Pharm - Lecture 9 - ganlionic blockers, Nero-muscular blockers Flashcards
What are the therapeutic uses of neuromuscular blocking agents (both competitive and non-competitive)?
1) Used as an adjuvant in surgical anesthesia to obtain relaxation of skeletal muscle (particularly the abdominal wall) to facilitate operative manipulations
2) used to facilitate intubation with a tracheal tube and to facilitate laryngoscopy/bronchoscopy
3) used to control severe muscle spasms
What is the mechanism for Competitive neuromuscular blocking agents? (non-depolorizing drugs)
Shared characteristics regarding absorption?
Shared characteristics regarding CNS penetration?
These drugs compete with Acetylcholine for unoccupied end-plate nicotinic receptors without activating the ion channel.
Poorly absorbed by GI
Can’t penetrate GI
What drugs are competitive neuromuscular blocking agents?
Rocuronium
Atracurium
Vecuronium
Pancuronium
What are the charactierstics of Rocuronium?
Duration and onset of action?
Elimination?
Cardiovascular effects?
Histamine release?
Duration of action: intermediate (30-60 minutes)
onset of action: rapid (1-2 minutes, can be used for tracheal intabation)
Elimination: liver metabolism
Cardiovascular effects: none
Histamine release: none
What are the charactierstics of Atracurium?
Duration of action? onset?
Elimination?
Cardiovascular effects?
Histamine release?
Duration of action: Intermediate (30-60)
Onset: 2-4 minutes
elimination: spontaniously degrades in plasma and by plasma esterase
Cardiovascular effects: minimal
Histamine release: slight
What are the charactierstics of Vecuronium?
Duration of action?
Elimination?
Cardiovascular effects?
Histamine release?
Duration of action: intermediate (60-90 minutes)
onset: 2-4 minutes
Elimination: liver metabolism
no cardiovascular or histamine response
What are the charactierstics of Pancuronium?
Duration of action?
Elimination?
Cardiovascular effects?
Histamine release?
Long duration of action (120-180 minutes)
Onset: 4-6 minutes
eliminated primarily by renal excretion
Slight increase in heart rate and blood pressure
slight histamine release
What is the mechanism of Depolorizing neuromuscular blockers?
Activate nicotinic receptors at the neuromuscular junction maintaining motor end plate depolorization and thus preventing transmision of another action potential
What drug is a depolarizing neuromuscular blocker?
Succinylcholine
What are the characteristics of succinylcholine? (split card up)
effects?
durration and onset of action?
mebaolization? (by pseydocholinsterase so genetic diferences means longer duration)
therapeutic use?
effects: muscle fasiculations followed by flaccid paralysis
Ultra short duration of action (5.8 minutes)
very rapid onset (1-1.5 minutes)
Metabolized by pseudocholinesterase
Used frequently to facilitate intubation with tracheal tube
What are the adverse effects and toxicty of Competitive neuromuscular blocking agents?
Prolonged apnea, cardiovascular collapse (rare, sometimes due to histamine release) and anaphylaxis
What are the adverse effects and toxicty of Depolarizing neuromuscular blocking agents?
1) prolonged apnea
2) malignant hyperthermia
3) post operative muscle pain
4) hyperkalemia
How can competitive antagonist toxicity/overdose be reversed?
acetylcholinesterase inhibitor (neostigmine or edrophonium)
can’t do this with depolarizing agents!
Why do neostigmine and edrophonium reverse the effect/decrease the duration of competitive neuromuscular blockade?
These two drugs are acetylcholinesterase inhibitors. By inhibiting acetylcholinesterase, you increase the concentration of acetylcholine and thus outcompete the competitive neuromuscular inhibitor
What drug must be used to conteract the effects of acetylcholinesterase inhibitors during surgery?
muscarinic receptor antagonist- usually glycopyrrolate (doesn’t penetrate CNS)
Need to do this to block muscarinic receptor actvity (bradycardia, GI/GU secretions/motility)
