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Anaesthesia > Muscle Relaxants > Flashcards

Muscle Relaxants Flashcards

1
Q

What enzyme breaks down acetylcholine (Ach) at the neuromuscular junction (NMJ)?

A

Acetylcholinesterase breaks down acetylcholine (Ach) at the NMJ.

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2
Q

What is the neurotransmitter at the neuromuscular junction?

A

The neurotransmitter at the neuromuscular junction is acetylcholine (Ach).

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3
Q

How is acetylcholine (Ach) formed?

A

Ach formation: Choline + acetyl co A (via choline acetyl transferase) → Ach.

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4
Q

How is acetylcholine destroyed?

A

Ach destruction: By acetylcholinesterase present in the synaptic cleft.

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5
Q

Describe the process of neuromuscular transmission.

A

Neuromuscular transmission: Depolarization of motor nerve → Ach release → Ach binds to receptors → muscle contraction.

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6
Q

What factors influence neuromuscular transmission (NMT)?

A

Factors: Prevent Ach synthesis (hemicholinium), prevent Ach release (↓ calcium, ↑ magnesium, botulism, aminoglycosides), deplete Ach stores, block Ach receptors, and block acetylcholinesterase action.

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7
Q

What are muscle relaxants?

A

Muscle relaxants are drugs used to impair neuromuscular transmission and provide skeletal muscle relaxation during anesthesia or critical care.

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8
Q

What are the indications for using muscle relaxants?

A

Indications: Facilitate tracheal intubation, ventilation, and surgical access.

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9
Q

What is the classification of depolarizing muscle relaxants?

A

Depolarizing MR: Resemble Ach, bind to receptors, cause initial depolarization (fasciculations), not metabolized by acetylcholinesterase.

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10
Q

Describe the depolarizing block mechanism of muscle relaxants.

A

Depolarizing block: Suxamethonium stimulates receptors causing fasciculations, then prevents Ach from reacting with receptors.

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11
Q

What is the classification of non-depolarizing muscle relaxants?

A

Non-depolarizing MR: Bind to Ach receptors without initial depolarization; exhibit fade and post-tetanic potentiation.

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12
Q

How is neuromuscular junction monitoring performed?

A

Monitoring NMJ: Using a peripheral nerve stimulator to assess responses to electrical stimuli.

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13
Q

What is the Train of Four (TOF) twitch test?

A

TOF twitches: 4 twitches at 2 Hz used to monitor neuromuscular block.

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14
Q

What are the TOF twitch results indicating different levels of muscle block?

A

TOF results: 3 twitches → 75% block, 2 twitches → 80%, 1 twitch → 90%, no twitch → 100% block.

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15
Q

What happens before muscle relaxants are administered?

A

Before MR administration: Ach crosses NMJ and stimulates receptors, producing full twitches.

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16
Q

What happens after a complete block with muscle relaxants?

A

After complete block: Non-depolarizing MR blocks Ach receptors, preventing further NMT, and no twitches are produced.

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17
Q

Describe the concept of “fade” in muscle relaxant usage.

A

Fade: Gradual decrease in twitch amplitude with non-depolarizing MR.

18
Q

What is post-tetanic facilitation?

A

Post-tetanic facilitation: Ach molecules increase in the synaptic cleft, enhancing subsequent twitch amplitude.

19
Q

What are the key properties of suxamethonium?

A

Suxamethonium: Fast onset, short duration, used in rapid sequence induction.

20
Q

What are the cardiovascular and muscular side effects of suxamethonium?

A

Side effects of suxamethonium: Bradycardia, fasciculations, increased intragastric pressure, hyperkalemia, malignant hyperthermia.

21
Q

How is suxamethonium metabolized?

A

Suxamethonium metabolism: By pseudocholinesterase; decreased in pregnancy, liver disease, and other conditions.

22
Q

What is the genetic enzyme defect associated with atypical pseudocholinesterase?

A

Atypical pseudocholinesterase: Genetic defect leading to prolonged apnea.

23
Q

What are the classifications of non-depolarizing muscle relaxants?

A

Non-depolarizing MR classifications: Benzylisoquinolines and aminosteroids.

24
Q

What are the key properties of atracurium?

A

Atracurium properties: CV stability, bronchospasm potential, metabolism by Hoffman’s degradation and ester hydrolysis.

25
Q

How is atracurium metabolized?

A

Atracurium metabolism: Hoffman degradation and ester hydrolysis.

26
Q

What are the key properties of cis-atracurium?

A

Cis-atracurium: Similar to atracurium but with fewer side effects and lower laudanosine production.

27
Q

What are the key properties of mivacurium?

A

Mivacurium: Rapid onset, short duration, metabolized by plasma cholinesterase.

28
Q

What are the key properties of doxacurium?

A

Doxacurium: Slow onset, long duration, used in prolonged surgeries.

29
Q

What are the key properties of pancuronium?

A

Pancuronium: Vagolytic effects, useful in shock, caution in hypertension.

30
Q

What are the key properties of vecuronium?

A

Vecuronium: CV stability, biliary and renal excretion.

31
Q

What are the key properties of pipecuronium?

A

Pipecuronium: CV stability, renal and biliary excretion.

32
Q

What are the key properties of rocuronium?

A

Rocuronium: Rapid onset, intermediate duration, reversed by Sugammadex.

33
Q

How are muscle relaxants further classified based on onset and duration?

A

Further classification: Rapid onset - Suxamethonium, Rocuronium; long duration - Pancuronium, Doxacurium.

34
Q

What agents are used to reverse the effects of muscle relaxants?

A

Reversal agents: Anticholinesterases (neostigmine) and Sugammadex.

35
Q

What are the effects of anticholinesterase drugs?

A

Anticholinesterase effects: Bradycardia, bronchospasm, increased secretions, CNS agitation.

36
Q

What is the recommended dose of neostigmine for reversal of muscle relaxants?

A

Neostigmine dose: 0.04 mg/kg, with anticholinergics like atropine or glycopyrrolate.

37
Q

How is clinical assessment of reversal of muscle relaxants conducted?

A

Clinical assessment of reversal: Head lift, mouth opening, tongue protrusion, and sustained hand grip.

38
Q

What is D-Tubocurarine, and what are its effects?

A

D-Tubocurarine: Causes histamine release, bronchospasm, ganglion blockade, and hypotension.

39
Q

Which muscle relaxants should be avoided in a hypertensive patient and why?

A

Avoid in hypertension: Pancuronium due to sympathomimetic effects; safe alternatives include atracurium or vecuronium.

40
Q

Which muscle relaxants should be avoided in an asthmatic patient, and how should residual muscle relaxants be reversed?

A

Avoid in asthma: Avoid histamine-releasing MR like atracurium; safe alternatives are rocuronium or vecuronium; reverse residual MR with neostigmine and anticholinergics.

Anaesthesia (16 decks)

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