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Year 1 > Pharmacology and physiology of the autonomic system > Flashcards

Pharmacology and physiology of the autonomic system Flashcards

1
Q

What is the role of the autonomic nervous system?

A

Branch of the CNS which has involuntary control over respiration, digestion and blood pressure.

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2
Q

What are the divisions of the autonomic nervous system?

A

Sympathetic, parasympathetic and enteric

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3
Q

What is the role of the enteric system?

A

Involuntary control of the gastric system.

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4
Q

What are M1 receptors?

A

Found in the CNS and the glands. Gs proteins which increases cAMP activity to activate phospholipase C -> IP3 which increases Ca2+ for increased membrane excitability and K+ conductance. It increases CNS excitability and gland secretion.

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5
Q

What are M2 receptors?

A

Found in the CNS and the atria of the heart. Gi protein which negatively reduces cAMP activity and reduces heart contraction and CNS excitability.

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6
Q

What are M3 receptors?

A

Found in the exocrine glands, smooth muscle of the GI tract. It is a Gs protein positively coupled to cAMP to increase Ca2+ availability and induce gland secretion and smooth muscle contraction.

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7
Q

What are M4 receptors?

A

Found in the CNS. Gi protein negatively coupled to cAMP but increases K+ conductance and reduces CNS excitability

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8
Q

What are M5 receptors?

A

Found in substantia nigra of the CNS. Gs protein positively coupled to cAMP to increases K+ conductivity. It has unknown effect.

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9
Q

How do nicotinic receptors respond to drugs?

A

They are previously in a closed state. When a drug binds they open. However, excessive dose over time can lead to it becoming desensitised and remaining closed unless a higher dose is given or withdrawal occurs.

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10
Q

Where are nicotinic receptors located?

A

In the muscles, ganglia and CNS.

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11
Q

Where is the (a3)2(B2)3 receptor located?

A

In muscles, ganglia and pre- or post-ganglionic neurons of the CNS. Induces release of acetylcholine and increases excitability and permeability of the membrane to the cations Na+ and K+

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12
Q

What is the (a7)5 receptor?

A

Present in the pre-or post ganglionic neurons of the CNS. It is a subtype of a nicotonic receptor which allow influx of Na+ or K+. It is implicated in Alzhiemer’s disease.

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13
Q

What are the muscle type nicotinic receptors?

A

(a3)2(B2)3 receptor which is found in the motor end plate to increase cation permeability and membrane excitability.

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14
Q

What are the ganglion nicotinic receptors located?

A

(a3)2(b2)3 which is found in ganglia such as pre-vertebral or paravertebral and increase membrane excitability or cation permeability

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15
Q

How do drugs affect the cholinergic system?

A

Inhibits acetylcholine uptake, packaging into vesicles, exocytosis of vesicles, acetylcholinesterase enzyme or action on post-synaptic receptors.

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16
Q

How is acetylcholine packaged into vesicles?

A

Via the ATP proton pump exchanger vAchT (vesicular acetylcholine transporter) which allows influx of Ach from synaptic cleft in exchange for H+

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17
Q

What is the rate limiting step in acetylcholine production?

A

Uptake of acetylcholine into the pre-synaptic cell.

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18
Q

What is vesamicol?

A

Inhibits the vAchT for packaging acetylcholine into vesicles.

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19
Q

What is hemicholinium?

A

Inhibits acetylcholine uptake into the pre-synaptic cell and reduces acetylcholine production.

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20
Q

What is botulinium?

A

Toxin released by bacteria used in beauty industry as botox which reduces exocytosis of vesicles of acetylcholine.

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21
Q

What are the type of cholinesterase inhibitors?

A

Reversible inhibitor which binds for a period of time to ACHesterase. Irreversible inhibitor which forms covalent bond with the enzyme to irreversibly inactive it.

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22
Q

How do irreversible cholinesterase inhibitors work?

A

Form covalent bond with ACHesterase which prevents reactivation

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23
Q

What is the role of organophosphate?

A

A pesticide which forms covalent bond with serine of acetylcholinesterase and irreversibly inactivates it.

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24
Q

What is the role of 2-PAM?

A

Treatment for pesticide poisoning by binding to organophosphate and prevent formation of covalent bond.

PRALIDOXIME

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25
Q

What are non-depolarising blocking agents and their use?

A

Non-depolarising blocking agents are muscarinic receptor antagonists which can act as muscle relaxants. They bind to the receptor and do not cause depolarisation, cannot be cleared by ACHesterase and lead to muscle paralysis in excess.

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26
Q

What are fast non-depolarising nicotinic agents?

A

Mivacurium

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27
Q

What are intermediate non-depolarising nicotinic agents?

A

Atracurium

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28
Q

What are slow non-depolarising nicotinic agents?

A

Pancuronium

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29
Q

What are depolarising blocking agents?

A

Bind to the muscarinic receptor and cause constant depolarisation and lead to muscle fasiculation and paralysis. It is used in anaesthesia.

29
Q

What are depolarising blocking agents?

A

Anaesthetic drug- Bind to the muscarinic receptor and cause constant depolarisation and lead to muscle fasiculation. Second stage is desensitisation of the receptor which leads to paralysis.

29
Q

What are depolarising blocking agents?

A

Bind to the muscarinic receptor and cause constant depolarisation and lead to muscle fasiculation and paralysis. It is used in anaesthesia.

30
Q

What is a short acting depolarising nicotinic agent?

A

Suxamethonium

31
Q

What are the muscarinic antagonists?

A

Non-depolarising neuromuscular agents. Includes atropine, tropicamide and scopolamine.

32
Q

What is atropine?

A

Muscarinic antagonist used to treat organophosphate poisoning AND BRADYCARDIA

33
Q

What is tropicamide?

A

A muscarinic antagonist used in opthalamology to reduce pupil constriction.

34
Q

What is scopolamine?

A

Muscarinic antagonist used for post surgery vomiting and muscle sickness

35
Q

What are the muscarinic agonists?

A

Pilocarpine which is used to reduce eye pressure to treat glaucoma.

36
Q

What is isoprenaline?

A

Synthetic form of noradrenaline

37
Q

How is tyrosine synthesised?

A

Phenylalanine-> tyrosine via phenylalanine hydroxylase

38
Q

How does the adrenal gland release catecholamines?

A

Pre-sympathetic ganglion leave the sympathetic trunk via the sphlancic nerve to act on the pre-vertebral ganglia of the adrenal medulla and act on chromaffin cells

39
Q

How many subclasses of Alpha 1 receptors are there?

A

A1a, A1b and A1d

40
Q

How many subclasses of Alpha 2 receptors are there?

A

A2a, A2b, A2c, and A2d

41
Q

How many B-adrenergic receptors are there?

A

3

42
Q

What are the effects of adrenergic agonists?

A

Increased tacycardia, hypertension, myadriasis (pupil dilation) , pallor and bronchodilation

43
Q

What are the a1 receptors?

A

Noradrenaline has the highest binding to this, then adrenaline, then isoprenaline. It increases cAMP activity -> phospholipase C to increase IP and DAG for Ca2+ release and increases contractility of the heart.

44
Q

What are the A1 agonists?

A

Phenyelphrine and methoxamine

45
Q

What are the a1 antagonists?

A

Praxosin and doxazosin

46
Q

What are the a2 receptors?

A

Adrenaline has the highest binding to this, then noradrenaline, then isoprenaline. It causes the reduction of cAMP activity but increases K+ channel activity.

47
Q

What are the A2 agonists?

A

Clonidine

48
Q

What are the A2 antagonists?

A

Yohimbine and idazoxan

49
Q

What are the B1 receptors?

A

Isoprenaline > noradrenalien > adrenlaine. Increases cAMP activity.

50
Q

What are B1 agonists?

A

Dobutamine and xamoterol

51
Q

What are the B1 antagonists?

A

Atenolol and metaprolol

52
Q

What are the B2 receptors?

A

Isoprenaline > adrenaline > noradrenaline. It increases cAMP activity.

53
Q

What are the B3 receptors?

A

Isoprenaline -> noradrenaline and adrenaline have equal effect. It increases cAMP activity.fOUND IN THE GALL BLADDER, ADIPOSE TISSUE AND URINARY BLADDDER

54
Q

How are adrenaline, noradrenaline and isoprenaline transported neuronal?

A

From the neuronal cell membrane via exocytosis. Noradrenaline -> adrenaline -> isoprenaline

55
Q

What inhibits neuronal transport of noradrenaline?

A

Cocaine and amphetamines

56
Q

What is the extraneuronal transport of noradrenaline?

A

Uptake of noradrenaline into non-neuronal cells, including dopamine and histamine.

57
Q

What inhibits extra-neuronal transport of noradrenaline?

A

Steroid hormones.

58
Q

What is the vesicular transport of noradrenaline?

A

Uptake of noradrenaline via vesicles including dopamine.

59
Q

What inhibits vesicular transport of noradrenaline?

A

Tetrabenazine and reserpine

60
Q

What inhibits noradrenaline synthesis?

A

Methyltyrosine

61
Q

What are uptake 1 blockers?

A

Prevent neuronal uptake of noradrenaline such as tricyclic drugs and cocaine.

62
Q

What is an example of a uptake blocker 1 tricyclic drug?

A

Despramine.

63
Q

What are sympathomimetic drugs?

A

Drugs which induce the activity of the sympathetic nervous system.

64
Q

What are indirectly acting sympathomimetics?

A

Tyramine, ingested with marmite, wine or cheese. For patients taking MAO inhibitors, it is problematic because tyramine is exchanged for noradrenaline via NET transport which allows noradrenaline to be released without synaptic transmission.

65
Q

What are the MAO inhibitors?

A

Non selective such as phenelezine, MAO A selective or MAO B selective.

66
Q

What is the effect of isoprenaline on the body?

A

Acts mainly on B-adrenergic as a vasodilator.

67
Q

What is the effect of adrenaline on the body?

A

Acts on both alpha and beta as vasodilator but increases HR

68
Q

What is the effect of noradrenaline?

A

Acts on mainly alpha adrenergic recepotrs and increases systolic and diastolic pressure as vasocontrictor.

69
Q

What are the a-adrenoreceptor antagonists side effects?

A

Failure for ejaculation, hypotension and tacycardia

70
Q

What are the b-adrenoreceptor antagonists and side effects?

A

Bronchoconstrction, cardiac failure and fatigue

Year 1 (191 decks)

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