TBR Bio Ch. 5 #34

[ajumobim]

Which drug could be given to counteract the effects of the antibody produced in myasthenia gravis?
A) an inhibitor of acetylcholinesterase
B) an immunostimulant
C) a paralytic agent, like curare
D) an inhibitor of acetylcholine synthase

I chose D initially. I get why the answer is A now because it says in the passage that the antibody may block the receptor or cause receptor breakdown, which would lead to less stimulation of the muscle cell and so we would need more ACh. But, in the beginning it says that myasthenia gravis is associated with weakness and fatigability due to repeated contraction. Wouldn't repeated contraction mean that there is an excess of acetylcholine in the synaptic cleft? Does anyone understand where my logic is wrong?

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[azor ahai]

Post the passage?

 

[Labrat07]

I'm guessing here but aren't acetylcholine synthase = acetycholine production. if you block that = no production = no action = no antibody. B and C you can ruled out since it's out of scope. I left with A and D. I ruled out D with that = left with A.

 

[NextStepTutor_3]

I'd also be interested in seeing the passage! Specifically, the last statement that you mentioned could be interpreted in two ways. We could assume that myasthenia gravis is associated with repeated contraction, causing weakness and fatigability. OR we could assume that an individual with myasthenia gravis would experience weakness and fatigue when he happens to contract his muscles repeatedly. Does this difference make sense? The first statement implies that the disease CAUSES extra contraction, which would lead to your interpretation that there's already too much acetylcholine in the synapse. However, I bet the wording of the passage points to the second interpretation. Why? Because outside knowledge shows that the first interpretation isn't correct - the antibodies produced in MG do attack/block the receptors on the postsynaptic cell. At no point do we have too MUCH acetylcholine, meaning that A would be our best bet to keep the ACh in the synapse long enough to contact the few functional receptors that remain.

Great question though! In these passages where we could either "inhibit the synthesis" or (to put it simply) "inhibit the inhibition," wording is everything. I think they probably just meant to say "people with MG get tired when they contract their muscles a lot," but it's certainly easy to read it differently.

 

[ajumobim]

@NextStepTutor_3 I tried taking a picture of it and uploading it, but the file was too large and I'm not computer-savvy at all lol. That difference makes a lot of sense though. Wow, that's really misleading! But, later on in the passage, it says "Antibodies to the acetycholine receptor have been found in 85% of patients with generalized myasthenia," which would allow you to get the correct answer. Unfortunately, I got tripped up by that first statement. Thanks for your help!

 

[Czarcasm]

@NextStepTutor_3 I tried taking a picture of it and uploading it, but the file was too large and I'm not computer-savvy at all lol. That difference makes a lot of sense though. Wow, that's really misleading! But, later on in the passage, it says "Antibodies to the acetycholine receptor have been found in 85% of patients with generalized myasthenia," which would allow you to get the correct answer. Unfortunately, I got tripped up by that first statement. Thanks for your help!

The passage suggests, that while the exact mechanism is not entirely known, the antibody somehow has a negative effect on the receptor itself (ie. reducing its function). They suggest 3 ways this can occur in the passage: the "antibody may block the receptor, it may cause faster receptor breakdown, or it may promote complement-mediated damage." Knowing this information, they are asking you to find an alternative solution to avoid this from happening. Unfortunately, antibody production is permanent once its been induced. Therefore, a reasonable treatment would be to somehow out-compete antibody binding all together, in order to prevent the decreased functionality or destruction of this Ach receptor. By moderately inhibiting acetylcholinesterase, we can increase Ach. In doing so, the two molecules (both the Ab and Ach) exhibit some form of competition. If we can increase the amount of Ach, we can essentially "dominate" the amount of antibody present. In otherwords, more Ach would bind, more often, as opposed to antibody binding (a negative effect). This is also ideal because, most molecular binding (such as Ach binding to AchR) is a reversible process of binding-unbinding. This essentially promotes the functionality of the receptor, while avoiding overstimulation and preventing its destruction or decreased functunality. This makes A the most logical answer.