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EDAIC Online course (BCSAC 2021) > Neuromuscular blocking agents > Flashcards

Neuromuscular blocking agents Flashcards

1
Q

Motor neurons?

A
  1. Ventral horn of spinal cord - Cell body
  2. Axons encapsulated in myeline sheeth to speed up nerve conduction
  3. Nodes of Ranvier facilotate saltatory conduction. Increase in conduction speed
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2
Q

NMJ?

A
  1. Contains; pre-synaptic terminal(nerve), synaptic cleft (20nm) & post synaptic receptor (Muscle)
  2. Pre-synaptic Ach release + Binding to post-synaptic nicotinic Ach receptors.
  3. The AchR are neurotransmitters-gated channels opens for 1ms
  4. Influx of sodium and efflux of potassium
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3
Q

Pre-synaptic nerve terminals ?

A
  1. They contain schwann cells (Structural function, nerve homeostasis & reinnervation)
  2. Neuronal Ach receptors (Prejunctional nicotinic receptors, 5 subunits, positive feedback role)
  3. Actylcholine
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4
Q

Acetylcholine formation?

A
  1. Acetyl-CoA + Choline

2. About 2 pools - Reserve vesicles (20%) & readily released vesicles (80%).

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5
Q

Sequence at pre-synaptic terminal ?

A
  1. Nerve impulses activate sodium channels
  2. Activation of P-type voltage-dependent calcium channels
  3. Influx of calcium into the cell
  4. Acetylcholine vesicles released
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6
Q

Synaptic cleft?

A
  1. Its about 20-50nm

2. Contains acetylcholinesterase - Ionic site, esteratic site (serine), hydrolysis (10000 molecules)

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7
Q

Post-junctional cleft?

A
  1. Consists folds and crests
  2. Folds: Very high density of Ach receptors
  3. Crests: Voltage gated sodium channels
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8
Q

Acetylcholine receptors?

A
  1. Nicotinic
  2. About 50million AchR/crest
  3. Protein of 5 polypeptide subunits in ring structre forming ionic channel
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9
Q

Types of Acetylcholine receptors?

A
  1. Mature/adult junctional AchR

2. Immature/fetal extrajunctional AchR

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10
Q

Mature/adult junctional AchR?

A
  1. Consists - 2-alpha, 1-beta, 1-delta & 1-Epsilon
  2. High conductivity
  3. Very short opening (1ms)
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11
Q

Immature/fetal extrajunctional AchR

A
  1. Consists - 2-alpha, 1-beta, 1-delta & 1-gamma
  2. Longer opening of channels
  3. Low conductance channel
  4. Develops after - Burns, sepsis, upper & lower motor neuron injury
  5. Sensitive to Sux
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12
Q

Upregulation of Immature/fetal extrajunctional AchR?

A
  1. Upper & lower motor neuron defects
  2. Prolonged chemical denervation (NMB, MgSO, clostridial toxins)
  3. Direct muscle trauma, tumour or inflammation
  4. Thermal injury
  5. Disuse atrophy
  6. Severe infection

All the above could upregulate AchR

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13
Q

Types of NMB drugs according to mechanism of action?

A
  1. Preventing Ach release (MgSO, aminoglycosides)
  2. Preventing Ach synthesis (Hemicholinum)
  3. Depleting Ach stores (Tetanus toxin)
  4. Blocking Ach receptors (rocuronium, atracurium)
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14
Q

Ideal NMB agent?

A

See picture..

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15
Q

Suxamethonium?

A
  1. It is 2 acetylcholine molecules joined by ester linkage
  2. About 10% excreted in urine and minimally hepatically metabolised
  3. Hydrolysed by plasma cholinesterase
  4. Causes depolarization of receptors
  5. Onset 60s, duration 2-3mins
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16
Q

Side effect of suxamethonium?

A
  1. Myalgia
  2. Cardiac arrhythmia
  3. Hyperkalaemia
  4. Increase IOP
  5. Anaphylaxis & MH
17
Q

Contraindications of Suxamethonium?

A
  1. Severe muscle trauma
  2. Burns > 24 hours - 18 months
  3. Muscle disease
18
Q

Non-depolarizing agents?

A

Aminosteroids and Benzylquinolinums

  1. Do not alter structural conformity of the AchR
  2. Reversible binding to alpha subunit via quaternary ammonium group
  3. Highly ionised, water soluble drugs, distributed in plasma and ECF - Small Vd
19
Q

Atracurium?

A
  1. About 0.5mg/kg, onset 2.5mins, lasting 20-35mins
  2. metabolised by ester hydrolysis (60%) & Hoffman degradation (40%)
  3. Hoffman - pH and temperature dependent.
  4. Laudanosine as an inactive metabolite - Epileptogenic properties.
  5. May cause histamine release / anaphylaxis
  6. Associated with critical illness myopathy
  7. No direct CVS effect
20
Q

Cisatracurium? (1 of 10 isomers of atracurium)

A
  1. Dose 0.15-0.2mg/kg, onset 2-3mins, duration 20-35mins
  2. Isomer of atracurium
  3. Reduced side effect
  4. About 3-4 times more potent than atracurium
  5. Hoffman degradation - Less laudanosine produced
  6. Does not release histamine
  7. Greater CVS stability
  8. useful for critical illness infusion
21
Q

Vecuronium?

A
  1. Dose 0.1mg/kg, onset 3-4mins, duration 30-45 mins
  2. Monoquaternary amine
  3. About 30% eliminated in urine
  4. Active metabolites (hepatic deacetylation)
  5. Avoid repeated doses in renal or hepatic failure
  6. No histamine release
  7. No CVS effect
  8. Partial affinity for sugammadex
22
Q

Rocuronium? Rapid onset curonium

A
  1. Dose 0.6mg/kg, onset 1-1.5mins, duration 30-45 mins
  2. About 6-8 times less potent than vecuronium
  3. Excreted unchanged in urine (30%) and bile (50%)
  4. Dependent on hepatic function
  5. No active metabolites
  6. Minimal histamine release
  7. Mild vagolytic properties - Increases HR
  8. Painful on injection and useful for critical illness infusion
23
Q

Factors affecting duration of non-DNMB agents ?

A
  1. Concomitant use of volatile agents
  2. pH (Acidosis)
  3. Temperature (Hypothermia)
  4. Age
  5. Hypokalaemia
  6. Hypocalcaemia
  7. Myasthenia gravis
  8. Hepatic & renal diseases
24
Q

Anticholinesterases ?

A
  1. Include; Neostigmine, Edrophonium, Pyridostigmine, Organophosphorous
  2. Inhibits acetylcholinesterases
  3. Prolongs half-life of Ach
  4. Muscarinic effects
25
Q

Cyclodextrans ? Sugammadex

A
  1. About 8 oligosccharides in a cylindrical structure.
  2. Lipophilic core and hydrophilic tail
  3. Encapsulates rocuronium
  4. Sug+Roc complex excreted in urine
  5. No muscarinic effects
  6. Prolonged QT interval and bradycardia reported
26
Q

Qualitative NMB monitoring ?

A
  1. Nerve stimulator
27
Q

Quantitative NMB monitoring ?

A
  1. Mechanomyography - Ulnar nerve stimulation - Gold standard
  2. Electromyography - Measures muscle AP following nerve stimulation - influenced by local temperature & diathermy
  3. Acceleromyography - Piezoelectric sensor - Acceleration of stimulated muscle

Newton’s second law of motion - F=ma

28
Q

Site for nerve stimulation?

A
  1. Adductor pollicis - Adduction of thumb
  2. Black -ve close to wrist and red +ve proximally
  3. Facial nerve - Less accurate than ulnar nerve. (Orbicularis oculi & corrugator supercilli)
29
Q

Differential muscle sensitivity?

A
  1. Fast in central muscles - Larynx & diaphragm

2. Slower in peripheral muscles - Adductor pollicis

30
Q

Times to receovery (fastest to slowest)?

A

Diaphragm > Laryngeal muscles > Corrugator supercilli > Abdominal muscles > Orbicularis oculi > Geniohyoid muscles > Adductor pollicis muscle.

31
Q

TOF?

A
  1. Supremaximal twitch at 2Hz (4 twitches in 2 secs)
  2. Twitches are 500ms apart
  3. No fade in depolarising agent
32
Q

Phase II block?

A
  1. After > 4mg/kg of Sux
  2. Repeat doses or infusion of Sux
  3. Fade is noted
  4. Post-tetanic potentiation
33
Q

TET? Tetanus

A
  1. Repetitive stimulation at high frequency 50-200Hz for 5 secs
  2. Fade with NDNMB increases
  3. Affects presynaptic AchR
34
Q

Post-tetanic count ?

A
  1. Tetanic stimulus 50Hz for 5 secs
  2. Followed 3secs later by ST stimuli at 1Hz for 20 secs
  3. Tetanus mobilises presynaptic Ach release
  4. Potentiates response to subsequent stimulation - Postetanic facilitation
  5. Assess deep NMB
35
Q

DBS ?

A
  1. Two mini tetanic bursts @ 50Hz within 0.75 sec apart
  2. Easy to subjectively assess fade
  3. No advantage over TOF
36
Q

Physiological conditions potentiating NMB?

A

See pictures

EDAIC Online course (BCSAC 2021) (35 decks)

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