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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
What is the maintenance dose for Succinylcholine?
0.1 mg/kg
26
What is the concentration of Succinylcholine?
20 mg/mL
27
What is the intubating dose for Rocuronium?
1 mg/kg
28
What is the maintenance dose for Rocuronium?
0.25 mg/kg
29
What is the concentration of Rocuronium?
10 mg/mL
30
What is the intubating dose of Vecuronium?
0.1 mg/kg 80 kg = 8 mg = 8 mL
31
What is the maintenance dose for Vecuronium?
0.01 mg/kg
32
What is the concentration of Vecuronium?
1 mg/mL
33
What is the concentration of Cisatracurium?
2 mg/mL
34
What is the dose for Neostigmine?
0.05 mg/kg *max dose of 5 mg
35
What is the concentration of Neostigmine?
1 mg/mL 1 mL per 20 kg 80 kg = 4 mL = 4 mg
36
What is the dose for Glycopyrrolate?
0.01 mg/kg
37
What is the concentration of Glycopyrrolate?
0.2 mg/mL (same mL as Neostigmine)
38
What is the dose for Sugammadex?
0-1 twitch: 4 mg/kg 2-4 twitches: 2 mg/kg immediately after NDMB: 16 mg/kg
39
What is the concentration of Sugammadex?
100 mg/mL
40
How many twitches do you need before administering Sugammadex?
minimum 1 twitch, ideally like 2 twitches
41
How is Hoffman elimination affected by blood pH and temperature?
faster with alkalosis and hyperthermia slower with acidosis and hypothermia
42
What drugs potentiate neuromuscular blockers?
volatile anesthetics antibiotics antidysrhythmics local anesthetics diuretics dantrolene cyclosporin tamoxifen
43
What electrolyte factors potentiate neuromuscular blockers?
increased Lithium increased Magnesium decreased Calcium decreased Potassium
44
Why does hypothermia potentiate neuromuscular blockade?
reduced metabolism and clearance
45
Which neuromuscular blockers block heart M2 receptors causing tachycardia?
Pancuronium and slightly Rocuronium
46
Which neuromuscular blockers stimulate heart M2 receptors causing bradycardia?
Succinylcholine
47
Which neuromuscular blockers stimulate the autonomic ganglia causing tachycardia?
Succinylcholine
48
What is the mechanism of action of extrajunctional nicotinic receptors?
stay open 4 times longer and upregulate leading to hyperkalemia
49
What are the standard subunits on a nicotinic receptor at the NMJ?
2 alpha, 1 beta, 1 delta, 1 epsilon
50
How and where is Acetylcholine synthesized?
AcetyleCoA + Choline + Choline Acetyltransferase -within the presynaptic nerve
51
How and where is Acetylcholine broken down?
Acetylcholine + water + Acetylcholinesterase -within the synapse
52
Which of the muscle relaxants are short acting?
Succinylcholine Mivacurium
53
Which of the muscle relaxants are intermediate acting?
Atracurium Cisatracurium Rocuronium Vecuronium
54
Which of the muscle relaxants are long acting?
Pancuronium
55
What are co-existing conditions that lower plasma cholinesterase?
atypical PCheE liver disease renal disease advanced age malnutrition pregnancy (high estrogen) burns neoplasm
56
What are drugs that lower plasma cholinesterase?
metoclopramide esmolol oral contraceptives MAO inhibitors cytotoxic drugs (N2 mustard & cyclophosphamide) anticholinesterase drugs (neostigmine, echothiophate, organophosphides)
57
What is a positive Dibucaine number and what is it's effect?
20 and below prolonged succinylcholine duration by 4-8 hours
58
Which muscle relaxant can cause malignant hyperthermia?
succinylcholine
59
In what patient injury should Succinylcholine be avoided?
open globe injury
60
What factors prolong Succinylcholine?
antibiotics (excluding cephalosporins) local anesthetics anticholinesterase agents increased extra cellular K+ increased extra cellular Mg+ inherited pseudo cholinesterase defect lithium
61
What are potential conditions that accentuate Succinylcholine Induced Hyperkalemia?
muscular dystrophy burns paralysis sepsis
62
What subunits does extrajunctional nicotinic receptors have?
2 gamma subunits (replaced epsilon) 5 alpha subunits
63
Do NDMRs cross the BBB and placenta?
No
64
Which NDMRs are eliminated by the liver?
Rocuronium Vecuronium
65
Which NDMRs are eliminated by the kidneys?
Pancuronium
66
Which NDMRs are eliminated by the plasma?
Atracurium Cisatracurium
67
Which muscle relaxants are most associated with anaphylaxis?
succinylcholine rocuronium
68
Which paralytic would you use in a patient with stage 3 kidney disease?
Cisatracurium *least renal elimination 16%
69
Which paralytic would you want to avoid in a patient with idiopathic hypertrophic subaortic stenosis?
pancuronium
70
How is the dose adjusted for a NDMR after administration of Succinylcholine?
1/2 intubating dose
71
What factors potentiate NDMRs?
aminoglycoside antibiotics local anesthetics volatiles hypothermia magnesium sulfate lithium loop diuretics antiarrhythmics dantrolene high Mg+ low Ca+ low K+
72
How does a patient with Myasthenia Gravis respond to muscle relaxers?
NDMR: sensitive Succ: resistant
73
How does a patient with muscle denervation injuries respond to muscle relaxers?
NDMR: resistant Succ: exaggerated response
74
Where is the best location to monitor onset of muscle relaxers?
facial nerve (orbicularis oculi or corrugator supercilii)
75
Where is the best location to monitor the recovery from muscle relaxers?
ulnar nerve (adductor pollicis) or posterior tibial nerve (flexor hallucis brevis)
76
What is the order from most to least resistant of the muscles in relation to muscle relaxers?
Vocal cords Diaphragm Orbicularis Oculi Abdominal Rectus Adductor Pollicis Masseter Pharyngeal Extra-ocular *Vocal Cords Die Out After Adding Muscle Paralysis Externally*
77
What mechanism is responsible for fade with TOF stimulation when using peripheral nerve stimulators and non-depolarizing muscle relaxants?
antagonism of presynaptic nicotinic receptors
78
What is the difference in a Phase 1 and Phase 2 block?
Phase 1: no fade, no post-tetanic potentiation Phase 2: fade, post-tetanic potentiation
79
What is the percentage of neuromuscular block in a patient with 4 equal twitches?
<70%
80
What are the most reliable test for recovery from blockade?
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
What is the reversal agent for Succinylcholine?
no reversal agent
82
What are the steps in NMJ?
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 2. Voltage-gated Ca+ channels are triggered to open and Ca+ flows in 3. Ca+ influx triggers synaptic vesicles to release Ach into the synaptic cleft via exocytosis 4. 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+ 5. The post-synaptic nerve terminal becomes more positive bringing membrane potential to -45 mV leading to depolarization 6. 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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