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Pharmacology Y2 > Neuromuscular Junction > Flashcards

Neuromuscular Junction Flashcards

1
Q

Why does acetylcholine have to be rapidly broken down and removed from the synapse?

A

To prevent desensitisation and repeated binding of the ACh receptors

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2
Q

What causes mEPPS?

A

Spontaneous vesicles of ACh that are released into the synapse, but does not cause enough depolarisation for an action potential to occur

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3
Q

Where do EPPs occur?

A

At the motor end plate, when enough neurotransmitter has been released into the synapse for an action potential to occur -> muscle twitch

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4
Q

EPPs are restricted to the ________ region

A

Endplate region

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4
Q

EPPs are restricted to the ________ region

A

Endplate region

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5
Q

What is the function of choline acetyl transferase?

A

Converts choline to acetylcholine

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6
Q

Name an ion that prevents the release of the vesicles of ACh into the synapse

A

Mg2+

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7
Q

What are present synaptic blockers?

A

Drugs that prevent the reuptake of choline into the presynaptic membrane

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8
Q

List 4 pre synaptic blockers

A

Hemicholinium
Botulinum toxin
Tetanus toxin
Aminoglycoside antibiotics

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9
Q

Where is botulinum toxin found?

A

Bad meat, fish, yoghurt

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10
Q

Where is botulinum toxin found?

A

Bad meat, fish, yoghurt

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11
Q

What is the mechanism of action of botulinum toxin?

A

Prevents neurotransmitter vesicles form binding to the presynaptic membrane
Interferes with Ca2+ activation

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12
Q

What is the mechanism of aminoglycoside antibiotics?

A

Interferes with Ca2+ activation in pre synaptic membrane

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13
Q

Which has more of an effect, botulinum toxin or tetanus toxin?

A

Botulinum toxin

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14
Q

What are post synaptic blockers?

A

Drugs that prevent the neurotransmitter from binding to the post synaptic membrane
Drugs that block the response of the neurotransmitter and receptor
Drugs that block the breakdown of the neurotransmitter

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15
Q

List 4 post synaptic blockers

A

Tubocurarine
Gallamine
Pancuronium
Suxamethonium

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16
Q

What is the mechanism of action for tubocurarine?

A

It is a competitive antagonist for ACh -> when bound it prevent ACh from binding

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17
Q

What is the mechanism of action for Anti AChE?

A

Blocks acetylcholinesterase from breaking down ACh, so it cannot be taken back into the pre synaptic membrane

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17
Q

What is the mechanism of action for Anti AChE?

A

Blocks acetylcholinesterase from breaking down ACh, so it cannot be taken back into the pre synaptic membrane

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18
Q

Describe the action of a competitive blocker

A

Competes with ACh for receptor sites., prevents ACh from binding

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19
Q

What is the mechanism of action of suxamethonium?

A

Binds to ACh receptor sites -> causes sustained depolarisation -> this inactivates Na+ channels -> muscle fibre cannot carry out action potentials

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20
Q

Describe the action of a depolarising blocker

A

Causes longer depolarisation to inactivate the Na+ channels so muscles fibre cannot cause new action potentials

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21
Q

Which causes fasciculation, competitive or depolarising blockers?

A

Depolarising blockers

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22
Q

Which causes hypotension due to ganglion block, competitive to depolarising blockers?

A

Competitive blockers

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23
Q

Which affects the eye, competitive or depolarising blockers?

A

Depolarising blockers

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24
Q

How do depolarising blockers affect the eye?

A

Eye muscles have multiple end plates, so a long depolarisation will cause compression of the eye ball in its socket

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25
Q

Which will have a greater effect as a blocker in myasthenia gravis, competitive or depolarising blockers?

A

Competitive blockers - most receptors will not be present in the first place
(the effect of depolarising blockers reduces as not as much depolarisation can occur with absent receptors)

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26
Q

Which has an effect on K+ plasma concentrations, competitive or depolarising blockers?

A

Depolarising blockers

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27
Q

How do depolarising blockers increase the K+ plasma concentrations?

A

Depolarising blockers will open the voltage gated K+ channels, so K+ leaves the cell and enters the plasma

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28
Q

Define fasciculation

A

Spontaneous and involuntary muscle contraction and relaxation

29
Q

Where are nicotinic receptors found in the nervous system?

A

In the autonomic ganglia synapses
In neuromuscular junctions to skeletal muscle
At the adrenal glands (direct attachment to the preganglionic neurone)

30
Q

Why do some drugs act on nicotinic ganglion receptors but not nicotinic muscle receptors?

A

The receptors differ in what amino acids make up the receptor subunits

30
Q

Why do some drugs act on nicotinic ganglion receptors but not nicotinic muscle receptors?

A

The receptors differ in what amino acids make up the receptor subunits

31
Q

Name 2 ganglion agonists

A

Nicotine
Tetramethyl ammonium

31
Q

Name 2 ganglion agonists

A

Nicotine
Tetramethyl ammonium

32
Q

Name a ganglion blocker

A

Hexamethonium

33
Q

Why is hexamethonium not used therapeutically anymore?

A

It does not distinguish between sympathetic and parasympathetic ganglia, therefore caused many undesirable side effects

34
Q

How many types of acetylcholinesterase are there?

A

2

35
Q

Name the 2 types of acetylcholinesterase

A

True AChE
Pseudo-AChE

36
Q

Name the 2 types of acetylcholinesterase

A

True AChE
Pseudo-AChE

37
Q

Where is true AChE found?

A

In synapses

38
Q

Where is pseudo-AChE found?

A

In plasma, breaks down AChE blockers

39
Q

Can AChE blockers differentiate between true and pseudo AChE?

A

No, they are both treated the same

40
Q

How many active sites are there on acetylcholinesterase?

A

2

41
Q

What are the 2 active sites of AChE?

A

Anionic site
Esteratic site

41
Q

What are the 2 active sites of AChE?

A

Anionic site
Esteratic site

42
Q

How does the esteratic site of AChE break down ACh?

A

Esteratic site is negatively charged -> ionic attraction to positively charged head of ACh

42
Q

How does the esteratic site of AChE break down ACh?

A

Esteratic site is negatively charged -> ionic attraction to positively charged head of ACh

43
Q

How does the anionic site of AChE break down ACh?

A

Reactive hydroxyl group at this site binds with the ester group of ACh -> choline dissociates -> enzyme is acetylated -> this bond then breaks to leave the enzyme, choline and acetic acid

44
Q

What are the 3 types of acetylcholinesterase blockers?

A

Short acting reversible
Long acting reversible
Irreversible

45
Q

Give an example of a short acting reversible AChE blocker

A

Edrophonium

46
Q

What is the mechanism of action of short acting AChE blockers?

A

Similar structure to ACh -> binds weakly to the anionic site of AChE then comes off

47
Q

What is the mechanism of action of short acting AChE blockers?

A

Similar structure to ACh -> binds weakly to the anionic site of AChE then comes off

48
Q

Give 2 examples of long acting reversible AChE blockers

A

Neostigmine
Pyridostigmine

48
Q

Give 2 examples of long acting reversible AChE blockers

A

Neostigmine
Pyridostigmine

49
Q

What is the mechanism of action of long acting reversible AChE blockers?

A

Positively charged group binds to anionic site -> Carbamyl group binds to esteratic site -> Cleaves -> hydrolysis of the carbamyl group to remove it from the enzyme is very slow -> enzyme cannot go on to break down other ACh quickly

50
Q

Give 2 examples of irreversible AChE blockers

A

DYFLOS / DFP
Novichok

51
Q

What is the action of DYFLOS irreversible AChE blocker at low concentrations?

A

Binds reversibly to the OH group in the esteratic site of AChE

52
Q

What is the action of DYFLOS irreversible AChE blocker at high concentrations?

A

Binds irreversibly to the OH group in the esteratic site of AChE

53
Q

What is the action of DYFLOS irreversible AChE blocker at high concentrations?

A

Binds irreversibly to the OH group in the esteratic site of AChE

54
Q

What is the result of DYFLOS irreversible AChE blocker?

A

Phosphorylates AChE so it can no longer break down ACh
Releases HF

55
Q

Name 2 reactivates of phosphorylates acetylcholinesterase

A

Pralidoxime
Di acetyl mono oxime

56
Q

Is constriction of the pupil parasympathetic or sympathetic?

A

Parasympathetic

57
Q

Is dilation of the pupil parasympathetic or sympathetic?

A

Sympathetic

58
Q

How can contraction of ciliary muscle in the eye help drain fluid in glaucoma?

A

Contraction of ciliary muscles opens the canal of Schlemm, which drains the fluid -> reduces intra ocular pressure

59
Q

What action to the parasympathetic and sympathetic nervous system could cause constriction of the ciliary muscles in the eye?

A

Parasympathetic agonists
Sympathetic antagonists

60
Q

How can cholinesterase blockers reduce glaucoma?

A

Increases the neurotransmitter effect for parasympathetic receptors -> causes constriction of the pupil

60
Q

How can cholinesterase blockers reduce glaucoma?

A

Increases the neurotransmitter effect for parasympathetic receptors -> causes constriction of the pupil

61
Q

What is a use of cholinesterase blockers in the GI tract?

A

Enhances muscle tone

62
Q

What is a use of cholinesterase blockers in the GI tract?

A

Enhances muscle tone

63
Q

What is a use of cholinesterase blockers in myasthenia gravis?

A

Prolongs time of ACh in the post synaptic cleft -> increases probability of ACh binding to receptor -> increased muscle response -> reduced muscle weakness

64
Q

What is a use of cholinesterase blockers after anaesthesia?

A

Used to enhance transmission to overcome the anaesthesia -> increased probability of ACh binding with cholinesterase blocker

65
Q

What is a diagnostic use of a short acting ACh blocker?

A

For diagnosis of myasthenia gravis

Pharmacology Y2 (9 decks)

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