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ans Flashcards

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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
What are some therapeutic uses of cholinesterase inhibitors?
eye treatment skeletal neuromuscular junction gastrointestinal system treatment of atropine poisoning
26
How is the eye treated by the use of cholinesterase inhibitors?
constriction of pupil decreases intraocular pressure in open-angle glaucoma
27
What are some long-acting, irreversible cholinesterase inhibitors?
organophosphates
28
How does organophosphates work?
phosphorylation of acetylcholinesterase inhibits the acetyl site thus acetylcholine cannot be cleaved and accumulate
29
What are the risks of organophosphates?
insecticides nerve gases
30
What is the risk of nerve gases?
deadly at low concentrations toxicity due to increase acetylcholine at cholinergic synapses persistent stimulation = neurotransmission paralysis
31
What are some signs of acute poisoning due to cholinesterase inhibitors?
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
What are the treatments for cholinesterase inhibitor poisoning?
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
Is atropine a muscarinic agonist or antagonist?
antagonist
34
What are the major pharmacological effects of atropine?
decrease sweating, salivation, lacrimation decrease gastrointestinal motility decrease gastric acid secretion decrease production of bronchial mucus bronchodilation increase heart rate
35
What are some side-effects of atropine?
dry mouth + skin urinary retention cycloplegia glaucoma depression hallucination increase body temp.
36
What are catecholamines?
hormones made by the adrenal glands
37
What enzyme synthesises tyrosine into dihydroxyphenylalanine?
tyrosine hydroxylase
38
What enzyme synthesises dihydroxyphenylalanine into dopamine?
DOPA decarboxylase
39
What enzyme synthesises dopamine into noradrenaline?
dopamine β-hydroxylase
40
What enzyme synthesises noradrenaline into adrenaline?
phenylethanolamine N-methyltransferase
41
What happens to noradrenaline in the synapse?
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
What synthesises adrenaline?
adrenal medulla
43
What are some modifications of noradrenaline?
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
What are the function of α1-receptors?
blood vessel = vasoconstriction lung = decrease secretion GI tract = decrease smooth muscle motility and tone eye = radial muscle contraction
45
What are the functions of β-receptors?
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
What are the different types of adrenergic drugs?
adrenoceptor agonists adrenoceptor antagonists adrenergic neurone blockers monoamine oxidase inhibitors
47
What classifies adrenoceptors?
molecular cloning of distinct protein moieties functional characteristics potencies of various stimulatory catecholamines
48
What is potencies of α-receptors to stimulatory catecholamines?
noradrenaline > adrenaline > isoprenaline
49
What is the potencies of β-receptors to various stimulatory catecholamines?
isoprenaline > adrenaline > noradrenaline
50
Where are α1 receptors found?
post-junctional sites
51
Where are most α2 receptors found?
pre-junctional sympathetic nerve endings
52
What does the activation of α2 receptors do?
inhibit noradrenaline release
53
Where are β1 receptors found in abundance?
heart and intestinal tract
54
Where are β2 receptors found in abundance?
respiratory tract, blood vessels and liver
55
What does β1 receptors trigger?
increase in heart rate and force
56
What does β2 receptors trigger?
relaxation of airway and vascular smooth muscle glycogenolysis/gluconeogenesis in the liver
57
What does the effect of adrenoceptor agonist depend on?
receptor selectivity of the drug adrenoceptor profile of the cell cellular response to receptor activation
58
What are the clinical uses of adrenaline?
anaphylactic reactions (β-adrenoceptors) cardiac arrest (β1-adrenoceptors) local anaesthetic solutions (α1-adrenoceptors)
59
How can adrenaline help during cardiac arrest?
helps restore cardiac rhythm
60
Why can adrenaline be used as a local anaesthetic?
vasoconstrictor effect increase duration of action decrease risk of systemic toxicity
61
What are sympathomimetic drugs?
stimulant compounds which mimic the effects of endogenous agonists of the SNS
62
What do indirect-acting sympathomimetics do?
no direct agonist activity but cause - release of noradrenaline - block noradrenaline uptake - inhibit noradrenaline metabolism
63
What is a mixed-acting sympathomimetics?
Ephedrine
64
What is the action of Ephedrine?
direct actions on adrenergic receptors releases noradrenaline from sympathetic nerves
65
Is Ephedrine a substrate for COMT or MAO?
no
66
What is Ephedrine used clinically for?
relieve nasal congestion (vasoconstrictor)
67
What are adrenoceptor antagonists?
prevent endogenous adrenoceptor agonists from binding to and stimulating adrenoceptors
68
α1-adrenoceptors antagonism can help treat?
hypertension
69
β1-adrenoceptor antagonism can help treat?
angina, arrhythmia, hypertension, post-myocardial infarcation
70
β-adrenoceptor antagonists are used to?
prevent endogenous adrenoceptor agonists from binding to and activating β-adrenoceptors
71
Most β-adrenoceptor antagonists end in?
-olol
72
What is an example of a β-adrenoceptor antagonists?
propranolol
73
What are the properties of propranolol?
non-selective antagonist oxymethylene bridge improves antagonists potency similar structure to β-agonists and local anaesthetics
74
What are the adverse effects of non-selective β-adrenoceptor antagonists?
may precipitate congestive heart failure (β1-blockade) may induce bronchoconstriction in asthmatics (β2-blockade) may potentiate hypoglyceamia in diabetics (β1-blockade)
75
What are adrenergic neurone blockers?
primarily block the release of noradrenaline from sympathetic neurones by inhibiting excitation-release coupling
76
What other major pharmacological actions contribute to sympathetic neuronal blockade?
taken up into sympathetic neurones via NET stored in vesicles released as false neurotransmitters
77
What is an example of an adrenergic neurone blocker?
Guanethidine

PHAR2200 (9 decks)

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