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Year 2 > Cholinergic Pharmacology > Flashcards

Cholinergic Pharmacology Flashcards

1
Q

What consists of the CND

A

Brain and Spinal Cord

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2
Q

Two parts of the PNS

A

Somatic (NMJ)

Autonomic

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3
Q

What chemical messengers are found in Somatic

A

ACh

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4
Q

What chemical messengers are found in autonomic

A

ACh and Noradrenaline

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5
Q

What chemical messenger acts in the Parasympathetic pathway

A

ACh

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6
Q

What neurotransmitter works in the sympathetic pathways

A

Noradrenaline

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7
Q

What can cholinergic receptors be categorised as

A

Nicotinic

Muscarinic

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8
Q

What type of receptor is Nicotinic

A

Ion channel

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9
Q

What type of receptor is Muscarinic

A

G-protein couples

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10
Q

Where are muscarinic receptors found

A

Parasympathetic system

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11
Q

Length of sympathetic preganglionic fibres vs parasympathetic

A

Sympathetic - shorter

Parasympathetic - longer

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12
Q

Why are sympathetic preganglionic shorter

A

Because the ganglia are closer to the spinal cord

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13
Q

Why are parasympathetic postganglionic fibres shorter

A

They synapse close to the target organ

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14
Q

What does ACh bind to in the somatic NS

A

Nicotinic receptors at the neuromuscular junction

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15
Q

Describe the processes that take place at the NMJ

A
  1. Acetyl CoA reacts with Choline to give ACh
  2. ACh stored in vesicles
  3. Vesicles fuses with membrane on pre-synapse
  4. ACh binds to Nicotinic cholingeric receptor
  5. Acetylcholinesterase breaks ACh to Choline and Acetate
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16
Q

Enzyme that catalyses process of choline + Acetyl CoA -> ACh

A

CAT (Choline acetyl transferase enzyme)

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17
Q

How does Botulinum Toxin effect the NMJ

A

Inhibits ACh vesicle release = paralysis by using proteases to degrade vesicle proteins

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18
Q

What two reasons do we use Botox for

A
  1. Cosmetic

2. Spasticity

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19
Q

Name a competitive NAChR antagonist

A
  1. Tubocurarine
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20
Q

How does Tubocurarine function

A
  1. Acts as a neuromuscular blockade by binding to 2 nicotinic ending sites preventing binding of ACh
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21
Q

Why do we give Tubocurarine

A

Has a muscle relaxant effect

2. Result in being conscious but aware of pain and paralysed

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22
Q

How do we reverse the block effect of Tubocurarine

A

Sugammadex

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23
Q

How does Sugammadex reverse block of Tubocurarine

A

Selective relaxant binding agent that encapsulates the blocker thereby preventing it from binding

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24
Q

Structure of Suxamethonium

A

2ACh stuck together

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25
How does Suzamethonium effect the NMJ
Desensitises the receptor causing paralysis of skeletal muscle
26
How fast does Suxamethonium act
Fast and for short duration
27
Why does Suxamethonium stay in the NMj for a while
Poor substrate for ACH esterase can only be broken down by plasma cholinesterase
28
Name a reversible ACh esterase inhibitor
Neostigmine
29
How does Neostigmine work
Blocks Cholinesterase increasing ACh at the synaptic cleft Remains for longer and stimulation lasts longer
30
When do we prescribe Neostigmine
Myasthenia Gravis - alors ACh to remain longer resulting in a stronger response
31
What is Myasthenia Gravis
Immune System produces antibodies against nAChR resulting in less receptors and weak skeletal muscles= response
32
How do irreversible inhibitors effect NMJs
Inhibit ACh Esterase causing ACh to build up Twitching, severe weakness and paralysis at NMJ
33
How does irreversible inhibition effect mAChR
``` Salivation Defecation Urination Bradycardia Hypotension ```
34
How does ACh accumulation from irreversible inhibition effect CNS
Confusion Loss of reflexes Convulsions Coma
35
Role of the autonomic nervous system
Fine tunes function of organs
36
Role of Pilocarpine
Stimulates saliva in patients with dry mouth Causes constrictor muscle and ciliary muscles to contract (miosis) Improved filtration of aqueous fluid Lowers intraocular pressure
37
What is Pilocarpine an agonist of
M3 (partial agonist)
38
Define miosis
Excessive constriction of pupil
39
When do we give Pilocarpine for adjusting intraocular pressure
For Glaucoma
40
What receptors mediate the parasympathetic pathway in the lungs
M3
41
What happens during excessive M3 receptor activation in the lung
Bronchoconstriction
42
Where is bronchoconstriction mediated by M3 seen
COPD | Asthma
43
What two types of antagonists do we have for M3 receptors in the lung
Ipratopium (short acting) and tiotropium (Long acting) | these act as bronchodilators
44
Each action in the bladder
Contraction of the bladder
45
Result of bladder agonist
More bladder contraction (urinary retention)
46
Result of using a bladder antagonist
Relaxes bladder
47
Example of a bladder agonist
Bethanechol
48
Example of a bladder antagonist
Oxynutinin
49
How does ACh effect the GI tract
Increase GI motility
50
What are mebeverine and scopolamine examples of
Gi antagonists
51
Why would we prescribe mebeverine and scopolamine
Irritable Bowel Syndrome
52
What is the adverse effects of muscarinic agonists
``` D- diarrhoea U- rination M- iosis B- Radycardia E- mesis L- agrimation S- alivation ```
53
What is a competitive antagonist at the nAChR at the autonomic ganglia
Hexamethonium
54
How does hexamethonium work
Blocks both the parasympathetic and sympathetic divisions of the autonomic nervous system
55
Does hexamethonium effect the NMJ
No
56
Four effects of parasympathetic autonomic block
1. Secretions reduced 2. Constipation 3. Urinart retention 4. Blurred vision
57
What is a sympathetic block a marker of at the autonomic level
Hypotension
58
When is hexamethonium given
As an antihypertensive
59
What does ACh regulate in the brain
Vomiting centre
60
What drug is given for motion sickness treatment and why
Scopolamine (anti-muscarininc)
61
How do we treat Parkinsons
Benxatropine blocks reuptake of ACh and increases dopamine at cleft
62
Why does Alzheimers occur
Lack of cholinergic neurones and reduction in ACh
63
How do we treat Alzheimers
Donepezil to inhibit ACh esterase increasing ACh in CNS (only works in CNS)

Year 2 (155 decks)

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