Skeletal Muscle Relaxants Flashcards
What is the MOA of neuromuscular blockers?
When are they used?
It has no known effects on…
Interfere with transmission at the NM end plate and lack CNS activity.
Used as adjuncts during anesthesia.
No known effects on consciousness or pain threshold.
Spasmolytic agents are often called…
What are they used for?
Centrally acting muscle relaxants.
To reduce spasticity in a variety of neurological conditions (LBP, fibromyalgia, muscle spasms)
What are the 2 basic mechanisms of NM blocking drugs?
What are the prototypes of each?
Non-depolarizing blockade: prevents access of ACh to its receptor and blocks depolarization.
-d-tubocurare
Depolarizing blockade: NM blockade that results from excess of a depolarizing agonist.
-succinylcholine
What is the ultra short-acting NM blocker?
What are the 3 long-acting NM blockers?
Succinylcholine
Doxacurium, Pancuronium, Pipecuronium
What are adverse-effects of NM blockers when taken in large doses?
The major reason for the adverse-effects of these drugs is due to…
Which drug is rarely used because of these adverse effects?
Profound hypotension and tachycardia with large doses.
Histamine release: bronchospasm, hypotension and salivary secretion.
Tubocurare.
Which drugs cause the least histamine release? (4)
Steroids: Pancuronium, Pipercuronium, Rocuronium, Vecuronium.
What is given to reverse the NMJ blockade?
What is given alongside to minimize the effects at mAChRs?
Cholinesterase inhibitors which antagonize non-depolarizing blockade by increasing the ACh at the NMJ (e.g. Neostigmine, Pyridostigmine, Edrophonium).
Anticholinergic drugs are often given with cholinesterase inhibitors to minimize the effects (Atropine, Glycopyrrolate).
What is the only clinically useful depolarizing blocking agent?
What reverses the NM blockade?
What is the MOA? (2)
Succinylcholine
Time
Phase 1 and Phase 2 desensitizing blocks.
Phase 1 block MOA =
What ensues as a result?
What augments it?
Succinylcholine’s effects are similar to ACh but produce a longer effect at the NMJ. Depolarized membranes remain depolarized and unresponsive to subsequent impulses.
Flaccid paralysis due to lack of repolarization.
Augmented by cholinesterase inhibitors.
Phase 2 block MOA =
How does the nAChR behave?
What is the Phase 2 block antagonized by?
Continued exposure to succinylcholine causes initial end plate depolarization to decrease and the membrane becomes repolarized.
It behaves as if in a prolonged closed state and becomes desensitized.
Antagonized by cholinesterase inhibitors.
What are the clinical uses of NM blockers? (4)
Surgical relaxation
Tracheal intubation
Control of ventilation
Treatment of convulsions
What dictates the use of NM blockers?
PKs of the drug.
The drugs of choice for rapid sequence intubation are those that…
What drugs? (3)
Act quickly!
Succinylcholine (Rocuronium, Vecuronium).
The drugs of choice used as adjuncts to general anesthesia for muscle relaxation are those that…
What drugs? (3)
Have longer duration.
Pancuronium (Atracurium, Cisatracurium).
Baclofen MOA
Centrally acting GABA-B agonist resulting in inhibition of excitatory NT release.
