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LCRS Pharmacology and Therapeutics > Neuromuscular blocking drugs > Flashcards

Neuromuscular blocking drugs Flashcards

1
Q

How is acetylcholine synthesised?

A

From acetyl CoA and Choline by choline acetyltransferase (CAT)

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2
Q

Where is CAT only found?

A

Cholinergic nerve terminals

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3
Q

What is the end plate potential?

A

The depolarisation of the membrane that occurs due to a receptor being stimulated and influx of sodium ions

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4
Q

The end plate potential is graded, what does that mean?

A

The size of the potential depends on how much acetylcholine is released and how many receptors are stimulated- once it reaches a threshold it will generate an action potential

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5
Q

Where is acetylcholinesterase found?

A

In the synaptic cleft bound to the basement membrane

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6
Q

What does acetylcholinesterase break acetylcholine down into?

A

Acetate and choline

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7
Q

What are the three main neuromuscular blockers?

A

Tubocurarine
Atracurium
Suxamethonium

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8
Q

What are the two main subtypes of nicotinic receptors?

A

Ganglionic (or neuronal)

Muscle

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9
Q

What do spasmolytics do?

A

Potentiate the actions of GABA

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10
Q

Name two spasmolytics and what they do?

A

Diazepam- facilitates GABA transmission

Baclofen- GABA receptor agonist

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11
Q

What conditions are spasmolytics useful for?

A

Some forms of cerebral palsy and spasticity following stroke

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12
Q

What do local anaesthetics act on?

A

Conduction of action potentials down motor neurones (use leads to muscle weakness)

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13
Q

What toxins interfere with acetylcholine release and how?

A

Neurotoxins- Toxic and lethal because they inhibit release of acetylcholine and block contraction of respiratory skeletal muscle causing death
Botulinum is the same

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14
Q

Which two types of drugs act on depolarisation of the motor end plate?

A

Depolarising- Suxamethonium

Non-depolarising- Tubocurarine

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15
Q

How does dantrolene work?

A

It is a spasmolytic that works in the muscle fibres themselves- this inhibits calcium release in the muscle fibre

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16
Q

Where do neuromuscular blocking drugs act?

A

Post-synaptically on nicotinic receptors on the motor end plate

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17
Q

If they are non depolarising, what sort of neuromuscular blocking drug are they?

A

Competitive nicotinic receptor antagonists e.g. tubocurarine and atracurium

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18
Q

If they are depolarising, what sort of neuromuscular blocking drug are they?

A

Nicotinic receptor agonists e.g. suxamethonium

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19
Q

What effect do these drugs have on consciousness and pain sensation?

A

None

20
Q

What do you always have to do when giving these drugs?

A

Assist respiration due to effect on respiratory muscles

21
Q

What is the structure of non-depolarising drugs like?

A

Big, bulky molecules with relatively restricted movement around the bonds

22
Q

What is the structure of suxamethonium like?

A

Made up of two acetylcholine molecules that are linked together

23
Q

What does the difference in structure between suxamethonium and non-depolarising drugs mean?

A

Suxamethonium is such more flexible and allows rotation

As it is made up of two acetylcholine units, one suxamethonium can bind to two alpha subunits and stimulate the receptor

24
Q

How does suxamethonium work?

A

It causes a phase 1 block- extended endplate depolarisation (overstimulation) which leads to a depolarisation block of the NMJ

25
Q

Suxamethonium causes fasciculations, what are these?

A

Individual fibre twitches as the suxamethonium begins to stimulate muscle fibres- this leads to flaccid paralysis- no muscle tone

26
Q

How is suxamethonium administered?

A

IV

27
Q

How long does the paralysis due to suxamethonium last?

A

5 minutes

28
Q

What is suxamethonium metabolised by?

A

Pseudocholinesterase in liver and plasma

29
Q

What is suxamethonium used for?

A

Endotracheal intubation- relaxes skeletal muscle of airways

Muscle relaxant for electroconvulsive therapy- treatment for severe clinical depression

30
Q

What are the unwanted effects of suxamethonium?

A

Post-op muscle pains due to fasciculations
Bradycardia- direct muscarinic effect on heart
Hyperkalaemia
Raised intraocular pressure- avoid for glaucoma

31
Q

What is tubocurarine?

A

Non-depolarising neuromuscular blocker

32
Q

What is the mechanism of action of tubocurarine?

A

Competitive nicotinic acetylcholine receptor antagonist

33
Q

What percentage block do you need to reach to achieve full relaxation of the muscles?

A

70-80%- at this point end plate potential won’t reach the threshold

34
Q

What are the effects of tubocurarine?

A

Same as suxamethonium including flaccid paralysis

35
Q

What is the certain sequence that skeletal muscles relax in?

A

Extrinsic eye muscles
Small muscles of the face, limbs and pharynx
Respiratory muscles

36
Q

What is the sequence of the skeletal muscle returning back to normal?

A

The opposite to the relaxing schedule:
Respiratory muscles
Small muscles of the face, limbs and pharynx
Extrinsic eye muscles

37
Q

What is tubocurarine used for?

A

Relaxation of skeletal muscles during surgical operations (less anaesthetic needed)
Permit artificial ventilation

38
Q

How can you reverse the actions of these non-depolarising neuromuscular blockers?

A

With anti-cholinesterase - They increase the concentration of acetylcholine so it can outcompete the antagonist

39
Q

What is an example of a reversible anti-cholinesterase?

A

Neostigmine

40
Q

Why do you give atropine when giving neostigmine?

A

With neostigmine, you increase acetylcholine concentration in all other cholinergic synapse so atropine will block muscarinic receptor over stimulation

41
Q

How are all NM blockers given?

A

IV

42
Q

How long does tubocurarine cause paralysis for?

A

40-60mins

43
Q

How does your body get rid of tubocurarine?

A

It isn’t metabolised at all, it is excreted in urine (70%) and bile (30%)

44
Q

What increases the duration of action of tubocurarine?

A

Impairment in hepatic or renal function

45
Q

What would you use if the patient did have hepatic or renal impairment?

A

Atracurium (15 min duration of action and isn’t affected by hepatic or renal function)

46
Q

What are the unwanted effects of tubocurarine?

A

Ganglion block
Histamine release from mast cells
Hypotension- due to ganglion blockade and histamine causes vasodilation
Tachycardia- reflex to hypotension
Bronchospasm- due to histamines
Excessive secretions- caused by histamine release
Apnoea- this is why you assist respiration

LCRS Pharmacology and Therapeutics (33 decks)

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