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Pharmacology > Skeletal Muscle Relaxants > Flashcards

Skeletal Muscle Relaxants Flashcards

1
Q

Types of Skeletal Muscle Relaxants

A

Neuromuscular blockers

  • Antagonists/ Non-depolarizing blockers
  • Agonists/ Depolarizing blockers

Spasmolytics

  • Chronic spasm agents
  • Acute spasm agents
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2
Q

Non-depolarizing blockers (types & names)

A
  1. Benzylisoquinolines
    - Tubocurarine
    - Atracurium
    - Cisatracurium
    - Mivacurium
  2. Ammonio Steroids
    - Pancuronium
    - Rocuronium
    - Vecuronium
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3
Q

MOA of Non-depolarizing Blockers

A

Competitive antagonists

  • causes motor weakness –>
  • skeletal muscles become totally flaccid & inexcitable to stimulation
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4
Q

Reversal of Non-depolarizing antagonists actions

A

Inc conc. of ACh in synapse

  • Neostigmine
  • Edrophonium
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5
Q

Classification of Non-depolarizing Muscle relaxants based on Duration of Action

A

Short-acting
- Mivacurium

Intermediate-acting

  • Atracurium
  • Cisatracurium
  • Rocuronium
  • Vecuronium

Long-acting

  • Tubocurarine
  • Pancuronium
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6
Q

Excretion of Non-depolarizing blockers

A
  1. Kidney – Long Half-life – Long Duration of Action

2. Liver – Short Half life – Short Duration of Action

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7
Q

Elimination mechanism & DOA of Benzylisoquinolones

A
  1. Mivacurium - Plasma pseudocholinesterase - 15 mins
  2. Atracurium - Enzymatic & Non-enzymatic ester hydrolysis - 45 mins
  3. Cisatracurium - Spontaneous (80%) & renal - 45 mins
  4. Tubocurarine - Renal & hepatic - 80 mins
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8
Q

Elimination mechanism & DOA of Ammonio steroids

A
  1. Rocuronium - Hepatic (80%) & Renal - 30 mins
  2. Vecuronium - Hepatic (80%) & Renal - 45 mins
  3. Pancuronium - Renal (80%) & Hepatic - 90 mins
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9
Q

Metabolism & AEs of Atracurium

A

Metabolite - Laudanosine

  • Hypotension
  • Seizures
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10
Q

Metabolism & AEs of Cisatracurium (Stereoisomer of Atracurium)

A

Metabolite = Laudanosine (much less than Atracurium)
- less histamine release

Replaced Atracurium in clinical practice

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11
Q

Metabolism of Mivacurium

A

Hydrolysis (inactivation) by Butyrylcholinesterase

  • not dependent on kidney or liver
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12
Q

Metabolism & uses of Rocuronium

A
  • Most rapid onset non-depolarizing blockers

- Used as an alternative to Succinylcholine for rapid sequence intubation

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13
Q

Depolarizing blockers (names)

A

-Succinylcholine (2 ACh molecules linked end-to-end)

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14
Q

MOA of Succinylcholine

A

Activates Nicotinic receptors –> depolarization of junction –> Unresponsiveness to additional impulses

  • Fasciculations
  • Flaccid paralysis
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15
Q

Time of onset & Duration of action of Succinylcholine

A

Time of onset = < 1 min

Duration of action = 5-10 mins (bc of rapid hydrolysis)

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16
Q

Metabolism/ Hydrolysis of Succinylcholine

A

Rapid hydrolysis by plasma Pseudocholinesterase

  • not effectively metabolized by Acetylcholinesterase
17
Q

Polymorphisms of Butyrylcholinesterase

A

Muscle blockade may be prolonged in pts. w/ abnormal variant of Butyrylcholineserase that uses Succinylcholine or Mivacurium.

18
Q

Treatment of pts. w/ Abnormal Butyrylcholinesterase & Succinylcholine or Mivacurium use

A

Mechanical ventilation until normal muscle function returns

19
Q

Pharmacokinetics of Neuromuscular blockers

A
  • Highly polar & poorly soluble in lipids
  • IV or IM use always (inactive if given by mouth)
  • Poor membrane penetration
  • Do not enter cells or cross the BBB
20
Q

AEs of Benzylisoquinolines

A

Hypotension

- Histamine release & ganglion blockade

21
Q

AEs of Ammonio steroids

A

Tachycardia –> Arrhythmias
- Muscarinic blockade (cardiac M2 receptors)

Pancuronium - Moderate tachycardia
- usually not a problem

22
Q

Drugs that causes Histamine release

A

Tubocurarine

Lesser extent

  • Mivacurium
  • Atracurium
23
Q

Drugs that cause Ganglion blockade

A

Tubocurarine
-block nicotinic receptors of Autonomic ganglia & adrenal medulla –>

  • Hypotension
  • Tachycardia
24
Q

AEs of Tubocurarine

A
  • Hypotension

- Tachycardia

25
Q

AEs of Depolarizing blockers (Succinylcholine)

A

Activates all autonomic cholinoceptors (nicotinic in SNS & PSNS and Muscarinic in heart)

  • Bradycardia
  • Histamine release
  • Muscle pain
  • Hyperkalemia
  • Inc. IOP
  • Inc intragastric pressure
  • Malignant hyperthermia
26
Q

CNS AEs of Muscle relaxants

A

NONE

- Unable to cross BBB

27
Q

Drugs that enhance Neuromuscular blockers

A
  • Inhaled anesthetics
  • Aminoglycosides
  • Tetracycline
28
Q

Diseases or Age that increase drug response

A
  • Myasthenia gravis

- Advanced age - Dec drug clearance

29
Q

Disease that Dec drug response

A

Severe burns & UMN disease - Proliferation of extra-junctional receptors
- Drug resistance

30
Q

Contraindication of Depolarizing Blockers

A
  1. Hx of malignant hyperthermia
  2. Hx of skeletal muscle myopathies
  3. Major burns
  4. Multiple traumas
  5. Denervation of skeletal muscles
  6. UMN injury
31
Q

Uses of Neuromuscular Blockers

A
  1. Adjuvants in surgical anesthesia

2. Succinylcholine - Endotracheal intubation & ECT

32
Q

Reversal of Non-depolarizing Blockers

A
  1. Neostigmine

2. edrophonium

33
Q

Bradycardia prevention

A
  1. Atropine

2. Glycopyrrolate

34
Q

Spasmolytic drug classes

A

Chronic use

  • CNS acting
  • Skeletal muscle acting

Acute use
- Centrally acting/ Brainstem

35
Q

Chronic use Spasmolytic Drugs (classes & names)

A
  1. Chronic use

CNS action

  • Diazepam (GABAa)
  • Baclofen (GABA agonists @ GABAb)
  • Tizanidine (a2-adrenoceptor agonist)

Skeletal muscle action

  • Dantrolene (Dec Ca release from SR)
  • Botulism toxin
36
Q

Acute use Spasmolytic drugs

A

Cyclobenzaprine (prototype)

  • centrally acting (level of brainstem)
  • use for relief of acute muscle spasm caused by local trauma or strain
  • Strong anti-muscarinic side effects
  • structurally related to TCAs

Pharmacology (16 decks)

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