Paralytics - Vecuronium Flashcards

1
Q

What is the recommended paralysis dose of Vecuronium?

a) 0.1 mg/kg IV based on ideal body weight (IBW)
b) 0.5 mg/kg IV based on ideal body weight (IBW)
c) 1 mg IV
d) 2 mg/kg IV based on actual body weight (ABW)

A

a) 0.1 mg/kg IV based on ideal body weight (IBW)

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2
Q

How do neuromuscular blocking drugs with quaternary ammonium groups affect renal function?

a) They cross renal tubules easily
b) They are metabolized in the renal tubules
c) Phase II block is observed in the renal tubules
d) They do not cross renal tubules

A

d) They do not cross renal tubules
(Phase II block)

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2
Q

What is the recommended defasciculating dose of Vecuronium when used in conjunction with Succinylcholine?

a) 0.1 mg/kg IV
b) 1 mg IV
c) 3 mg IV
d) 5 mg IV

A

b) 1 mg IV

1 mg IV 3 minutes before Succinylcholine

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3
Q

Which of the following statements accurately describe the pharmacokinetics Vecuronium with quaternary ammonium groups? (Select 3)

a) They are highly ionized and water-soluble
b) Their volume of distribution is limited to the extracellular fluid (ECF)
c) They readily cross the blood-brain barrier (BBB)
d) They do not cross the blood-brain barrier (BBB)

A

a) They are highly ionized and water-soluble,
b) Their volume of distribution is limited to the extracellular fluid (ECF),
d) They do not cross the blood-brain barrier (BBB)

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3
Q

What is the concentration of Vecuronium in a 10 mL syringe containing 10 mg of the drug?

a) 1 mg/mL
b) 2 mg/mL
c) 0.5 mg/mL
d) 10 mg/mL

A

a) 1 mg/mL

Concentration: 10mg in 10mL syringe= 1mg/mL

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3
Q

What percentage of Vecuronium is eliminated by the kidneys and liver, respectively?

a) 10% by kidneys and 90% by liver
b) 50% by kidneys and 50% by liver
c) 70% by kidneys and 30% by liver
d) 20% by kidneys and 80% by liver

A

b) 50% by kidneys and 50% by liver

Kane NMBD:
Hepatic metabolism
Principle organ of elimination
3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)

Renal excretion
Approx 30% appears unchanged (*70% metabolized in liver)
Renal dysfunction
Elimination ½ time prolonged

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4
Q

What is the primary mechanism of action of Veuronium? (Select 2)

a) Binds to nicotinic acetylcholine receptors at the neuromuscular junction
b) Opens monovalent cation channels
c) Prevents the opening of monovalent cation channels
d) Enhances depolarization at the neuromuscular junction

A

a) Binds to nicotinic acetylcholine receptors at the neuromuscular junction,

c) Prevents the opening of monovalent cation channels

MOA: Binds to nicotinic acetylcholine receptors at synaptic end plate and prevents opening of monovalent cation channels, thus preventing depolarization. Quaternary ammonium groups (Highly ionized, H2O sol). VD limited to ECF. No crossing BBB, renal tubules (Phase II block)

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5
Q

What is the typical onset time for Vecuronium?

a) 1-2 minutes
b) 3-4 minutes
c) 5-6 minutes
d) 7-8 minutes

A

b) 3-4 minutes

Tx Wes reference:
2-3 min

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6
Q

How is Vecuronium metabolized? Select 2

a) Vecuronium is metabolized to 3-desacetylvecuronium, which is 50% as potent as the parent drug.
b) The 3-desacetylvecuronium metabolite is further metabolized to an inactive form.
c) Vecuronium is exclusively metabolized by the kidneys.
d) The active metabolite 3-desacetylvecuronium contributes to the drug’s effect for an extended duration.

A

a) Vecuronium is metabolized to 3-desacetylvecuronium, which is 50% as potent as the parent drug,

b) The 3-desacetylvecuronium metabolite is further metabolized to an inactive form

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7
Q

What is the half-life of Vecuronium?

a) 15 minutes
b) 30 minutes
c) 45 minutes
d) 60 minutes

A

c) 45 minutes

Tx Wes reference:
duration: 45-90 min

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8
Q

How is Vecuronium primarily metabolized in the body? (Select 2)

a) Hepatic metabolism
b) Renal metabolism
c) Metabolism to 3-desacetylvecuronium
d) Metabolism to an active metabolite

A

a) Hepatic metabolism,
c) Metabolism to 3-desacetylvecuronium

Elimination: hepatic metabolism c 3-desacetylvecuronium metabolite (50% as potent), but further metabolized to inactive metabolite; 50% eliminated by kidneys and 50% elimination by liver

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9
Q

What are the potential issues with using Vecuronium in the post-anesthesia care unit (PACU)? (Select 2)

a) Prolonged neuromuscular blockade leading to hypercarbia
b) Increased risk of immediate recurarization
c) Rapid recovery of neuromuscular function
d) Vicious cycle of worsening blockade and hypercarbia

A

a) Prolonged neuromuscular blockade leading to hypercarbia,
d) Vicious cycle of worsening blockade and hypercarbia

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9
Q

Vecuronium is classified as which type of neuromuscular blocking drug? (Select 2)

a) Aminosteroid NMBD
b) Benzylisoquinolinium NMBD
c) Depolarizing NMBD
d) Non-depolarizing NMBD

A

a) Aminosteroid NMBD
d) Non-depolarizing NMBD

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10
Q

Why should Vecuronium be used with caution in patients with renal or liver impairment? (Select 2)

a) It can lead to prolonged neuromuscular blockade due to altered metabolism and elimination.
b) It has a reduced onset time in these patients.
c) It may result in recurarization due to prolonged effects.
d) It is associated with increased risk of hypercarbia in the post-anesthesia care unit (PACU).

A

a) It can lead to prolonged neuromuscular blockade due to altered metabolism and elimination,

c) It may result in recurarization due to prolonged effects

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11
Q

What considerations should be made when using Vecuronium in the ICU? (Select 2)

a) Prolonged use can lead to tolerance, reducing neuromuscular response.
b) Long-term use can result in recurarization.
c) Tolerance may lead to dysregulation of neuromuscular function.
d) Short-term use is typically sufficient for critical care situations.

A

a) Prolonged use can lead to tolerance, reducing neuromuscular response,
c) Tolerance may lead to dysregulation of neuromuscular function

C/I: Don’t use with renal/liver pts d/t prolonged effect and recurarization;

PACU hypercarbia after Vec prolongs blockade (vicious cycle);

ICU prolonged use= tolerance (Rec dysfxn/ paralysis)

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12
Q

How does acidosis affect neuromuscular blockade? (Select 2)

a) Acidosis can prolong the duration of neuromuscular blockade if it occurs after administration of NMBDs.
b) Acidosis shortens the duration of neuromuscular blockade.
c) It can enhance the neuromuscular blocking effect of NMBDs.
d) Acidosis has no impact on neuromuscular blockade.

A

a) Acidosis can prolong the duration of neuromuscular blockade if it occurs after administration of NMBDs,

c) It can enhance the neuromuscular blocking effect of NMBDs

13
Q

How does pregnancy affect the pharmacokinetics of Vecuronium? (Select 2)

a) Clearance of NMBDs is increased during the third trimester due to progesterone.
b) NMBDs have a prolonged duration of action early postpartum.
c) NMBDs have no significant changes in pharmacokinetics during pregnancy.
d) Clearance of NMBDs is reduced during the third trimester.

A

a) Clearance of NMBDs is increased during the third trimester due to progesterone,

b) NMBDs have a prolonged duration of action early postpartum

14
Q

What factors can lead to prolonged neuromuscular blockade in patients with obesity? (Select all that apply)

a) Increased volume of distribution in obese patients.
b) Decreased clearance of NMBDs due to increased adipose tissue.
c) Prolonged duration of blockade due to altered pharmacokinetics.
d) Faster elimination of NMBDs due to higher metabolism.

A

*could be A & B too

c) Prolonged duration of blockade due to altered pharmacokinetics

15
Q

Which of the following are true regarding the side effects of neuromuscular blocking drugs (NMBDs) that do not release histamine? (Select 2)

a) They do not cause histamine release.
b) They can lead to vagal input, which may affect heart rate.
c) Histamine release from NMBDs is a common side effect.

A

a) They do not cause histamine release,

b) They can lead to vagal input, which may affect heart rate,

16
Q

How might the administration of opiates interact with the effects of Vecuronium that cause vagal input? (Select 2)

a) Opiates may exacerbate the vagal effects of NMBDs, leading to bradycardia.
b) Opiates can prevent the vagal effects of NMBDs, reducing bradycardia.
c) In severe cases, vagal effects can progress from bradycardia to asystole.
d) Opiates have no impact on the vagal effects of NMBDs.

A

a) Opiates may exacerbate the vagal effects of NMBDs, leading to bradycardia,

c) In severe cases, vagal effects can progress from bradycardia to asystole

S/E: No histamine release, but also vagal input. Unchecked if opiates given (brady to asystole in some cases)

17
Q

· Paralytics Information to know

-Why you shouldn’t give sux after you’ve reversed a patient? If reversed with Neostigmine, this will cause a reduction in pseudocholinesterase activity and prolonged block. Also, reversal of a nondepolarizer will increase Ach at the synapse causing cholinergic syndrome and an increased depolarization of Succ. Possibility of phase II block

-Know how to monitor twitching in a stroke/paralyzed patient

A