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Human Diseases > W2 9 Automic Pharmacology > Flashcards

W2 9 Automic Pharmacology Flashcards

1
Q

Basic anatomy of the ANS (pg 81)

A

Parasympathetic NS - preganglionic neurone with ACh, postganglionic neurone ACh
Sympathetic NS - preganglionic ACh, postganglionic NAd

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2
Q

What are cholinergic nerves?

A

Nerves that use acetylcholine as a neurotransmitter

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3
Q

Brief process of nerve transmission for cholinergic nerves (6 steps that will be explained in detail)

A

Supply of transmitter precursor
Synthesis of transmitter
Storage of transmitter
Release of transmitter
Inactivation of transmitter
Feedback (inhibition of release)

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4
Q

How is acetylcholine supplied for cholinergic transmission?

A

Nerves can’t make choline it is taken up from the blood, comes from diet at liver. Uptake into nerve endings via a high-affinity carrier. Sodium dependent process.

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5
Q

What is hemicholinium?

A

A competitive inhibitor of the choline carrier, causes activity-dependent block of cholinergic transmission due to the depletion of ACh stores.
Although ChAT inhibitors are not used clinically.

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6
Q

How is ACh synthesised?

A

Choline + acetyl CoA —> acetylcholine + CoA
Catalysed by choline acetyltransferase (ChAT)

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7
Q

Where does ChAT occur?

A

Occurs in the nerve cytoplasm

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8
Q

How is ACh stored?

A

Store is maintained by an energy-dependent pump. ACh is packaged into vesicles.
(Drugs can inhibit transport but not used clinically, vesamicol).

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9
Q

How is ACh released?

A

Requires entry of Ca2+ into the nerve ending. Occurs by exocytosis: fusion of vesicle membrane with the cell membrane.

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10
Q

What drugs affect the release of ACh?

A

Release is blocked by botulinum toxin.

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11
Q

What is botulinum toxin used for clinically?

A

Blepharospasm, salivary drooling, axillary hyperhidrosis, achalasia (oesophageal spasm), cosmetic reasons
Is a biological warfare agent

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12
Q

How is ACh removed from the synaptic cleft?

A

Acetylcholine —> acetate + choline
Hydrolysed by acetylcholinesterase (AChE)
Non-reversible reaction

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13
Q

Where is AChE present?

A

Present in nerve and muscle cells, red cell membrane. Mainly bound to cell membranes or basement membranes. A soluble form is secreted from neurones into CSF.

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14
Q

When do cholinesterase inhibitors work?

A

Only works if there is a pre-existing tonic release of ACh. Inhibitor to allow the released ACh to be in sufficient quantity to outcompete the antagonist. Normally used after a competitive nicotinic receptor antagonist, to overcome the neuromuscular blockade.

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15
Q

Clinically, what are the most important actions of cholinesterase inhibitors?

A

Skeletal muscle (treatment of MG, reverse neuromuscular blockade)
CNS (treatment of alzeimers, boost cholinergic transmission)
Eye (treatment of glaucoma, pupillary constriction)

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16
Q

Examples of cholinesterase inhibitors

A

Neostigmine

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17
Q

What do cholinesterase inhibitors do?

A

Amplify parasympathetic transmission

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18
Q

Why is butyrylcholinesterase?

A

A non-specific cholinesterase found in blood plasma. It will breakdown ACh. Metabolises some drugs eg suxamethonium.

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19
Q

Cholinergic nerves have presynaptic receptors. What feedback is there inhibiting further release in the cholinergic nerve systems?

A

ACh (muscarinic) inhibits release of ACh (enteric)
ACh (nicotinic) increases the release of ACh (motor)
ATP, adenosine ninjibit release ACh
Morphine (opioids) inhibit release (autonomic) ACh
Noradrenaline inhibits release (autonomic) ACh, but increases motor release.

20
Q

Why does taking morphine lead to constipation?

A

They inhibit autonomic ACh release. Most parasympathetic post-ganglionic neurones have opioid receptors on them, so morphine inhibits autonomic and enteric NS.

21
Q

What is Myasthenia Gravis?

A

Muscle weakness and rapid fatigue (affecting eyelids first - ptosis)

22
Q

What causes MG?

A

Caused by autoantibodies to skeletal nicotinic receptors

23
Q

How is MG treated?

A

Neostigmine

24
Q

What is atropine?

A

A muscarinic receptor antagonist, blocks nerves response to ACh.

25
Q

What effects does atropine have?

A

Increases parasympathetic activity, which reduces airway diameter, increases GIT activity, increases secretions in the lungs.

26
Q

Acetylcholine release and modulation

A

Image pg84

27
Q

Where is ACh the transmitter at which sites?

A
  1. Motor nerve endings in skeletal muscle
  2. Preganglionic autonomic
  3. Postganglionic parasympathetic (eg vagus to the heart)
  4. Postganglionic sympathetic (eg symp. vasoconstrictor)
28
Q

Which cells must have receptors for acetylcholine?

A

Skeletal muscle, heart and sympathetic ganglion cells

29
Q

What are skeletal muscle nicotinic receptors selectively antagonised by?

A

Decamethonium, pancuronium etc

30
Q

What are autonomic ganglia (and CNS) nicotinic receptors selectively antagonised by?

A

Hexamethonium

31
Q

Hexamethonium used to be used to treat hypertension. What were the problems?

A
  1. Very poorly absorbed from the gut so had to be given via injection
  2. Not only blocked sympathetic ganglia, but also parasympathetic ganglia to give unpredictable side effects.
32
Q

What is the mechanism of action of hexamethonium?

A

Blocks the ion channel, stopping sodium and calcium ions from getting into the cell

33
Q

What distinguishes channel block from competitive block?

A

Channel block:
Use dependent block
Block becomes more effective as membrane is hyperpolwrised

34
Q

How do nicotinic receptor antagonists work?

A

Transiently stimulate ganglia and motor end-plate, if given briefly at high concentrations.
However receptors rapidly desensitise, and so these agonists can end-up inhibiting ganglionic transmission if given at low concentrations for a ‘long time’. Ganglia are no longer targeted clinically.
(Do I even need this card)

35
Q

What are muscarinic receptors?

A

G-protein couple receptors

36
Q

What are the 3 main classes of muscarinic receptors?

A

M1 stomach, salivary glands
M2 cardiac
M3 smooth muscle

37
Q

What are the clinical uses of antimuscarinic drugs (with the drug used)

A

Asthma (ipratropium)
Bradycardia (atropine)
Decrease gut motility, decrease secretions (pirenzapine)
During operations: decrease decreases in airways, decrease AChEI side effects (atropine)
To dilate pupils (tropicamide)
Urinary incontience (oxybutynin)
Motion sickness (hyoscine)

38
Q

What are the parasympathetic effects that antimuscarinics reverse?

A

In asthma they inhibit parasympathetic bronchoconstriction
Opposes PNS slowing of heart rate for bradycardia
In eyes PNS usually causes pupillary constriction

39
Q

Examples of muscarinic agonists (parasympathomimetics)

A

ACh (endogenous), muscarine, pilocarpine

40
Q

Effects of parasympathomimetics

A

Cardiovascular - decreased HR, cardiac output
Smooth muscle - contracts, vascular dilates via endothelium
Exocrine glands - secrete - sweating, lacrimation, salivation, bronchial secretion

41
Q

How do parasympathomimetics affect blood pressure?

A

Endothelial cells produce NO when seeing a muscarinic agonist. These cause release of vasodilators and travel to smooth muscle cells causing them to dilate. So peripheral vasodilation, causing fall in blood pressure.

42
Q

What are the effects of muscarine agonists?

A

Increased secretions (salivations), increased gut motility, slowing of the heart, bronchoconstriction, urinary frequency, constriction of pupils, vasodilation (via activation of endothelial receptors)

43
Q

What drugs can have similar effects to muscarine agonists?

A

Many of the same effects present with acetylcholinesterase inhibition.

44
Q

Clinical uses of muscarinic agonists?

A

Pilocarpine - topically for glaucoma - through action on ciliary muscle and hence increasing aqueous humor drainage

45
Q

What is the difference between nicotinic and muscarinic receptors?

A

Nicotinic are ligand-gated ion channels
Muscarinic are G-protein coupled receptors

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