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Principles of Therapy > Theme 5 - Nervous System > Flashcards

Theme 5 - Nervous System Flashcards

1
Q

What are the main functions of the autonomic nervous system?

A

Cause consistency of internal environment (homeostasis)
Includes all involuntary efferent neurons
Controls subconscious effectors

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2
Q

What are the 3 divisions of the autonomic nervous system?

A

enteric
parasympathetic
sympathetic

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3
Q

What is the difference between sympathetic and parasympathetic nervous system?

A

Sympathetic - fight or flight

Parasympathetic - rest and digest

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4
Q

What are the neurotransmitters in the sympathetic nervous system?

A

Adrenergic: noradrenaline

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5
Q

What are the neurotransmitters in the parasympathetic nervous system?

A

Cholinergic: acetylcholine

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6
Q

What are the receptors involved in cholinergic neurotransmission?

A

Nicotinic and muscarinic

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7
Q

What are the 2 types of nicotinic receptors and where are they located?

A

NN - autonomic ganglia

NM - skeletal muscle

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8
Q

What are the 3 types of muscarinic receptors and where are they located?

A

M1 - gastric parietal (secretes gastric acid)
M2 - heart
M3 - glands/smooth muscle

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9
Q

What are the receptors involved in adrenergic neurotransmission?

A

Alpha and beta

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10
Q

What are the 2 types of alpha receptors and where are they located?

A

alpha-1: postsynaptic neurons (esp. smooth muscle)

alpha-2: presynaptic neurons (autoreceptors)

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11
Q

What are the 2 main types of beta receptors and where are they located?

A

beta-1: intestinal smooth muscle and heart

beta-2: bronchial, uterine, vascular smooth muscle

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12
Q

What is the effect of alpha receptor stimulation

A

excitatory, except smooth muscle in gut and eye constriction

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13
Q

What is the effect of beta receptor stimulation

A

inhibitory, except in heart

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14
Q

What is the response of the parasympathetic and sympathetic nervous system on the EYES?

A

Parasympathetic: constricts pupils
Sympathetic: dilates pupile

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15
Q

What is the response of the parasympathetic and sympathetic nervous system on the HEART?

A

Parasympathetic: beats slowly
Sympathetic: beats faster and stronger

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16
Q

What is the response of the parasympathetic and sympathetic nervous system on the LUNGS?

A

Parasympathetic: constricts airways
Sympathetic: relaxes airways, deep breathing

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17
Q

What is the response of the parasympathetic and sympathetic nervous system on the DIGESTION?

A

Parasympathetic: stimulates
Sympathetic: inhibits

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18
Q

What is the response of the parasympathetic and sympathetic nervous system on the MUSCLES?

A

Parasympathetic: reduces blood flow to skeletal muscle
Sympathetic: increases blood flow to skeletal muscles

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19
Q

How does glucose and choline enter the neuron?

A

facilitated transport

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20
Q

With which ion is choline uptake associated with?

A

Na+

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21
Q

What is glucose converted into in the mitochondria?

A

Acetyl-CoA

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22
Q

What 2 components combine in the cytoplasm to form acetylcholine and what enzyme is it catalysed by?

A

Acetyl-CoA and choline

enzyme: choline acetyltransferase

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23
Q

What transports ACh into vesicles for storage?

A

VAT - vesicle-associated transporter

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24
Q

What activates VAMPS and SNAPS?

A

influx of Ca2+ into neuron

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25
Q

What do activated VAMPS and SNAPS cause?

A

exocytosis of ACh, dopamine, noradrenaline into synaptic cleft (vesicle contents)

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26
Q

What happens to ACh in axonal cleft?

A

binds to receptors and depolarisation occurs

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27
Q

How does the concentration of ACh in synaptic cleft decrease?

A

Enzyme acetylcholineesterase hydrolyses ACh to choline and acetate

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28
Q

What happens to choline and acetate after it has been hydrolysed?

A

Choline recycled back to neuron (becomes ACh again)

Acetate used for metabolic purposes

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29
Q

How much ACh reaches circulation

A

Virtually none, plasmaesterases in blood deactivate ACh immediately

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30
Q

What does tyrosine transform into?

A

dopa, then dopamine

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31
Q

Which enzyme transforms tyrosine into dopamine?

A

Tyrosine hydroxylase

32
Q

What transports dopamine into vesicles for storage?

A

VMAT - vesicle monoamine transporter

33
Q

Which enzyme turns dopamine into noradrenaline?

A

b-hydroxylase

34
Q

Which enzyme converts noradrenaline into adrenaline

A

Phenylethanolamine N-methyl transferase (only in adrenal medulla)

35
Q

How is NA removed from synaptic cleft?

A

Binds to adenoceptors of target cell
Noradrenaline transporter
There is no enzyme in synaptic cleft like acetylcholineesterase

36
Q

What are the 3 ways NA is deactivated?

A
  • Reuptake by adrenergic neuron (like choline)
  • Removal by circulation (like plasmaesterases) and degradation in liver
  • Reuptake 2 = active transport in effector cells followed by enzymatic degradation
37
Q

Which 2 enzymes degrade catecholamines?

A

COMT (Catechol – oxygen – methyltransferase)

MAO (Mono aminoxidase)

38
Q

What are the 3 clinical uses of sympathomimetic Drugs (adrenergic agonists)?

A

Increase blood pressure

Cause constriction of blood vessels in mucosa

39
Q

Name the catecholamines

A

Isoprenaline, adrenaline, noradrenaline, dopamine

40
Q

Name a β1-adrenergic agonist

A

Dobutamine

41
Q 
What type of drugs are these:
Salbutamol 
Orciprenaline
Salmeterol
Formoterol
A

β2-adrenergic agonists

42
Q

Name an α-receptor agonist

A

Phenylephrine

43
Q 
What type of drugs are these:
Ephedrine
Phenylpropanolamine
Amphetamine
Naphazoline and Oxymetazoline
A

Indirect/Mixed action adrenergic agonists

44
Q

List 3 α-antagonists

A

Phenoxybenzamine (α1&raquo_space;» α2)
Phentolamine (α1=α2)
Prazosin (α1)

45
Q 
What type of drugs are these?
Propanalol
Timolol
Pindolol
Metaprolol
Atenolol
A

β-antagonists (non- selective)

46
Q

Name a α and β-antagonist

47
Q

Name 2 direct acting muscarinic agonists

A

Muscarin and Pilocarpine

48
Q

What is the collective name for indirect acting muscarinic agonists?

A

Cholinesterase inhibitors (stop the breakdown of ACh)

49
Q 
What type of drugs are these?
Edrophonium
Neostigmine
Physostigmine
Pyridostigmine bromide
A

cholinesterase inhibitors

50
Q

Which drug is also a nicotonic agonist?

A

Neostigmine

51
Q

What is the antidote for atropine poisoning?

A

Physiostigmine

52
Q 
What type of drugs are these?
Atropine 
Scopolamine
Ipratropium
Cyclopentolate
Propantheline
A

muscarinic antagonists/blockers

53
Q

Which receptors do neuromuscular blockers block?

A

nicotinic cholinergic receptors (NM>NN)

54
Q

Which Non-polarising muscle relaxant is no longer used?

A

d-Tubocurarine (curare)

55
Q

List 6 Non-polarising muscle relaxants

A
  1. Pancuronium chloride
  2. Vecuronium bromide
  3. Atracurium besilate
  4. Cisatracurium besilate
  5. Mivacurium chloride
  6. Rocuronium bromide
56
Q

What are the 2 types of neuromuscular blockers?

A

Non-polarising muscle relaxants

Depolarising muscle relaxants

57
Q

What is the main function of neuromuscular blockers?

A

General anaesthetics

58
Q

What type of drugs are Non-polarising muscle relaxants

A

Nicotinic receptor agonists

59
Q

How do Non-polarising muscle relaxants work?

A

They compete with ACh for NM receptors, cause skeletal muscle relaxation

60
Q

What reverses the effect of Non-polarising muscle relaxants?

A

cholinesterase inhibitors

61
Q

What must be added to cholinesterase inhibitors when reversing the effects of Non-polarising muscle relaxants?

A

antimuscarinic drug (atropine)

62
Q

Name a Depolarising muscle relaxant

A

Succinylcholine

63
Q

What happens in a Phase I block of a Depolarising muscle relaxant?

A

Drug binds to NM receptor and occupies for 3-5mins, this prevents repolarisation of membrane

64
Q

What happens in a Phase II block of a Depolarising muscle relaxant?

A

After repeated doses (bad)

Repolarisation takes place slowly while receptors remain occupied, receptor becomes desensitised to effect of ACh

65
Q

What are the Disadvantages/dangers of Depolarising muscle relaxants?

A

Some patients are abnormally sensitive

66
Q

What are local anaesthetics?

A

Drugs used to prevent pain by causing a reversible block of conduction along nerve fibres

67
Q

Where are local anaesthetics administered?

A

Locally where pharmacological action is desired

68
Q

Which part of a local anaesthetic penetrates the interior of the axon?

A

lipophilic base

69
Q

What happens to local anaesthetic once it reaches the axon?

A

It becomes protonated

70
Q

What do local anaesthetics bind to?

A

receptors in Na+ channel

71
Q

What happens when local anaesthetics bind to Na+ channel?

A

It inactivates the channel at resting potential, so depolarisation does not occur and a nerve block occurs

72
Q

What is the Rate of absorption of local anaesthetics dependant on?

A

Site of administration
Dose
Specific drug

73
Q

What is often added to LA solutions?

A

vasoconctrictors (adrenaline, noradrenaline, felipressin)

74
Q

Why are vasoconctrictors added to LA solutions?

A

Reduces systemic absorption

75
Q

Where do the main side effects of LA occur?

A

Cardiovascular system and CNS

76
Q

Name 3 ester local anaesthetics

A

cocaine, benzocaine, oxybuprocaine

77
Q

Name 4 amine local anaesthetics

A

lignocaine, lidocaine, prilocaine, bupivacaine

Principles of Therapy (10 decks)

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