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PHAR2200 > ans > Flashcards

ans Flashcards

1
Q

What is the neurotransmitter at the preganglionic neuron of the sympathetic ns?

A

Acetylcholine

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2
Q

What is the neurotransmitter at the post ganglionic neuron of the sympathetic ns?

A

Noradrenaline

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3
Q

What are the target receptors for the sympathetic ns?

A

alpha and beta receptors

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4
Q

What is the neurotransmitter at the pre ganglionic neuron of the parasympathetic ns?

A

Acetylcholine

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5
Q

What is the neurotransmitter of the post ganglionic neuron of the parasympathetic ns?

A

Acetylcholine

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6
Q

What is the target receptor for the parasympathetic ns?

A

muscarinic acetylcholine receptors

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7
Q

What is the parasympathetic nerve effects of the heart?

A

Decrease rate (bradycardia)
Decrease force of contraction

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8
Q

What is the parasympathetic effect on the lungs?

A

Bronchoconstriction, secretion

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9
Q

What is the parasympathetic effect on the GI tract?

A

increase tone motility of small and large intestines
increase secretion of saliva and gastric acid

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10
Q

What is the parasympathetic effect on the glands?

A

increase sweating, salivation, lacrimation

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11
Q

What is the parasympathetic effect on the eye?

A

sphincter muscle contraction, ciliary muscle contraction

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12
Q

What is the parasympathetic effect on the blood vessels?

A

most blood not innervated
may be vasodilation in some

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13
Q

How is acetylcholine formed?

A

choline + acetyl-co-enzyme A = acetylcholine

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14
Q

What enzyme forms acetylcholine?

A

choline acetyltransferase

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15
Q

Does muscarine stimulate nicotinic receptors?

A

false

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16
Q

What is muscarine selective for?

A

muscarinic receptors

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17
Q

What is nicotine selective for?

A

nicotinic receptors

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18
Q

What is the uses of muscarinic agonists?

A

open angle glaucoma
urinary retention
paralytic ileus

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19
Q

How is open angle glaucoma treated with muscarinic agonists?

A

increases intraocular pressure
dilate pupil impairs aqueous humour drainage
cholinergic agonist constricts pupil

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20
Q

What is the mechanism of ACh-Est?

A

has two sites - anionic and esteratic to breakdown Acetylcholine

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21
Q

What are cholinesterase inhibitors?

A

inhibit the catalytic activity of cholinesterase enzymes

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22
Q

What do cholinesterase enzyme catalyse?

A

hydrolysis of acetylcholine

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23
Q

What are some short-acting reversible cholinesterase inhibitors?

A

edrophonium

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24
Q

What are some long-acting reversible cholinesterase inhibitors?

A

carbamylated intermediates, physostigmine; neostigmine

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25
Q

What are some therapeutic uses of cholinesterase inhibitors?

A

eye treatment
skeletal neuromuscular junction
gastrointestinal system
treatment of atropine poisoning

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26
Q

How is the eye treated by the use of cholinesterase inhibitors?

A

constriction of pupil
decreases intraocular pressure in open-angle glaucoma

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27
Q

What are some long-acting, irreversible cholinesterase inhibitors?

A

organophosphates

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28
Q

How does organophosphates work?

A

phosphorylation of acetylcholinesterase inhibits the acetyl site thus acetylcholine cannot be cleaved and accumulate

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29
Q

What are the risks of organophosphates?

A

insecticides
nerve gases

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30
Q

What is the risk of nerve gases?

A

deadly at low concentrations
toxicity due to increase acetylcholine at cholinergic synapses
persistent stimulation = neurotransmission paralysis

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31
Q

What are some signs of acute poisoning due to cholinesterase inhibitors?

A

bronchoconstriction, accumulation of respiratory secretions, weakened or paralysed respiratory muscles, central respiratory paralysis
bradycardia
sweating, salivation, lacrimation
constriction of the pupils
increase gastrointestinal activity

32
Q

What are the treatments for cholinesterase inhibitor poisoning?

A

stop exposure
assist respiration
administer cholinergic antagonist, e.g. atropine
administer pralidoxime (organopshophate poisoning)
administer anticonvulsant
monitor for cardiac irregularities
administer diazepam (treat agitation + sedation)

33
Q

Is atropine a muscarinic agonist or antagonist?

A

antagonist

34
Q

What are the major pharmacological effects of atropine?

A

decrease sweating, salivation, lacrimation
decrease gastrointestinal motility
decrease gastric acid secretion
decrease production of bronchial mucus
bronchodilation
increase heart rate

35
Q

What are some side-effects of atropine?

A

dry mouth + skin
urinary retention
cycloplegia
glaucoma
depression
hallucination
increase body temp.

36
Q

What are catecholamines?

A

hormones made by the adrenal glands

37
Q

What enzyme synthesises tyrosine into dihydroxyphenylalanine?

A

tyrosine hydroxylase

38
Q

What enzyme synthesises dihydroxyphenylalanine into dopamine?

A

DOPA decarboxylase

39
Q

What enzyme synthesises dopamine into noradrenaline?

A

dopamine β-hydroxylase

40
Q

What enzyme synthesises noradrenaline into adrenaline?

A

phenylethanolamine N-methyltransferase

41
Q

What happens to noradrenaline in the synapse?

A
  1. diffuses and has no role
  2. bind to pre-junction α2 receptors = inhibition of noradrenaline
  3. diffuse and stimulate post-junctional α and β receptors
  4. taken up by NET
  5. taken up by ENT at post-junctional cell
42
Q

What synthesises adrenaline?

A

adrenal medulla

43
Q

What are some modifications of noradrenaline?

A

increase bulkiness of substituents on the N-atom = resistance to monoamine oxidase (MAO)
modification of catechol -OH groups = resistance to catechol-O-methyl transferase (COMT)

44
Q

What are the function of α1-receptors?

A

blood vessel = vasoconstriction
lung = decrease secretion
GI tract = decrease smooth muscle motility and tone
eye = radial muscle contraction

45
Q

What are the functions of β-receptors?

A

heart = increase rate and force of contraction
blood vessels = vasodilation
GI tract = decrease smooth muscle motility and tone
lung = bronchodilation, increase secretion
eye = ciliary muscle relaxation

46
Q

What are the different types of adrenergic drugs?

A

adrenoceptor agonists
adrenoceptor antagonists
adrenergic neurone blockers
monoamine oxidase inhibitors

47
Q

What classifies adrenoceptors?

A

molecular cloning of distinct protein moieties
functional characteristics
potencies of various stimulatory catecholamines

48
Q

What is potencies of α-receptors to stimulatory catecholamines?

A

noradrenaline > adrenaline > isoprenaline

49
Q

What is the potencies of β-receptors to various stimulatory catecholamines?

A

isoprenaline > adrenaline > noradrenaline

50
Q

Where are α1 receptors found?

A

post-junctional sites

51
Q

Where are most α2 receptors found?

A

pre-junctional sympathetic nerve endings

52
Q

What does the activation of α2 receptors do?

A

inhibit noradrenaline release

53
Q

Where are β1 receptors found in abundance?

A

heart and intestinal tract

54
Q

Where are β2 receptors found in abundance?

A

respiratory tract, blood vessels and liver

55
Q

What does β1 receptors trigger?

A

increase in heart rate and force

56
Q

What does β2 receptors trigger?

A

relaxation of airway and vascular smooth muscle
glycogenolysis/gluconeogenesis in the liver

57
Q

What does the effect of adrenoceptor agonist depend on?

A

receptor selectivity of the drug
adrenoceptor profile of the cell
cellular response to receptor activation

58
Q

What are the clinical uses of adrenaline?

A

anaphylactic reactions (β-adrenoceptors)
cardiac arrest (β1-adrenoceptors)
local anaesthetic solutions (α1-adrenoceptors)

59
Q

How can adrenaline help during cardiac arrest?

A

helps restore cardiac rhythm

60
Q

Why can adrenaline be used as a local anaesthetic?

A

vasoconstrictor effect
increase duration of action
decrease risk of systemic toxicity

61
Q

What are sympathomimetic drugs?

A

stimulant compounds which mimic the effects of endogenous agonists of the SNS

62
Q

What do indirect-acting sympathomimetics do?

A

no direct agonist activity but cause
- release of noradrenaline
- block noradrenaline uptake
- inhibit noradrenaline metabolism

63
Q

What is a mixed-acting sympathomimetics?

A

Ephedrine

64
Q

What is the action of Ephedrine?

A

direct actions on adrenergic receptors
releases noradrenaline from sympathetic nerves

65
Q

Is Ephedrine a substrate for COMT or MAO?

A

no

66
Q

What is Ephedrine used clinically for?

A

relieve nasal congestion (vasoconstrictor)

67
Q

What are adrenoceptor antagonists?

A

prevent endogenous adrenoceptor agonists from binding to and stimulating adrenoceptors

68
Q

α1-adrenoceptors antagonism can help treat?

A

hypertension

69
Q

β1-adrenoceptor antagonism can help treat?

A

angina, arrhythmia, hypertension, post-myocardial infarcation

70
Q

β-adrenoceptor antagonists are used to?

A

prevent endogenous adrenoceptor agonists from binding to and activating β-adrenoceptors

71
Q

Most β-adrenoceptor antagonists end in?

A

-olol

72
Q

What is an example of a β-adrenoceptor antagonists?

A

propranolol

73
Q

What are the properties of propranolol?

A

non-selective antagonist
oxymethylene bridge improves antagonists potency
similar structure to β-agonists and local anaesthetics

74
Q

What are the adverse effects of non-selective β-adrenoceptor antagonists?

A

may precipitate congestive heart failure (β1-blockade)
may induce bronchoconstriction in asthmatics (β2-blockade)
may potentiate hypoglyceamia in diabetics (β1-blockade)

75
Q

What are adrenergic neurone blockers?

A

primarily block the release of noradrenaline from sympathetic neurones by inhibiting excitation-release coupling

76
Q

What other major pharmacological actions contribute to sympathetic neuronal blockade?

A

taken up into sympathetic neurones via NET
stored in vesicles
released as false neurotransmitters

77
Q

What is an example of an adrenergic neurone blocker?

A

Guanethidine

PHAR2200 (9 decks)

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