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ESA 2- Membranes and Receptors > The Autonomic Nervous System and Pharmokinetics > Flashcards

The Autonomic Nervous System and Pharmokinetics Flashcards

1
Q

What is the ANS comprised of?

A

A series of two neurones, one pre-ganglionic and one post-ganglionic

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2
Q

What is the ganglion?

A

The collection of cell bodies in the PNS

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3
Q

Where do the neurones in the ANS have their cell bodies?

A

One in the CNS, one in the PNS

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4
Q

What do neurones in the ANS exert action via?

A

Smooth muscle
Viscera
Secretory glands

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5
Q

What is the thoraco-lumbar outflow part of?

A

The sympathetic nervous system

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6
Q

Where do the nerve fibres that contribute to the thoraco-lumbar outflow have their cell bodies?

A

In all 12 thoracic sections and the first 2 lumbar sections

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7
Q

How long are the nerve fibres in the thoraco-lumbar outflow?

A

Short pre-ganglionic nerve fibre

Long post-ganglionic nerve fibre

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8
Q

Where can the nerve fibres synapse in the thoraco-lumbar outflow?

A

May synapse at the same level as origin (paravertebral origin)
May synapse at different level to origin
May not synapse in paravertebral chain

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9
Q

What kind of neurones are the pre-ganglionic in the thoraco-lumbar outflow?

A

Cholinergenic (ACh)

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10
Q

What do the post-ganglionic neurones in the thoraco-lumbar outflow express?

A

Nicotinic receptors

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11
Q

What kind of neurones are the post-ganglionic in the thoraco-lumbar outflow?

A

Noradrenergic (NA)

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12
Q

What are the classes of adrenoreceptors?

A

Alpha (1 and 2)

Beta (1 and 2)

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13
Q

What is the exception to the rules of the thoraco-lumbar rules?

A

Some synapses are cholinergic- perspiration and ejaculation pathways

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14
Q

What is the cranio-sacral outflow part of?

A

The parasympathetic nervous system

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15
Q

How long are the nerve fibres in the cranio-sacral outflow?

A

Long pre-ganglionic nerve fibre

Short post-ganglionic nerve fibre

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16
Q

What kind of neurones are the pre-ganglionic in the cranio-sacral outflow?

A

Cholinergic

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17
Q

What do the post-ganglionic neurones in the cranio-sacral outflow express?

A

Nicotinic receptors

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18
Q

What kind of neurones are the post-ganglionic in the cranio-sacral outflow?

A

Cholinergic

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19
Q

What synthesises acetylcholine?

A

The enzyme choline acetyltransferase (CAT)

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20
Q

What is acetylcholine synthesised from?

A

Choline and the metabolic intermediate Acetyl-CoA

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21
Q

Where is acetylcholine synthesised?

A

In the cytoplasm of cholinergic terminals

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22
Q

What happens to acetylcholine once synthesised?

A

Some is degraded by cytoplasmic cholinesterase

The majority is transported into synaptic vesicles by an indirect active transport mechanism

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23
Q

What do cholinergic terminals possess?

A

Numerous vesicles contain high concentrations (>100mM) of ACh

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24
Q

How can ACh be released from cholinergic terminal vesicles?

A

By Ca mediated exocytosis

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25
Q

What happens to released ACh?

A

It can interact with both pre- and postsynaptic cholinoreceptors

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26
Q

What is the opportunity for ACh to interact with receptors limited by?

A

ACh in the synaptic cleft being acted upon by cholinesterase, which rapidly degrades ACh to choline and acetate

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27
Q

Where is the activity of cholinesterase highest?

A

At fast (nicotinic) cholinergic synapses

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28
Q

What is the result of cholinesterase at cholinergic synapses?

A

The synaptic cleft half-life of ACh is only a few milliseconds

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29
Q

What recaptures most choline?

A

A choline transporter present in the synaptic terminal

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30
Q

What is noradrenaline synthesised from?

A

Tyrosine

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31
Q

Where is noradrenaline synthesised?

A

Within the nerve terminal

32
Q

What is the rate limiting enzyme in noradrenaline synthesis?

A

Tyrosine hydroxylase

33
Q

Where is the enzyme dopamine ß-hydroxylase located?

A

Within synaptic vesicles

34
Q

What does dopamine ß-hydroxylase do?

A

Transports newly synthesised dopamine into the vesicle prior to its conversion to noradrenaline

35
Q

What does dopamine ß-hydroxylase recognise?

A

Dopamine and noradrenaline

36
Q

What does dopamine ß-hydroxylase recognising dopamine and noradrenaline allow for?

A

It’s recycling following release and reuptake

37
Q

At what level is cytoplasmic NA concentration under most circumstances?

A

Low

38
Q

At what level is intravesicular NA concentration under most circumstances?

A

Very high (0.5-1.0M)

39
Q

Why is a very high intravesicular NA concentration possible?

A

Because the vesicular transporter exploits a H-ATPase-generated cytoplasm-vesicle H-gradient to move catecholamines against their concentration gradient

40
Q

What is cytoplasmic NA susceptible?

A

Enzymatic breakdown by monoamine oxidase

41
Q

How is tyrosine converted to noradrenaline?

A

Tyrosine -> dopa -> dopamine -> noradrenaline

42
Q

How is NA released?

A

Ca mediated exocytosis

43
Q

What can released noradrenaline interact with?

A

Both pre- and postsynaptic adrenoreceptors

44
Q

What is the opportunity for noradrenaline to interact with adrenoreceptors limited by?

A

A high affinity reuptake system, Uptake 1

45
Q

What does uptake 1 act to do?

A

Rapidly remove NA from the synaptic cleft, rapidly decreasing the localised concentration and terminating its actions

46
Q

What happens to any NA escaping from the synaptic cleft?

A

It is removed from the extracellular space by another, widespread, lower affinity reuptake system, uptake 2

47
Q

What is ACh and NA release triggered by?

A

Depolarisation of the nerve terminal membrane, Ca entry, and fusion of vesicles with the pre synaptic membrane (Ca mediated exocytosis)

48
Q

What drugs act on cholinergic nerve terminals?

A

Nicotinic cholinoceptor antagonists
Muscarinic cholioceptor agonists
Muscarinic cholinoceptor antagonists
Cholinesterase inhibitors

49
Q

How do agents that interfere with cholinergic transmission and are of therapeutic use generally act?

A

By interaction with cholinoceptors

50
Q

What is the exception to agents interfering with cholinergic transmission acting by interaction with cholinoceptors?

A

Cholinesterase inhibitors

51
Q

How are cholinesterase inhibitors used therapeutically?

A

They decrease the rate of ACh degradation, and so prolong the lifetime of ACh within the synaptic cleft

52
Q

What drugs act on adrenergic nerve terminals?

A 
α-methyl-tyrosine 
α-methyl-DOPA
CarbiDOPA
Adrenergic blocking drugs 
Indirectly-acting sympathomimetic agents (IASAs)
Uptake 1 inhibitors
53
Q

What does α-methyl-tyrosine do?

A

Completely inhibits tyrosine hydroxylase, and therefore blocks de novo synthesis of noradrenaline

54
Q

What is the clinical use of α-methyl-tyrosine?

A

Inhibits NA synthesis in pheochromocytoma

55
Q

What is α-methyl-DOPA taken up by?

A

Adrenergic neurones

56
Q

What happens do α-methyl-DOPA when taken up by adrenergic neurones?

A

It is converted to α-methyl-noradrenaline

57
Q

How is α-methyl-DOPA differ from a true neurotransmitter?

A

It is poorly metabolised

58
Q

What is the result of α-methyl-DOPA being poorly metabolised?

A

It accumulates in the synaptic vesicles of noradrenergic terminals

59
Q

How is α-methyl-DOPA released from synaptic vesicles?

A

Ca mediated exocytosis

60
Q

What happens when α-methyl-DOPA is released from synaptic vesicles?

A

It preferentially activates pre-synaptic α2 receptors

61
Q

What happens when α-methyl-DOPA activates pre-synaptic α2 receptors?

A

The ßγ subunit of the α2 receptor inhibits the VOCC, reducing Ca mediated neurotransmitter release

62
Q

What does carbiDOPA do?

A

Inhibits DOPA decarboxylase in the periphery, but not in the CNS

63
Q

Why does carbiDOPA not inhibit DOPA decarboxylase in the CNS?

A

It does not cross the BBB

64
Q

What is carbiDOPA used for?

A

In combination with L-DOPA in the treatment of Parkinson’s disease

65
Q

Where are adrenergic blocking drugs selectively concentrated?

A

In terminals

66
Q

How are adrenergic blocking drugs selectively concentrated in terminals?

A

By uptake 1

67
Q

How do adrenergic blocking drugs act?

A

Via a variety of mechanisms, including a local anaesthetic action reducing impulse conduction and Ca mediated exocytosis and repletion of NA from synaptic vesicles

68
Q

Why are adrenergic blocking drugs rarely used therapeutically?

A

Because of their severe side effects, including postural hypotension

69
Q

What are IASAs structurally related to?

A

NA

70
Q

Why are IASAs though to exert their actions by additional/other methods to NA?

A

Because they are only weak agonists at adrenoreceptors

71
Q

What happens to IASAs?

A

They are recognised and transported into the adrenergic terminal by Uptake 1 and taken up into the synaptic vesicles

72
Q

What happens to NA displaced by IASAs?

A

It can leak into the synaptic cleft, by a mechanism unrelated to Ca mediated exocytosis

73
Q

What is the extent to which NA leaks into the synaptic cleft greatly enhanced by?

A

The inhibition of the NA-degrading enzyme MAO

74
Q

What do uptake 1 inhibitors comprise?

A

An important class of therapeutic agents, the tricyclic antidepressants

75
Q

How do uptake 1 inhibitors exert their therapeutic action?

A

Centrally

76
Q

What are the unwanted side effects of tricylic antidepressants?

A

Their possible peripheral actions, e.g. tachycardia and cardiac dysrhythmias

ESA 2- Membranes and Receptors (13 decks)

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