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2-Anesthesia Pharm Exam 2 > Nondepolarizing NMBDs > Flashcards

Nondepolarizing NMBDs Flashcards

1
Q

What is the action of Nondepolarizing NMBDs?

A

act as competitive antagonists by binding to the α subunits of the nAChR

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2
Q

What do the Nondepolarizing NMBDs bind to?

A

to one of the α subunits

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3
Q

What does Nondepolarizing NMBDs binding cause?

A

doesn’t open channel, blocks depolarization

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4
Q

What are the classifications of Nondepolarizing NMBDs?

A

Chemical class & Duration of action

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5
Q

What are the different chemical class of Nondepolarizing NMBDs?

A

steroidal, benzylisoquinolinium

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6
Q

In general, dose of ________ ED95 is used to facilitate tracheal intubation and dose of ______ of the ED95 is used to maintain neuromuscular blockade

A

2-3x; 10%

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7
Q

What substance was the basis for development of the benzylisoquinolinium-type muscle relaxants? What historical impact did it have?

A

Curare (South American Indians’ arrow poisons)

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8
Q

What is tubocurarine? What was its only clinical use?

A

not currently in use anymore d/t side effects,

De-fasciculating dose (priming dose) 3 mg- primary purpose when it was used

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9
Q

What Benzylisoquinolinium Compounds are currently in use? (3)

A

Atracurium, Cisatracurium, Mivacuronium

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10
Q

What is the structure of Atracurium (Tracrium)?

A

Racemic mixture of 10 stereoisomers

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11
Q

What is the metabolism of Atracurium (Tracrium)?

A

Undergoes spontaneous degradation at physiologic temperature and pH by Hoffman elimination and can also undergo ester hydrolysis

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12
Q

What does metabolism of Atracurium (Tracrium) yield (2)?

A

yielding laudanosine and a monoquaternary acrylate as metabolites

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13
Q

What is laudanosine? What is its clearance?

A

is liver dependent for clearance, with 70% excreted in bile (excretion of this metabolite is impaired in patients with biliary obstruction)

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14
Q

What is the permeability of Atracurium (Tracrium) to the BBB and CNS?

A

Crosses blood brain barrier and has CNS stimulating properties

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15
Q

What can Atracurium (Tracrium) cause the release of?

A

histamine release

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16
Q

What is a potential quality of Atracurium (Tracrium) ?

A

Neuroprotective qualities?

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17
Q

What is the intubating dose of Atracurium (Tracrium)?

A

0.5 mg/kg

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18
Q

What is the onset of Atracurium (Tracrium)?

A

2-4 minutes

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19
Q

What is the duration of action of Atracurium (Tracrium)?

A

30-60 min. (intermediate acting)

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20
Q

What is the subsequent dose of Atracurium (Tracrium)?

A

0.1-0.2 mg/kg

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21
Q

What is the chemical structure of Cisatracurium (Nimbex)?

A

Cis isomer of atracurium

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22
Q

What is the potency of Cisatracurium (Nimbex)?

A

4-5 times more potent than atracurium

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23
Q

What is the metabolism of Cisatracurium (Nimbex)?

A

Metabolized by Hoffman elimination to laudanosine and a monoquaternary alcohol metabolite

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24
Q

How much of hoffman elimination accounts for the clearance of Cisatracurium (Nimbex)?

A

Hoffman elimination accounts for 77% of the total clearance and 23% is drug is cleared through organ-dependent means (renal elimination = 16%)

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25
Q

Does Cisatracurium (Nimbex) under ester hydrolysis?

A

Does not undergo ester hydrolysis

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26
Q

Does Cisatracurium (Nimbex) cause histamine release?

A

No

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27
Q

What is the induction dose of Cisatracurium (Nimbex)?

A

0.1 mg/kg

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28
Q

What is the onset of Cisatracurium (Nimbex)?

A

2-4 minutes

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29
Q

What is the duration of action of Cisatracurium (Nimbex)?

A

30-60 min. (intermediate acting)

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30
Q

What is the subsequent dose of Cisatracurium (Nimbex)?

A

0.03 mg/kg

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31
Q

What is the only short short-acting nondepolarizing neuromuscular blocking drug available?

A

Mivacurium (Mivacron), (left the market in 2006, reintroduced in 2016)

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32
Q

What is the chemical structure of Mivacurium (Mivacron)?

A

Mix of 3 stereoisomers

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33
Q

What is the metabolism of Mivacurium (Mivacron)?

A

Metabolized by butyrylcholinesterase (plasma cholinesterase/pseudocholinesterase)

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34
Q

What is the rate of metabolism of Mivacurium (Mivacron)?

A

at about 70-88% of the rate of succinylcholine to a monoester, a dicarboxylate acid

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35
Q

What can Mivacurium (Mivacron) produced? When?

A

May produce histamine release, if administered rapidly

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36
Q

What is the intubation dose of Mivacurium (Mivacron)?

A

0.25 mg/kg given over 15 seconds

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37
Q

What is the onset of Mivacurium (Mivacron)?

A

2-3 minutes

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38
Q

What is the duration of action of Mivacurium (Mivacron)?

A

15-20 min. (short acting)

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39
Q

What is the subsequent dose of Mivacurium (Mivacron)?

A

0.1 mg/kg

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40
Q

What are the sterodial compounds (Aminosteroids) of NMBDs currently in practice?

A

Pancuronium, Vecuronium, Rocuronium

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41
Q

What is the potency of Pancuronium (Pavulon)?

A

Potent, long-acting

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42
Q

What properties does Pancuronium (Pavulon) have (2)?

A

Possesses vagolytic (increased HR) and butrylcholinesterase-inhibiting properties

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43
Q

How is Pancuronium (Pavulon) cleared? (2)

A

40-60% cleared by the kidneys & 11% excreted in the bile

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44
Q

How is Pancuronium (Pavulon) metabolized?

A

15-20% metabolized by deacetylation in the liver

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45
Q

What is true about Pancuronium (Pavulon) metabolites?

A

Metabolites are less potent as neuromuscular blockers and are excreted in urine

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46
Q

What important about the Pancuronium (Pavulon) accumulation?

A

Accumulation of the 3-OH metabolites responsible for the prolongation of the duration of the block produced by pancuronium

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47
Q

What is the intubating dose of Pancuronium (Pavulon)?

A

0.08 - 0.1 mg/kg

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48
Q

What is the onset of Pancuronium (Pavulon)?

A

2-4 minutes

49
Q

What is the duration of action of Pancuronium (Pavulon)?

A

60-90 min. (long acting)

50
Q

What is the subsequent dose of Pancuronium (Pavulon)?

A

0.015- 0.1 mg/kg

51
Q

What are the characteristics of Vecuronium (Norcuron) that makes it slightly different then Pancuronium (Pavulon)?

A
  • A slight decrease in potency
  • Loss of the vagolytic properties of pancuronium
  • Molecular instability in solution (explains shorter duration of action)
  • Increased lipid solubility (greater biliary elimination of vecuronium than pancuronium)
52
Q

What is the principle elimination of Vecuronium (Norcuron)?

A
  • Liver principal organ of elimination

- 30-40% cleared in the bile

53
Q

Vecuronium (Norcuron): Renal excretion accounts for excretion of _______ of the administered dose

A

30%

54
Q

What is the duration of action based off of for Vecuronium (Norcuron)?

A

Duration of action is dependent primarily on hepatic function and to a lesser extent, renal function

55
Q

What can contribute to prolonged neuromuscular blockade from vecuronium?

A

During prolonged administration, the metabolite 3-OH may contribute to prolonged neuromuscular blockade

56
Q

3-OH has ______ the neuromuscular blocking potency of vecuronium

A

80%

57
Q

What is the intubating dose of Vecuronium (Norcuron)?

A

0.1 mg/kg

58
Q

What is the onset of Vecuronium (Norcuron)?

A

2-4 minutes – you will have to bag/mask vent the patient until the onset of action

59
Q

What is the duration of action of Vecuronium (Norcuron)?

A

30-60 min. (intermediate acting)

60
Q

What is the subseqent dose of Vecuronium (Norcuron)?

A

0.01-0.015 mg/kg

61
Q

What is the characteristics of Vecuronium (Norcuron) storage?

A

Prepared as a powder, must be reconstituted

62
Q

What duration class is Rocuronium (Zemuron)?

A

Intermediate acting

63
Q

What is the recovery of Rocuronium (Zemuron)?

A

Moderate recovery

64
Q

What is the onset of Rocuronium (Zemuron)? What is its onset compared to other NMBD?

A
  • Faster onset than pancuronium or vecuronium

- Time to maximum block is 1.7 minutes

65
Q

What is the potency of Rocuronium (Zemuron)?

A

6 times less potent than vecuronium

66
Q

What is the primarily elimination of Rocuronium (Zemuron)? (2)

A

Primarily eliminated by the liver and excreted in the bile

67
Q

Approximately _______ of rocuronium is excreted unchanged in the urine

A

30%

68
Q

What is the storage of Rocuronium (Zemuron)?

A

At room temperature, rocuronium is stable for 60 days (is usually refridgerated)

69
Q

What is the intubating dose of Rocuronium (Zemuron)?

A

0.6 mg/kg

70
Q

What is the onset of Rocuronium (Zemuron)?

A

1-1.5 minutes

71
Q

What is the RSI dose of Rocuronium (Zemuron)?

A

0.6-1.2 mg/kg provides good to excellent intubating conditions in 45-90 seconds

72
Q

What is the duration of action of Rocuronium (Zemuron)?

A

30-60 min. (intermediate acting)

73
Q

What is the maintenance dose of Rocuronium (Zemuron)?

A

0.1-0.2 mg/kg

74
Q

What effect can two successive injections of nondepolarizing muscle relaxants have?

A

can decrease the onset of muscle paralysis

75
Q

What is the priming dose?

A

A small sub-paralytic “priming” dose is injected about 3 minutes before the full intubating dose

76
Q

What is the effect of the priming dose?

A

The priming dose, by occupying a small number of receptors, speeds the onset of effect with the subsequent dose

77
Q

What is possible to achieve by priming?

A

By priming, it is possible to achieve onset times in the range of one minute

78
Q

What can most patients show signs of following a priming dose?

A

As with defasciculation and SCh, some patients may show signs of weakness following the priming dose

79
Q

Who do we need to be careful using priming doses with?

A

Careful with vulnerable patients- become very anxious and remember this! (“I can’t breathe”)

80
Q

What is drug potency expressed in?

A

terms of the dose-response relationship

81
Q

What is potency?

A

Potency is expressed as the dose of drug required to produce an effect

82
Q

What is potency in relationship to Nondepolarizing NMBDs?

A
  • 50% or 95% depression of twitch height (ED50 and ED95)

- ED50 is a more robust parameter

83
Q

What effect does inhalational anesthetics have on nondepolarizing neuromuscular blockers.

A

Inhalational anesthetics potentiate the neuromuscular blocking effect

84
Q

What is required regarding the dose of nondepolarizing NMBDs with inhalational anesthetics?

A

Decrease in the required dosage of neuromuscular blocker and prolongation of both the duration of action of the relaxant and recovery from neuromuscular block

85
Q

What effects the magnitude of potentiate?

A

is dependent upon the duration of inhalational anesthesia, the specific inhalational agent used, and the concentration of inhalational agent used

86
Q

Rank the order of common anesthesia meds and their potentiate of non depolarizing NMBDs?

A

desflurane > sevofurane > isoflurane > halothane > nitrous oxide-barbiturate-opioid or propofol anesthesia

87
Q

What is the mechanism of action for potentation of inhalational anesthetics and non depolarizing NMBDs?

A
  • Central effect on alpha motorneurons and interneuronal synapsis
  • Inhibition of postsynaptic nicotinic acetylcholine receptors
  • Augmentation of the antagonist’s affinity at the receptor site
88
Q

What are some antibiotic examples that can potentiate neuromuscular blockade?

A

Aminoglycoside antibiotics, Polymyxins

Lincomycin and clindamycin, Tetracyclines

89
Q

What are some Aminoglycoside antibiotic examples that can potentiate neuromuscular blockade?

A

Gentamycin, Streptomycin, Tobramycin

90
Q

What is the MOA of Lincomycin and clindamycin potentiation of non depolarizing NMBDs?

A

Primarily inhibit the prejunctional release of acetylcholine and depresses postjunctional nicotinic acetylcholine receptor sensitivity to acetylcholine

91
Q

What is the activity of Tetracyclines potentiation of non depolarizing NMBDs?

A

Exhibit postjunctional activity only

92
Q

What effect does hypothermia and magnesium sulfate have on nondepolarizing neuromuscular blocking agents?

A

potentiates the neuromuscular blockade induced by nondepolarizing neuromuscular blocking agents

93
Q

What is the MOA of magnesium on potentiate nondepolarizing neuromuscular blocking agents?

A
  • Mechanism of action may be pharmacokinetic, pharmacodynamic or both
  • High magnesium concentrations inhibit calcium channels at the presynaptic nerve terminals that trigger the release of acetycholine
94
Q

What do local anesthetics have on neuromuscular block?

A

in larger doses potentiate neuromuscular block

95
Q

_________ also potentiates the neuromuscular block

A

Quinidine

96
Q

What is a factor that makes pts more resistant to nondepolarizing muscle blockers?

A

Patients receiving chronic anticonvulsant therapy

97
Q

What is the MOA of chronic anticonvulsant therapy on Decreasing Potency of Neuromuscular Blocking Agents?

A

Attributed to increased clearance, increased binding of the neuromuscular blockers to alpha1 acid glycoproteins, and/or upregulation of neuromuscular acetylcholine receptors

98
Q

What is needed for pts receiving anticonvulsant therapy and need a neuromuscular blockade?

A

Need increased doses to achieve complete neuromuscular blockade

99
Q

What is the relationship between hyperparathyroidism and hypercalecemia to atracurium?

A

In patients with hyperparathyroidism, hypercalcemia is associated with decreased sensitivity to atracurium and a resulting shortened duration of neuromuscular blockade

100
Q

What effect does increased calcium have on tubocurarine and pancuronium?

A

Increased calcium concentrations decrease the sensitivity to tubocurarine and pancuronium

101
Q

What determines the speed of onset of action to to the potency of the nondepolarizing blocker?

A

The speed of onset of action is inversely proportional to the potency of the nondepolarizing blocker

102
Q

Low potency is predictive of a _______onset

A

rapid onset (rocuronium)

103
Q

High potency is predictive of a ______ onset

A

slow onset (tubocurarine)

“Per equipotent doses: more molecules exist in solution for the lower potency drug”

104
Q

What two medications cause autonomic effects?

A

Tubocurarine & Pancurornium

105
Q

What is the autonomic effects of Tubocurarine?

A

Associated with marked ganglion blockade resulting in hypotension

106
Q

What is the autonomic effects of Tubocurarine from histamine release? (4)

A

causes flushing, hypotension, reflex tachycardia, bronchospasm

107
Q

What is the autonomic effects of Pancurornium? (2)

A
  • Direct vagolytic effect

- May stimulate catecholamine release from adrenergic nerve terminals

108
Q

What three NMBD cause histamine release?

A

Mivacurium, atracurium, and tubocuranine

109
Q

What are the clinical signs of histamine release? (4)

A

Skin flushing, decreases in blood pressure, decreases in systemic vascular resistance, increases in heart rate

110
Q

When are clinical signs of histamine release are seen?

A

when plasma concentrations of histamine increase 200-300% below baseline

111
Q

What is the duration of histamine release?

A

Short duration of 1-5 minutes, dose related

112
Q

What can occur with histamine release in those with reactive airway disease?

A

Histamine release may result in increased airway resistance and bronchospasm in patients with reactive airway disease

113
Q

What are the probabilities of Anaphylactic or anaphylactoid reactions during anesthesia?

A

estimated to occur in 1:1,000 to 1:25,000 administrations

114
Q

What is the mortality rate of Anaphylactic or anaphylactoid reactions?

A

Associated mortality rate of 5%

115
Q

What immune component is associated with anaphylactic or anaphylactoid reactions?

A

IgE mediated

116
Q

What is the most common cause of anaphylaxis during anesthesia?

A

who experienced allergic reactions: neuromuscular blocking drugs > antibiotics

117
Q

What medications are most commonly associated with Anaphylactic reactions?

A

Succinylcholine and rocuronium most frequently involved

118
Q

____________ and ________ less frequently involved in Anaphylactic reactions.

A

Pancuronium and cisatracurium

119
Q

Review Neuromuscular Blocking Agent Elimination: Summary

A

Slide 64

2-Anesthesia Pharm Exam 2 (6 decks)

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