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Flashcards in Neuromuscular Blocking Drugs Deck (25)
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1

Describe how impulses are transmitted across synapses.

Action potential propagates along the presynaptic neurone -> depolarisation of presynaptic membrane -> opening of voltage gated calcium channels -> calcium influx -> vesicle exocytosis

2

What type of receptor is found at the neuromuscular junction?

Nicotinic acetylcholine receptors

3

Where are these receptors found on the muscle fibre?

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

4

Where is acetylcholinesterase found?

It is bound to the basement membrane in the synaptic cleft

5

State the three main neuromuscule blockers.

Tubocurarine
Atracurium
Suxamethonium

6

State the two main types of nicotinic acetylcholine receptor.

Ganglionic
Muscle

7

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

2

8

What are the two types of neuromuscular blocker?

Depolarising
Non-depolarising

9

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

Depolarising = suxamethonium = nicotinic acetylcholine receptor AGONIST
Non-depolarising = tubocurarine + atracurium = nicotinic acetylcholine receptor antagonist

10

How do NM blockers affect consciousness and pain sensation?

They do NOT

11

What must you always do when giving NM blockers?

Assist respiration because of their effect on respiratory muscle action

12

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

Non-depolarising = big, bulky molecules with limited movement around their bonds
Suxamethonium = made up of two acetylcholine molecules that are linked together. This is more flexible and allows rotation. As it is madeup of two acetylcholine molecules it can binds to the two alpha subunits and activate the receptor.

13

Describe the mechanism of action suxamethonium.

Suxamethonium is a nicotinic receptor agonist.
It causes an extended end plate depolarisation leading to a depolarising block of the NMJ
This is a phase 1 block
NOTE: it is not metabolised as rapidly as acetylcholine so it will remain bound to the nicotinic receptors making them switch off due to overstimulation

14

What does suxamethonium normally cause before causing the flaccid paralysis?

Fasciculations – individual fibre twitches as the suxamethonium begins to stimulate the nicotinic receptor (remember it is an agonist)

15

What is the duration of paralysis of suxamethonium?

5 mins

16

How is suxamethonium metabolised?

It is metabolised by pseudocholinesterase (butyrylcholinesterase) in the liver and plasma

17

What are some uses of suxamethonium?

Endotracheal intubation – relaxes the muscles of the airways
Muscle relaxant for electroconvulsive therapy – treatment for severe clinical depression

18

State and explain four unwanted effects of suxamethonium.

Post-operative muscle pains
 Due to initial fasciculations
Hyperkalaemia
 If there is soft tissue injury or burns you will lose some neurones innervating the tissuea
 Then you will get upregulation of receptors in the skeletal muscle – deinnervation supersensitivity
 So if you give suxamethonium you get an exaggerated response with a bigger influx of sodium and bigger efflux of potassium
Bradycardia
 This is due to the direct muscarinic action on the heart
 This effects tends to be prevented because suxamethonium is usually given after GA and hence following administration of atropine (muscarinic antagonist) in the pre-med
Raised intraocular pressure
 AVOID for eye injuries and glaucoma

19

Describe the mechanism of action of tubocurarine.

Tubocurarine is a competitive nicotinic acetylcholine receptor antagonist.
You only need 70-80% block to achieve full relaxation of the muscles
If you block this proportion of the receptors then the end-plate potential generated will NOT reach the threshold

20

State two uses of tubocurarine.

Relaxation of muscles during surgical operations (this means that less general anaesthetic is needed)
Permit artificial ventilation

21

How can the actions of NM blockers be reversed?

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

22

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

Atropine
Giving physostigmine will raise the synaptic concentration of acetylcholine at ALL cholinergic synapses (not just the neuromuscular junctions) so you need some atropine to block these unwanted effects

23

How are all NM blockers administered?

Intravenously

24

What is the duration of paralysis of tubocurarine?

40 mins

25

State some unwanted effects of tubocurarine.

MAIN EFFECTS: ganglion block + histamine release from mast cells cause most of the unwanted effects
 HYPOTENSION – histamine can act on H1 receptors and cause vasodilation
 TACHYCARDIA – reflex tachycardia in response to hypotension
 BRONCHOSPASM – caused by histamine release
 EXCESSIVE SECRETIONS (bronchial and salivary) – histamine release
 APNOEA – which is why you assist respiration