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Flashcards in NMJ blockers Deck (15):

Atracurium (Tracrium®)

non-depolarizing NMJ blocker
Time to onset of action 2-4 min
-degraded by temp/pH-dependent Hofmann reaction.
-not metabolized by enzymes and may be useful for patients with liver and/or renal failure.


Mivacurium (Mivacron®)

non-depolarizing NMJ blocker
Short duration of action (12-18 min)
Benzylisoquinoline, Time to onset of action: 2-4 min
*metabolized by plasma
cholinesterase (why short duration)*
-Problems if given when decreased plasma cholinesterase activity
Pts with liver disease or nutritional deficiencies may have abnormal plasma cholinesterase activity. Flushing of the face and neck is common.


Rocuronium (Zemuron®)

non-depolarizing NMJ blocker
Intermediate Duration of action (30-60 min)
Steroidal structure, Liver metabolism
*Time to onset of action: very rapid (1-2 min) similar to succinylcholine and used to rapidly relax laryngeal and jaw muscles for tracheal intubation*


Succinylcholine (Anectine®)

depolarizing NMJ blocker
Duration (5-8 min); Time to onset; 1-1.5 min – very fast
*Used for very short procedures (e.g. intubation)
*initial fasciculations mostly in the chest and abdomen,
occur immediately after drug admin
-no antidote, (like non-depol NMJ blockers)


NMJ blocker uses

GA adjuncts in sx: Cause the complete relaxation of skeletal muscle
-no CNS effects; only given IV


1st muscles to be blocked/affected ??

small rapid moving muscles → limb trunk muscles → intercostal muscles → lastly, the diaphragm
*recovery in reverse order, diaphragm is 1st to regain function


Botox is used to treat ??

blephorospasm (involuntary eyelid closing), strabismus (eye spasms) and wrinkle treatment


Non-depolarizing (competitive) NMJ blockers characteristics

Not metabolized by AChE
-Competitive inhibitors of ACh binding to ACh receptor at NMJ
-antiAChE agents (e.g. neostigmine) reverse NMJ block by non-depolarizing NMJ blockers


general non-depolarizing (competitive) NMJ blocker SEs

Prolonged apnea, histamine release (bronchospasm, hypotension)


Benzylisoquinonlines ( “___curium” name) SEs

Histamine release, few vagal/ganglionic blocking effects


Steroidal compounds (“___curonium” name) SEs

-Block of ganglionic muscarinic receptors can occur resulting in tachycardia due to effects on vagus
-Vecuronium and rocuronium are newer agents with little or no associated tachycardia or histamine release


succinylcholine metabolism

Degraded by plasma choline esterase (e.g. butyrylcholinesterase)
Problems with decreased butyrylcholineesterase: atypical or deficient plasma cholinesterase, hepatic or liver disease, nutritional deficiencies


succinylcholine MOA

alters electro-chemical driving forces: excessive opening of nicotinic ACh receptors by SCh results in decreased electro- chemical driving forces and therefore less positive ion entry in presence of ACh resulting in less muscle response to motor neuron activity.
-this is phase I: single dose, fast onset; neostigmine augments blocking action of SCh


Phase II SCh

after prolonged infusion or dosing 10X of normal dose (5 mg/kg); slow onset
-MP: -80mV
-Neostigmine antagonizes SCh block


botulinum toxin

besides wrinkles, for
blephorospasm – involuntary closing of eyelid and strabismus – deviation of eye position that cannot be overcome
MOA: prevent release of presynaptic ACh at NMJ
SEs: upregulation of post-synaptic nicotinic ACh receptors at previous injection site(s) resulting in increased wrinkles and ptosis - eyelid droop