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Apex > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

How many subunits comprise the postsynaptic nicotinic receptor at the NMJ?

A

5

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2
Q

Which subunits does acetylcholine bind to on the postsynaptic receptor?

A

Alpha and Alpha

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3
Q

How many acetylcholine molecules are required to activate postsynaptic nicotinic receptors?

A

Two, one for each alpha subunit

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4
Q

Why don’t anions pass through the pores opened during postsynaptic receptor stimulation?

A

The negative charge within the channel repels them

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5
Q

What are extrajunctional receptors?

A

Acetylcholine receptors that are dysfunctional and exist outside of the normal NMJ

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6
Q

In the event of a denervation injury, when should Succinylcholine be avoided?

A

Beginning 24-48 hours after the original injury, and extending 6-12 months. For burns, could be years if they still have contractures

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7
Q

How does the proliferation of extrajunctional receptors impact non-depolarizing NMB?

A

It makes patients less sensitive, because there are more receptors that require blocking

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8
Q

What happens when acetylcholine in the NMJ junction stimulates PREsynaptic Ach receptors?

A

It mobilizes stockpiled acetylcholine to the front line, so the cell is prepared to fire again

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9
Q

What role does calcium play in presynaptic cells?

A

Calcium influx destabilizes the proteins that hold acetylcholine in place, allowing exocytosis of acetylcholine

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10
Q

A phase one block is characterized by:

A

No post-tetanic potentiation

Constant diminished response to double burst stimulation

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11
Q

A phase two block is characterized by:

A

Fade with tetany
Prolonged duration

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12
Q

What is the best location to measure onset of blockade?

A

Orbicularis (Facial Nerve)

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13
Q

What is the best location to measure recovery from blockade?

A

Adductor Pollicis (Ulnar Nerve)

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14
Q

What are the best qualitative tests for recovery from blockade?

A

Tetany for > 5 seconds without fade

Head lift > 5 seconds

Holding tongue depressor in teeth against force

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15
Q

Central muscles are ______ resistant to paralytics than peripheral muscles

A

Central muscles are more resistant than peripheral muscles

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16
Q

Where on the body should you place the nerve stimulator to measure onset of blockade?

A
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17
Q

Where on the body should you place the nerve stimulator to measure recovery from blockade?

A
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18
Q

The genioglossus muscle doesn’t resume full function until the TOF is:

A

> 0.9!!! This means any amount of residual blockade will cause airway obstruction

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19
Q

Which response to succinylcholine is more common in adults: tachy or bradycardia?

A

Tachy in adults, because Succinylcholine mimics the effects of Ach at the SYMPATHETIC GANGLIA, causing an increase in SNS tone

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20
Q

Which response to succinylcholine is more common in pediatrics: tachy or bradycardia?

A

Bradycardia in peds
Succinylcholine stimulates M2 receptors in the SA node

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21
Q

What increases the risk of bradycardia in pediatrics?

A

Repeat doses. The reason is, it’s actually the metabolite of Succ that’s usually the culprit. Giving a repeat dose increases serum levels of the metabolite

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22
Q

If a pediatric patient requires a repeat dose of succinylcholine, what else should be given

A

Atropine or glyco

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23
Q

How much does Succinylcholine increase serum potassium levels

A

0.5-1 mEq/L for up to 10-15 min

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24
Q

Since succinylcholine increases intragastric pressure, does it increase the risk of aspiration?

A

No. It also increases LES tone, so the two cancel each other out

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25
Q

What is the role of Acetylcholinesterase?

A

It breaks down Ach in the NMJ

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26
Q

What is the role of pseudocholinesterase?

A

It breaks down Succ, Mivacurium, and the ester LAs

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27
Q

What are alternate names for pseudocholinesterase?

A
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28
Q

What are alternate names for acetylcholinesterase?

A
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29
Q

Where is pseudocholinesterase produced?

A

in the liver

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30
Q

What effect does late-stage pregnancy have on pseudocholinesterase?

A

It decreases Pseudocholinesterase activity, which will prolong the effects of Succ

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31
Q

What effect does obesity have on pseudocholinesterase?

A

It increases pseudocholinesterase activity, which will shorten the duration of succinylcholine

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32
Q

Will a patient with myasthenia gravis have an increase or decreased response to succinylcholine?

A

Decreased, because there are fewer receptors and therefore getting a full fasciculation is difficult

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33
Q

Which drugs decrease pseudocholinesterase activity?

A

Esmolol
Edrophonium
Metoclopramide

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34
Q

What are five key conditions that reduce pseudocholinesterase activity?

A
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35
Q

What is dibucaine?

A

It’s an amide local anesthetic that’s used to test pseudocholinesterase activity

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36
Q

What does a dibucaine number of 70-80 mean?

A

Typical homozygous

(AKA normal)

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37
Q

What does a dibucaine number of 50-60 mean?

A

Heterozygous variant

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38
Q

What does a dibucaine number of 20-30 mean?

A

Homozygous Atypical

(AKA completely abnormal)

39
Q

What is the best treatment for a patient with prolonged paralysis from succinylcholine?

A

Sedation, ventilation, and time

40
Q

How long will a patient with heterozygous pseudocholinesterase deficiency remain paralyzed after receiving succinylcholine?

A

20-30 min

41
Q

How long will a patient with homozygous pseudocholinesterase deficiency remain paralyzed after receiving succinylcholine?

A

4-8 hours

42
Q

Which diseases increase the risk of succinylcholine-induced hyperkalemia?

A
43
Q

Which disease increase sensitivity to Succinylcholine?

A
44
Q

The ED95 in NMBs is defined as:

A

The dose at which there is a 95% reduction in twitch height

45
Q

What dose of an NMB is required for intubation?

A

2-3x the ED95

46
Q

What is the intubating dose of Cisatracurium?

A

0.1 mg/kg

47
Q

What is the intubating dose of Vecuronium?

A

0.1 mg/kg

48
Q

What is the intubating dose of Atracurium?

A

0.5 mg/kg

49
Q

What is the intubating dose of Rocuronium?

A

0.6 mg/kg

50
Q

What is the longest-acting NMB?

A

Pancuronium at 85 minutes!

51
Q

What is the shortest acting NMB?

A

Mivacurium at 18 minutes

52
Q

What are the two classes of non-depolarizers?

A

Benzylisoquinoliniums
AND
Aminosteroid

53
Q

Name the benzylisoquinolinium NMBs

A

The -curiums

54
Q

Name the aminosteroid NMBs

A

The -oniums

55
Q

Metabolism of which drugs is less likely to be effected with renal insufficiency?

A

The Benzyls, because they undergo spontaneous degradation in the plasma

56
Q

Which NMB is eliminated by Hoffman Elimination?

A

Cisatracurium (77%)
Atracurium (30%)

57
Q

Which NMB is metabolized by pseudocholinesterase?

A

Mivacurium

58
Q

How is hoffman elimination impacted by temperature?

A

Alkalosis and hyperthermia: FASTER

Acidosis and Hypothermia: SLOWER

59
Q

Which NMBs produce laudanosine?

A

Atracurium and Cisatracurium

Laudanosine can cause seizures with prolonged use

60
Q

What is Rocuronium’s primary method of elimination?

A

It undergoes almost no metabolism in the liver. It’s eliminated as a whole molecule through biliary excretion

Only 10-25% of it is renally excreted

61
Q

Which aminosteroid is primarily eliminated renally?

A

Pancuronium (85%)

62
Q

Name two NMBs that don’t produce any active metabolites

A

Rocuronium and Mivacurium

63
Q

How does serum calcium impact NMB potentiation?

A

Hypocalcemia increases potentiation (no calcium, no contraction)

64
Q

How does serum lithium impact NMB potentiation?

A

Elevated serum lithium increases NMB potency

65
Q

How does magnesium impact NMB potentiation?

A

An increase in Mg competes with Ca, resulting in less Ach mobilization in the presynaptic nerve terminals

66
Q

How does serum potassium impact NMB potentiation?

A

Just like Ca. Decreased K means increased paralysis

67
Q

Which inhaled anesthetic potentiates paralysis the most?

A

Desflurane

68
Q

Which NMBs cause histamine release?

A

Succinylcholine
Atracurium
Mivacurium

69
Q

What are the cardiovascular effects of Pancuronium?

A

It has a vagolytic effect.

It inhibits M2 receptors in the heart, causing tachycardia and catecholamine release

70
Q

Which patients absolutely should not receive Pancuronium?

A

Patients with HOCM

71
Q

What is the most common cause of allergic reactions in the OR?

A

NMBs

72
Q

Which NMBs have the highest rates of anaphylaxis?

A

Succ and Roc

73
Q

What serum lab value is used to assess an allergic reaction?

A

Tryptase levels

74
Q

Exposure to _______ can increase the risk of sensitivity to NMBs

A

Soaps or cosmetics. Someone who has a lot of allergies to topical things may be more at risk

75
Q

There are three AchE inhibitors that are used to reverse NMBs:

A

Edrophonium
Neostigmine
Pyridostigmine

76
Q

AchE inhibitors reverse the effects of NMBs in two ways:

A

Enzyme Inhibition
Presynaptic Effects

77
Q

AchE breaks Ach into:

A

Acetate and Choline

78
Q

How do AchE inhibitors impact pseudocholinesterase?

A

Neostigmine and Pyridostigmine inhibit pseudocholinesterase

Edrophonium does not

79
Q

What would happen if you gave succinylcholine after reversing Roc with Neostigmine?

A

The effect of the succ would be prolonged, because it inhibits Pseudocholinesterase

80
Q

Edrophonium is best paired with _______

A

Atropine

81
Q

Glycopyrrolate is best paired with ________

A

neostigmine or pyridostigmine

82
Q

What is the dose of edrophonium?

A

0.5 - 1 mg/kg

83
Q

What is the dose of neostigmine?

A

0.05 mg/kg

84
Q

What is the dose of pyridostigmine?

A

0.1 - 0.3 mg/kg

85
Q

What is the onset time of edrophonium?

A

1-2 minutes

86
Q

What is the onset time of neostigmine?

A

5-15 min

87
Q

What is the onset time of pyridostigmine?

A

10 - 20 min

88
Q

Should the dose of AchE inhibitors be increased in patients with renal failure?

A

No. Renal failures prolongs the MOA for both NMBs and AchE inhibitors, so you can dose them the same

89
Q

What is the dose of intrathecal neostigmine?

A

50-100 mcg

90
Q

What are the side effects of intrathecal neostigmine?

A

Nausea, vomiting, prolonged sensory and motor block

91
Q

Which AchE decreases postoperative shivering?

A

Physostigmine

It actually works better than demerol or clonidine

92
Q

What are the general side effects of AchE inhibitors?

A

Bradycardia
Bronchoconstriction
Nausea
Vomiting
Miosis

93
Q

If you reversed a patient with sugammadex, when can you re-paralyze with Rocuronium?

A

If they received less than 4 mg/kg:

5 min - 4 hrs: 1.5 mg/kg Roc

> 4hrs: 0.6 mg/kg Roc

If they received 16 mg/kg, you have to wait 24 hours

94
Q

There is only one AchE inhibitor that crosses the BBB:

A

Physostigmine

You can give this for symptomatic confusion from scopolamine

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