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Anesthesia Pharm > NMBAs > Flashcards

NMBAs Flashcards

1
Q

Which disease lead to the upregulation of extrajunctional receptors?

A

Severe sepsis

Muscular Dystrophy

Skeletal Muscle Trauma

Burns

Motor Neuron Injury (upper and lower)

Tetanus

CVA

Spinal Cord Injury

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2
Q

Why is the presence of extrajunctional receptors problematic with succinylcholine?

A

Extrajunctional receptors are way more sensitive to succ. They remain open longer and allow more sodium to enter the cell. This augments potassium leak and may lead to life threatening hyperkalemia

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3
Q

What is the primary treatment for hyperkalemia for Succinylcholine?

A

Calcium Chloride (raises the threshold potential)

Hyperventilation (create an alkalotic state to move K into the cell)

Sodium Bicarb (create an alkalotic state to move K into the cell)

Glucose + Insulin (insulin shifts K intracellularly)

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4
Q

Patients with extrajunctional receptors are sensitive to ______ and resistant to ______

A

They’re sensitive to Succinylcholine

They’re resistant to Non-depolarizers

BECAUSE there are MORE RECEPTORS for the nonedepolarizer to block

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5
Q

How long should succinylcholine be avoided if the patient has had a disease resulting in upregulation of extrajunctional receptors?

A

24-48 hours

BUT with burns it should be longer (1-2 years)

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6
Q

Which NMBA does not cause fade?

A

Succinylcholine

All the nondepolarizers produce fade

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7
Q

Why doesn’t succinylcholine produce fade?

A

Succinylcholine binds to the presynaptic receptor just like Ach would. It mobilizes the stockpile of Ach in the presynaptic cells just like Ach.

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8
Q

What causes fade?

A

In normal presynaptic cells, Ach released into the synaptic cleft binds with presynaptic receptors and mobilizes Ach stockpiles so they’re available to be released with subsequent depolarizations

Nondepolarizers BLOCK both pre and post synaptic receptor, so with each depolarization the amount of Ach in the cleft decreases

By contrast, succinylcholine AGONIZES both pre and postsynaptic alpha subunits

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9
Q

What distinguishes between a Phase 1 and Phase 2 block?

A

Phase 1 block has no fade (think succinylcholine)

Phase 2 block has no fade (think nondepolarizers)

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10
Q

There are two situations in which succinylcholine may cause a Phase 2 block:

A
  1. The dose is greater than 7-10 mg/kg
  2. It’s running as an infusion for 30-60 min
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11
Q

Which is more resistant to paralytics: central or peripheral mucles?

A

Central are more resistant

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12
Q

You should measure recovery at which muscle?

A

A peripheral one (because it will recover slower)

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13
Q

You should measure onset at which muscle?

A

A central one, because it will take longer to be affected

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14
Q

Full recovery does not occur until a TOF ratio is:

A

Greater than 0.9 at the adductor policis

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15
Q

Molecularly, Succinylcholine is made up of:

A

two acetylcholine molecules

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16
Q

What are the cardiovascular effects of Succinylcholine, and why?

A

Bradycardia (more common in children)

Tachycardia (more common in adults)

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17
Q

By how much does serum K increase with Succinylcholine administration in a normal patient?

A

0.5 - 1 mEq/L

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18
Q

How does Succinylcholine impact IOP?

A

Increase intraocular pressure

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19
Q

What should you do if you have a patient that requires RSI but has an open ocular injury?

A

At the end of the day, a traumatic or delayed intubation raises IOP more than succ

Always prioritize the airway

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20
Q

What should you do if a patient develops masseter spasm after succinylcholine?

A

Nothing, unless there are other s/s of MH

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21
Q

What’s the difference between pseudocholinesterase and acetylcholinesterase?

A

Pseudo metabolizes Succ, Mivarium, and the Ester LAs

Acetylcholinesterase metabolizes Acetylcholine ONLY

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22
Q

What are some other names for acetylcholinesterase?

A

Genuine

Type 1

True

Specific

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23
Q

What are some other names for pseudocholinesterase?

A

Butyrylcholinesterase

Type 2

False

Plasma Cholinesterase

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24
Q

Acetylcholinesterases are found:

Pseudocholinesterases are found:

A

Acetyl: the NMJ

Pseudo: the Plasma

P is for plasam

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25
Q

Where is pseudocholinesterase produced?

A

in the liver

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26
Q

What % reduction in pseudocholinesterase will cause neuromuscular dysfunction?

A

Symptoms begin at 60% reduction and are severe at 20% reduction

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27
Q

What is the role of pseudocholinesterase in the CNS?

A

It isn’t found in the CNS

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28
Q

Since succinylcholine’s duration is so short, even if it’s prolonged it usually isn’t clinically relevant. The exception is:

A

Patients with atypical pseudocholinesterase

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29
Q

What is the definitive test for atypical pseudocholinesterase?

A

The Dibucaine Test

30
Q

What is the best treatment for someone who is having a prolonged duration of succinylcholine and is suspected to have atypical pseudocholinesterase?

A

Whole blood and FFP both have pseudocholinesterase in them

BUT

the best option is just to leave to mechanically ventilated and sedated until it wears off in 4-8 hours

31
Q

Why is succinylcholine contraindicated in pediatric cases?

A

Because they could have undiagnosed muscular dystrophy, leading to a hyperkalemic rhabdomyolysis

32
Q

How is DMD inherited?

A

X linked recessive

33
Q

DMD results in the absence of ______

A

Dystrophin, which anchors actin and myosin to the cell membrane

34
Q

The absence of Dystrophin causes:

A

trauma to the sarcolemma, resulting in increased membrane permeability (lots of potassium moving out of the cell, and lots of calcium moving into it)

35
Q

Who has the highest incidence of myalgia following succinylcholine administration?

A

Young adults (women more so than men), undergoing ambulatory surgery

36
Q

Who has the lowest incidence of myalgia from succinylcholine?

A

The very young and very old

pregnant women

37
Q

How long does myalgia persist after succinylcholine use?

A

24-48 hours

38
Q

What can be done to reduce the risk of myalgia with succinylcholine?

A

NSAIDs

Lidocaine 1.5 mg/kg

Using a higher dose (rather than low dose)

39
Q

Are opioids helpful with succinylcholine myalgia?

A

no

40
Q

What amount of a nondepolarizing NMBA is required to limit fasciculations?

A

1/10 of the ED95

Must be given 3-5 minutes before

41
Q

If you want to use a nondepolarizer to prevent myalgia, how should the succinylcholine dose be adjusted?

A

Increased by 1.5-2 mg/kg

42
Q

Who should NOT receive a defasciculation dose?

A

patients with pre-existing muscle disease (like myasthenia gravis)

43
Q

Which diseases are associated with hyperkalemia from succinylcholine?

A

Guillain Barre

HyperPP

MS

44
Q

For NMBAs, the ED95 is defined as:

A

the dose at which there is a 95% decrease in twitch height

45
Q

What dose of NMBAs is required for tracheal intubation?

A

1-2x the ED95 of that drug

46
Q

There are two classes of Non-Depolarizing NMBs:

A
  1. Benzylisoquinolinium
  2. Aminosteroids
47
Q

List the Benzylisoquinolinium NMBAs

A

All of the -curiums:

Atracurium

Cisatracurium

Mivacurium

48
Q

List the Aminosteroid NMBAs

A

All of the -oniums

Rocuronium

Vecuronium

Pancuronium

49
Q

How is atracurium metabolized?

A

33% Hofmann

66% Nonspecific esterases

50
Q

Does atypical pseudocholinesterase alter atracurium metabolism?

A

NO! nonspecific plasma esterases are NOT THE SAME THING as pseudocholinesterases

51
Q

How is cisatracurium metabolized?

A

Hofmann

52
Q

How is Mivacurium metabolized?

A

Pseudocholinesterase

This is why it has such a short duration of action

53
Q

What is Hofmann elimination?

A

a base-catalyzed reaction that is dependent on pH and temperature

54
Q

What makes hofmann elimination faster?

What makes it slower?

A

Faster with alkalosis and hyperthermia

Slower with acidosis and hypothermia

55
Q

Which aminosteroid NMBA does not undergo hepatic deacetylation?

A

Rocuronium

56
Q

There are only two NMBAs that do not have metabolites:

A

Rocuronium

Mivacurium

57
Q

Which NMBA relies on renal elimination THE MOST?

A

Pancuronium (85%)

58
Q

Which NMBAs produce laudanosine metabolites?

A

Cisatracurium

Atracurium

59
Q

What drugs prolong NMBAs?

A

Volatile anesthetics

Aminoglycosides

Dantrolene

60
Q

Which inhaled anesthetic potentiates NMBAs the most?

A

Des

61
Q

What are four electrolyte disorders that potentiate neuromuscular blockade?

A

Decreased K

Decreased Ca

Increased Mg

Increased Li

62
Q

Why does hypothermia potentiate NMBA?

A

reduces the metabolism and clearance of neuromuscular blockers

63
Q

Which patients should not receive pancuronium? Why?

A

Anybody who can’t tolerate a higher heart rate

Pancuronium is vagolytic

64
Q

Which NMBAs cause histamine release?

A

SAM

Succinylcholine

Atracurium

Mivacurium

65
Q

what do cardiac M2 receptors control?

A

They’re parasympathetic

Stimulation causes bradycardia

Blockade causes tachycardia

66
Q

Which NMBAs stimulate M2 cardiac receptors?

A

Succinylcholine

67
Q

Which NMBAs blockade cardiac M2 receptors?

A

Pancuronium (moderate)

Rocuronium (slight)

68
Q

Which NMBA can cause tachycardia by stimulating the autonomic ganglion?

A

Succinylcholine

69
Q

What is the most common cause of perioperative anaphylaxis?

A

NMBAs

70
Q

There are two NMBAs that can cause anaphylaxis:

A

succinylcholine (most common)

Rocuronium

71
Q

What enzyme is measured to diagnose anaphylaxis?

A

Tryptase, which is released from mast cells during degranulation

Anesthesia Pharm (12 decks)

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