Why neostigmine isn't effective in phase I of succinlycholine? - USMLE Forums
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Old 07-08-2013
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Default Why neostigmine isn't effective in phase I of succinlycholine?

Hi,
Why choline esterase inhibitors (e.g., neostigmine) are not effective in phase I of succinlycholine action? FA says it may increase the depolarization.
Why they only work in phase 2, not phase 1?
Thanks
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Old 07-08-2013
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Quote:
Originally Posted by melboghdady View Post
Hi,
Why choline esterase inhibitors (e.g., neostigmine) are not effective in phase I of succinlycholine action? FA says it may increase the depolarization.
Why they only work in phase 2, not phase 1?
Thanks
The details are too intense!!! But if you're interested, page 19 on this link: http://faculty.washington.edu/ramaiahr/3BChapter_13.pdf

I tried to read it, but gave me a headache!!!!

For USMLE purposes, I think it's safe to just know (in terms of REVERSAL OF BLOCKADE.........

1) Neostigmine WORSEN'S the depolarization in phase I. This is logical, because Phase I, is basically when you already have depolarization taking place (action of succinylcholine)...causing fasciculations, and when prolonged... it will ultimately cause a flaccid paralysis (via desensitization). So it's logical to see why an 'acetylcholinersterate inhibitor' would add to this prolonged 'depolarizing' effect via action of Ach on the Nm receptor.

in other words: Neostigmine worsens phase I. Or as FA puts it: the BLOCKADE is potentiated by cholinesterase inhibitors. Remember, the goal is to REVERSE the blockade ---> Neostimgine doesn't do this!! it Worsens it!

Again, Phase I is known as "the phase of prolonged depolarization". So adding an AchE Inhibitor, would add to this effect, and would make that process worse.



2) Now this is where it gets a little fuzzy. Kaplan seems to pretty much say that IT IS NOT POSSIBLE to reverse phase II with 'AchE Inhibitor'. But according to FA: 'antidote of phase II consists of neostigmine'

You can sort of see the point kaplan is trying to make: if the Receptors are desensitized, then how can you stimulate them with Ach!!!?????

But you can also see the point with FA...despite the desnsitization, increase amounts of ACh, and falling levels of succinylcholine would eventually reverse the blockade (because not all cells would be phase II depolarized i suppose)




I'm sure there is a better answer to this question out there...but those probably are found in anesthesiology books, and at this point...i'm sticking to FA!!! If anybody does know the specifics, and doesn't mind sharing, please enlighten us!!!!!






in a nutshell: I think its perfectly safe to logically conclude: neostigmine has NO EFFECT on phase 1 depolarization of the Blockade. and in fact, potentiates it (makes it worse).

And that, Phase II blockade, can be reversed with Neostigmine (as per FA). But, Kaplan does raise a good point - how can Neostigmine have an effect on the phase II desensitized receptors???

I guess in this case, knowing the concepts is more important than knowing the details. If you know why FA might be correct, and why KAPLAN might be correct, you're in good shape in terms of getting concepts down!

Last edited by ReggieMiller; 07-08-2013 at 07:28 AM.
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Thanks doctor for the great help
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Old 07-08-2013
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yw! in fact, i like answering questions here, because it reinforces concepts, and its a good way to review!
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