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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
Which affects the eye, competitive or depolarising blockers?
Depolarising blockers
24
How do depolarising blockers affect the eye?
Eye muscles have multiple end plates, so a long depolarisation will cause compression of the eye ball in its socket
25
Which will have a greater effect as a blocker in myasthenia gravis, competitive or depolarising blockers?
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)
26
Which has an effect on K+ plasma concentrations, competitive or depolarising blockers?
Depolarising blockers
27
How do depolarising blockers increase the K+ plasma concentrations?
Depolarising blockers will open the voltage gated K+ channels, so K+ leaves the cell and enters the plasma
28
Define fasciculation
Spontaneous and involuntary muscle contraction and relaxation
29
Where are nicotinic receptors found in the nervous system?
In the autonomic ganglia synapses In neuromuscular junctions to skeletal muscle At the adrenal glands (direct attachment to the preganglionic neurone)
30
Why do some drugs act on nicotinic ganglion receptors but not nicotinic muscle receptors?
The receptors differ in what amino acids make up the receptor subunits
30
Why do some drugs act on nicotinic ganglion receptors but not nicotinic muscle receptors?
The receptors differ in what amino acids make up the receptor subunits
31
Name 2 ganglion agonists
Nicotine Tetramethyl ammonium
31
Name 2 ganglion agonists
Nicotine Tetramethyl ammonium
32
Name a ganglion blocker
Hexamethonium
33
Why is hexamethonium not used therapeutically anymore?
It does not distinguish between sympathetic and parasympathetic ganglia, therefore caused many undesirable side effects
34
How many types of acetylcholinesterase are there?
2
35
Name the 2 types of acetylcholinesterase
True AChE Pseudo-AChE
36
Name the 2 types of acetylcholinesterase
True AChE Pseudo-AChE
37
Where is true AChE found?
In synapses
38
Where is pseudo-AChE found?
In plasma, breaks down AChE blockers
39
Can AChE blockers differentiate between true and pseudo AChE?
No, they are both treated the same
40
How many active sites are there on acetylcholinesterase?
2
41
What are the 2 active sites of AChE?
Anionic site Esteratic site
41
What are the 2 active sites of AChE?
Anionic site Esteratic site
42
How does the esteratic site of AChE break down ACh?
Esteratic site is negatively charged -> ionic attraction to positively charged head of ACh
42
How does the esteratic site of AChE break down ACh?
Esteratic site is negatively charged -> ionic attraction to positively charged head of ACh
43
How does the anionic site of AChE break down ACh?
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
What are the 3 types of acetylcholinesterase blockers?
Short acting reversible Long acting reversible Irreversible
45
Give an example of a short acting reversible AChE blocker
Edrophonium
46
What is the mechanism of action of short acting AChE blockers?
Similar structure to ACh -> binds weakly to the anionic site of AChE then comes off
47
What is the mechanism of action of short acting AChE blockers?
Similar structure to ACh -> binds weakly to the anionic site of AChE then comes off
48
Give 2 examples of long acting reversible AChE blockers
Neostigmine Pyridostigmine
48
Give 2 examples of long acting reversible AChE blockers
Neostigmine Pyridostigmine
49
What is the mechanism of action of long acting reversible AChE blockers?
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
Give 2 examples of irreversible AChE blockers
DYFLOS / DFP Novichok
51
What is the action of DYFLOS irreversible AChE blocker at low concentrations?
Binds reversibly to the OH group in the esteratic site of AChE
52
What is the action of DYFLOS irreversible AChE blocker at high concentrations?
Binds irreversibly to the OH group in the esteratic site of AChE
53
What is the action of DYFLOS irreversible AChE blocker at high concentrations?
Binds irreversibly to the OH group in the esteratic site of AChE
54
What is the result of DYFLOS irreversible AChE blocker?
Phosphorylates AChE so it can no longer break down ACh Releases HF
55
Name 2 reactivates of phosphorylates acetylcholinesterase
Pralidoxime Di acetyl mono oxime
56
Is constriction of the pupil parasympathetic or sympathetic?
Parasympathetic
57
Is dilation of the pupil parasympathetic or sympathetic?
Sympathetic
58
How can contraction of ciliary muscle in the eye help drain fluid in glaucoma?
Contraction of ciliary muscles opens the canal of Schlemm, which drains the fluid -> reduces intra ocular pressure
59
What action to the parasympathetic and sympathetic nervous system could cause constriction of the ciliary muscles in the eye?
Parasympathetic agonists Sympathetic antagonists
60
How can cholinesterase blockers reduce glaucoma?
Increases the neurotransmitter effect for parasympathetic receptors -> causes constriction of the pupil
60
How can cholinesterase blockers reduce glaucoma?
Increases the neurotransmitter effect for parasympathetic receptors -> causes constriction of the pupil
61
What is a use of cholinesterase blockers in the GI tract?
Enhances muscle tone
62
What is a use of cholinesterase blockers in the GI tract?
Enhances muscle tone
63
What is a use of cholinesterase blockers in myasthenia gravis?
Prolongs time of ACh in the post synaptic cleft -> increases probability of ACh binding to receptor -> increased muscle response -> reduced muscle weakness
64
What is a use of cholinesterase blockers after anaesthesia?
Used to enhance transmission to overcome the anaesthesia -> increased probability of ACh binding with cholinesterase blocker
65
What is a diagnostic use of a short acting ACh blocker?
For diagnosis of myasthenia gravis

Pharmacology Y2 (9 decks)

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