Neuromuscular blocking drugs Flashcards

1
Q

Why are these drugs used?

A

To cause muscle paralysis with intubation (esp. suxamethonium b/c fast onset + short duration) + abdominal surgery (less anaesthetia used) and to assis ventilation in intensive care

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2
Q

Competitive blockers are also known as _____ and examples are ___

A

non-depolarising curares, e.g. tubocurarine, vecuronium, pancuronium + atracurium

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3
Q

Competitive blocker characteristics

A

High affinity for nAChR’s -> long residence in binding site so ACh release can’t effect synaptic potential -> too small to elicit a.p.

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4
Q

Features of competitive block:

A
  1. Relaxation without preliminary excitation of muscles
  2. Relaxant effect antagonised by anticholinesterases
  3. Tetanic “fade” more pronounced
  4. Myastenia gravis patients (autoimmune loss of ACh receptors) normally sensitive
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5
Q

Why may a cholinesterase blocker be used against a competitive blocker?

A

Reverse the administration of a competitive blocker as the duration of these blockers is quite long

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6
Q

Only example of a depolarising blocker

A

Suxamethonium = agonist of nAChr

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7
Q

How is suxamethonium different to ACh

A

Resistant to hydrolysis by local cholinesterase so can bind and rebind to receptor -> sustained depol of endplate muscle fibre

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8
Q

Why does mucle fibre membrane become inexcitable after initial a.p. with suxamethonium

A

Na channels around endplate inactive can’t generate ap

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9
Q

Features of depolarisation block:

A
  1. Initial fasciculation -> endplate depol. causes excitation of muscle fibres -: post-op muscle pain
  2. Block not relieved by anticholinesterases
  3. Myasthenia gravis patients insensitive to blocking action
  4. Action at endplate causes release of K+ from muscle cells -> hypokalaemia
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10
Q

Why can K+ release from suxamethonium be dangerous?

A

If plasma K+ already high (in severe burns or crush injuries) or if K+ release enhanced (disease/ injuries causing denervation)

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11
Q

Suxamethoniums relationship with cholinesterase

A

CHE from PLASMA. so action lasts only 5 mins

- If plasma CHE level low, action can be prolonged to several hours

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12
Q

Causes of low plasma CHE

A

Genetic abnormality due to mutation or liver disease, malnutrition or use of anticholinesterase drugs

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13
Q

What terrible side effect can be seen if suxamethnoium is used with GA’s in a susceptible patient and why are they susceptible

A

Malignant hyperthermia, someone with a mutation in calcium release channel on SR since calcium release produces persistent muscle spasm and hyperthermia

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14
Q

3 compounds that block cholinergic transmission

A
  1. Botulinum toxin
  2. hemincholinium
  3. streptomycin
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15
Q

Botulinum toxin origins

A

High molecular weight protein produced by an anaerobic bacillus (clostridium botulinum) which can grow in badly tined food -> rare but highly dangerous cause of food poisoning

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16
Q

Potency of botulinum toxin

A

Letal dose 70. ig and its effects are long lasting (weeks)

17
Q

Botulinum toxin mech of action and uses

A

Blocks release of ACh at NMJ and ganglia without affecting postsynaptic mech’s -: prolonged relief of muscle spas min dystonia in severe localised excessive sudoration

18
Q

Hemicholinium characteristics

A
  • Structurally similar to choline
19
Q

Hemicholinium mech of action and uses

A
  • competitively inhibits uptake of choline by cholinergic nerve terminals
  • > active, carrier-mediated transport
  • > causes terminals to run short of choline, so ACh synthesis can’t keep up with release
  • Action - slow -> mainly experimental
20
Q

Streptomycin is a ____ antibiotic

A

aminoglycoside

21
Q

Streptomycin means of action and side effect

A

Inhibit ACh by blocking Ca entry -> weakness as a side effect + potentiates action of neuromuscular blocking agents in anaesthetia