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Old 09-20-2012
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Post local anesthetic mechanism

q) can someone please explain the original action of local anesthetics
it acts on inactivated sodium channels or activated sodium channels...?

kaplan video tells acts on inactivated sodium and F.A-2012 tells they act on activated sodium channels ...is kaplan wrong or F.A wrong..?

checked in errata too they haven't changed anything.......and also they removed the causalgia of malignant hyperthermia for inhaled anaesthetics in errata......can also explain about this..?

thank you
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Old 09-20-2012
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Don't remember exactly but if you remember voltage gated sodium channels have M gate and h gate and sometimes one is closed while other is open as in resting stage M gate is closed but h gate is open.
May be both books are right but its just the matter of which gate is open.
Ya i know i am not clarifying stuff as i am confused too but may be u can try thinking that way and ya when you get the reason explain me too
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Originally Posted by koolkiller88 View Post
Don't remember exactly but if you remember voltage gated sodium channels have M gate and h gate and sometimes one is closed while other is open as in resting stage M gate is closed but h gate is open.
May be both books are right but its just the matter of which gate is open.
Ya i know i am not clarifying stuff as i am confused too but may be u can try thinking that way and ya when you get the reason explain me too
thanks for replying.....ya i saw the video again it says inactivated channel

1)resting phase-----------M gate close, h gate open( no conductance)
2)activated sodium channels------M gate open ,h gate open (depolarization---phase 1)

3)inactivated sodium channels-------M gate open, h gate close (repolarization)

it's already discussed in this forum...but i'm unable to conclude from it coz in the lecture he clearly mentioned it around 6-7 times acting on inactivated sodium channels......have a look
Mechanism of Local Anesthetics
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Oh thats quite a big explanation and i lost it in mid way.

Actually our main purpose here is to prevent depolarization. So, no further action potential is transmitted.
So local anesthesia should work on inactivated Na+ channels to prevent further action potential.
If local anesthesia work on activated Na+ channel then that would keep them depolarized (don't think it would help in anesthetic effect anyhow)

Remember morphine and other opoids also bind to opoid receptors and keep them hyperpolarized and prevent pain transmission.

May be that can be the reasoning but not sure.
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Quote:
Originally Posted by koolkiller88 View Post
Oh thats quite a big explanation and i lost it in mid way.

Actually our main purpose here is to prevent depolarization. So, no further action potential is transmitted.
So local anesthesia should work on inactivated Na+ channels to prevent further action potential.
If local anesthesia work on activated Na+ channel then that would keep them depolarized (don't think it would help in anesthetic effect anyhow)

Remember morphine and other opoids also bind to opoid receptors and keep them hyperpolarized and prevent pain transmission.

May be that can be the reasoning but not sure.
thanks again.....ya may be ur right.........they prevent depolarization......but they do by blocking inactivated channels(remember h channels allow some depolarization but not equal to threshold as they are slow channels---that's the reason used in post MI)......
f.a says they block activated channels preferentially( kaplan video says ----block inactivated channels preferentially)......also in video he states..."a fish toxin(bungarotoxin) acts by blocking activated extracellular sodium channels which is exactly opposite to local anesthetics".......

wikipedia also tells.... acts on inactivated sodium channels like video
only F.A tells it differently........so tell me which one to follow:sorry:
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Originally Posted by venky2600 View Post
thanks again.....ya may be ur right.........they prevent depolarization......but they do by blocking inactivated channels(remember h channels allow some depolarization but not equal to threshold as they are slow channels---that's the reason used in post MI)......
f.a says they block activated channels preferentially( kaplan video says ----block inactivated channels preferentially)......also in video he states..."a fish toxin(bungarotoxin) acts by blocking activated extracellular sodium channels which is exactly opposite to local anesthetics".......

wikipedia also tells.... acts on inactivated sodium channels like video
only F.A tells it differently........so tell me which one to follow:sorry:
Local Anesthetics

Read this thread dude. It might help. I think Kaplan and wiki is more accurate regarding this matter.
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Originally Posted by koolkiller88 View Post
Local Anesthetics

Read this thread dude. It might help. I think Kaplan and wiki is more accurate regarding this matter.
thanks again...........so after such detailed long post i decided not to trust everything with F.A
and wat abt dantrolene thing in F.A?......did you correct it from errata( they removed abt dantrolene use in inhalational agents.....)
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Jeez, have the same confusion. So what's the consensus guys? We go with inactivated channels?
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Originally Posted by dockhi View Post
Jeez, have the same confusion. So what's the consensus guys? We go with inactivated channels?
i would like to go with inactivated channels....as it is mentioned in miller anesthesia text too( as f.a is a review book)......but i keep on wondering this point haven't changed since 2010 edition F.A....it implies controversy exist
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Quote:
Originally Posted by venky2600 View Post
thanks again...........so after such detailed long post i decided not to trust everything with F.A
and wat abt dantrolene thing in F.A?......did you correct it from errata( they removed abt dantrolene use in inhalational agents.....)
Thanks for telling. I didn't paid attention to this blunder.
According to errata malignant hyperthermia rare in inhaled anesthesia (should be removed)
but i cross checked with kaplan and they also says dantrolene is used for malignant hyperthermia caused by both inhalation anesthesia and succinylcholine.
So i think errata of pg 476 is not exactly an errata

According to kaplan videos also malignant hyperthermia is potential complication of halothane use.
So
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Agreed with koolkiller,
That page is confusing in FA. (The only page replete with confusions!) Will choose Kaplan then. Done confusing myself more about this
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ya....errata made some changes like unhappy triad well....but i think some changes need errata again
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Quote:
Originally Posted by venky2600 View Post
ya....errata made some changes like unhappy triad well....but i think some changes need errata again
Hahaha... FA should publish errata's errata now.. Seems errata ver. 12.0.01


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Default Unhappy triad

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Originally Posted by venky2600 View Post
ya....errata made some changes like unhappy triad well....but i think some changes need errata again
Hey thanks for mentioning again
about unhappy triad
FA errata is right about it.
As it states: medial meniscus and MCL attached together so tear together.

Wiki also states that
Unhappy triad includes:
MCL, ACL, medial meniscus (but due to lateral force lateral meniscus is also get teared- know as O'Donoghue triad)

I just Did a question in UW which states that
Due to lateral knee injury (doesn't specify about unhappy triad)-
ACL, MCL and meniscus get affected (So I think due to injury issue saying "meniscus injury" would be most appropriate.
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Quote:
Originally Posted by koolkiller88 View Post
Hey thanks for mentioning again
about unhappy triad
FA errata is right about it.
As it states: medial meniscus and MCL attached together so tear together.

Wiki also states that
Unhappy triad includes:
MCL, ACL, medial meniscus (but due to lateral force lateral meniscus is also get teared- know as O'Donoghue triad)

I just Did a question in UW which states that
Due to lateral knee injury (doesn't specify about unhappy triad)-
ACL, MCL and meniscus get affected (So I think due to injury issue saying "meniscus injury" would be most appropriate.
ya i also checked when i first read F.A, it's little controversy and came to know from many sites that lat.meniscus more common than medial meniscus(though both are common indeed)
but now we have to stick to f.a...as it clearly errated not lateral...
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