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Apex Review > Neuromuscular blockers 4 > Flashcards

Neuromuscular blockers 4 Flashcards

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
Q

Electrolytes that potentiate neuromuscular drugs include:

A

increased lithium
increased magnesium
decreased calcium
decreased potassium

26
Q

Drugs that potentiate neuromuscular drugs include

A

volatile anesthetics
antibiotics
antidysrhythmics
local anesthetics
diuretics
other drugs: dantrolene, cylcosporin, tamoxifen

27
Q

Which local anesthetics potentiate neuromuscular drugs?

A

probably all of them

28
Q

Which diuretics potentiate neuromuscular drugs?

A

furosemide

29
Q

What other drugs potentiate neuromuscular drugs?

A

dantrolene, cyclosporin, tamoxifen

30
Q

Which antidysrhythmics potentiate neuromuscular drugs?

A

verapamil, amlodipine, lidocaine, quinidine

31
Q

Which antibiotics potentiate neuromuscular durgs?

A

aminoglycosides
polymyxins
clindamycin
lincomycin
tetracycline

32
Q

Which inhaled anesthetic potentiates NMBs the most?

A

desflurane

33
Q

Which inhaled anesthetic potentiates NMBs the least?

A

nitrous oxide

34
Q

Which condition precludes the use of pancuronium?
a. aortic regurgitation
b. hypertrophic cardiomyopathy
c. first degree AV block
d. bradycardia

A

b. hypertrophic cardiomyopathy

35
Q

Pancuronium is a _____-

A

vagolytic (it increases heart rate)

36
Q

________, ___________, ____________ release histamine

A

succinylcholine, atracurium, & mivacurium

37
Q

The release of histamine leads to

A

tachycardia & vasodilation

38
Q

Patients who are ___________________ should not receive histamine-releasing drugs unless the clinical benefits outweighs the risk.

A

sensitive to a higher heart rate or reduced afterload

39
Q

Succinylcholine stimulates ________________ which can produce tachycardia

A

autonomic ganglia

40
Q

Succinylcholine can also stimulate ______________ which can produce bradycardia

A

M2 receptors in the SA node

41
Q

Pancuronium is unique in that it has a _________ effect in the SA node

A

vagolytic effect & stimulates the release of catecholamines

42
Q

The patient with ___________ should not receive pancuronium

A

hypertrophic cardiomyopathy

43
Q

Which neuromuscular blocker is MOST likely to cause anaphylaxis?
a. atracurium
b. cisatracurium
c. succinylcholine
d. rocuronium

A

c. succinylcholine

44
Q

__________________________ are the most common cause of perioperative allergic reactions

A

Neuromuscular blockers

45
Q

Which NMBs are associated with the highest incidence of anaphylaxis?

A

succinylcholine & rocuronium

46
Q

Do neuromuscular blocker drugs have cross-sensitivity?

A

yes, may occur in up to 70% of those who have experienced a previous allergic response

47
Q

How do allergic reactions develop as a result of NMBs?

A

the structures of NMBs contain one or more antigenic quaternary ammonium groups that interact with IgE causing mast cell and basophil degranulation

48
Q

It’s possible that sensitivity to any NMBs can develop following

A

exposure to soaps or cosmetics (because they contain antigenic quaternary ammonium groups)

49
Q

What enzyme is measured to diagnose an anaphylactic reaction?

A

tryptase (an elevated tryptase level reflects mast cell and basophil degranulation (peaks between 15-120 minutes after exposure

Apex Review (224 decks)

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