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Discussion Starter · #1 ·
A patient in the operating room undergoes rapid sequence intubation to prevent aspiration of gastric contents. During this rapid induction, he is given a standard intravenous (IV) dose of muscle relaxant “X.” The patient is then given a standard IV dose of vecuronium to maintain muscle relaxation during surgery. At the end of the surgical procedure, more than an hour later, the anesthesiologist administers a standard IV dose of neostigmine. However, the patient does not respond and continues to display too much muscle paralysis to permit safe extubation. Drug X was most likely which of the following?


A. Dantrolene
B. Pancuronium
C. Succinylcholine
D. Midazolam
E. Tubocurarine

I heard USMLE testing more anesthesia qns so I got this one for you to practice....
 

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some info i got googling!!

Mechanism of action of succinyl choline:

phase 1 block

  • Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's nicotinic sodium channel; sodium moves into the cell, a disorganised depolarisation of the motor end plate occurs and calcium is released from the sarcoplasmic reticulum. This results in fasciculation.
  • In the normal muscle, following depolarisation, acetylcholine is rapidly hydrolysed by acetylcholinesterase and the muscle cell is able to 'reset' ready for the next signal.
  • Suxamethonium has a longer duration of effect than acetylcholine and is not hydrolysed by acetylcholinesterase. It does not allow the muscle cell to 'reset' and keeps the 'new' resting membrane potential below threshold. When acetylcholine binds to an already depolarised receptor it cannot cause further depolarisation.
  • Calcium is removed from the muscle cell cytosol independent of repolarisation (depolarization signalling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculation.

phase 2 block

  • Following infusion or repeated doses of suxamethonium, phase 2 block may occur.
  • The receptor blockade takes on characteristics of a non-depolarising neuromuscular block (ie. fade in response to nerve stimulation, however unlike non-depolarizing neuromuscular blocking agents it cannot be reversed
 

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Discussion Starter · #7 ·
Mechanism of action of succinyl choline:

phase 1 block

  • Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's nicotinic sodium channel; sodium moves into the cell, a disorganised depolarisation of the motor end plate occurs and calcium is released from the sarcoplasmic reticulum. This results in fasciculation.
  • In the normal muscle, following depolarisation, acetylcholine is rapidly hydrolysed by acetylcholinesterase and the muscle cell is able to 'reset' ready for the next signal.
  • Suxamethonium has a longer duration of effect than acetylcholine and is not hydrolysed by acetylcholinesterase. It does not allow the muscle cell to 'reset' and keeps the 'new' resting membrane potential below threshold. When acetylcholine binds to an already depolarised receptor it cannot cause further depolarisation.
  • Calcium is removed from the muscle cell cytosol independent of repolarisation (depolarization signalling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculation.

phase 2 block

  • Following infusion or repeated doses of suxamethonium, phase 2 block may occur.
  • The receptor blockade takes on characteristics of a non-depolarising neuromuscular block (ie. fade in response to nerve stimulation, however unlike non-depolarizing neuromuscular blocking agents it cannot be reversed
Man You rocked :scared:

Very nicely explained. No need for further info.. Thankz bro.
 

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A patient in the operating room undergoes rapid sequence intubation to prevent aspiration of gastric contents. During this rapid induction, he is given a standard intravenous (IV) dose of muscle relaxant "X." The patient is then given a standard IV dose of vecuronium to maintain muscle relaxation during surgery. At the end of the surgical procedure, more than an hour later, the anesthesiologist administers a standard IV dose of neostigmine. However, the patient does not respond and continues to display too much muscle paralysis to permit safe extubation. Drug X was most likely which of the following?

A. Dantrolene
B. Pancuronium
C. Succinylcholine
D. Midazolam
E. Tubocurarine

I heard USMLE testing more anesthesia qns so I got this one for you to practice....
Sorry, but I don´t get this qs.

I understand that drug X is Succi...but he only received one dose of succi, so we are not in phase II block. He received Vecuronium, which means that the muscular response (twitch) came back (the cholinesterases were functioning ok) - you always have to check the twitches first......So, why he still have muscle paralysis ... the only thing that I can think of is that the patient received Pancuronium instead of vecuronium (standard IV dose of neostigmine after one hour is not enough) :eek:
 
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