AP reaches the end of the motor neuron; Ca influxes; vesicle exocytosis; ACh is released
Describe the role of the Action Potential in the NMJ.
upon binding to a nicotinic receptor, sodium comes into the cell and stimulates a motor end plate potential; if large, AP is propagated along the entire muscle fiber causing contraction
Describe what happens when ACh binds to Nicotinic Receptors (nAChR).
surgical relaxation, endotracheal intubation, ventilation control, epileptic patients
What are the clinical applications of NMBs? (4)
diaphragm; first
The _______ is the last muscle to be paralyzed and the _______ to recover.
look-alike packaging/labeling, look-alike drug names, unsafe mnemonics, orders entered wrong, knowledge deficit
What are common dispensing errors involved with NM blockers? (5)
antagonists that mimic ACh; depolarizing blocker- receptor desensitization
How is muscle contraction blocked? (2)
cisatracurium, vecuronium, rocuronium
What are the Non-depolarizing, short/intermediate-acting NM blockers? (3)
pancuronium
What is the Non-depolarizing, Long-acting NM blocker?
succinylcholine
What is the Depolarizing NM blocker?
neostigmine, pyridostigmine, edrophonium
What are the ACh esterase inhibitors? (3)
competitive AChR antagonist; compete for nAChR binding at muscle membrane in NMJ end plate
Non-depolarizing NM blocker MOA? (3)
large doses can enter the pore of ion channel causing a more intense blockade that weakens NM transmission; can block pre-synaptic Na+ channels interfering with ACh release
What are the additional MOA's of Non-depolarizing NM blockers? (2)
elimination half-life
The DoA of NM blockers strongly correlates with ___________.
c
Which is the least potent?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
c
Which has the quickest onset?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
a
Which is a potent stereoisomer of Atracurium?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
laudanosine
What is the active, toxic metabolite of Cisatracurium?
a
Which is the most commonly used?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
b
Which has a duration of action of 1 hour?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
b
Which can cause tachycardia?
a) Cisatracurium
b) Pancuronium
c) Rocuronium
d) Vecuronium
inhibit AChE and directly increase ACh release
Neostigmine/Pyridostigmine MOA?
more rapid onset than other reversals; less effective in presence of potent NM blockade
Edrophonium characteristics? (2)
rapidly encapsulates and inactivates the NM blockers; forms a complex that is excreted in the urine
Sugammadex MOA?
rocuronium, vecuronium
Which NM blockers is Sugammadex approved for? (2)
hypersensitivity reaction, anaphylaxis, encapsulates progesterone
Sugammadex AE's? (3)
AChR agonist; depolarizes membrane in the same manner as ACh; causes transient contractions/fasciculations and persistent stimulation that results in closure/inactivation of Na+ channels-flaccid paralysis
Succinylcholine MOA?
the membrane will gradually repolarize, but neurotransmission will remain blocked; resulting in receptor desensitization
If a patient receives multiple boluses of Succinylcholine, what will occur?
quick; short
Succinylcholine has ______ onset of action and a ______ duration of action.
short procedures; emergencies when immediate airway reopening is required
When is Succinylcholine best used? (2)
false; most is metabolized by plasma cholinesterase
A large amount of Succinylcholine reaches the NMJ. T/F?
hyperkalemia, muscle pain, bradycardia
AE's of Succinylcholine? (3)
volatile anesthetics (halothane); malignant hyperthermia; due to abnormal release of calcium
Succinylcholine + _______ = ?
malignant hyperthermia
-rare autosomal dominant disorder that leads to life-threatening
hypercatabolic state
dantrolene
What is given to treat Malignant Hyperthermia?
massive muscle contraction, lactic acid production/metabolic acidosis, tachycardia, increased body temp
Malignant Hyperthermia symptoms? (4)