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PHAR0002 > Neuromuscular Blockers, Other Synaptic Targets (lecture 7) > Flashcards

Neuromuscular Blockers, Other Synaptic Targets (lecture 7) Flashcards

1
Q

Why is suxamethonin useful?

A

It has the most rapid onset of any of the neuromuscular blocking drugs

It is ideal if fast onset and brief duration of action is required (e.g. in tracheal intubation)

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2
Q

Where does beta-bungarotoxin come from?

A

Snake venom (krait)

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3
Q

What is the relative potency of neuromuscular blockers compared to?

A

Tubocurarine (relative potency = 1)

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4
Q

What is the duration of action of suxamethonin?

A

Few minutes

Broken down by esterases

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5
Q

What is the difference between non-depolarising, competitive blockers (NDC) and depolarising, non-competitive blockers (DNC)?

A

NDC - act as competitive (ACh) antagonists

DNC - act as ACh receptor agonists

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6
Q

Describe the action of non-depolarising, competitive blockers

A
  1. NDC competes with ACh for binding site
  2. Decreasing [ACh] bound
  3. This decreases EPP below threshold
  4. No AP generated
  5. = transmission failure
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7
Q

Describe the action of depolarising, non-competitive blockers

A
  1. Act as ACh receptor agonists, compete with ACh and bind to receptor
  2. Generating an action potential
  3. However, they are not broken down by acetylcholinesterase
  4. Causing prolonged depolarisation of the muscle end-plate which cannot then repolarise
  5. Causing asynchronous muscle contraction
  6. Eventually the blockers directly block the channel or cause receptor desensitisation
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8
Q

What is the action of beta-bungarotoxin compared with alpha-bungarotoxin?

A

Beta enters the nerve terminal on the presynaptic site

Alpha binds irreversibly to ACh receptors ont he postsynaptic membrane - preventing ACh binding

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9
Q

What is suxamethonin used in?

A

Intubation

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10
Q

What is suxamethonin broken down by?

A

Esterases

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11
Q

What is scoline apnoea?

A

Patients with mutant esterases (genetic variation) which cannot metabolise and therefore prolong the effect of suxamethonin

It is only apparent at the end of an operation

They are kept anesthetised and ventilated in a high dependency unit until this muscle relaxant is cleared by other slower means and the patient begins breathing spontaneously.

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12
Q

What is botulinum toxin used for?

A
  1. To prevent spasticity
  2. To stop wrinkles (prevents muscle contraction in the face)
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13
Q

What is a potentiator of neurotransmitter release?

A

K+ channel blockers

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14
Q

What do K+ channel blockers cause?

A

A prolonged duration of AP
Thus increasing NT release (due to inc [Ca2+])

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15
Q

What do divalent cations do?

A

Block Ca2+ channels to prevent the release of NTs

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16
Q

What are the relative potencies of non-depolarising neuromuscular blockers compared to ?

A

Tubocurarine (relative potency =1)

17
Q

What are the 2 types of neuromuscular blockers / muscle relaxants?

A
  1. Non-depolarising, competitive blockers (NDC)
  2. Depolarising, non-competitive blockers (DNC)
18
Q

What are neuromuscular blockers?

A

Drugs that block NT release at the neuromuscular junction

19
Q

What are Decamethonium and Suxethonium used for?

A

Experimental use only

20
Q

What is the relative potency and duration of action of PANCURONIUM (NDC)?

A

RP = 5

Medium duration of action

21
Q

What is the relative potency and duration of action of VECURONIUM (NDC)?

A

RP = 3

Short-medium duration of action (<20 mins)

22
Q

What is the relative potency and duration of action of ALCURONIUM (NDC)?

A

RP = 1

Medium-long duration of action

23
Q

What is the relative potency and duration of action of ATRACURIUM (NDC)?

A

RP = 0.9

Medium duration of action

24
Q

What are 3 examples of toxins?

A
  1. Botulinum toxin
  2. Beta-bungarotoxin
  3. Tetrodotoxin
25
Q

What are 3 examples of depolarising non-competitive neuromuscular blockers (DNC)?

A
  1. Suxamethonium
  2. Decamethonium
  3. Suxethonium
26
Q

What are 3 examples of aminoglycoside antibiotics?

A
  1. Streptomycin
  2. Neomycin
  3. Kanamycin
27
Q

What are 2 examples of K+ channel blockers?

A
  1. Tetraethylammonium (TEA)
  2. 4-aminopyridine
28
Q

What er 2 examples of experimentally used (only) NDCs?

A
  1. Tubocurarine
    RP = 1
    Medium-long duration of action (20-30 mins)
  2. Gallamine
    RP = 0.2
    Medium duration of action
29
Q

How does botulinum toxin (Botox) work?

A
  1. Enters the presynaptic nerve terminal
  2. Protease destroys proteins of the nerve terminal needed for the secretory vesicles (containing neurotransmitter) to fuse with the membrane
  3. Preventing the release of neurotransmitter out of the presynaptic neurone and into the synaptic cleft
30
Q

How do you reverse the effect of NDCs?

A

Increase [ACh] by using acetylcholinesterase inhibitor to prevent the breakdown of ACh molecules

31
Q

Describe the structure of suxamethonin (example of DNC)

A

Made of 2 associated ACh molecules

PHAR0002 (20 decks)

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