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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
Q

what does low calcium cause (side effect)?

A

muscle weakness

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26
Q

how is Ach synthesized?

A

motor nerve ending by acetylation of choline which is controlled by choline acetylase enzyme

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27
Q

how is Ach rapidly hydrolyzed?

A

acetylcholinesterase (AChE) converts it to acetic acid and choline

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28
Q

how long does rapid hydrolysis of Ach take?

A

<15 milliseconds ms (prevents the sustained depolarization of the NMJ)

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29
Q

WHERE are presynaptic prejunctional nAchRs (receptors)?

A

on the motor NERVE ending

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30
Q

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)

A

tetanic fade*, fasciculations with SCh, short-lived contractions before blockade with SCh

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31
Q

WHERE are extrajunctional (perijunctional) nAchRs (receptors)?

A

throughout the muscle cell itself

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32
Q

WHAT are extrajunctional (perijunctional) nAchRs (receptors)?

A

typically found in fetus (fetal receptors)

proliferation occurs when muscle is damaged, diseased, or denervated (stroke, paralysis, burn, immobilization, muscular dystrophy)

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33
Q

how much longer do extrajunctional (perijunctional) nAchRs (receptors) channels remain open?

A

4x as long, greater risk for HYPERKALEMIA

Potassium is coming out (stroke, crush injuries/trauma, long term injuries)

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34
Q

WHERE are postsynaptic receptors found?

A

junctional folds of the muscle membrane (transmembrane)

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35
Q

what 5 linear protein subunits make up postsynaptic receptors?

A

2 alpha, 1 beta, 1 delta, 1 epsilon

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36
Q

the binding of Ach to the 2 alpha sites causes the receptor to undergo change to open a channel for?

A

cations

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37
Q

what leaves the cell to cause depolarization?

A

potassium

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38
Q

what enters the cell to cause depolarization?

A

calcium and sodium

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39
Q

what is a depolarizing blocker?

A

attaches to both alpha sites, mimics ACh, and causes depolarization

example: Succ

40
Q

what is a nondepolarizing blocker?

A

attaches to ONE alpha site, to prevent ACh from binding, and thus prevents depolarization

41
Q

where does a channel blockade work at?

A

physically block an open channel or a closed channel around the EXTRACELLULAR ENTRANCE

42
Q

what is onset time?

A

time from administration to maximum effect

43
Q

what is clinical duration?

A

time from administration to 25% recovery of twitch response

44
Q

what is total duration?

A

time from administration to 90% recovery of twitch response

45
Q

recovery index

A

time from 25% to 75% recovery of twitch response

46
Q

ED95

A

the dose needed to produce 95% suppression of single twitch response

47
Q

what are 4 objectives of clinical monitoring of NM function?

A

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
Q

how does monitoring for NMB occur?

A

Electrical stimulation of the PERIPHERAL motor nerve to observe the muscular contractions in response.

49
Q

why is it important to place leads appropriately*

A

if you apply to muscle and not the nerve, it will retract regardless (false positive)

50
Q

what does the ulnar nerve stimulate*

A

adductor pollicis brevis muscle in the thumb

51
Q

what color lead needs to be on the nerve?

A

black

52
Q

what does the posterior tibial nerve stimulation cause*

A

PLANTAR flexion of the big toe (NOT the whole foot)

think “PPPosterior PPPlantar”

53
Q

what does the lateral popliteal/peroneal nerve stimulation cause*

A

DORSI flexion of the WHOLE foot

54
Q

what does the facial nerve stimulate*

A

orbicularis oculi or the frontalis

55
Q

where should you place electrodes for facial nerve stimulation?

A

place BLACK lead near the tragus of the ear

56
Q

what does response seen in orbicularis oculi reflect*

A

onset of laryngeal muscle relaxation

(similar to laryngeal muscle, rapidly moving, both are highly vascular, helps determine when to get the ETT in)

57
Q

why should you prefer ulnar nerve for recovery verses orbicularis oculi?

A

possible to overdose relaxant/overestimate recovery from block

58
Q

Order of ONSET for NMB?

A

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
Q

Order of RECOVERY for NMB?

A

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
Q

3 signs of residual paralysis
or
first signs of relaxation?

A

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
Q

enzyme that rapidly hydrolyzes Ach (<15 milliseconds) into acetic acid and choline

A

acetylcholinesterase

62
Q

what is the preferred stimulation for lower extremities

A

lateral popliteal/peroneal

dorsiflexion of foot

63
Q

reflects ONSET of laryngeal muscle relaxation (they are both rapidly moving and highly vascularized)

(best for sensing ONSET of NMB)

A

orbicularis oculi

64
Q

If using OO, it is possible to ______dose the relaxant, _______estimate recovery, and _________estimate the blockade*

A

OVERdose relaxant
OVERestimate recovery
UNDERestimate blockade

65
Q

1 Hz = __ second

A

1 second

66
Q

types of nerve stimulation:
there is no control

A

single twitch

67
Q

types of nerve stimulation:
ideal for maintenance phase and when to re-dose

A

TOF

68
Q

2/4 means ___% block
3/4 means ___% block
4/4 means ___-___% block

A

2/4 means 90% block
3/4 means 80% block
4/4 means 70-75% block

69
Q

headlift on TOF: not an indication of recovery ____ or ____% *

A

50 or 60%

70
Q

types of nerve stimulation:
easier to detect fade (1st and 4th twitch)

A

double burst

71
Q

types of nerve stimulation:
best indication of recovery

A

tetanic stimulation (tetanus)
painful
Wait at least 10 minutes between! To avoid false info (due to increased Ach)

72
Q

Post-tetanic twitches of 10 coincides with __st twitch of TOF

A

PTT 10= 1st twitch TOF

73
Q

Post-tetanic twitch of 1 means ___ minutes (intermediate) or ____ minutes (long acting) until TOF has its 1st twitch

A

8 minutes for intermediate
30 minutes for long-acting

74
Q

what is the indication of recovery for NMB*

A

sustained tetanus with no fade

75
Q

ALWAYS assess baseline twitches after giving _____, and before ______

A

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
Q

Guidelines for Reversal:
No twitches*

A

Do not attempt to reverse! (could prolong/accentuate/enhance it by the anticholinesterase)

77
Q

Guidelines for Reversal:
1 twitch*

A

30 minutes

78
Q

Guidelines for Reversal:
2-3 twitches*

A

4-12 minutes

79
Q

Guidelines for Reversal:
4 twitches*

A

2 minutes (edrophonium)
5 minutes (neostigmine)

80
Q

what side effect can occur for Succs, especially on second dose*

A

bradycardia (parasympathetic response)

81
Q

what are the 3 sympathetic side effects of Succs*

A

INCREASED HR, BP, SVR

82
Q

LACK of fade of tetanus
MINIMAL fade of TOF
NO PTT
blockade is accentuated by anticholinesterase

A

phase I

83
Q

fade
blockade is attenuated by anticholinesterase

A

phase II

84
Q

Destroys (metabolizes) Sch

A

plasma cholinesterase = psuedocholinesterase

85
Q

Dibucaine 80: homozygous normal: ___ to ___ min*

A

5 to 10 min

86
Q

Dibucaine 40-60: heterozygous atypical: ___ min*

A

30 min

87
Q

Dibucaine 20: homozygous atypical: >___ hours*

A

> 3 hours

88
Q

anticholinesterase drugs lead to ___________ Succs

A

prolonged Sch

  • Insecticides
  • Myasthenia gravis medications
  • Glaucoma medications
  • Chemo drugs
  • Alzheimer’s medications (not clinically significant)
89
Q

Inhibitors of Plasma Cholinesterase lead to ______________ Sch

A

metoclopramide (reglan)

90
Q

dose for _______ body weight for Sch

A

TOTAL body weight

obese patients have increased plasma cholinesterase activity, leading to SHORTENED Sch

91
Q

what is the increase in hyperkalemia for Sch*

A

0.5 to 1

92
Q

how long AFTER burns do you not use Sch

A

24 hours

93
Q

myalgia is most likely with*

A

young
healthy
females
who ambulate after surgery

94
Q

bad side effects of Sch

A

histamine
masseter spasm
malignant hyperthermia
myoglobinuria/rhabdomyolysis
myalgia
hyperkalemia
increased ICP, IOP, intragastric

95
Q

Defasciculating Dose:
1/___th of intubating dose of NMB

A

1/10 of intubating dose

96
Q

Defasciculating Dose:
If you give the nondepolarizer, then you need to __________ the Sch dose*

A

increase the Sch dose

97
Q

what side effect is NOT effected by defasciculating dose for Sch*

A

hyperkalemia

Pharm 1 (9 decks)

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