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Anaesthesiology > Muscle Relaxants > Flashcards

Muscle Relaxants Flashcards

1
Q

Define action potential

A

This is a certain fast transitory and propagating of the resting membrane potential

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2
Q

What are the phases of action potential?

A

Depolarization.
Overshoots.
Repolarization

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3
Q

What happens during hypopolarization?

A

This is the initial increase of the membrane, potential to the volume of the threshold, potential the threshold, potential open voltage gated sodium channels, and causes a large influx of sodium ions, leading to depolarization

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4
Q

What happens during depolarization?

A

There’s a significant increase in sodium inside the cell, causing an increase in the electro positivity of the cell leading to the overshoot phase

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5
Q

What happens during the overshoot phase of action potential?

A

The sodium permeability across the cell membrane decreases because the sodium channels begin to close. The overshoot value of the cell potential causes potassium channel voltage gates to open, which causes a large potassium efflux , decreasing the electro positivity of the cell. This is the repolarization phase.

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6
Q

What is the function of the repolarization phase of action potential?

A

Repolarization serves a purpose of restoring the resting membrane potential. It’s always leads to hyperpolarization first but soon after that, the membrane establishes the values of membrane potential resting membrane potential.

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7
Q

What is the purpose of muscle relaxants?

A

Muscle relaxation refers to the suppression of the resting muscle tone and stretch reflex

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8
Q

What are the components of motor unit?

A

Each motor nerve fiber (motor neuron), innervates several muscle fibers (muscle cells)

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9
Q

What is the name of the chemical messenger that stimulates action potentials

A

Acetylcholine

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10
Q

What’s the name of the enzyme that promotes the production of acetylcholine

A

Choline acetyltransferase

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11
Q

What effect does acetylcholine have on the post synaptic neuron?

A

It causes an influx of sodium ions leading to depolarization of the cell

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12
Q

What happens to acetylcholine after it stimulates the post synaptic neuron?

A

Acetylcholine becomes hydrolyzed by acetyl colonist, is presence within the impolite

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13
Q

Where is the major site of action of neuromuscular relaxant agents?

A

Cholinergic-nicotinic, receptors on the motor end plates

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14
Q

What are the two subgroups of neuromuscular blocking agents?

A

Nondepolarizing.
Depolarizing

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15
Q

What is the mechanism of action of nondepolarizing muscle relaxants?

A

They are competitive.
They bind reversibly with the cholinergic-nicotinic sites without opening the acetylcholine ion gated channel

This does not cause depolarization and reduces the number of receptors available for ACh to bind to and cause depolarization.

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16
Q

The action of nondepolarizing relaxants can be reversed with what compound

A

AntiAcetylcholinesterases

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17
Q

What is the MOA of antiacetylcholinesterases

A

Inhibits the hydrolysis of acetylcholine by acetylcholinesterases

The concentration of acetylcholine increases thus competing with the no. Depolarizing muscle relaxants for the receptors

You have to wait until Fasciculations are observed before administering the reversal agent

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18
Q

True or false

Both depolarizing and non depolarizing muscle relaxants are Acetycholine analogues

A

True

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19
Q

What are non-depolarizing muscle relaxants

A

Competitive neuromuscular blocking agents

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20
Q

List two groups of Non-depolarizing neuromuscular blocking agents

A

Benzylisoquinolonium compounds (Curiums)

Steroids
(Coniums)

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21
Q

Most Benzylisoquinoloniums release histamines and cause hypotension except……

A

Cisatracurium

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22
Q

What is the main side effect seen in Benzylisoquinoloniums (type of non-depolarizing neuromuscular agent)

A

Histamine release
Hypotension

Except Cisatracurium

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23
Q

True or false

Steroid non-depolarizing neuromuscular blocking agents cause histamine release and hypotension

A

False

This is seen with Benzylisoquinoloniums

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24
Q

List three examples of Benzylisoquinoloniums

A

Atracurium
Cisatracurium (NIMBEX)
Mivacurium

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25
Q

What is the pharmacological name for Nimbex and how did it get its name

A

Cisatracurium
NIMBEX- excellent neuromuscular blocker

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26
Q

Which benzylisoquinolonium compound is short acting?

A

Mivacurium (minicurium lol)

15-20mins

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27
Q

List two intermediate acting benzylisoquinoloniums

A

Atracurium 20-40 mins
Cisatracurium 40-60 mins

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28
Q

When is the onset of action of Atracurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

1.5-2mins

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29
Q

When is the onset of action of Cisatracurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

2-3 mins

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30
Q

When is the onset of action of Mivacurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

2-3mins

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31
Q

What is the duration of action of Atracurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

20-40 intermediate

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32
Q

When is the duration of action of Cisatracurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

40-60 mins intermediate

33
Q

When is the duration of action of Mivacurium
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

15-20mins - short acting

34
Q

How is Atracurium metabolized
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

Hoffman Élimination

35
Q

How is Cisatracurium metabolized
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

Hoffman Élimination

36
Q

How is Mivacurium metabolized
(A non-depolarizing muscle relaxant from the benzylisoquinolonium family)

A

Plasma Cholinesterase

37
Q

What is Hoffman Élimination?

A

Hoffman elimination is a temperature and pH-dependent process and is slowed by acidosis and hypothermia. The remainder is metabolized via ester hydrolysis by non-specific esterases in the plasma that are unrelated to pseudocholinesterase

38
Q

Should you use Atracurium in Asthmatic patients for neuromuscular blockade?

A

No, as it causes histamine release, Nimbex (Cisatracurium) should be considered instead

39
Q

Atracurium should not be used in hypertension patients, what is the alternative

A

Cisatracurium (stereoisomer of Atracurium) - as it has no effect on the BP

40
Q

List 4 advantages that Cisatracurium(Nimbex) has over Atracurium

A
  • No effect on BP (can be used in HTN)
  • No histamine release (can be used in asthma)
  • more potent
  • longer duration
41
Q

What is the name of the ONLY short-acting nondepolarizing muscle relaxant

A

Mivacurium

42
Q

List 3 steroid non-depolarizing muscle relaxants

A

Rocuronium
Vecuronium
Pancuronium

43
Q

What is the main advantage of Rocuronium?

A

It has a quick onset (1.5 mins) and can be used in Rapid Sequence Induction (just like suxamethonium)

44
Q

List two intermediate acting non-depolarizing muscle relaxants

A

Rocuronium
Vecuronium (30-40mins)

45
Q

List one long acting non-depolarizing muscle relaxants in

A

Pancuronium (90-120mins)

46
Q

What is the onset of action for Rocuronium (Steroidal non-desolating muscle relaxant)?

A

1.5mins

47
Q

What is the onset of action for Vecuronium (Steroidal non-desolating muscle relaxant)?

A

2-3mins

48
Q

What is the onset of action for Pancuronium (Steroidal non-desolating muscle relaxant)?

A

3-5mins

49
Q

How is Vencuronium metabolized

A

By the liver

50
Q

What are the systemic effects of Rocuronium and Vecuronium (non-depolarizing muscle relaxants)

A

No histamine release
No hypotension
No Tachycardia

51
Q

What are the systemic effects of Pancuronium (non-depolarizing muscle relaxants)

A

Sinus tachycardia +/- inc. BP
Little /no histamine release

52
Q

True or false

You can use Pancuronium when an increase in BP or HR is desired

A

True

(Do not use in hypertensives!)

53
Q

List the two main uses of non-depolarizing muscle relaxants

A

To facilitate tracheal intubation in non-urgent situations

Following suxamethonium to maintain muscle relaxation during surgery

54
Q

What is the reversal agent for Non-depolarizing neuromuscular relaxant

A

Neostigmine (anticholintesterase)

Although the recovery of normal neuromuscular function will eventually occur spontaneously after these drugs, it is often accelerated by the administration of an anticholinesterase is like neostigmine

55
Q

What combination of drugs are administered during the reversal of a non-depolarizing muscle relaxant?

A

Anticholinesterase
Vagolytic Agent

56
Q

List three anticholinesterases

A

Neostigmine
Pyridostigmine
Edrophonium

57
Q

List two vagolytic agents combined with anticholinesterases during the reversal of non-depolarizing agents

A

Glycopyrrolate (antisialagogue)
Atropine

58
Q

What role do vagolytic agents play when they are combined with anticholinesterases during the reversal of non-depolarizing agents

A

They are used for counteracting bradycardia caused by the increased Ach at muscarinic receptors, resulting from the anticholinesterase

59
Q

What is the mechanism of action of anticholinesterase?

A

It’s inhibits enzyme degradation of ACH in increasing ACH at nicotinic muscarinic, receptors and displaces non-polarized muscle relaxants as a competitive inhibitor.
Muscarinic effects of reversing agents include unwanted bradycardia salivation and increased bowel peristalsis that’s why we give vagal agents in conjunction

60
Q

What is the dose of Neostigmine administered when combined with anticholinesterases during the reversal of non-depolarizing agents

A

0.04-0.08 mg/kg

61
Q

What is the recommended Anticholinergic/vagolytic used with Neostigmine during the reversal of non-depolarizing agents

A

Glycopyrrolate

62
Q

What is the recommended dose of the Anticholinergic/vagolytic Glycopyrrolate used with Neostigmine during the reversal of non-depolarizing agents

A

0.2mg

63
Q

Name the only depolarizing neuromuscular relaxant that is currently used in clinical practice

A

Suxamethonium (succinylcholine-Sch)

64
Q

What is the moa of suxamethonium

A

It mimics ACh and binds to Ach receptors causing prolonged depolarization- the muscle relaxes/stops contracting BUT remains depolarized rendering it unable to be excited and contract

65
Q

There are two phases of depolarizing muscle relaxants block
Phase I and Phase II

Describe Phase I

A

This occurs when the receptors are occupied by the succinylcholine molecules, depolarization persist, muscle transmission is interrupted, and the muscle remains flaccid.

Recovery from this block depends on the washout of the succinylcholine molecules from the area and elimination from the body.

66
Q

There are two phases of depolarizing muscle relaxants block
Phase I and Phase II

Describe Phase II

A

This occurs if the phase 1 block is maintained with continuous infusion or repeated injections of a depolarizing agent is performed, and the receptors become insensitive to the normal action of acetylcholine , even after the relaxant molecules are removed from the junctional area.
Phase 2 block is reversible with anticholinesterases

67
Q

What is the intubating dose of suxamethonium in adults?

A

1.5mg/kg

68
Q

What is the hallmark presentation after the induction of a muscle relaxant

A

After induction there is a short period of muscle Fasciculations as the membrane is depolarized, followed by muscle paralysis

69
Q

What is the drug of choice used to facilitate tracheal intubation in patients likely to regurgitate and aspirate, as part of the RSI

A

Suxamethonium

70
Q

When is normal neuromuscular transmission restored when Suxamethonium is used?

A

3-6 mins
No reversing agent

However if phase II blockade is achieved antiacetylcholinesterase can be used

71
Q

When is normal neuromuscular transmission restored when suxamethonium is used ?

A

After 3-6 mins
No reversing agent

However, if phase II block is achieved anticholinesterase can be used

72
Q

How does recovery from suxamethonium occur spontaneously?

A

This is because suxamethonium is hydrolysed by the enzyme plasma cholinesterase (pseudocholinesterase)

73
Q

List 8 side effects of suxamethonium

A
  • Arrythmias
  • Hyperkalemia
  • Malignant Hyperthermia
  • Increased Intraocular pressure
  • Increased ICP
  • Increased Intragastric pressure
  • Muscle Pain and Fasciculations
  • Histamine Release
74
Q

How does suxamethonium cause hyperkalemia ?

A

Depolarization of an increased number of receptors by such May lead to massive release of potassium out of muscle cells :

Recall: Potassium is pumped out of the cells during depolarization

75
Q

Which patients are at risk for hyperkalemia when using suxamethonium

A
  • Burn patients 3weeks to 3mons after injury
  • muscle dystrophy eg: Duchene
  • Crush injury
  • Severe closed head injury
76
Q

List 5 indications for suxamethonium

A
  • assist intubation
  • increased risk of aspiration (RSI)
  • short procedure
  • Electroconvulsive therapy
  • Laryngospasm
77
Q

List 4 absolute contraindications for suxamethonium

A
  • allergic
  • positive h/o malignant hyperthermia
  • myotonia
  • high risk for hyperkalemia
78
Q

List 4 relative contraindications for suxamethonium use

A
  • h/o pseudocholinesterase deficiency
  • myasthenia gravis
  • open eye injury
79
Q

Apart from Neostigmine, list one more reversal agent for Rocuronium

A

Sugammadex

Anaesthesiology (10 decks)

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