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Pharmacology Exam 2 > Muscle Relaxants > Flashcards

Muscle Relaxants Flashcards

1
Q

What NDMBs are benzylisoquinolines?

A

Atracurium & Cisatracurium

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2
Q

What NDMBs are aminosteroids?

A

Rocuronium, Vecuronium, and Pancuronium

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3
Q

What muscle relaxant is a depolarizing muscle blocker?

A

Succinylcholine

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4
Q

What are the two agents commonly used together to reverse muscle relaxants?

A

Neostigmine (anticholinesterase)
Glycopyrrolate (anticholinergic)

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5
Q

How is Atracurium metabolized?

A

Primary: Ester hydrolysis
Secondary: Hoffman elimination

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6
Q

How is Cisatracurium metabolized?

A

Primary: Hoffman elimination

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7
Q

Which NDMB is best for renal failure patients?

A

Cisatracurium
*only 16% renal elimination

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8
Q

Which NDMB should be avoided for patients with aortic stenosis?

A

Pancuronium
*tachycardia occludes LVOT which decreases CO and BP

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9
Q

Which NDMBs do not have active metabolites?

A

Rocuronium (no metabolism)
Mivacurium (pseudocholinesterase)

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10
Q

Which NDMBs have active metabolites that can lead to seizures? Which one is worse?

A

Atracurium (worst) & Cisatracurium

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11
Q

Which NDMBs are dependent on hepatic/renal function for metabolism and elimination?

A

Aminosteroids (Roc, Vec, Panc)
Biliary: Vec & Roc
Renal: Panc

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12
Q

How is Succinylcholine metabolized?

A

plasma cholinesterase (pseudocholinesterase)

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13
Q

Which muscle relaxants are primarily eliminated by metabolism?

A

Succinylcholine, Atracurium, Cisatracurium

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14
Q

Which muscle relaxants are primarily eliminated by the liver?

A

Vecuronium, Rocuronium

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15
Q

Which muscle relaxants are primarily eliminated by the kidneys?

A

Pancuronium

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16
Q

Which muscle relaxants cause histamine release?

A

Atracurium, Mivacurium, Succinylcholine
*Atracurium most associated with, may lead to hypotension and tachycardia

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17
Q

Which muscle relaxant is most associated with tachycardia?

A

Pancuronium
moderate blockade heart M2 (stimulates release and blocks reuptake of catecholamines)

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18
Q

Which muscle relaxants are most associated with anaphylaxis?

A

Succinylcholine & Rocuronium

(Lesser: Atracurium, Cisatracurium & Vecuronium)

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19
Q

Which muscle relaxant is most associated with bradycardia?

A

Succinylcholine
stimulation heart M2

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20
Q

What is the intubating dose of Atracurium?

A

0.5 mg/kg

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21
Q

What is the maintenance dose of Atracurium?

A

0.1 mg/kg

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22
Q

What is the intubating dose of Cisatracurium?

A

0.1 mg/kg

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23
Q

What is the maintenance dose of Cisatracurium?

A

0.05 mg/kg

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24
Q

What is the intubating dose for Succinylcholine?

A

1 mg/kg

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25
Q

What is the maintenance dose for Succinylcholine?

A

0.1 mg/kg

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26
Q

What is the concentration of Succinylcholine?

A

20 mg/mL

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27
Q

What is the intubating dose for Rocuronium?

A

1 mg/kg

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28
Q

What is the maintenance dose for Rocuronium?

A

0.25 mg/kg

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29
Q

What is the concentration of Rocuronium?

A

10 mg/mL

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30
Q

What is the intubating dose of Vecuronium?

A

0.1 mg/kg

80 kg = 8 mg = 8 mL

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31
Q

What is the maintenance dose for Vecuronium?

A

0.01 mg/kg

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32
Q

What is the concentration of Vecuronium?

A

1 mg/mL

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33
Q

What is the concentration of Cisatracurium?

34
Q

What is the dose for Neostigmine?

A

0.05 mg/kg
*max dose of 5 mg

35
Q

What is the concentration of Neostigmine?

A

1 mg/mL

1 mL per 20 kg
80 kg = 4 mL = 4 mg

36
Q

What is the dose for Glycopyrrolate?

A

0.01 mg/kg

37
Q

What is the concentration of Glycopyrrolate?

A

0.2 mg/mL
(same mL as Neostigmine)

38
Q

What is the dose for Sugammadex?

A

0-1 twitch: 4 mg/kg
2-4 twitches: 2 mg/kg
immediately after NDMB: 16 mg/kg

39
Q

What is the concentration of Sugammadex?

40
Q

How many twitches do you need before administering Sugammadex?

A

minimum 1 twitch, ideally like 2 twitches

41
Q

How is Hoffman elimination affected by blood pH and temperature?

A

faster with alkalosis and hyperthermia
slower with acidosis and hypothermia

42
Q

What drugs potentiate neuromuscular blockers?

A

volatile anesthetics
antibiotics
antidysrhythmics
local anesthetics
diuretics
dantrolene
cyclosporin
tamoxifen

43
Q

What electrolyte factors potentiate neuromuscular blockers?

A

increased Lithium
increased Magnesium

decreased Calcium
decreased Potassium

44
Q

Why does hypothermia potentiate neuromuscular blockade?

A

reduced metabolism and clearance

45
Q

Which neuromuscular blockers block heart M2 receptors causing tachycardia?

A

Pancuronium and slightly Rocuronium

46
Q

Which neuromuscular blockers stimulate heart M2 receptors causing bradycardia?

A

Succinylcholine

47
Q

Which neuromuscular blockers stimulate the autonomic ganglia causing tachycardia?

A

Succinylcholine

48
Q

What is the mechanism of action of extrajunctional nicotinic receptors?

A

stay open 4 times longer and upregulate leading to hyperkalemia

49
Q

What are the standard subunits on a nicotinic receptor at the NMJ?

A

2 alpha, 1 beta, 1 delta, 1 epsilon

50
Q

How and where is Acetylcholine synthesized?

A

AcetyleCoA + Choline + Choline Acetyltransferase
-within the presynaptic nerve

51
Q

How and where is Acetylcholine broken down?

A

Acetylcholine + water + Acetylcholinesterase
-within the synapse

52
Q

Which of the muscle relaxants are short acting?

A

Succinylcholine
Mivacurium

53
Q

Which of the muscle relaxants are intermediate acting?

A

Atracurium
Cisatracurium
Rocuronium
Vecuronium

54
Q

Which of the muscle relaxants are long acting?

A

Pancuronium

55
Q

What are co-existing conditions that lower plasma cholinesterase?

A

atypical PCheE
liver disease
renal disease
advanced age
malnutrition
pregnancy (high estrogen)
burns
neoplasm

56
Q

What are drugs that lower plasma cholinesterase?

A

metoclopramide
esmolol
oral contraceptives
MAO inhibitors
cytotoxic drugs (N2 mustard & cyclophosphamide)
anticholinesterase drugs (neostigmine, echothiophate, organophosphides)

57
Q

What is a positive Dibucaine number and what is it’s effect?

A

20 and below
prolonged succinylcholine duration by 4-8 hours

58
Q

Which muscle relaxant can cause malignant hyperthermia?

A

succinylcholine

59
Q

In what patient injury should Succinylcholine be avoided?

A

open globe injury

60
Q

What factors prolong Succinylcholine?

A

antibiotics (excluding cephalosporins)
local anesthetics
anticholinesterase agents
increased extra cellular K+
increased extra cellular Mg+
inherited pseudo cholinesterase defect
lithium

61
Q

What are potential conditions that accentuate Succinylcholine Induced Hyperkalemia?

A

muscular dystrophy
burns
paralysis
sepsis

62
Q

What subunits does extrajunctional nicotinic receptors have?

A

2 gamma subunits (replaced epsilon)
5 alpha subunits

63
Q

Do NDMRs cross the BBB and placenta?

64
Q

Which NDMRs are eliminated by the liver?

A

Rocuronium
Vecuronium

65
Q

Which NDMRs are eliminated by the kidneys?

A

Pancuronium

66
Q

Which NDMRs are eliminated by the plasma?

A

Atracurium
Cisatracurium

67
Q

Which muscle relaxants are most associated with anaphylaxis?

A

succinylcholine
rocuronium

68
Q

Which paralytic would you use in a patient with stage 3 kidney disease?

A

Cisatracurium
*least renal elimination 16%

69
Q

Which paralytic would you want to avoid in a patient with idiopathic hypertrophic subaortic stenosis?

A

pancuronium

70
Q

How is the dose adjusted for a NDMR after administration of Succinylcholine?

A

1/2 intubating dose

71
Q

What factors potentiate NDMRs?

A

aminoglycoside antibiotics
local anesthetics
volatiles
hypothermia
magnesium sulfate
lithium
loop diuretics
antiarrhythmics
dantrolene

high Mg+
low Ca+
low K+

72
Q

How does a patient with Myasthenia Gravis respond to muscle relaxers?

A

NDMR: sensitive
Succ: resistant

73
Q

How does a patient with muscle denervation injuries respond to muscle relaxers?

A

NDMR: resistant
Succ: exaggerated response

74
Q

Where is the best location to monitor onset of muscle relaxers?

A

facial nerve (orbicularis oculi or corrugator supercilii)

75
Q

Where is the best location to monitor the recovery from muscle relaxers?

A

ulnar nerve (adductor pollicis) or posterior tibial nerve (flexor hallucis brevis)

76
Q

What is the order from most to least resistant of the muscles in relation to muscle relaxers?

A

Vocal cords
Diaphragm
Orbicularis Oculi
Abdominal Rectus
Adductor Pollicis
Masseter
Pharyngeal
Extra-ocular

Vocal Cords Die Out After Adding Muscle Paralysis Externally

77
Q

What mechanism is responsible for fade with TOF stimulation when using peripheral nerve stimulators and non-depolarizing muscle relaxants?

A

antagonism of presynaptic nicotinic receptors

78
Q

What is the difference in a Phase 1 and Phase 2 block?

A

Phase 1: no fade, no post-tetanic potentiation
Phase 2: fade, post-tetanic potentiation

79
Q

What is the percentage of neuromuscular block in a patient with 4 equal twitches?

80
Q

What are the most reliable test for recovery from blockade?

A
  1. sustained jaw clench on tongue blade
  2. handgrip same as pre-induction
  3. head lift >5 seconds
  4. inspiratory force better than 40 cm H2O
81
Q

What is the reversal agent for Succinylcholine?

A

no reversal agent

82
Q

What are the steps in NMJ?

A
  1. Resting membrane potential: -90 mV
  2. Action potential reaches axon terminal, Na+ channel opens with influx of Na+ into presynaptic cell moving threshold potential to -45 mV leading to depolarization
  3. Voltage-gated Ca+ channels are triggered to open and Ca+ flows in
  4. Ca+ influx triggers synaptic vesicles to release Ach into the synaptic cleft via exocytosis
  5. Ach binds post sypnaptic nicotinic receptors causing Na+ and Ca+ to influx and K+ to efflux and pre-synaptic nicotinic receptors causing influx of Ca+
  6. The post-synaptic nerve terminal becomes more positive bringing membrane potential to -45 mV leading to depolarization
  7. Ach is broken down by Acetylcholinesterase (AchE) into acetate which diffuses away and choline which goes back to the presynaptic nerve to be recycled

Pharmacology Exam 2 (5 decks)

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