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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
What is the role of Acetylcholinesterase?
It breaks down Ach in the NMJ
26
What is the role of pseudocholinesterase?
It breaks down Succ, Mivacurium, and the ester LAs
27
What are alternate names for pseudocholinesterase?
28
What are alternate names for acetylcholinesterase?
29
Where is pseudocholinesterase produced?
in the liver
30
What effect does late-stage pregnancy have on pseudocholinesterase?
It decreases Pseudocholinesterase activity, which will prolong the effects of Succ
31
What effect does obesity have on pseudocholinesterase?
It increases pseudocholinesterase activity, which will shorten the duration of succinylcholine
32
Will a patient with myasthenia gravis have an increase or decreased response to succinylcholine?
Decreased, because there are fewer receptors and therefore getting a full fasciculation is difficult
33
Which drugs decrease pseudocholinesterase activity?
Esmolol Edrophonium Metoclopramide
34
What are five key conditions that reduce pseudocholinesterase activity?
35
What is dibucaine?
It's an amide local anesthetic that's used to test pseudocholinesterase activity
36
What does a dibucaine number of 70-80 mean?
Typical homozygous (AKA normal)
37
What does a dibucaine number of 50-60 mean?
Heterozygous variant
38
What does a dibucaine number of 20-30 mean?
Homozygous Atypical (AKA completely abnormal)
39
What is the best treatment for a patient with prolonged paralysis from succinylcholine?
Sedation, ventilation, and time
40
How long will a patient with heterozygous pseudocholinesterase deficiency remain paralyzed after receiving succinylcholine?
20-30 min
41
How long will a patient with homozygous pseudocholinesterase deficiency remain paralyzed after receiving succinylcholine?
4-8 hours
42
Which diseases increase the risk of succinylcholine-induced hyperkalemia?
43
Which disease increase sensitivity to Succinylcholine?
44
The ED95 in NMBs is defined as:
The dose at which there is a 95% reduction in twitch height
45
What dose of an NMB is required for intubation?
2-3x the ED95
46
What is the intubating dose of Cisatracurium?
0.1 mg/kg
47
What is the intubating dose of Vecuronium?
0.1 mg/kg
48
What is the intubating dose of Atracurium?
0.5 mg/kg
49
What is the intubating dose of Rocuronium?
0.6 mg/kg
50
What is the longest-acting NMB?
Pancuronium at 85 minutes!
51
What is the shortest acting NMB?
Mivacurium at 18 minutes
52
What are the two classes of non-depolarizers?
Benzylisoquinoliniums AND Aminosteroid
53
Name the benzylisoquinolinium NMBs
The -curiums
54
Name the aminosteroid NMBs
The -oniums
55
Metabolism of which drugs is less likely to be effected with renal insufficiency?
The Benzyls, because they undergo spontaneous degradation in the plasma
56
Which NMB is eliminated by Hoffman Elimination?
Cisatracurium (77%) Atracurium (30%)
57
Which NMB is metabolized by pseudocholinesterase?
Mivacurium
58
How is hoffman elimination impacted by temperature?
Alkalosis and hyperthermia: FASTER Acidosis and Hypothermia: SLOWER
59
Which NMBs produce laudanosine?
Atracurium and Cisatracurium Laudanosine can cause seizures with prolonged use
60
What is Rocuronium's primary method of elimination?
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
Which aminosteroid is primarily eliminated renally?
Pancuronium (85%)
62
Name two NMBs that don't produce any active metabolites
Rocuronium and Mivacurium
63
How does serum calcium impact NMB potentiation?
Hypocalcemia increases potentiation (no calcium, no contraction)
64
How does serum lithium impact NMB potentiation?
Elevated serum lithium increases NMB potency
65
How does magnesium impact NMB potentiation?
An increase in Mg competes with Ca, resulting in less Ach mobilization in the presynaptic nerve terminals
66
How does serum potassium impact NMB potentiation?
Just like Ca. Decreased K means increased paralysis
67
Which inhaled anesthetic potentiates paralysis the most?
Desflurane
68
Which NMBs cause histamine release?
Succinylcholine Atracurium Mivacurium
69
What are the cardiovascular effects of Pancuronium?
It has a vagolytic effect. It inhibits M2 receptors in the heart, causing tachycardia and catecholamine release
70
Which patients absolutely should not receive Pancuronium?
Patients with HOCM
71
What is the most common cause of allergic reactions in the OR?
NMBs
72
Which NMBs have the highest rates of anaphylaxis?
Succ and Roc
73
What serum lab value is used to assess an allergic reaction?
Tryptase levels
74
Exposure to _______ can increase the risk of sensitivity to NMBs
Soaps or cosmetics. Someone who has a lot of allergies to topical things may be more at risk
75
There are three AchE inhibitors that are used to reverse NMBs:
Edrophonium Neostigmine Pyridostigmine
76
AchE inhibitors reverse the effects of NMBs in two ways:
Enzyme Inhibition Presynaptic Effects
77
AchE breaks Ach into:
Acetate and Choline
78
How do AchE inhibitors impact pseudocholinesterase?
Neostigmine and Pyridostigmine inhibit pseudocholinesterase Edrophonium does not
79
What would happen if you gave succinylcholine after reversing Roc with Neostigmine?
The effect of the succ would be prolonged, because it inhibits Pseudocholinesterase
80
Edrophonium is best paired with _______
Atropine
81
Glycopyrrolate is best paired with ________
neostigmine or pyridostigmine
82
What is the dose of edrophonium?
0.5 - 1 mg/kg
83
What is the dose of neostigmine?
0.05 mg/kg
84
What is the dose of pyridostigmine?
0.1 - 0.3 mg/kg
85
What is the onset time of edrophonium?
1-2 minutes
86
What is the onset time of neostigmine?
5-15 min
87
What is the onset time of pyridostigmine?
10 - 20 min
88
Should the dose of AchE inhibitors be increased in patients with renal failure?
No. Renal failures prolongs the MOA for both NMBs and AchE inhibitors, so you can dose them the same
89
What is the dose of intrathecal neostigmine?
50-100 mcg
90
What are the side effects of intrathecal neostigmine?
Nausea, vomiting, prolonged sensory and motor block
91
Which AchE decreases postoperative shivering?
Physostigmine It actually works better than demerol or clonidine
92
What are the general side effects of AchE inhibitors?
Bradycardia Bronchoconstriction Nausea Vomiting Miosis
93
If you reversed a patient with sugammadex, when can you re-paralyze with Rocuronium?
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
There is only one AchE inhibitor that crosses the BBB:
Physostigmine You can give this for symptomatic confusion from scopolamine

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