CPTP 2.7 ANS

Question 1

Muscarinic receptor locations

M1, M2 and M3

Answer 1

M1 - neural
M2 - cardiac
M3 - SM in lungs, GI tract, iris and most glands

Question 2

Actions of Gs protein

Answer 2

Activates adenylyl cyclase

Activates Ca2+ channels

Question 3

Actions of Gi protein

Answer 3

Inhibits adenylyl cyclase
Activates K+ channels

Binds to M2 receptor

Question 4

Action of Gq protein

Answer 4

Activates phospholipase C

Binds to M1 and M3 receptors

Question 5

M2 (parasympathetic) receptor

Effector organ? Its parasympathetic response?

Answer 5

Heart muscle

Decrease HR

Question 6

M3 receptor

Effector organs and their parasympathetic response?

Answer 6

Salivary glands - watery secretion
Lungs - bronchoconstriction
Stomach - increased secretions and motility
eye - constriction of pupil and increased outflow of aqueous humour

Question 7

what is glaucoma

Answer 7

increase in aqueous humour and so causing increased pressure in the eyes

Results in optic nerve damage

Question 8

mechanism of action of neurotransmitter

Answer 8

1. synthesis (choline + AcCoA = ACh)
2. storage in vesicles
3. Exocytic release (Ca2+ influx causes vesicle migration followed by release of ACh)
4. Receptor binding (muscarinic/ nicotinic) followed by ion influx and action potential)
5. Termination (breakdown in synapse by acetylcholine esterase (AChE)
6. Recycling

Question 9

What is the function of AChE?

Answer 9

break down ACh and form acetate and choline

Question 10

Anti-cholinergic drug

Answer 10

e.g. Neostigmine

Inhibit AChE to prolong duration of action of ACh

Question 11

A drug to treat glaucoma

Answer 11

Topical pilocarpine

causes the ciliary muscle to contract, opening the trabecular meshwork. This action facilitates the rate that aqueous humour leaves the eye to decrease intraocular pressure

Question 12

Why do muscarinic antagonists need localised administration?

Answer 12

Due to the widespread distribution of muscarinic receptors, systematically administered antimuscarinics have multiple effects.

Question 13

Clinical use of muscarinic antagonist in ophthalmology

Answer 13

Atropine or tropicamide

To dilate the pupil and paralyse accommodation to enable eye examination

Topical administration

Question 14

Clinical use of muscarinic antagonist in respiratory

Answer 14

Ipratropium or tiotropium (by inhalation)

To treat asthma/ COPD
Dilation of bronchial smooth muscle

Question 15

Clinical use of muscarinic antagonist in cardiology

Answer 15

Atropine (IV)

Treatment of sinus bradycardia e.g. after MI

Question 16

The major side effects of antimuscarinic drugs

Answer 16

blurred vision
mydriasis
urinary retention
confusion
constipation
dry mouth
headache
exacerbation of glaucoma

Question 17

action of neuronal nicotinic agonist and its clinical use

Answer 17

Activate both sym- and para- nervous system

Effect is autonomic confusion therefore neuronal nicotinic agonists are not clinically useful

Question 18

Action of neuronal nicotinic antagonist

Answer 18

Causes loss of sympathetic and parasympathetic reflexes especially in cardiac tissue

Question 19

What is suxamthonium?

Answer 19

Muscular nicotinic agonist

Question 20

Action of muscular nicotinic agonist

Answer 20

• Long lasting depolarisation leading to blocking effect
• Used for muscle relaxation during surgery
• Broken down by a plasma cholinesterase to inactive metabolites
• Longer duration of effect than acetylcholine (as it is not hydrolysed by AChE)

Question 21

Action of muscular nicotinic antagonist

Answer 21

e. g. atracurium
- used to induce muscle relaxation during surgery or intensive care
- competitive antagonist
- action reversed by anticholinesterases