NMB reversal agents Flashcards
what type of bond is formed when edrophonium binds to the anionic site in acetylcholinesterase
electrostatic
how does edrophonium, neostigmine, and pyridostigmine work
reversibly inhibits AchE which inadvertently increases Ach at the NMJ.
which drugs inhibit pseudocholinesterase
neostigmine and pyridostigmine (not edrophonium, which inhibits AchE)
2 ways that AchE inhibitor increases concentration of Ach at nicotinic receptor
- enzyme inhibition
- presynaptic effects
AchE inhibiting drugs bind to and inhibit AchE by interacting with these sites in 1 of 3 ways
- electrostatic attachment
- formation of carbamyl esters
- phosphorylation
how Ach is inhibited: electrostatic attachment
type of inhibition:
examples:
type of inhibition: competitive
examples: edrophonium
how Ach is inhibited: formation of carbamyl esters
type of inhibition:
examples:
type of inhibition: competitive
examples: neostigmine, pyridostigmine, physostigmine
how Ach is inhibited: phosphorylation
type of inhibition:
examples:
type of inhibition: non competitive
examples: organophosphates, echothiopate
how Ach is inhibited: phosphorylation
type of inhibition:
examples:
type of inhibition: non competitive
examples: organophosphates, echothiopate
primary MOA of edrophonium is most likely
presynaptic (more Ach avail stimulates release of more Ach)
edrophonium
dose
onset
DOA
metabolism and elimination
best pairing
dose: .5-1mg/kg
onset: 1-2m
DOA: 30-60m
metabolism and elimination: renal 75%, liver 25%
best pairing: atropine
neostigmine
dose
onset
DOA
metabolism and elimination
best pairing
dose: .02-.07mg/kg
onset: 5-15m
DOA: 45-90m
metabolism and elimination: renal 50% liver 50%
best pairing: glyco
pyridostigmine
dose
onset
DOA
metabolism and elimination
best pairing
dose: .1-.3
onset: 10-20m
DOA: 60-120m
metabolism and elimination: renal 75% liver 25%
best pairing: glyco
renal failure and AchE
prolongs DOA of AchE and NMB but no need to re dose anything
quarternary amine AchE’s
edrophonium, neostigmine, pyridostigmine
which AchE can you use for postop shivering
physostigmine 40mcg/kg
by increasing Ach availability, AchE’s produce these PSNS SE’s
DUMBBELLS
Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Emesis
Lacrimation (increased tear production)
Laxation (elimination of fecal waste)
Salivation
compared to atropine, glyco is more likely to produce
xerostomia (dry mouth)
review scopolamine, atropine, and glyco in terms of how much each (in comparison to each other)
increases HR
smooth muscle relaxation
sedation
antisialagogue
mydriasis and cycloplegia
prevent motion induced nausea
decreases gastric H+ secretion
why does glyco not possess CNS activity
it is a quarternary amine
best to least antagonized drug with sugammadex
roc>vec>panc
how is sugammadex excreted
unchanged via kidneys
finish this chart
(dose per twitch response)
use patients ______ body weight to dose sugammadex
actual
what if the patient needs to be re dosed after 16mg/kg sugammadex within 24h?
use non amino steroid NMB (atracurium, cis, mivacurium) or succ
what if the patient needs to be re dosed after <4mg/kg sugammadex has been given?
sugammadex in last 5m-4h–>1.2mg/kg roc
>4 hours ago: .6mg/kg roc or .1mg/kg vec
how long does sugammadex reduce effectiveness of contraceptives
7 days
4 drugs that decrease shivering in the PACU
physostigmine
meperidine
clonidine
dexmedetomidine
does glyco cause sedation or mydriasis or prevent nausea
no
