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Foundations & Anatomy First year > Autonomic and NMJ Pharmacology > Flashcards

Autonomic and NMJ Pharmacology Flashcards

1
Q

How many types of cholinergic receptors exist?

A

2, ionotropic (ion channel nicotinic receptor) and metabotropic (g-protein)

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2
Q

How many types of adrenergic receptors exist?

A

3, they are all metabotropic

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3
Q

What is the function of presynaptic autoreceptors?

A

Once bound to the transmitter, they will inhibit voltage gated Calcium channels and reduce further transmitter release

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4
Q

Where is the neurotransmitter usually metabolised?

A

Within the cell or in glia

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5
Q

What are the two synapsing components of the NMJ?

A

Efferent motor neurones and the skeletal muscle

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6
Q

Give examples of how you could stop the NMJ synapses working well?

A

Stop acetylcholine being packaged into vesicles
Stop vesicle release by blocking calcium channels
Stop vesicle release by preventing vesicle fusion
Blocking post synaptic nicotinic receptors
Use an agonist to keep these receptors open, causes brief muscle twitching and then paralysis as voltage gated channels stay in their refractory state

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7
Q

How can you make the NMJ synapses work better?

A

Stop the breakdown of acetylcholine by blocking the enzyme acetylcholinesterase

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8
Q

What can depolarizing and non-depolarizing blockers causing paralysis help do clinically?

A

Surgical procedures, controlling spasms in tetanus

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9
Q

What can anticholinesterases be used for clinically?

A

Treating myasthenic conditions
Reversing action of non-depolarizing blockers
Stops the breakdown of Ach by blocking the acetylcholinesterase so it hangs around in the synaptic cleft for longer.

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10
Q

How can you stop transmission in the ANS at the ganglion ?
(Ganglion is midway synapse on ANS systems)

A

The receptors are nicotinic as in NMJ so
1. Inhibit choline synthesis
2. Black calcium channels, preventing exocytosis
3. Block vesicle fusion
4. Block nicotinic receptor
Depolarising or non-depolarising (depolarising is disorganised and releases Ca2+ messengers)

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11
Q

Why can you activate nicotinic receptors at the ganglion using Nicotine but not at the NMJ?

A

Nicotine is more potent at the ganglion

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12
Q

Why are there no clinical applications of ganglionic transmission modulation?

A

Drugs modulate parasympathetic and parasympathetic ganglionic transmission and probably NMJ transmission too, producing complex actions with many side-effects

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13
Q

What is the effect of muscarinic agonists?

A

Mimics the effect of the parasympathetic nervous system

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14
Q

What is the effect of a muscarinic antagonist?

A

Blocks the effect of the parasympathetic system

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15
Q

What is gluacoma characterised by?

A

High intraoccular pressure

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16
Q

How can you inhibit post ganglionic sympathetic transmission?

A

Block enzymes that produce noradrenaline
Stop the Noradrenaline being packaged into vesicles
Introduce fake transmitter which doesn’t have the same effect as NA
Inhibit release by activating presynaptic autoreceptors (inhibiting voltage gated calcium channels and therefore inhibiting calcium dependant exocytosis)

17
Q

What are sympathomimetics and give examples?

A

Things that make the sympathetic post ganglionic synapses work better
Some sypathomematics indirectly trigger the release of NA - amphetamine
Some sympathomematics are agonists of NA which activate specific alpha and beta receptors
Things that stop the breakdown of NA have little effect because they are inactivated by uptake, and the breakdown only occurs inside cells.

18
Q

What is a clinical application of a alpha 1 agonist?

A

Stops watery secretions in the mouth and airways, used as decongestants and to dilate the pupil

19
Q

What is a clinical application of a alpha 2 agonist?

A

Treatment of hypertension- reduces heart rate and strength of contraction

20
Q

What is a clinical application of a beta 2 agonist?

A

Treatment of asthma, relaxes the muscles in the airways of the lungs

21
Q

What is a clinical application of a beta 1 antagonist?

A

Treatment of hypertension, angina, arrhythmias and gluacoma, reduces the production of aqueous humour.

22
Q

What is noteworthy about parasympathetic muscarinic antagonists?

A

Not selective and will block all three types of muscarinic receptor – M1, M2 and M3

23
Q

What is the effect of hemicholinium?

A

Blocks choline transport and so stops acetylcholine being packaged into the vesicles - affects all choline synapses

24
Q

What is the effect of suxamethoneum?

A

Blocks acetylcholine receptors. It acts as an agonist so keeps the ion channel open. Causes voltage gated channels to open - brief muscle twitching and then paralysis - channels remain in their refractory state.

25
Q

What is the effect of 3,4 aminopyridine?

A

Blocks voltage gated potassium channels so stops repolarization - continuous release of acetylcholine because there is a prolonged calcium action potential

26
Q

What is the effect of Eserine?

A

Stops the breakdown of acetylcholine by blocking acetlycholine esterase

27
Q

What is the effect of mecylamine?

A

Non-depolarising nicotinic receptor blocker?

28
Q

How do you improve ganglionic transmission?

A

Activate nicotinic receptors - more potent at ganglia than the NMJ

29
Q

What can reduce the production of aqueous humour?

A

Alpha agonists and beta blockers

30
Q

What is the effect of carbidopa?

A

Blocks the enzymes that produce NA (affects sympathetic post ganglionic transmission)

31
Q

What is the effect of resperine?

A

Blocks the transporters that fill the vesicles with NA (affects sympathetic post ganglionic transmission)

32
Q

What is the effect of methyldopa?

A

False transmitter, also activates inhibatory presynaptic autoreceptors (affects sympathetic transmission)

33
Q

What is the effect of doxazosin or propanolol?

A

Block post synaptic receptors (affects sympathetic post ganglionic transmission)

34
Q

What is the effect of cocaine, on the sympathetic post ganglionic transmission?

A

Causes an increase in the noradrenaline in the synaptic cleft

35
Q

Give example of noradrenaline agonist molecules

A

Phenylephrine and salbutamol

36
Q

What type of agonist is a mydriatic?

A

Alpha 1 (dilates the pupil)

37
Q

Which synapses are used in somatic system?

A

NMJs

38
Q

Give an overview of synaptic transmission

A
  1. Synthesis and packaging of Ach neurotransmitter
    1. Action potential reaches axon terminals
    2. Voltage-gated Ca2+ channels open
    3. Calcium-dependent exocytosis occurs
    4. Diffusion of neurotransmitter across cleft
    5. Binds to ionotropic and metabotropic receptors
    6. Presynaptic autoreceptors pick up neurotransmitter and inhibit release
    7. Uptake of neurotransmitter by glia or neurons (acetylcholinesterase in NMJ) - inactivated
  2. Metabolisation of neurotransmitter

Foundations & Anatomy First year (104 decks)

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