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Farmer > Choliomimetics > Flashcards

Choliomimetics Flashcards

1
Q

Describe the synthesis of acetylcholine.

A

Acetylcholine is synthesised from Acetyl CoA and choline via choline acetyltransferase (CAT)

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2
Q

Why are the receptors described as nicotinic and muscarinic?

A

Muscarinic effects are those that can be replicated by muscarine
Nicotinic effects are those that an be replicated by nicotine
Comes from amanita muscaria and nicotiana tabacum

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3
Q

What can be given to abolish muscarinic effects?

A

Atropine (competitive muscarinic antagonist)

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4
Q

State where you would find the different types of muscarinic receptor.

A

M1 – salivary glands, CNS, stomach
M2 – heart
M3 – salivary glands, bronchial/visceral smooth muscle, eyes, and sweat glands
M4 and M5 are found in the CNS

NOTE: muscarinic receptors are generally excitatory except for on the heart

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5
Q

What type of receptor are all muscarinic receptors?

A

7TM

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6
Q

What is the difference in the G-protein receptors of M1, M3 and M5 compared to M2 and M4?

A

M1, M3 and M5 = Gq protein linked receptors – they stimulate PLC which increases IP3 and DAG
(Odd numbers = Odd name)

M2 and M4 = Gi protein linked receptors (inhibitory) – they decrease the production of cAMP

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7
Q

Describe the structure of nicotinic receptors. What determines its ligand binding properties?

A

Nicotinic receptors consist of 5 subunits (alpha, beta, gamma, delta or epsilon)
The combination of subunits determines its ligand binding properties.

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8
Q

What are the two main types of nicotinic receptor? Describe their subunit composition.

A 
Muscle = 2 alpha + beta + delta + epsilon 
Ganglion = 2 alpha + 3 beta
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9
Q

How do the effects of acetylcholine on nicotinic receptors compare to its effects on muscarinic receptors?

A

The effects of acetylcholine are relatively weak on nicotinic compared to muscarinic

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10
Q

What three effects does muscarinic stimulation have on the eye?

A

Contraction of the ciliary muscle (accommodate for near vision)

Constriction of sphincter pupillae (circular muscle of the eye) – this constricts the pupil and increases drainage of intraocular fluid

Lacrimation (tears)

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11
Q

What is glaucoma?

A

Sustained raised intraocular pressure – this can cause damage to the optic nerves and retina and can lead to blindness

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12
Q

Where is aqueous humour produced? Describe its passage through the eye.

A

The capillaries in the ciliary body produce aqueous humour
Aqueous humour passes anteriorly into the anterior chamber and is then drained through the canals of Schlemm into the venous system

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13
Q

What is the role of aqueous humour?

A

Provides oxygen and nutrients to the cornea and lens because they don’t have a blood supply

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14
Q

What happens in Angle-closure glaucoma?

A

Increased pressure reduces the angle between the cornea and the iris, which decreases the drainage of intraocular fluid through the canals of Schlemm

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15
Q

What are the effects of giving a muscarinic agonist to people with Angle-closure glaucoma?

A

This causes constriction of sphincter pupillae and opens up the angle to increase the drainage of intraocular fluid

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16
Q

Describe, in detail (including the mechanism), the muscarinic effects on the heart.

A

Binding of acetylcholine to the M2 receptors (Gi protein linked receptor) causes a decrease in cAMP production
This triggers a decrease in Ca2+ influx, which leads to a decrease in cardiac output
It also triggers an increase in K+ efflux, which leads to a decrease in heart rate

17
Q

Describe the muscarinic effects on the vasculature.

A

No direct parasympathetic innervation of vessels
However, there are muscarinic receptors on endothelial cells. When stimulated, it triggers NO production from endothelium, causing vasodilation and TPR decrease

18
Q

Summarise the muscarinic effects on the cardiovascular system.

A

Decrease in heart rate
Decrease in cardiac output (due to decreased atrial contraction)
Decrease in total peripheral resistance (due to vasodilation)
Decrease in blood pressure

19
Q

Describe the muscarinic effects on non-vascular smooth muscle.

A

It is the opposite of muscarinic effects on vascular smooth muscle
It causes CONTRACTION of non-vascular smooth muscle
Lungs – bronchoconstriction
GI tract – increased motility
Bladder – increased bladder emptying

20
Q

Describe the muscarinic effects on exocrine glands.

A

Salivation
Increased bronchial secretions
Increased GI secretions (including gastric HCl production)
Increased sweating (sympathetic-mediated)

21
Q

What are the two types of cholinomimetic drug?

A

Directly Acting – muscarinic agonists

Indirectly Acting – acetylcholinesterase inhibitors -> increase the synaptic concentration of acetylcholine

22
Q

State two types of muscarinic receptor agonists and give an example of each.

A

Choline Esters – Bethanechol (M3 selective agonist used to increase gut motility and bladder emptying)

Alkaloids – Pilocarpine (non-selective muscarinic agonist used to reduce pressure in eye e.g. Glaucoma, acts on postganglionic parasympathetic synapses)

23
Q

What are some side effects of pilocarpine?

A

Blurred vision – Constricts pupil/induces accommodation
Hypotension – Increases NO production in endothelium
Sweating – Increases Ach activation of Sweat glands
Respiratory difficulty – Increases bronchoconstriction
GI disturbance and pain – Increases gut motility

24
Q

What are some side effects of Bethanechol?

A

Same side effects as pilocarpine as well as possible bradycardia and nausea

25
Q

What is the half life of pilocarpine and bethanechol?

A

3-4 Hours

26
Q

What are the two types of cholinesterase?

A

Acetylcholinesterase – found in ALL cholinergic synapses, highly selective for acetylcholine, rapid

Butyrylcholinesterase – Not in synapses, in plasma and many tissues, broad specificity, hydrolyses other esters e.g. suxamethonium, shows genetic variation

27
Q

State the effects of low, moderate and high doses of cholinesterase inhibitors.

A

LOW – enhances muscarinic effects
MODERATE – further enhances muscarinic effects + increases transmission at ALL autonomic ganglia (nicotinic receptors)
HIGH – depolarising block at autonomic ganglia and NMJ (the nicotinic receptors get overstimulated so they shut down)

28
Q

What are the two types of anticholinesterase? Give examples of each.

A

Reversible – physostigmine, neostigmine, donepezil

Irreversible – ecothiopate, dyflos, sarin

29
Q

Describe the mechanism of action of reversible anticholinesterases.

A

Reversible anticholinesterases donate a CARBAMYL group, which blocks the active site of the acetylcholinesterase
Carbamyl groups are removed by slow hydrolysis (takes mins rather than milliseconds)

30
Q

What is physostigmine used to treat?

A

Glaucoma (It has a half-life of about 30 mins, shorter than Pilocarpine or Bethanechol)

31
Q

What type of poisoning is physostigmine used to treat?

A

Atropine poisoning (because it increases the synaptic concentration of acetylcholine so it can outcompete the atropine)

32
Q

What type of compound are irreversible anticholinesterases?

A

Organophosphates

33
Q

Describe the mechanism of action of irreversible anticholinesterases.

A

They rapidly react with the enzyme active site, leaving a large blocking group. The blocking group is stable and resistant to hydrolysis so recovery requires the production of new enzymes

34
Q

What is ecothiopate used to treat?

A

Glaucoma

35
Q

State some side-effects of ecothiopate.

A

Same as Bethanechol without nausea – Its final physiological effect is the same, so it shouldn’t be shocking that they have similar side effects

36
Q

What type of anticholinesterases can cross the blood-brain barrier?

A

Non-polar

37
Q

Describe the effects of low and high doses of anticholinesterase drugs on CNS activity.

A

Low – CNS excitation with the possibility of convulsions

High – unconsciousness, respiratory depression and death

38
Q

State two anticholinesterases that are used to treat Alzheimer’s disease

A

Donepezil

Tacrine

39
Q

Describe the treatment of organophosphate poisoning

A

IV atropine – this blocks the muscarinic receptors, reducing effect of raised synaptic ACh concentration

Patient is put on a ventilator because of respiratory depression caused by excess ACh at the synapse (causing depolarising block)

If treated in first few hours, patient should be given IV Pralidoxime in conjunction with atropine, Pralidoxime is an oxime which can unblock the enzymes

Farmer (33 decks)

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