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Pharmacology > Neuromuscular blocking drugs > Flashcards

Neuromuscular blocking drugs Flashcards

(38 cards)

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1
Q

What is ACh synthesised from and which enzyme does this?

A

acetyl CoA and choline

choline acetyltransferase (CAT)

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2
Q

Where is CAT found?

A

only in cholinergic nerve terminals

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3
Q

What happens to ACh after it has acted on the receptors?

A

its broken down by acteylcholinesterase into choline and acetic acid and then reuptaken into the presynaptic nerve terminal

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4
Q

Where does the ACh bind at neuromuscular junctions?

A

Nicotonic acetylcholine receptors on the end plate (usually in the middle of the fibres)

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5
Q

Describe how nicotinic receptors work

A

they are ion linked channels - when the receptor is stimulated sodium ions influx

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6
Q

What is end plate potential?

A

Voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the NMJ

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7
Q

Where is the acetylcholinesterase bound?

A

to the basement membrane in the synaptic cleft

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8
Q

What are the three main neuromuscular blockers?

A

tubocurarine
atracurium
suxamethonium

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9
Q

What are the two main types of nicotinic receptors?

A

ganglionic (neuronal)

muscle (skeletal)

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10
Q

Describe the structure of the nicotinic receptor

A

membrane spanning

  • 5 subunits
  • 2 alpha subunits
  • these alpha subunits found on the top of the receptor either side must be activated for receptor activation
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11
Q

How many molecules of ACh are needed to activate the nicotinic receptor?

A

2

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12
Q

What is diazepam and how does it work?

A

a spasmolytic

  • it facilitates GABA transmission
  • useful in cerebral palsy and spasticity after strokes etc.
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13
Q

Where do local anaesthetics work?

A

affect the conduction of AP down neurones

- unwanted SE caused when a motor neurone is affected and muscle weakness can occur

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14
Q

What does botulinum toxin do?

A

It inhibits the release of ACh so blocks the contraction of respiratory skeletal muscle therefore can be lethal (neurotoxins)

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15
Q

What are the two types of neuromuscular blocking drugs and where do they act?

A

Depolarising - Suxamethonium

Non-Depolarising - Tubocurarine

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16
Q

Are neuromuscular drugs post or pre-synaptic acting?

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A

post - they act on the nicotinic receptors on the motor end plate

17
Q

What are non-depolarising drugs and how do they work?

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A

Competitive nicotinic receptor antagonist

18
Q

What are depolarising drugs and how do they work?

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A

Nicotinic receptor agonists

19
Q

Do neuromuscular blocking drugs affect conciousness, pain? What should be done when they are given and why?

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A
  • NO
  • NO
  • Assist respiration as it affect respiratory muscles
20
Q

Describe the structures of non depolarising drugs

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A

big, bulky with relatively restricted motion around the bonds

21
Q

Describe the structure of suxamethonium

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A

made of two ACh molecules

  • flexible and allows rotation
  • one can stimulate the receptor alone
22
Q

How does suxamethonium work?

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A

It causes an extended end plate depolarisation -> leads to a depolarisation block of the NMJ

This is called a phase 1 block

  • If you give a patient suxamethonium, it will slowly seep into the muscle fibres
  • It will stimulate the nicotinic receptors
  • It isn’t metabolised as rapidly as acetylcholine
  • So it will remain bound to the nicotinic receptors and very quickly these receptors will switch off
  • This is a depolarisation block caused by overstimulation
23
Q

What can suxamethonium lead to?

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A

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

24
Q

Describe the pharmacokinetics of suxamethonium

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A

Route: Intravenous (highly charged)

Duration of paralysis: 5 minutes (short-lived)

Metabolised by pseudocholinesterase in the liver and plasma

25
What are the uses of suxamethonium?
Endotracheal Intubation: It relaxes the skeletal muscle of the airways Muscle Relaxant for Electroconvulsive Therapy: This is a treatment for severe clinical depression
26
What are some unwanted effects of suxamethonium?
Post-operative muscle pains – This is due to the initial fasciculations Bradycardia – This is due to the direct muscarinic action on the heart. But this effects tends to be prevented by the fact that suxamethonium is generally given after general anaesthetic when patients would have had atropine (competitive muscarinic antagonist) in their pre-med Hyperkalaemia Raised Intraocular Pressure – avoid for eye injuries and glaucoma Flaccid paralysis Fasciculations
27
Why does suxamethonium cause hyperkalaemia?
Soft tissue injury or burns can lead to ventricular arrhythmias/cardiac arrest. If there is a burn/soft tissue injury, you lose some of the neurones innervating the muscle and so you get upregulation of the receptors in the skeletal muscle = deinnervation supersensitivity. So if you give suxamethonium you will get an exaggerated response. You get bigger influx of sodium and bigger efflux of potassium
28
What is tubocurarine?
Non-depolarising neuromuscular blocker Naturally occurring ammonium compound (alkaloid) found in South American plant
29
How does tubocurarine work?
Competitive nicotinic acetylcholine receptor antagonist - You need about 70-80% block to achieve full relaxation of the muscles - If you block this proportion of receptors, the end-plate potential generated won’t reach the threshold
30
What are the effects of tubocurarine?
- The effects are the same as suxamethonium | - This also produces flaccid paralysis
31
How does recovery of muscles occur following tubocurarine?
The skeletal muscles relax in a certain sequence and they get back to normal in the opposite order: - Extrinsic eye muscles (relaxes first, gets back to normal last) - Small muscles of the face, limbs, pharynx - Respiratory muscles (relaxes last, gets back to normal first)
32
What is the effect of tubocurarine on the NM transmission?
You get a little shoulder in the action potential which is the end-plate potential If tubocurarine has been given, you get the beginning of the depolarisation but the depolarisation is too small to trigger an action potential
33
What are the uses of tubocurarine?
Relaxation of skeletal muscles during surgical operations (less anaesthetic needed). This is because the NM blocker has taken the role of making the muscles relax so the dose of the GA can be lower Permit Artificial Ventilation
34
How can the effects of non-depolarising neuromuscular drugs be reversed?
anti cholinesterases e.g. neostigmine (Giving neostigmine increases ACh conc in all other cholinergic synpases so give atroping with it to block muscarinic over stimulation)
35
Describe the pharmacokinetics of tubocurarine
- All the neuromuscular blockers are given intravenously (highly charged) - Does not cross the BBB or placenta - Long duration of paralysis: 40-60 mins - Not metabolised at all - It is excreted in the urine (70%) and the bile (30%) - If there is impairment in hepatic or renal function, the duration of action of tubocurarine is increas
36
Which drug should be given in place of tubocurarine if the patients has liver or kidney impairment?
atracurium as not affected by liver or kidney function It is chemically unstable molecule and due to the pH of the plasma it gets hydrolysed into two inactive fragments
37
What are the unwanted effects of tubocurarine?
- Ganglion block – it could block some of the nicotinic receptors in the ganglia - Histamine release from mast cells - Hypotension (due to ganglion blockade and histamine acting on the H1 receptors causing vasodilation) - Tachycardia (May lead to arrhythmias, this is a reflex in response to the hypotension or could also be due to the blockade of vagal ganglia) - Bronchospasm (caused by the histamine release) - Excessive secretions (bronchial and salivary, caused by the histamine release) Apnoea
38
Which two mechanisms cause the majority of unwanted effects of tubocurarine?
ganglion blockade and histamine release from mast cells

Pharmacology (26 decks)

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