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Pharm 1 > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

what is the mechanism of action of NMD?

A

prevents muscle contraction by interfering with the transmission of an action potential from the nerve ending to the muscle

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2
Q

where does the NMD work specifically?

A

at the junction between nerve and muscle

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3
Q

what are the 5 uses of NMD?

A

1) Facilitate endotracheal intubation
2) Decrease muscle tone to provide appropriate operating conditions (abd surgical case)
3) To alleviate muscle activity with ECT (seizure)
4) To allow balanced anesthesia without patient movement
5) To assist in controlled ventilatory patients in the ICU

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4
Q

what type of terminal does a NMD impulse arrive at?

A

motor nerve terminal

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5
Q

What influx causes vesicles to adhere to the PREsynaptic membrane and rupture to release acetylcholine (ACh) into the cleft?

A

Calcium

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6
Q

what type of receptor does ACh diffuses across the synaptic cleft/synapse/gap/junction to?

A

nicotinic (cholinergic) receptor

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7
Q

what is another name for nicotinic receptor?

A

cholinergic

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8
Q

what type of sites does Ach bind to on the POSTsynaptic receptor? (causes the ion channel to open)

A

alpha (MUST BIND TO BOTH)

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9
Q

Sodium and potassium ions move through the channel causing depolarization of what?

A

motor end plate membrane

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10
Q

what is the change in the transmembrane potential to reach threshold potential (2 different numbers)?

A

-90mV to -45 mV – threshold potential

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11
Q

The action potential spreads over the surfaces of the muscle fibers causing ___________?

A

contraction

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12
Q

what comes IN the cell during an action potential?

A

sodium

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13
Q

what goes OUT of the cell during an action potential?

A

potassium

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14
Q

how is muscle contraction initiated?

A

excitation-contraction coupling

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15
Q

what is Ach metabolized by?

A

acetylcholinesterase (AChE), a local acetylcholine enzyme (which is contained in the postsynaptic membrane)

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16
Q

what would low calcium cause?

A

decreased release in Ach

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17
Q

is NMD local or systemic?

A

local, not really going out into plasma

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18
Q

what type of NMD blocks the alpha site so that the muscle cant do anything

A

Curare alkaloids

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19
Q

what is the only depolarizing NMB?

A

Succinylcholine

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20
Q

how does succinylcholine work?

A

attaches to the alpha site, causes the muscle to depoliarize just like normal, but then once its depolarized it cant repolarize until the succ diffuses

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21
Q

how is release of acetylcholine triggered?

A

increases in the concentrations of free calcium ions in nerve terminals

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22
Q

what is Ach

A

a primary neurotransmitter

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23
Q

what is the principal site of action of neuromuscular blocking agents

A

Neuromuscular junction

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24
Q

what drug inhibits release of Ach

A

magnesium (think it works opposite of calcium)

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25
what does low calcium cause (side effect)?
muscle weakness
26
how is Ach synthesized?
motor nerve ending by acetylation of choline which is controlled by choline acetylase enzyme
27
how is Ach rapidly hydrolyzed?
acetylcholinesterase (AChE) converts it to acetic acid and choline
28
how long does rapid hydrolysis of Ach take?
<15 milliseconds ms (prevents the sustained depolarization of the NMJ)
29
WHERE are presynaptic prejunctional nAchRs (receptors)?
on the motor NERVE ending
30
what is indirect evidence of the activation mobilizes additional ACh for subsequent release (blockade of these receptors causes a decrease in the release of ACh)
tetanic fade*, fasciculations with SCh, short-lived contractions before blockade with SCh
31
WHERE are extrajunctional (perijunctional) nAchRs (receptors)?
throughout the muscle cell itself
32
WHAT are extrajunctional (perijunctional) nAchRs (receptors)?
typically found in fetus (fetal receptors) proliferation occurs when muscle is damaged, diseased, or denervated (stroke, paralysis, burn, immobilization, muscular dystrophy)
33
how much longer do extrajunctional (perijunctional) nAchRs (receptors) channels remain open?
4x as long, greater risk for HYPERKALEMIA Potassium is coming out (stroke, crush injuries/trauma, long term injuries)
34
WHERE are postsynaptic receptors found?
junctional folds of the muscle membrane (transmembrane)
35
what 5 linear protein subunits make up postsynaptic receptors?
2 alpha, 1 beta, 1 delta, 1 epsilon
36
the binding of Ach to the 2 alpha sites causes the receptor to undergo change to open a channel for?
cations
37
what leaves the cell to cause depolarization?
potassium
38
what enters the cell to cause depolarization?
calcium and sodium
39
what is a depolarizing blocker?
attaches to both alpha sites, mimics ACh, and causes depolarization example: Succ
40
what is a nondepolarizing blocker?
attaches to ONE alpha site, to prevent ACh from binding, and thus prevents depolarization
41
where does a channel blockade work at?
physically block an open channel or a closed channel around the EXTRACELLULAR ENTRANCE
42
what is onset time?
time from administration to maximum effect
43
what is clinical duration?
time from administration to 25% recovery of twitch response
44
what is total duration?
time from administration to 90% recovery of twitch response
45
recovery index
time from 25% to 75% recovery of twitch response
46
ED95
the dose needed to produce 95% suppression of single twitch response
47
what are 4 objectives of clinical monitoring of NM function?
1) Titration of dosage of NMB to desired effect 2) Monitor for unusual resistance or sensitivity or prolonged action of a NMB 3) Evaluation of reversibility 4) Determine recovery from block in conjunction with clinical evaluation
48
how does monitoring for NMB occur?
Electrical stimulation of the PERIPHERAL motor nerve to observe the muscular contractions in response.
49
why is it important to place leads appropriately*
if you apply to muscle and not the nerve, it will retract regardless (false positive)
50
what does the ulnar nerve stimulate*
adductor pollicis brevis muscle in the thumb
51
what color lead needs to be on the nerve?
black
52
what does the posterior tibial nerve stimulation cause*
PLANTAR flexion of the big toe (NOT the whole foot) think "PPPosterior PPPlantar"
53
what does the lateral popliteal/peroneal nerve stimulation cause*
DORSI flexion of the WHOLE foot
54
what does the facial nerve stimulate*
orbicularis oculi or the frontalis
55
where should you place electrodes for facial nerve stimulation?
place BLACK lead near the tragus of the ear
56
what does response seen in orbicularis oculi reflect*
onset of laryngeal muscle relaxation (similar to laryngeal muscle, rapidly moving, both are highly vascular, helps determine when to get the ETT in)
57
why should you prefer ulnar nerve for recovery verses orbicularis oculi?
possible to overdose relaxant/overestimate recovery from block
58
Order of ONSET for NMB?
1) Small, rapidly moving muscles such as eyes, fingers 2) Trunk, abdominal muscles, long muscles with mostly slow fibers such as adductor pollicis 3) Intercostal and diaphragm
59
Order of RECOVERY for NMB?
1) Intercostal and diaphragm 2) Small, rapidly moving muscles such as eyes, fingers 3) Trunk, abdominal muscles, long muscles with mostly slow fibers such as adductor pollicis
60
3 signs of residual paralysis or first signs of relaxation?
1) Inability to focus vision, keep eyelids open; will have double vision 2) inability to swallow 3) Inability to phonate/make sound *however, hearing is INTENSIFIED (small muscles of the ear are relaxed)
61
enzyme that rapidly hydrolyzes Ach (<15 milliseconds) into acetic acid and choline
acetylcholinesterase
62
what is the preferred stimulation for lower extremities
lateral popliteal/peroneal dorsiflexion of foot
63
reflects ONSET of laryngeal muscle relaxation (they are both rapidly moving and highly vascularized) (best for sensing ONSET of NMB)
orbicularis oculi
64
If using OO, it is possible to ______dose the relaxant, _______estimate recovery, and _________estimate the blockade*
OVERdose relaxant OVERestimate recovery UNDERestimate blockade
65
1 Hz = __ second
1 second
66
types of nerve stimulation: there is no control
single twitch
67
types of nerve stimulation: ideal for maintenance phase and when to re-dose
TOF
68
2/4 means ___% block 3/4 means ___% block 4/4 means ___-___% block
2/4 means 90% block 3/4 means 80% block 4/4 means 70-75% block
69
headlift on TOF: not an indication of recovery ____ or ____% *
50 or 60%
70
types of nerve stimulation: easier to detect fade (1st and 4th twitch)
double burst
71
types of nerve stimulation: best indication of recovery
tetanic stimulation (tetanus) painful Wait at least 10 minutes between! To avoid false info (due to increased Ach)
72
Post-tetanic twitches of 10 coincides with __st twitch of TOF
PTT 10= 1st twitch TOF
73
Post-tetanic twitch of 1 means ___ minutes (intermediate) or ____ minutes (long acting) until TOF has its 1st twitch
8 minutes for intermediate 30 minutes for long-acting
74
what is the indication of recovery for NMB*
sustained tetanus with no fade
75
ALWAYS assess baseline twitches after giving _____, and before ______
after giving Succs before NMB (there is potential issue with Sch and atypical plasma cholinesterase and you need to know the source of what is wrong)
76
Guidelines for Reversal: No twitches*
Do not attempt to reverse! (could prolong/accentuate/enhance it by the anticholinesterase)
77
Guidelines for Reversal: 1 twitch*
30 minutes
78
Guidelines for Reversal: 2-3 twitches*
4-12 minutes
79
Guidelines for Reversal: 4 twitches*
2 minutes (edrophonium) 5 minutes (neostigmine)
80
what side effect can occur for Succs, especially on second dose*
bradycardia (parasympathetic response)
81
what are the 3 sympathetic side effects of Succs*
INCREASED HR, BP, SVR
82
LACK of fade of tetanus MINIMAL fade of TOF NO PTT blockade is accentuated by anticholinesterase
phase I
83
fade blockade is attenuated by anticholinesterase
phase II
84
Destroys (metabolizes) Sch
plasma cholinesterase = psuedocholinesterase
85
Dibucaine 80: homozygous normal: ___ to ___ min*
5 to 10 min
86
Dibucaine 40-60: heterozygous atypical: ___ min*
30 min
87
Dibucaine 20: homozygous atypical: >___ hours*
>3 hours
88
anticholinesterase drugs lead to ___________ Succs
prolonged Sch * Insecticides * Myasthenia gravis medications * Glaucoma medications * Chemo drugs * Alzheimer’s medications (not clinically significant)
89
Inhibitors of Plasma Cholinesterase lead to ______________ Sch
metoclopramide (reglan)
90
dose for _______ body weight for Sch
TOTAL body weight obese patients have increased plasma cholinesterase activity, leading to SHORTENED Sch
91
what is the increase in hyperkalemia for Sch*
0.5 to 1
92
how long AFTER burns do you not use Sch
24 hours
93
myalgia is most likely with*
young healthy females who ambulate after surgery
94
bad side effects of Sch
histamine masseter spasm malignant hyperthermia myoglobinuria/rhabdomyolysis myalgia hyperkalemia increased ICP, IOP, intragastric
95
Defasciculating Dose: 1/___th of intubating dose of NMB
1/10 of intubating dose
96
Defasciculating Dose: If you give the nondepolarizer, then you need to __________ the Sch dose*
increase the Sch dose
97
what side effect is NOT effected by defasciculating dose for Sch*
hyperkalemia

Pharm 1 (9 decks)

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