NMJ pharm Flashcards by laura gibbons

nondepolarizing NM blocking agents

isoquinoline derivatives

steroid derivates

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Nondepolarizing isoquinoline derivatives

Cisatracurium
tubocurarine 
atracurium
doxacurium
metocurine
mivacurium

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nondepolarizing steroids derivatives

pancuronium
pipecuronium
recuroinum
vecuronium

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depolarizing NM blocking agents

succinylcholine

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mm relaxants/spasmolytics

dantorlene

botulinum

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AChEinhibitors

echotophate
edrophonium
neostigmine
physostigmine
pyridostigmine
ambenonium
donepezil
galantamine
rivastigmine
tacrine

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antimuscarinic compounds

atropine

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cholinesterase reactivators

pralidoxime

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neuromuscular blockers

antinicotinic drugs
interfere with NMJ do not have CNS activity
adjuncts to general anesthesia for mm relaxation
all are highly polar and inactive orally so must be administered parenterally

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spasmolytics

used to reduce spasticity in a variety of neurological conditions
aka ‘centrally acting’ mm relaxants

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neuromuscular blocking agents MOA

competitive antagonists at nAChR

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which mm are affected first?

smaller mm, larger mm (diaphragm) are last to be affected and first to recover

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reversal of neuromuscular blockade

AChE inhibitors
neostigmine and pyridostigmine
edrophonium (less effective)
administer anticholinergic agents with AChE inhibitors to minimize adverse cholinergic effects effects d/t increased ACh at mAChR

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adverse effects of nondepolarizing agents

some produce H2 -> wheals, bronchospasm, hypotension, bronchial and salivary secretion can co-administer antiH2
large doses tubocurarine and metocurine can prodcuce AChR blockade at autonomic ganglia and adrenal medulla -> hypotension and tachy
b/c tubocurariene causes sign H2 release not really used anymore

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NM blockers and anesthetics

inhaled anesthetics potentiate the NM blockade produced by nondepolarizing mm relaxants
dose dependent

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NM blockers and abx

aminoglycosides enhance NM blockade

some abx reduce release of ACh

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aminoglycosides

gentamicin
tobramycin
amikacin
streptomycin

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phenytoin and carbamazepine

significantly increase requirement for nondepolarizing NMBAs by unknown mech

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NMBAs in pts >70

must be reduced d/t decreased metabolism and clearance

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pts with severe burns and UMN disease

resistant to NMBAs likely d/t decreased nAChRs

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atracurium

intermediate acting
breakdown product laudanosine can cross BBB and cause seizures 
only an issue with prolonged Tx
can be used in renal or hepatic failure
less H2 release

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cisatracurium

isomer of atracurium, but 3x as potent
intermediate acting with fewer side effects
can used used with significant renal/hepatic failure
devoid of CV efects

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micacurium

shortest duration of action of all nondepolarizing agents
large dose can cause profound H2 release and CV effects
not really used

intermediate acting steroid derivatives

vecuronium and rocuronium
more depend on biliary excretion or hepatic meta and used more often then long acting steroid derivatives
low H2 release

long acting derivatives

pancuronium pipcuronium low H2 release

prolonged steroidal derivative use

several days | 3-hydroxy metabolite can cause prolonged paralysis b/c has longer half life

pancuronium

intermediate onset, long acting, high potency | DOC for pts w/normal renal and hepatic fnx requiring paralysis >1hr

rocuronium

most rapid onset, intermediate acting, and low potency alternative to succinylcholine devoid of CV effects

vecuronium

slower onset, intermediate duration, high potnecy acceptable alternative to competitive nondepolarizing blocker to rocuronium commonly used in critically ill pts for >24hrs no CV effects

succinylcholine

only depolarizing blocking drug used clinically

PK of succinylcholine

ultra-short acting d/t rapid hydrolysis and inactivation by plasmacholinesterase so only small percentage of dose reaches NMJ not effectively metabolized by AChE at NMJ

PD of succinylcholine

phase 1: depolarizing-> mm contraction -> cannot be redepolarized -> flaccid paralysis phase 2: desensitization of AChR

uses of succinylcholine

rapid sequence induction (emergency surgery) and for quick surgical procedures

reversal of succinylcholine

plasma cholinesterases

CV adverse effects of succinylcholine

cardiac arrythmias when administered with halothane anesthesia neg inotropic and chronotropic effects large doses can cause pos inotropic and chronotropic effects

other adverse effects of succinylcholine

``` hyperkalemia (most common) increased intraocular pressure increased intraepigastric pressure mm pain H2 release ```

hyperkalemia

most common adverse effect of succinylcholine pts with burns, nn damage, NM disase, closed head injury, and truama are more at risk for hyperkalemia which can lead to cardiac arrest

CI to succinylcholine

personal or FHx of MH myopathies associated with elevated CPK acute phase of injury, majro burns, multiple trauma, neuro injury

black box warning of succinylcholine

cardiac arrest d/t rhabdomylosis with hyperkalemia usually males <8yrs

succinylcholine and anesthetics

dantrolene MOA

inhibits RyR

adverse rxns dantrolene

mm weakness sedation hepatits (don't give orally if pt has hep)

dantrolene uses

butyrylcholinesterase

aka pseudocholinesterase or plasma cholinesterase synthesized by liver absent in NMJ and CNS also inhibited by cholinesterase inhibitors

3 subgroups of AChE inhibitors

alcohols carbamic acid esters (carbamates) organophosphates

alcohols

contain alcohol and quaternary ammonium group- positively charged edrophonium bind noncovalently and reversibly

carbamates

quaternary or tertiary ammonium groups (pos or neutral) neostigmine, pyridostigmine, physostigmine, and carbaryl bind noncovalently and reversibly

organophosphates

neutral and highly lipid soluble | bind covalently and irreversibly

quaternary and charged AChE inhibitors

parenteral administration no CNS duration determined by stability of inhibitor-enzyme complex, not meta or excretion neostigmine, pyridostigmine, edrophonium, echothiophate, ambenonium

tertiary and uncharged AChE inhibitors

well absorbed from all sites CNS more toxic then quaternary physostigmine, donepezil, tacrine, rivastigmine, galantamine

organophosphates

lipid soluble very toxic everywhere must regenerate AChE

alcohols duration of action

relatively weak interactions and short lived 2-10min

carbamic acid esters duration of action

2-step hydrolysis | 2nd step- formation of covalent bond requires 30min-6hrs

uses of AChE inhibitors

``` MG reversal of pharm paralysis glaucoma dementia antimuscarinic antidote ```

succinylcholine and AChE inhibitors

phase 1 block enhanced by AChE inhibitors | phase 2 block inhibited

beta blockers and AChE inhibitors

enhanced bradycardia

systemic corticosteroids and AChE inhibitors

enhance mm weakness seen in MG