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PT 1 > L17 Neuromuscular Relaxants > Flashcards

L17 Neuromuscular Relaxants Flashcards

1
Q

What are the 5 indications for neuromuscular relaxants?

A
  1. Treatment of spastic muscle conditions
  2. Relaxation of larynx for endotracheal intubation
  3. Prevent muscle contraction during ECT
  4. Relaxation of chest during mechanical ventilation
  5. Adjuvant to anesthesia during surgery
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2
Q

What do neuromuscular relaxants do?

A

Selectively block the nicotinic receptors at the neuromuscular junction

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3
Q

Describe the process of neurotransmission at NMJs.

A

ACh is released from pre-synaptic vesicles into the synapse. 2 ACh bind to nicotinic receptors. This opens cation channels and increases Na+ and K+ conductance, producing an end plate potential (EPP). EPPs are summed, leading to AP generation and propagation. The AP propagates down T-tubules, activating L-type Ca2+ channels. Ca2+ is released by ryanodine receptors; this leads to cross-bridge formation.

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4
Q

What is an action-potential dependent increase in intracellular calcium followed by a decrease due to sequestration by the SR?

A

Muscle twitch

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5
Q

What is the reduced ability to lower calcium between stimulations due to increased frequency of stimulation that leads to incomplete relaxation?

A

Clonus

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6
Q

What is a tetanic contraction?

A

No appreciable reduction in intracellular calcium between stimuli leading to a physiological muscle contraction

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7
Q

Upon what does propagation of the AP generated by AchR agonist binding depend?

A

The availability of voltage-gated Na+ channels in the resting state

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8
Q

What are the two types of neuromuscular relaxants acting on nicotinic recepotrs?

A
  1. Non-depolarizing agents (curare drugs)

2. Depolarizing agents (succinylcholine)

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9
Q

Proper skeletal muscle contraction requires what 5 things?

A
  1. ACh release
  2. Available nicotinic receptors
  3. Summation of EPPs to produce an AP
  4. Fast Na+ channels in the resting state
  5. Increased intracellular calcium
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10
Q

What is the mechanism of action of non-depolarizing drugs (curare drugs)?

A
  1. Competitive antagonist at nicotinic ACh receptors; prevents depolarization and EPPs
  2. Overcome by excess ACh through tetanic stimulation and cholinesterase inhibitors
  3. At higher concentrations, they block the channel pore and are less sensitive to excess ACh
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11
Q

Describe the clinical characteristics of curare drugs (distribution; BBB; half life, receptor reserve)

A
  1. Rapid distribution
  2. Do not cross BBB
  3. Half life depends on drug elimination: Renal > hepatic > plasma cholinesterase
  4. Large receptor reserve; thus, must occupy a large portion of receptors to prvent muscle twitch
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12
Q

What are the 5 curare drugs?

A
  1. Pancuronium
  2. Tubocurarine
  3. Vecuronium
  4. Rocuronium
  5. Mivacurium
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13
Q

The biological half-life of curare drugs is ___ (longer, shorter) than the duration of action.

A

Longer

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14
Q

The percentage of receptors that must be blocked by curare drugs before an effect is observed is directly related to ___. Describe the relative ___ in different organs.

A

Receptor reserve; Respiratory muscle and muscles of coarse movement&raquo_space; Muscles of the face and eyes (Block fine muscles first, then large limbs, then respiratory muscles)

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15
Q

What are the toxicities of non-depolarizing muscle relaxants?

A
  1. Non-analgesic

2. Apnea

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16
Q

What are the indications of non-depolarizing muscle relaxants?

A
  1. Muscle relaxation for surgical procedures
  2. Endotrachel intubation (rocuronium, mivacurium)
  3. Reduced resistance during ventilation
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17
Q

What is in important drug interaction with non-depolarizing muscle relaxants?

A

Enhances effect of inhalation anesthetics

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18
Q

What are chemical antidotes to non-depolarizing muscle relaxants?

A
  1. Cholinesterase inhibitors (neostigmine)

2. Muscarinic blockers to minimize effect of cholineserase inhibitor (glycopyrrolate)

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19
Q

What is the Phase I mechanism of action of depolarizing blocking agents?

A

Phase I: succinylcholine binds to the nicotinic receptor, causing depolarization with sustained contractions. Plasma cholinesterase is not available at the synapse, therefore depolarization is prolonged. Voltage-gated Na+ channels are inactivated and cannot regain their resting state until the membrane is repolarized. No further AP can be propagated, resulting in flaccid paralysis.

20
Q

What is the Phase II mechanism of action of depolarizing blocking agents?

A

Occurs after prolonged exposure to succinylcholine. The membrane repolarizes. Despite this, it remains desensitized.

21
Q

What augments Phase I blockage?

A

Cholinesterase inhibitors

22
Q

Compare the onset of action of depolarizing and non-depolarizing drugs.

A

Depolarizing drugs have a more rapid onset of action than non-depolarizing agents

23
Q

What metabolizes depolarizing drugs? What happens if there is a genetic variant of this metabolic agent?

A

Plasma cholinesterase; prolongation of drug action

24
Q

How is the action of depolarizing drugs terminated?

A

Diffusion of drug away from motor end plate

25
Q

What are the clinical manifestations of depolarizing drugs?

A

Muscle fasciculations (arm, neck, leg, diaphragm) followed by neuromuscular blockade

26
Q

What are the indications of depolarizing agents?

A
  1. Endotracheal intubation

2. Suppression of muscle contraction during ECST

27
Q

What are the toxicities of depolarizing agents?

A
  1. Non-analgesic
  2. Apnea
  3. Hyperkalemia immediately after burns/several days after widespread tissue injury (due to K+ release from motor endplate)
28
Q

What are the contraindications of depolarizing agents?

A
  1. Family history of malignant hyperthermia
29
Q

What are the antidotes to depolarizing agents (Phase I and Phase II)?

A

Phase I: time for diffusion

Phase II: cholinesterase inhibitors

30
Q

What are the indications of spasmolytic drugs?

A

Heightened skeletal muscle tone due to:

  1. Release from inhibitory supraspinal control
  2. Increased activity of facilitory pathways
  3. Increased excitability of alpha and gamma motor systems
31
Q

What is the goal of spasmolytic therapy?

A
  1. Reduce 1a afferent-mediated stretch reflex

2. Enhance activity of inhibitory internuncial neurons

32
Q

What are the 4 spasmolytic drugs?

A
  1. Baclofen
  2. Benzodiazepines (diazepam, clonazepam)
  3. Tizanidine
  4. Dantrolene
33
Q

What is the mechanism of action of Baclofen?

A

Direct agonist of GABA B receptors expressed on excitatory 1a afferent nerve terminals; activation of these receptors inhibits N-type Ca2+ channels and thus NT release from 1a-afferents; also reduces substance P release in the spinal cord

34
Q

What are the indications of baclofen?

A
  1. Multiple sclerosis
35
Q

What are the toxicities of baclofen?

A
  1. Drowsiness
36
Q

How can baclofen side effects be mitigated?

A

Intrathecal administration

37
Q

What is the mechanism of action of benzodiazepines?

A

Positive allosteric modulators of GABA A receptors, increases GABA-mediated Cl- influx, leading to pre-synaptic inhibition

38
Q

What are the indications of benzodiazepines?

A
  1. Spinal spasticity

2. MS

39
Q

What are the toxicities of benzodiazepines?

A

Sedation and drowsiness

40
Q

What is the mechanism of action of tizanidine?

A

Alpha-2 adrenergic agonist, mediates pre- and post-synaptic inhibition in SC

41
Q

What are the indications of tizanidine?

A
  1. MS

2. Spinal spasticitiy

42
Q

What are the toxicities of tizanidine?

A
  1. Drowsiness

2. Hypotension

43
Q

What is the mechanism of action of dantrolene?

A

Blocks Ca2+ release from SR of skeletal muscle

44
Q

What are the indications of dantrolene?

A
  1. Spasticity due to stroke, SC injury, MS, or cerebral palsy
  2. Malignant hyperthermia
45
Q

What are the toxicities of dantrolene?

A
  1. Muscle weakness

2. Sedation

PT 1 (34 decks)

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