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YR2 LCRS Pharm > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

Describe how impulses are transmitted across synapses.

A 
AP propagates along presynaptic neurone
Depolarisation of presynaptic membrane
Opening of VGCC
Ca2+ influx
Vesicle exocytosis
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2
Q

What type of receptor is found at the neuromuscular junction?

A

Nicotinic acetylcholine receptors

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3
Q

Where are nicotinic receptors found on the muscle fibre?

A

Motor end plate (usually in the middle of muscle fibres)

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4
Q

What does depolarisation of the membrane on muscle fibres cause? Describe the character of this depolarisation.

A

Change in end plate potential
This is a graded potential, thus is dependent on the amount of ACh released + the number of receptors stimulated
Once the EPP reaches a threshold, it generates an AP that propagates in both directions along the muscle fibre

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5
Q

Where is acetylcholinesterase found?

A

Bound to the BM in the synaptic cleft

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6
Q

State the 3 main neuromuscular blockers.

A

Tubocurarine
Atracurium
Suxamethonium

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7
Q

State the 2 main types of nicotinic acetylcholine receptor.

A

Ganglionic

Muscle

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8
Q

Describe the structure of nicotinic acetylcholine receptors.

A

Consist of 5 subunits (alpha, beta, gamma, delta, epsilon)

Always 2 alpha subunits, which bind to ACh + activate the receptor

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9
Q

How many molecules of acetylcholine are required to activate one nicotinic acetylcholine receptor?

A

2

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10
Q

Name two drugs that are used as spasmolytics and describe their action.

A

Diazepam
Baclofen
Both facilitate GABA transmission
Work in spinal cord to reduce generation of APs

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11
Q

Give 2 examples of conditions in which spasmolytics may be used.

A

Certain forms of cerebral palsy

Spasticity following strokes

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12
Q

What do local anaesthetics have their effect on?

A

Conduction of AP’s in motor neurones (injecting LA’s to a motor neurone causes muscle relaxation + weakness)

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13
Q

Describe the action of neurotoxins.

A

Inhibit the release of ACh + hence block contraction of respiratory skeletal muscle causing death

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14
Q

What are the two types of neuromuscular blocker?

A

Depolarising

Non-depolarising

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15
Q

Name a spasmolytic that has a different action to diazepam + baclofen

A

Dantrolene

Acts in muscle fibres themselves by inhibiting Ca2+ release from SR in the muscle fibre

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16
Q

Describe the difference in mechanism of action between depolarising and non-depolarising NM blockers. Which NM blockers fall into each category?

A 
Depolarising = suxamethonium = nicotinic ACh receptor AGONIST  
Non-depolarising = tubocurarine + atracurium = nicotinic ACh receptor antagonist
17
Q

How do NM blockers affect consciousness and pain sensation?

A

They do NOT

18
Q

What must you always do when giving NM blockers?

A

Assist respiration because of their effect on respiratory muscle action

19
Q

Describe the difference in structure between non-depolarising and depolarising NM blockers?

A 
Non-depolarising = big, bulky molecules with limited movement around their bonds  
Suxamethonium = made up of 2 ACh molecules linked together: more flexible + allows rotation. As it is made up of 2 ACh molecules it binds to the 2 alpha subunits + activates the receptor.
20
Q

Describe the mechanism of action suxamethonium.

A

=nicotinic receptor agonist.
Causes an extended end plate depolarisation leading to a depolarising block of the NMJ = a “phase 1 block”
Not metabolised as rapidly as ACh so will remain bound to receptors making them switch off due to overstimulation
Results in FLACCID PARALYSIS

21
Q

What does suxamethonium normally cause before causing the flaccid paralysis?

A

Fasciculations: individual fibre twitches as the suxamethonium begins to stimulate the nicotinic receptor

22
Q

What is the duration of paralysis of suxamethonium?

A

5 mins (short)

23
Q

How is suxamethonium metabolised?

A

By pseudocholinesterase in the liver + plasma

24
Q

What are some uses of suxamethonium?

A

Endotracheal intubation: relaxes muscles of the airways

Muscle relaxant for electroconvulsive therapy: treatment for severe clinical depression

25
Q

State and explain 4 unwanted effects of suxamethonium.

A

Post-operative muscle pains (Due to initial fasciculations)
Hyperkalaemia: soft tissue injury/ burns results in loss of some neurones innervating the tissue, + upregulation of receptors in skeletal muscle= deinnervation supersensitivity, causes exaggerated response with a bigger influx of Na+ + bigger efflux of K+
Bradycardia: due to direct muscarinic action on the heart (usually prevented by atropine (muscarinic antagonist) in the pre-med)
Raised intraocular pressure: AVOID for eye injuries + glaucoma

26
Q

Describe the mechanism of action of tubocurarine.

A

Competitive nicotinic ACh receptor antagonist.

70-80% block to achieve full relaxation of the muscles

27
Q

Describe the order of relaxation of skeletal muscles and the order in which they return back to normal when given tubocurarine.

A

Causes flaccid paralysis.
Order:
Extrinsic eye muscles (1st to relax, last to go back to normal)
Small muscles of the face, limbs + pharynx
Respiratory muscles

28
Q

State 2 uses of tubocurarine.

A

Relaxation of muscles during surgical operations (so less GA is needed)
Permit artificial ventilation

29
Q

How can the actions of NM blockers be reversed?

A

Give an anti-cholinesterase (e.g. physostigmine)

30
Q

What else must you give with this drug when trying to reverse the actions of NM blockers?

A

Atropine
Giving physostigmine will raise the synaptic concentration of ACh at ALL cholinergic synapses (not just NMJ’s) so need atropine to block these unwanted effects

31
Q

How are all NM blockers administered?

A

Intravenously

32
Q

What is the duration of paralysis of tubocurarine?

A

1-2 hours (long)

33
Q

Describe the metabolism and excretion of tubocurarine?

A

NOT metabolised at all

Excreted in the urine (70%) + bile (30%)

34
Q

Under which conditions would you get an increased duration of action of tubocurarine? What would you change under these conditions?

A

Impairment of hepatic or renal function increases duration of action
Under these conditions use ATRACURIUM (15 min duration) + is NOT affected by liver or kidney function

35
Q

State 5 unwanted effects of tubocurarine.

A

Ganglion block + histamine release from mast cells cause most of the unwanted effects
HYPOTENSION: histamine acts on H1 receptors, causes vasodilation + ganglion blockade
TACHYCARDIA: reflex tachycardia in response to hypotension + blockade of vagal ganglion
BRONCHOSPASM: caused by histamine release
EXCESSIVE SECRETIONS (bronchial + salivary): histamine release
APNOEA: so need to assist respiration

YR2 LCRS Pharm (34 decks)

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