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29 Cards in this Set
- Front
- Back
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What is the most used NMJ blocker? Main advantage? Disadvantage?
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Succinylcholine or Suxamethonium
Advantage: fast onset and short duration Disadvantage: muscle pain |
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What is the structure of the Succinylcholine compound?
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Two acetylcholine molecules linked by their acetyl groups.
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Succinylcholine imitates the action of _____ at the _____ acting on muscle type _____ receptors.
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ACh
Neuromuscular Jnxn Nicotinic receptors |
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Is Sux depolarizing or non-depolarizing?
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depolarizing
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If Sux imitates ACh, is it also degraded by acetylcholinesterase?
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No, it is degraded by butyrylcholinesterase, a plasma cholinesterase.
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What is the first thing that happens after Sux binds to the nicotinic ACh receptor?
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Binding results in the opening of the receptor's nicotinic sodium channel. Sodium then moves into the cell, causing a disorganized depolarization of the motor end plate, and calcium is then released from the sarcoplasmic reticulum. This results in a muscle twitch.
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If Sux causes a muscle twitch, how in the world does it result in relaxation?
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Well, in the normal muscle, ACh is rapidy hydrolyzed and the muscle cell can 'reset' and be ready for next signal. Sux has a longer duration of effect than ACh, so muscle cell cannot reset and thus keeps the 'new' resting membrane potential below threshold. When ACh binds to an already depolarized receptor it cannot cause further depolarization. Calcium is removed from the muscle cell cytosol regardless of depolarization. As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. Thus, muscle flaccidity!!!
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Butyrylcholinesterase is a plasma cholinesterase and is not present at motor cell end-plate. So, what happens to the Sux that binds at the end-plate?
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The effect is terminated by diffusion away from motor end-plate.
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What does it mean to say "depolarizing" muscle relaxant?
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These agents act by depolarizing the plasma membrane of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.
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How do non-depolarizing muscle relaxants work?
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They block the agonist, ACh, from binding nicotinic receptors, thereby preventing depolarization.
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Which non-depolarizing blocker is entirely metabolized in the liver?
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Rocuronium
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Which non-depolarizing blocker is excreted entirely by the kidney?
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Gallamine
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Is d-Tubocurarine excreted by the kidney?
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50-60% excreted by the kidney, and the rest probably in bile.
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What is the danger with drugs that are either metabolized in the liver or excreted by the kidney?
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Duration of action can become dangerously extended in people with renal/hepatic failure.
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Clearance of which blocker's metabolites is not affected by liver/kidney functions?
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Mivacurium
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What is the prototype of a non-depolarizing NMJ blocker?
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Tubocurarine
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In small clinical doses, the non-depolarizing NMJ blockers do what?
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They act predominantly at the nicotinic receptor site to block ACh.
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And at higher doses?
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They can block prejunctional Na channels thereby decreasing ACh release.
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Is transient relief of non-depolarizing blockers possible?
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Yes, by increasing ACh levels at the synaptic cleft (ie use cholinesterase inhibitors).
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T/F Late in phase II block by depolarizing NMJ blocker, the characteristics of the blockade are almost identical to those of non-depolarizing blockers.
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True. At this point, tetanus is not sustained, and the action can be reversed by AChE inhibitors.
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What effect will administration of succinylcholine have on tubocurarine action?
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Antagonistic (duh)
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What will be the effect of neostigmine on the action of tubocurarine?
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Also antagonistic.
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What is the initial excitatory effect on skeletal muscle after administering tubocurarine?
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None yo.
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Response to a tetanic stimulus after administration of tubocurarine?
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Unsustained (meaning that's it's not sustained)
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What is the rate of recovery from tubocurarine?
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30-60 mins (ie 30 mins to one hour)
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What happens if you administer tubocurarine during Phase I of succinylcholine blockade? And during Phase 2?
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Phase I: antagonistic
Phase II: augmented (be be synergistic) |
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What happens if you administer neostigmine during Phase I of succinylcholine blockade? And phase II?
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Phase I: augmented
II: antagonistic |
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What is the initial excitatory effect on skeletal muscle of succinylcholine blockade?
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Fasciculations
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What is the response to a tetanic stimulus during phase I of succinylcholine blockade? Phase II?
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Phase I: sustained
Phase II: unsustained |
