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pharm > 10. Neuromuscular blocking drugs > Flashcards

10. Neuromuscular blocking drugs Flashcards

1
Q

what are the targets for acetylcholine at neuromuscular junctions?

A

nicotinic acetylcholine receptors on the end plate

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2
Q

what happens when nicotinic receptors are stimulated?

A
  • nicotinic receptors are ion channel linked
  1. conformational change and sodium ion influx
  2. depolarisation of the membrane (end plate potential)
  3. action potential generated when threshold is reached
  4. propagation of the AP in both directions
  5. acetylcholinesterase is bound to the basement membrane in the synaptic cleft and breaks down acetylcholine to acetate and choline
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3
Q

what are the 3 main neuromuscular blockers?

A
  • tubocurarine
  • atracurium
  • suxamethonium
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4
Q

what are the 2 main subtypes of nicotinic receptors?

A
  • ganglionic (or neuronal)

- muscle

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5
Q

describe the nicotinic acetylcholine receptor

A
  • span the membrane
  • 5 subunits
  • 2 a-subunits
  • a-subunits must bind to ACh for the receptor to be activated THEREFORE 2 ACh molecules needed to activate receptor
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6
Q

name 2 spasmolytic drugs and their actions

A
  1. diazepam - facilitates GABA transmission
  2. baclofen - GABA receptor agonist
    (3. dantrolene - reduces release of Ca2+ from SR)
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7
Q

what are diazepam and baclofen useful in?

A

some forms of cerebral palsy and spasticity following stroke

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8
Q

what is an unwanted effect of local anaesthetic?

A

muscle weakness

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9
Q

what drugs and toxins can interfere with ACh release?

A
  • neurotoxins - inhibit release of ACh

- botulinum toxin

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10
Q

where do neuromuscular blocking drugs work?

A

on the nicotinic receptors on the motor end plate (post-synaptically)

depolarising nicotinic receptor agonists - suxamethonium

non-depolarising competitive nicotinic receptor antagonists - tubocurarine, atracurium

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11
Q

what do neuromuscular blocking drugs NOT affect?

A
  • consciousness

- pain sensation

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12
Q

what should be done when giving neuromuscular blocking drugs?

A

assist respiration due to effects on the respiratory muscles

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13
Q

what is the structure of non-depolarising neuromuscular blocking drugs?

A

big, bulky molecules with restricted movement around the bonds

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14
Q

what is the structure of suxamethonium?

A

2 acetylcholine molecules linked together

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15
Q

what is the mechanism of action of suxamethonium?

A
  • causes an extended end plate depolarisation -> leads to a depolarisation block of the NMJ
  • isn’t metabolised as rapidly as ACh so will remain bound to the nicotinic receptors and will cause the receptors to quickly switch off (depolarisation block caused by overstimulation)
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16
Q

what are fasciculations and what causes them?

A

individual fibre twitches as the suxamethonium begins to stimulate nicotinic receptors, leading to flaccid paralysis

17
Q

what are the pharmacokinetics of suxamethonium?

A
  • intravenous route
  • 5min duration of paralysis
  • metabolised by pseudocholinesterase in the liver and plasma
18
Q

what are the uses of suxamethonium?

A
  • endotracheal intubation (relaxes the skeletal muscle of the airways)
  • muscle relaxant for electroconvulsive therapy (treatment for severe clinical depression)
19
Q

what are the unwanted effects of suxamethonium?

A
  • post-operative muscle pains due to fasciculations
  • bradycardia due to the direct muscarinic action on the heart
  • hyperkalaemia
  • raised intraocular pressure
20
Q

why does suxamethonium cause hyperkalaemia?

A
  • soft tissue injury/burns can lead to ventricular arrhythmias/cardiac arrest
  • during a burn/soft tissue injury you lose some of the neurones innervating the muscle and there is upregulation of the receptors in the skeletal muscle = denervation supersensitivity
  • giving suxamethonium will result in an exaggerated response leading to a bigger influx of sodium and bigger efflux of potassium
21
Q

describe tubocurarine

A
  • non-depolarising neuromuscular blocker

- naturally occurring ammonium compound (alkaloid) found in South American plant

22
Q

what is the mechanism of action of tubocurarine?

A
  • competitive nicotinic acetylcholine receptor antagonist
  • 70-80% block is necessary to achieve full relaxation of the muscle as this will ensure the end-plate potential generated will not reach the threshold
23
Q

what are the effects of tubocurarine?

A
  • same as suxamethonium
  • flaccid paralysis
  • skeletal muscles relax in a certain sequence and go back to normal in the opposite order:
    1. extrinsic eye muscles
    2. small muscles of the face, limbs, pharynx
    3. respiratory muscles
24
Q

what are the uses of tubocurarine?

A
  • relaxation of skeletal muscles during surgical operations (less anaesthetic needed)
  • permit artificial ventilation
25
Q

how can the actions of non-depolarising neuromuscular blockers be reversed?

A

anticholinesterases e.g. neostigmine (reversible anticholinesterase) to increase the [ACh] so it can outcompete

26
Q

what should be given alongside anticholinesterases?

A

atropine as anticholinesterases will increase [ACh] in all other cholinergic synapses so atropine will block the muscarinic receptor overstimulation

27
Q

what are the pharmacokinetics of tubocurarine?

A
  • intravenously given
  • does not cross BBB or placenta
  • 40-60min duration of paralysis
  • not metabolised at all
  • excreted in urine (70%) and bile (30%)
  • duration of action increases during hepatic/renal dysfunction
28
Q

what would be used instead of tubocurarine in the case of hepatic/renal impairment and why?

A

ATRACURIUM

  • chemically unstable molecule
  • 15min duration of action
  • gets hydrolysed into 2 inactive fragments due to the pH of the plasma
  • not affected by liver/kidney function
29
Q

what are the unwanted effects of tubocurarine?

A
  • ganglion block
  • histamine release from mast cells
  • hypotension (BP can drop due to ganglion blockade, histamine can act on the H1 receptors on the vasculature to cause vasodilation)
  • tachycardia (reflex in response to hypotension)
  • bronchospasm caused by histamine release
  • excessive secretions (bronchial and salivary) caused by histamine release
  • apnoea
30
Q

what are the unwanted effects of tubocurarine mainly due to?

A

ganglion blockade and histamine release from mast cells

pharm (32 decks)

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