaine also induces vasospasm (not that that particularly has anything to do with it). Metoprolol may have been correct if the peak maintained a constant magnitude but had a greater width.

As for tyramine, as far as I'm aware, that merely increases the release of more catecholamines, which would have caused vasoconstriction when it was first administered, but we can see the vasoconstriction only occurs after NE is added.

 

[you.old]

@Phloston Did you get Filgrastim/Sargramostim right? Which one did you choose?

 

[Phloston]

@Phloston Did you get Filgrastim/Sargramostim right? Which one did you choose?

Lol. You're asking me about an NBME that I did three years ago and have probably repressed. What was the question?

 

[you.old]

@Phloston This thread seems to be getting activated every 2-3 years. Lol.
Did NBME 6 offline today (Had to do offline coz it's already taken down) (score: 189/200)
This was the question:
A 31-year-old man with AIDS is reveiving HAART. Lab studies show significant myelosuppression and a decreased plasma HIV-mRNA burden. To counteract this toxicity (rather than modify his ART), he begins treatment with a hematopoietic GF. 30 min later, he develops dyspnea, severe muscle pain, vomiting, and sinus tachycardia, his blood pressure is 80/40 mmHg. Which of the following hematopoietic GFs most likely caused these new findings?
A) EPO
B) Filgrastim
C) PDGF
D) Sargramostim
E) Thrombopoietin
(BTW, what was your score on the extended feedback? Just a memory refresher, your predicted NBME6 score was 252 (12 days out) and you were jetlagged. Cheers)