Neuromuscular blockers 4 Flashcards

(49 cards)

1
Q

What are the two classes of nondepolarizing neuromuscular blockers?

A

aminosteroid compounds: rocuronium, vecuronium, pancuronium
benzylisoquinolinium compounds: atracurium, cisatracurium, mivacurium

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2
Q

Hofmann elimination is base-catalyzed reaction that’s dependent on

A

normal blood pH & temperature

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3
Q

Benzylisoquinolinium compounds undergo

A

spontaneous degradation in the plasma (Hofmann elimination & non-specific plasma esterases)

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4
Q

___________ is a metabolite of both atracurium and cisatracurium

A

Laudanosine (more so w/ atracurium)

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5
Q

Laudanosine can produce

A

seizures (CNS stimulant)

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6
Q

The termination of action for aminosteroid neuromuscular blockers depends on

A

hepatic metabolism
biliary excretion
and/or renal excretion

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7
Q

________________ compounds are better choices for patients with hepatic or renal dysfunction.

A

Benzylisoquinolinium

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8
Q

Atracurium is hydrolyzed by

A

Hofmann elimination (33%) & non-specific plasma esterases (66%)

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9
Q

Cisatracurium metabolism is dependent on

A

Hofmann elimination

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10
Q

Mivacurium is metabolized by

A

pseudocholinesterase (explains it’s relatively short DOA)

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11
Q

Hofmann elimination is faster with

A

alkalosis & hyperthermia

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12
Q

Hofmann elimination is slower with

A

acidosis and hypothermia

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13
Q

Is the metabolite laudanosine a concern in the OR?

A

no; only concerned with prolonged infusion in the ICU

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14
Q

Rocuronium is eliminated through

A

biliary excretion as an unchanged molecule

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15
Q

Vecuronium undergoes

A

hepatic deacetylation to 3-OH vecuronium (1/2 as potent as parent compound but rapidly metabolized)

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16
Q

Pancuronium undergoes

A

hepatic deacetylation to 3-OH pancuronium (1/2 as potent as parent compound)

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17
Q

Rocuronium is metabolized

A

it’s not!
eliminated via the liver >70% & renal elimination 10-25% & biliary excretion

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18
Q

Vecuronium is metabolized

A

via the liver (30-40%)

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19
Q

Pancuronium is metabolized via the

A

liver (10-20%)

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20
Q

List 4 neuromuscular blockers that undergo organ-independent elimination?

A

atracurium
cisatracurium
mivacurium
succinylcholine

21
Q

Which drugs potentiate neuromuscular blockade? select 3
a. desflurane
b. gentamycin
c. phenytoin
d. mannitol
e. dantrolene
f. hydrocortisone

A

a. desflurane
b. gentamycin
e. dantrolene

22
Q

Factors that potentiate neuromuscular blockade increase

A

the difficulty of reversal as well as the risk of residual weakness

23
Q

What are the three groups of potentiating factors for neuromuscular blockade?

A

drugs
electrolytes
patient factors

24
Q

Patient factors that potentiate neuromuscular drugs include?

A

hypothermia (decreases metabolism & clearance)
gender (women are more sensitive to the effects of NMBs)

25
Electrolytes that potentiate neuromuscular drugs include:
increased lithium increased magnesium decreased calcium decreased potassium
26
Drugs that potentiate neuromuscular drugs include
volatile anesthetics antibiotics antidysrhythmics local anesthetics diuretics other drugs: dantrolene, cylcosporin, tamoxifen
27
Which local anesthetics potentiate neuromuscular drugs?
probably all of them
28
Which diuretics potentiate neuromuscular drugs?
furosemide
29
What other drugs potentiate neuromuscular drugs?
dantrolene, cyclosporin, tamoxifen
30
Which antidysrhythmics potentiate neuromuscular drugs?
verapamil, amlodipine, lidocaine, quinidine
31
Which antibiotics potentiate neuromuscular durgs?
aminoglycosides polymyxins clindamycin lincomycin tetracycline
32
Which inhaled anesthetic potentiates NMBs the most?
desflurane
33
Which inhaled anesthetic potentiates NMBs the least?
nitrous oxide
34
Which condition precludes the use of pancuronium? a. aortic regurgitation b. hypertrophic cardiomyopathy c. first degree AV block d. bradycardia
b. hypertrophic cardiomyopathy
35
Pancuronium is a _____-
vagolytic (it increases heart rate)
36
________, ___________, ____________ release histamine
succinylcholine, atracurium, & mivacurium
37
The release of histamine leads to
tachycardia & vasodilation
38
Patients who are ___________________ should not receive histamine-releasing drugs unless the clinical benefits outweighs the risk.
sensitive to a higher heart rate or reduced afterload
39
Succinylcholine stimulates ________________ which can produce tachycardia
autonomic ganglia
40
Succinylcholine can also stimulate ______________ which can produce bradycardia
M2 receptors in the SA node
41
Pancuronium is unique in that it has a _________ effect in the SA node
vagolytic effect & stimulates the release of catecholamines
42
The patient with ___________ should not receive pancuronium
hypertrophic cardiomyopathy
43
Which neuromuscular blocker is MOST likely to cause anaphylaxis? a. atracurium b. cisatracurium c. succinylcholine d. rocuronium
c. succinylcholine
44
__________________________ are the most common cause of perioperative allergic reactions
Neuromuscular blockers
45
Which NMBs are associated with the highest incidence of anaphylaxis?
succinylcholine & rocuronium
46
Do neuromuscular blocker drugs have cross-sensitivity?
yes, may occur in up to 70% of those who have experienced a previous allergic response
47
How do allergic reactions develop as a result of NMBs?
the structures of NMBs contain one or more antigenic quaternary ammonium groups that interact with IgE causing mast cell and basophil degranulation
48
It's possible that sensitivity to any NMBs can develop following
exposure to soaps or cosmetics (because they contain antigenic quaternary ammonium groups)
49
What enzyme is measured to diagnose an anaphylactic reaction?
tryptase (an elevated tryptase level reflects mast cell and basophil degranulation (peaks between 15-120 minutes after exposure