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PA20016 > The somatic nervous system 1 > Flashcards

The somatic nervous system 1 Flashcards

1
Q

Where are cell bodies in the somatic nervous system?

A

In the brain stem.

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2
Q

What is the somatic nervous system?

A

Conscious decisions sending signals to leg muscles, postural muscles etc. and outside bits of the eyes.

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3
Q

What neurotransmitter and receptor is involved in the somatic nervous system?

A

ACh on nicotinic receptors.

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4
Q

What is a motor unit?

A

The motor neuron and the muscle fibre it innervates.

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5
Q

Is the motor neuron myelinated in the somatic nervous system?

A

Yes - there is rapid conduction down the motor neurons.

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6
Q

What happens when an action potential is conducted along a motor nerve?

A

There is depolarisation and an influx of calcium at the nerve terminal. ACH released into the synapse and binds to nicotinic receptors.

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7
Q

What is ACh metabolised by?

A

Acetylcholine esterases.

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8
Q

What subunits do the nicotinic receptors contain?

A

Alpha, beta, delta and gamma subunits.

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9
Q

How many sites does ACh bind to on nicotinic receptors?

A

Two sites.

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10
Q

What are the two sites of Na+ influx at the neuromuscular junction end plate?

A

ACh binding to receptors causes Na+ influx which generates an end plate potential, which then initiates the opening of proximal voltage gated Na+ channels. This causes amplification of ion influx and action potential in the muscle cell.

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11
Q

How is the signal at an NMJ terminated?

A

ACh esterase.

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12
Q

What is the idea of excitation-contraction coupling in skeletal muscle?

A

A Na+ driven action potential opens L-type calcium channels, which stimulates Ca2+ induced Ca2+ release from intracellular stores.

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13
Q

How does smooth and skeletal muscle contraction differ?

A

Skeletal muscle contraction is due to nicotinic receptors and ion influx, whereas smooth muscle contraction is due to g protein coupled and muscarinic receptors - more of the contraction is due to phospholipase C.

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14
Q

What is the most common way to interfere with cholinergic transmission?

A

Blocking nicotinic cholingergic receptors at NMJs.

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15
Q

How can ACh be decreased at NMJs?

A

Inhibit ACh synthesis or release.

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16
Q

How can ACh be increased/the effect increased at the NMJ?

A

Enhanced nicotinic effects.

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17
Q

What may induction motor reflexes interfere with in surgery?

A

Insertion of tubes for the surgery.

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18
Q

Why might muscle spasm occur in surgery?

A

Mechanical manipulation of limbs and nerves.

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19
Q

When are reflexes suppressed in anaesthesia?

A

Not until deep anaesthesia.

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20
Q

What can be used to make it easier to insert tubes during surgery?

A

Transient neuromuscular blockers.

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21
Q

What do neuromuscular junction blocking drugs interfere with?

A

The post-synaptic action of ACh.

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22
Q

What are the differences between non-depolarising agents and depolarising blocking agents?

A

Non-depolarising - ACh receptor antagonists (no efficacy), whereas depolarising are weak nicotinic agonists.

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23
Q

How do depolarising blocking agents work?

A

They cause depolarisation weakly, but then remain bound so depolarisation cannot occur again.

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24
Q

What is curare?

A

A non-depolarising agent that is a mixture of alkaloids found in south american plants, including d-tubocurarine.

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25
Q

What effect does curare have?

A

It causes paralysis by blocking neuromuscular transmission, but not nerve conduction or muscle contractility.

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26
Q

What is curare originally used for?

A

Poison arrows by indigenous south american peoples.

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27
Q

Why is curare safe to eat animals that have been poisoned with it?

A

It doesn’t cross the GI tract for long.

28
Q

What action does d-tubocararine have?

A

It binds to nicotinic receptors are NMJs as an antagonist.

29
Q

Why does tubocararine need to block a lot of receptors to have any effect?

A

Much more ACh is released than needed, so most receptors (90%) need to blocked to have an effect.

30
Q

What synthetic derivatives of d-tubocararine are now used clinically?

A

Atracurium, pancuronium and gallium.

31
Q

What effect does tubocararine have on neuromuscular transmission?

A

Nerve stimulation normally initiates end-plate potential which initiates an action potential. Tubocurarine reduces the end plate potential amplitude so that no action potential is generated.

32
Q

Why do clinically used non-depolarising NM blocking drugs ideally have shorter durations of action?

A

You don’t want a high level of block after the surgery has been completed.

33
Q

What is duration of non-depolarising NM blocking drugs determined by?

A

Susceptibility to cholinesterases and clearance - half life.

34
Q

What is alpha-bungarotoxin?

A

It irreversibly binds to the nicotinic ACh receptors at the NMJ, and inhibits ACh binding.

35
Q

What is alpha-bungarotoxin useful for?

A

Receptor studies.

36
Q

What are some of the unwanted effects of non-depolarising blockers?

A

Hypotension, histamine release from mast cells, respiratory failure.

37
Q

Why is hypotension a side effect of non-depolarising blockers?

A

There is ganglion blockade as the agents are selective but not specific, so will affect transmission at the ganglion as well at the NMJ.

38
Q

What effect can histamine release from mast cells due to non-depolarising blockers have?

A

It can cause bronchospasm in sensitive individuals. It is not related to the nicotinic receptor.

39
Q

What are some common depolarising blocking agents?

A

Decamethonium, suxamethonium.

40
Q

What is the mechanism of depolarising blocking agents?

A

They initially bind and activate the nicotinic receptor and open the end plate voltage sensitive Na+ channels to depolarise the muscle. This is maintained at the end-plate and there is a loss of electrical excitability. As the molecules are present in the synapse longer than ACh, the receptors stays open and cannot be depolarised again.

41
Q

What is the depolarising block (phase I) caused by depolarising agents?

A

(Na+ channels) The muscle is held in the depolarised state, and the sodium channels are refractory and are no longer open. The muscle becomes flaccid as Ca2+ is taken into the stores.

42
Q

What are the three states of the sodium channel?

A

Resting, active and inactive.

43
Q

What are the two gates of the sodium channel?

A

Gate v (voltage dependent) and gate t (time dependent).

44
Q

How do the states of the sodium channel, in terms of gate opening and closing?

A

In the resting state, v is closed whilst t is open. In the active state, v opens when the surrounding membrane is depolarised and t closes soon after to inactive the channel. In the inactive state, v remains open whilst t is closed.

45
Q

What are the two phases of the block caused by depolarising agents?

A

Depolarising block (I) and desensitisation block (II).

46
Q

What is the densensitisation block?

A

(ACh nicotinic) Persistent stimulation leads to receptor desensitisation - this doesn’t normally occur with ACh as it is rapidly removed. The muscle partially repolarises but transmission remains blocked.

47
Q

How do depolarising agents differ to ACh?

A

Depolarising agents are removed a lot more slowly than ACh.

48
Q

What are the states of nicotinic ACh receptors?

A

Resting, resting with agonist bound (but channel closed), active with channel open, desensitized without agonist, desensitized with agonist bound.

49
Q

What are the advantages of depolarising neuromuscular blockers?

A

They have rapid onset and a short duration of action, they can be used for surgery during pregnancy (doesn’t cross blood-placenta barrier - doesn’t affect newborn respiration) and are less likely to elicit histamine release.

50
Q

What are some of the unwanted effects/dangers of depolarising drugs?

A

Bradycardia, potassium release, post-operative pain, increased intraocular pressure, prolonged paralysis, malignant hyperthermia.

51
Q

Why is bradycardia an effect of depolarising drugs?

A

Direct muscarinic action.

52
Q

Why is potassium release an effect of depolarising drugs?

A

There is an increase in cation permeability at the end plate that causes loss of K+. This results in hyperkalemia that can cause ventricular dysrhythmia.

53
Q

Why is there an increase in intraocular pressure when using depolarising drugs?

A

There is contraction of extra-ocular muscles.

54
Q

What are some other uses of neuromuscular blocking drugs?

A

Electroconvulsive therapy - depolarisation of the brain but not the muscles, lethal injections. They can be used for lethal injections to prevent spasm - implies a more peaceful death.

55
Q

What are the key differences between non-depolarising and depolarising agents?

A

Non-depolarising block can be reversed by increasing ACh concentration, depolarising blocks produce initial fasciculation (small twitches), suxamethonium (depolarising) is hydrolysed by plasma cholinesterase and is shorter-acting than tubocurarine.

56
Q

What can genetic polymorphisms in esterases result in?

A

Prolonged action.

57
Q

How can neuromuscular blocker’s action be reversed?

A

Neostigmine - an AChesterase inhibitor that raises ACh in the synapse. This reverses the non-depolarising block and potentiates the depolarising block.

58
Q

What are the characteristics of neostigmine?

A

It is a quaternary ammonium compound that competes with ACh on cholinesterase. It is lipid insoluble and does not cross the blood-brain barrier.

59
Q

What is the action/onset of neostigmine?

A

It has an onset of within a minute, a peak in 10 minutes and a duration of 20-30 minutes.

60
Q

How is neostigmine removed from the body?

A

It is metabolized by plasma esterases. The elimination half-life is prolonged in renal disease.

61
Q

What nervous system does neostigmine stimulate?

A

The parasympathetic nervous system due to enhanced ACh.

62
Q

What can neostigmine cause, due to parasympathetic stimulation?

A

Bradycardia - there is cardiac arrest after high doses.

63
Q

What side effects can neostigmine have after surgery?

A

Postoperative nausea and vomiting, GI disturbance.

64
Q

Why are antimuscarinics used with neostigmine?

A

Overcome the problems of this - these block out the adverse effects due to ACh effects at non-muscular junctions.

65
Q

How else can neuromuscular blocker’s action be reversed?

A

Sugammadex - it chelates aminosteriod non-depolarising blockers.

66
Q

What is the benefit is using sugammadex?

A

It avoids the use of cholinesterase inhibitors and avoids the use of depolarising agents - it can remove the non-depolarizing blocker without the adverse effects on the autonomic nervous system.

67
Q

Why is neostigmine not used all the time?

A

It is expensive.

PA20016 (10 decks)

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