black widow spider venom

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Miracoli

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A biopsy of the neuromuscular junction from a patient who was bitten by a black widow spider provides the following information: (1) the postsynaptic nerve terminals respond normally to ACh injected into the synaptic cleft, and (2) neither presynaptic depolarization nor high external Ca can elicit EPSP’s (or EJPs) or muscle contraction. Based on this information, the molecular action of the black widow toxin is MOST likely to:
A. block the postsynaptic ACh receptor.
B. prevent miniature epp’s from combining into a normal epp’s.
C. block K permeation through the ACh receptor so that this channel becomes highly Na selective.
D. block ACh-esterase within the synaptic cleft.
E. does not allow the vesicles in the presynaptic terminals to fuse normally in order to release Ach.
 
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Fatalis said:
B
the venom causes a huge release of ach then the stores are exhausted so you cant release any neurotrasmitter; hence you wont be able to form any mini EPPs
Click to expand...

But the stem says the post synaptic membrane responds appropriately when ACh is injected into the cleft. Isn't that leading you to answer E?
 
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I think the toxin causes an Ach release, like @Fatalis said.

-Exogenous Ach still works on the post-synaptic receptor because it is still functional.

-The issue is that when you are trying to induce pre-synaptic release (via Calcium or depolarization), you get no result because the toxin has caused a massive Ach release that depleted endogenous stores.
 
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I think the question wants you to forego what you were taught about the black widow venom in class and focus on the criteria they are giving you. Anything that deals with post synaptic can be ruled out and then this leaves you with B and E. MiniEPPs are innate phenomena that happens regardless and some combine to form an EPP, this can't be helped but only stopped if there is no transmitter available, this is a plausible answer but criteria (2) states that no matter how much you push it it can't elicit a release, (I would choose this if there are no better answers or no more information given about the patient pre-biopsy) BUT, E fits both criteria if there are no/destroyed docking mechanism and therefore the most plausible and best answer.

The focus is the last sentence stating that you Base it on this information.
 
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Dr najeeb discussed this in one of his lectures and the answer is E as far as i remember.
 
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Questions like this are a little ridiculous.

For Step 2CK, Conrad Fischer, in MTB2, makes a point that the black widow spider causes hypocalcaemia and tetany, whereas the brown recluse spider causes abdominal pain.

I didn't think vesicles themselves could be depleted.

Maybe the black widow upregulates calcium consumption presynaptically (which is why the ACh release and tetany occur), leading to calcium depletion (hypocalcaemia and failure of vesicular fusion) that cannot be compensated for acutely merely with calcium.

Calcium gluconate is the treatment, so we're clearly trying to restore presynaptic calcium.

Vesicles wouldn't bind to the membrane without calcium (same process as in phototransduction). So E would be right. But once again, ridiculous question.
 
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001100010010011 said:
I think the toxin causes an Ach release, like @Fatalis said.

-Exogenous Ach still works on the post-synaptic receptor because it is still functional.

-The issue is that when you are trying to induce pre-synaptic release (via Calcium or depolarization), you get no result because the toxin has caused a massive Ach release that depleted endogenous stores.
Click to expand...

So are you saying answer B? Or answer E? MEPPs/EPPs occur only on the motor end plate in response to ACh. They have nothing to do, per se, with what is going on in the presynaptic membrane.
 
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ulikedaggers said:
So are you saying answer B? Or answer E? MEPPs/EPPs occur only on the motor end plate in response to ACh. They have nothing to do, per se, with what is going on in the presynaptic membrane.
Click to expand...

I am going to go with the consensus: E. I originally thought B because we're all taught that the venom causes Ach release.

Good talk, everyone.
 
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Ah I was wondering why people were saying B. I haven't learned anything about BWT yet so there was no conflicting knowledge in my head.
 
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Phloston said:
Questions like this are a little ridiculous.

For Step 2CK, Conrad Fischer, in MTB2, makes a point that the black widow spider causes hypocalcaemia and tetany, whereas the brown recluse spider causes abdominal pain.

I didn't think vesicles themselves could be depleted.

Maybe the black widow upregulates calcium consumption presynaptically (which is why the ACh release and tetany occur), leading to calcium depletion (hypocalcaemia and failure of vesicular fusion) that cannot be compensated for acutely merely with calcium.

Calcium gluconate is the treatment, so we're clearly trying to restore presynaptic calcium.

Vesicles wouldn't bind to the membrane without calcium (same process as in phototransduction). So E would be right. But once again, ridiculous question.
Click to expand...

why is this a ridiculous question?
 
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sanj238 said:
why is this a ridiculous question?
Click to expand...


I don't think it is. I think people when they first see this question they want to quickly revert to their previous knowledge because thats what they expect to be tested on. However, this question is a question that tests your logical reasoning skills not your previous knowledge about the black widow venom. That's why they put that clause in the last sentence, to emphasize what it wants you to focus on. It wants you to focus on your knowledge of nerve terminals NOT toxins and then choose the best answers. This is that type of question that 250+ scorers in the Official Step 1 thread talk about that can't be taught. In my opinion.
 
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GangaMaster said:
I don't think it is. I think people when they first see this question they want to quickly revert to their previous knowledge because thats what they expect to be tested on. However, this question is a question that tests your logical reasoning skills not your previous knowledge about the black widow venom. That's why they put that clause in the last sentence, to emphasize what it wants you to focus on. It wants you to focus on your knowledge of nerve terminals NOT toxins and then choose the best answers. This is that type of question that 250+ scorers in the Official Step 1 thread talk about that can't be taught. In my opinion.
Click to expand...

Reminds me of the type of questions on the old NBME forms (1-4) that were retired for a reason.
 
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Despite any testing of the logical reasoning of neurophysiology, the combination of the stem and correct answer give you the opposite impression of what the toxin actually does, unless you're an infectious disease spec

The clinical relevance is that black widow toxin causes hypocalcaemia and tetany. These patients experience painful spasms and need to be treated with calcium gluconate.

Good questions make a full circle around a clinical point. This question should reword the point about calcium to say something like "despite treatment with increased extracellular calcium, there was no response..."

Either way, I'm not here to fight questions. But I'm just pointing out that this one is characteristic of old NBME ones, as well as some still floating around on the real Step1 unfortunately.
 
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Phloston said:
Despite any testing of the logical reasoning of neurophysiology, the combination of the stem and correct answer give you the opposite impression of what the toxin actually does, unless you're an infectious disease spec

The clinical relevance is that black widow toxin causes hypocalcaemia and tetany. These patients experience painful spasms and need to be treated with calcium gluconate.

Good questions make a full circle around a clinical point. This question should reword the point about calcium to say something like "despite treatment with increased extracellular calcium, there was no response..."

Either way, I'm not here to fight questions. But I'm just pointing out that this one is characteristic of old NBME ones, as well as some still floating around on the real Step1 unfortunately.
Click to expand...

I still dont see it. whether it makes a full circle or not, I would still be able to clearly see what they are asking which is all that matters right...
 
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EE is correct.
The wording of the stem of the question is good , but difficult to choose between B and E.
-The primary toxin (alpha-latrotoxin) acts as a transmembrane pore and allows calcium influx into the cells.
-Alpha-latrotoxin, a large protein toxin, found in black widow spiders causes pokes in the PM and destabilizes cell membranes by opening (acts as) Calcium channels resulting in a massive influx of calcium at the axon terminal causing massive exocytosis of acetylcholine and norepinephrine from nerve terminals, depleting its stores of acetylcholine from presynaptic nerve terminals.. Clinically,Black widow spider causes painful muscle spasms with severe abdominal pain,, hypocalcaemia and tetany, followed by weakness. The treatment is Calcium gluconate and Black widow spider (Latrodectus mactans) antivenom called lexicomp


Thank you for participation
For more explanation about membrane potential check here
http://www.usmleforum.com/files/forum/2014/1/767949.php
 
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Miracoli said:
http://www.usmleforum.com/files/forum/2014/1/767949.php
Click to expand...

The only thing worse than the terrible advice, mis-information, bad english, rampant intellectual thievery, and clingyness of those users on that website is the incredibly nauseating color scheme.

This question is based on wrong information. Black widow spider toxin causes excessive release of neurotransmitters like Ach (http://www.ncbi.nlm.nih.gov/pubmed/15066411), clearly vesicles are fusing.

I've got a similar style of question:
In a recent independent evaluation 2+2 was found to equal 5.
What does 2+2=?

A)1
B)2
C)3
D)4
E)Radiohead
F)5

A cool question would be like someone in a lab puts black widow spider venom on a specimen and runs a train of four on it.
 
Last edited:
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Modeselektor said:
The only thing worse than the terrible advice, mis-information, bad english, rampant intellectual thievery, and clingyness of those users on that website is the incredibly nauseating color scheme.

This question is based on wrong information. Black widow spider toxin causes excessive release of neurotransmitters like Ach (http://www.ncbi.nlm.nih.gov/pubmed/15066411), clearly vesicles are fusing.
Click to expand...

I laughed out loud--great description of that forum.

I also went on a pubmed search, found a similar article, shook my head because of the existential crisis that this question caused me and walked away from my computer.
 
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Modeselektor said:
The only thing worse than the terrible advice, mis-information, bad english, rampant intellectual thievery, and clingyness of those users on that website is the incredibly nauseating color scheme..
Click to expand...

You are doing misinformation here, i did not find the question from usmleforum.com 🙂 I posted the question because it was difficult for me too. It is not my problem if you do not like a website, I am just a user (of websites for usmle).
 
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Miracoli said:
EE is correct.
The wording of the stem of the question is good , but difficult to choose between B and E.

take home message about black widow spider
-The primary toxin (alpha-latrotoxin) acts as a transmembrane pore and allows calcium influx into the cells.
-Alpha-latrotoxin, a large protein toxin, found in black widow spiders causes pokes in the PM and destabilizes cell membranes by opening (acts as) Calcium channels resulting in a massive influx of calcium at the axon terminal causing massive exocytosis of acetylcholine and norepinephrine from nerve terminals, depleting its stores of acetylcholine from presynaptic nerve terminals.. Clinically,Black widow spider causes painful muscle spasms with severe abdominal pain,, hypocalcaemia and tetany, followed by weakness. The treatment is Calcium gluconate and Black widow spider (Latrodectus mactans) antivenom called lexicomp


Thank you for participation
For more explanation about membrane potential check here
http://www.usmleforum.com/files/forum/2014/1/767949.php
Click to expand...
 
Upvote 0 Downvote
 
Last edited:
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