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@usmlestudystep nd md2012 : i think 2 reads of FA should be done before starting nbme..what are your views? please share..
nd guys..i've read goljan once but many ppl here on forum prefer pathoma..is it better ? nd pathoma videos are available online? i mean any link?
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@xako i think that utube vid link explains .
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Is there anyone struggling with Physio? Like me.
Jus wana knw hw r u guys dealing with it. I started listening 2 Dr.Kudrat .. makes a lot more sense now than my first read.
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Do u guys can answer all these ques people upload in this forum..i cant answer most of them..and some people r so good they answer all of them correctly..dont how can i get better in just one month..
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Guys FA says local anesthetics bind to sodium channel in ACTIVE state
Kaplan says it binds to INACTIVATED Na channels like Class IA antiarrhythmics,
I assume in FA it is a mistake... ????
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@xako22
There are two fundamental mechanisms of inhibition. Na+ currents are reduced by local anesthetics primarily because the drug-bound channels fail to open. Investigations with neutral and cationic compounds show that the channel-activation process is disrupted by local anesthetics. 27, 28 A sodium channel inhibited by a local anesthetic is functionally similar to an inactivated channel; both inactivation and anesthetic binding prevent the complete conformational changes of the activation process by partially immobilizing the channel. 29 Blockade of the ion-conducting pore, the second mechanism, plays a part in channel inhibition, but the contribution from this action seems minor.
Are inactivated channels essential for local anesthetic binding and action? No, because when inactivation is prevented by various chemical reagents or toxins, there is only a small change in the tonic and phasic actions of local anesthetics. 30 Phasic channel inhibition occurs during depolarizations that are as short as neuronal impulses (1-5 ms) because local anesthetics bind more rapidly and with higher affinity to activated channels (some open, some in intermediate activated conformations preceding the open state) than to resting channels. During longer depolarizations, additional binding to drug-free inactivated channels also can occur 17, 25 ; this mode of binding probably accounts for much of the cardiotherapeutic action of local anesthetic-like class I antiarrhythmics.