Unit 5 - NMB Reversals & Anticholinergics Flashcards
what metabolizes succs
pseudocholinesterase
acetylcholinesterase inhibitors that antagonize pseudocholinesterase
neostigmine & pyridostigmine (not edrophonium)
where is AChE concentrated
around nicotinic receptors at NMJ
acetylcholinesterase inhibitors that inhibit AChE
Edrophonium, neostigmine, and pyridostigmine
how do acetylcholinesterase inhibitors antagonize block with NDNMB
inc. concentration of ACh at NMJ
more ACh available to antagonize the block
2 ways AChE inhibitors increase ACh at nicotinic receptor
1) enzyme inhibition, 2) presynaptic effects
Primary mechanism of edrophonium
most likely presynaptic
MOA of edrophonium
- forms electrostatic bond at anionic site and a noncovalent H+ bond at the esteratic site (short duration of action, H+ bonds are weak)
- competitive
2 possible mechanisms of presynaptic action:
- Similar to succs, AChE inhibitors stimulate presynaptic receptor = additional ACh release
- Inhibition of AChE near presynaptic receptor increases ACh concentration in that region
is a dose adjustment of AChE inhibitors needed for renal failure
nope - duration of NMBs also prolonged
effect of mixing AChE inhibitors
additive effect
neostigmine antagonism is faster in children or adults?
infants & children
which AChE inhibitor(s) pass the BBB
only Physostigmine (tertiary amine)
Edrophonium, neostigmine, & pyridostigmine are quaternary amines (do not
risks of extubating with TOF ratio < 0.9
↑ risk airway obstruction, hypoxemic events, postop pulm. complications
effect of giving AChE inhibitor at full recovery
paradoxical muscle weakness