Kruse DSA: agents that act on the NMJ Flashcards
What are the nondepolarizing neuromuscular blocking drugs?
- atracurium
- cisatracurium
- doxacurium
- metocurine
- mivacurium
- tubocurarine
- Pancuronium
- pipercuronium
- rocuronium
- vecuronium
What is the ONE depolarizing neurmuscular blocking drug?
-succinylcholine
Muscle relaxants?
- Dantrolene
- Botulinum toxin
Acetylcholinesterase inhibitors
- abenomium
- donepezil
- echothiophate
- edrophonium
- galantamine
- neostigmine
- physostigmine
- Pyridostigmine
- rivastigmine
- tacrine
Antimuscarinic compunds
- atropine
- glycopyrrolate
Cholinesterase reactivators
-pralidoxime
What do nondepolarizing NM blocking agents do?
- act as antagonists of the nAChR
- prototype: d-tubocurarine
What do depolarizing NM blocking agents do?
- blockad by excess of a depolarizing agonist (ACh)
- prototype: succinylcholine
What are all NM blocking drugs structurally similar to?
-acetylchoine… makes sense
How must NM blocking drugs be administered?
-parenterally because they are highly polar and inactive orally
PK of nondepolarizing NM blocking agents?
- fast distribution, slow elimination
- poor solubility
- if excreted by kidney, longer half life than when excreted by liver
- all steroidal muscle relaxants are metabolized to active metabolites
MOA for ND (non depolarizing) NM blocking agents?
- competitive antagonists at the nAChR
- least potent have fastes onset and shortest duration of action
- larger muscles recover better and are most resistant
How doe we reverse the NM blockade?
- add ACh! a natural agonist of the nAChR
- or succinylcholine
What cholinesterase inhibitors could we had to reverse effects of NM blockade?
-pyridostigmine or neostigmine
What is coadministered with cholineesterase inhibitors to minimize adverse cholinergic effects caused by increase in ACh concentration at mAChRs?
-Anticholinergic agents like glycopyrrolate or atropine
Adverse effects of Nondepolarizing agents?
- histamine release (bronchospasms and hypotension)
- d tubocurarine causes a lot of this so we don’t use it anymore
What do anesthetics do with NM blockade?
-potentiate it
How do abx react with NM blockings
-aminoglycosides enhance NM blockade
-
In what disease is NM blockade by nondepolarizing muscle relaxants enhanced?
-myasthenia gravis
Atracurium
- intermediate-acting NM blocker
- inactivated by spontaneous breakdown (hoffmann elimination)
- Laudanosine will cause seizure bc it crosses BBB
- usually short term use in OR so nbd
- *less histamine release than other nondepolarizing agents
Cisatracurium
- intermediate acting stereoisomer of atracurium with fewer side effects
- can be used even with significant renal and hepatic impairment
- virtually devoid of CV effects
Doxacurium
- long acting ND muscle relaxant eliminated by the kidney
- not often used because of the long-l;asting effects as well as high degree of elimination by the kidney (not used in pts with renal failure)
- no CV effects
Mivacurium
- Shortest duration of action, slower onset of action than succinylcholine
- if you use toomuch to speed onset, get profound histamine release and subsequent CV effects
- metabolism by plasma cholinesterase (pt’s with renal failure have less of this)
Steroid derivatives
-the intermediate active steroid muscle relaxants (vecuronium, rocuronium) tend to be more dependent on biliary excretion or hepatic metabolism for their elminiation and are more likeyl to be used clinically than long acting steroid relaxants (pancuronium pipecuronium