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ANS pharmacology Flashcards

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1
Q

M1 receptor location

A

neural –> CNS, peripheral ganglia

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2
Q

M1 receptor function

A

CNS excitation, gastric secretion

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3
Q

M2 receptor location

A

cardiac –> atria, conducting tissue, presynaptic terminals

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4
Q

M2 receptor function

A

cardiac inhibition, presynaptic inhibition

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5
Q

M3 receptor location

A

glandular –> exocrine gland, smooth muscle, vascular endothelium

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6
Q

M3 function

A

gland secretion, smooth muscle contraction, vasodilation

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7
Q

Carbachol

A

muscarinic receptor agonist with long lasting effect, carbamoyl group replacing acetyl group on acetylcholine

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8
Q

methacholine

A

muscarinic receptor agonist with methyl side chain, higher selectivity towards muscarinic than nicotinic receptor

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9
Q

bethanechol

A

muscarinic receptor agonist with carbamyl group + methyl side chain –> long lasting + higher selectivity towards muscarinic receptors than nicotinic receptors

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10
Q

What is glaucoma?

A

increased intraocular pressure e.g. accumulation of aqueous humour, obstruction of canal of schlemm

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11
Q

Pilocarpine

A

Treating glaucoma: M3 muscarinic receptor agonist

  • induce contraction of iris circular muscle improve aqueous humour outflow by expanding filtration angle
  • induce contraction of ciliary muscle exerting tension –> opening trabecular network and promoting fluid movement into canal of schlemm
  • muscarinic receptors are widespread –> agonist have many side effects and thus seldomly used
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12
Q

atropine

A

muscarinic antagonist

- too long lasting

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13
Q

tropicamide

A

atropine-like muscarinic antagonist

  • block M3 receptors to inhibit constriction of iris circular muscle –> mydriasis, abolishing light reflex –> easy viewing of retina during eye exam and surgery
  • also inhibit constriction of ciliary muscle –> abolish eye accommodation
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14
Q

tiotropium

A

inhibit M3 receptor to suppress reflex airway constriction

- given by aerosol to treat asthma and obstructive pulmonary disease

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15
Q

atropine

A

block M2 receptor to treat sinus bradycardia e.g. after MI

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16
Q

pirenzipine

A

M1-selective antagonist reducing gastric acid secretion –> treat peptic ulcer

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17
Q

hyoscine butylbromide

A

quaternary agents used as antispasmodic to treat GI hypermotility
- not absorbed well and tend to stay in GI

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18
Q

hyoscine, scopolamine

A

block M1-3
Anaesthetic premedication
- reduce secretion and reflex bronchoconstriction –> ensure clear airway
- prevent bradycardia
- go through BBB - weak sedative effect in addition to anaesthetics
- also treat motion sickness

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19
Q

benztropine

A
  • selective M1 antagonist –> block central cholinergic activity –> treat parkinsonism
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20
Q

trimetaphan

A

blocking ganglionic nicotinic receptor –> produce short-term lowering of blood pressure
- receptor antagonism –> bind to agonist binding domain

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21
Q

hexamethonium

A

block ganglionic nicotinic receptor by block opening of Na+ channel

  • reduce sympathetic tone of blood vessel and heart –> reduce BP
  • no longer used
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22
Q

Botulinum toxin

A
  • bind to presynaptic membrane of cholinergic synapse –> degrade SNAP-25 of SNARE protein –> inhibit exocytosis of acetylcholine
  • progressively paralysis parasympathetic and motor system –> respiratory failure
  • antitoxin only effective if given before symptoms appear
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23
Q

small dose of botulinum toxin can treat

A
  • upper motor neurone syndrome –> cause abnormal muscle tone
  • focal hyperhidrosis (excess sweating)
  • blepharospasm - persistent and disabling eyelid spasm
  • strabismus - cross eye
  • chronic migraine - unilateral headache
  • bruxism - teeth grinding
  • botox - reduce skin wrinkles
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24
Q

butyrylcholinesterase

A
  • widely distributed with broad substrate specificity

- hydrolyze ester-containing drugs e.g. procaine, suxamethonium

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25
edrophonium
short-duration antiAchE - form readily reversible ionic bond with esteratic site
26
neostigmine
medium duration antiAchE | forming carbamate ester - slowly hydrolysed from esteratic site
27
dyflos
long duration antiAchE | phosphate ester is very stable
28
pralidoxime
AchE reactivator given in case of moderate to severe antiAchE poisoning --> only effective before aging occur
29
Benzodiazepine
diazepam, lorazepam, midazolam prevent convulsion
30
myasthenia gravis
weakness and fatigue of muscle caused by reduction of nicotinic receptor at skeletal neuromuscular junction
31
diagnosis of myasthenia gravis
short-acting edrophonium produce improvement on muscle strength
32
treatment of myasthenia gravis
medium-duration neostigmine
33
reverse non-depolarising neuromuscular block e.g. tubocurarine
neostigmine - medium acting
34
long acting insecticides and nerve gases
dyflos --> severe poisoning
35
anticholinesterase poisoning !!
muscarinic - M1/3 - sludge - M2 - slow heart rate, bradycardia and hypotension - M3 - bronchoconstriction, vasodilation via NO production, miosis CNS - convulsion, depression, unconsciousness, respiratory failure nicotinic - initial stimulation increase sympathetic tone --> hypertension --> later become depolarisation block leading to hypotension - initial skeletal muscle twitch (fasciculation) --> later become depolarisation block and paralysis at neuromuscular junction
36
a1-adrenoreceptor mechanism
Gq protein --> activate phospholipase C --> increase intracellular Ca2+ --> vasoconstriction
37
a2-adrenoreceptor mechanism
Gi protein --> lower cAMP --> lower [Ca2+]i --> lower [K+] --> inhibit noradrenaline release (autoreceptor)
38
b1/2/3-adrenoreceptor mechanism
Gs protein --> increase cAMP --> increase heart rate and contractility / bronchodilation + vasodilation / lipolysis
39
a1-adrenoreceptor agonist
phenylephrine
40
a2-adrenoreceptor agonist
clonidine --> reduce further release of NA
41
b1-adrenoreceptor agonist
dobutamine
42
b2-adrenoreceptor agonist
salbutamol
43
terbutaline
b2-adrenoreceptor agonist
44
competitive reversible a1 antagonist
phentolamine
45
irreversible a1 antagonist
phenoxybenzamine
46
long acting a1 antagonist
terazosin
47
selective a1a antagonist
tamsulosin
48
a2 antagonist
yohimbine
49
propanolol
block b1 and b2 adrenoreceptor
50
cardioselective b-blockers
metoprolol and atenolol - higher affinity for b1 than b2
51
3rd generation b-blocker
carvedilol - block b1,b2 and a1 blocking leading to vasodilation --> extra effect on reducing BP
52
biosynthesis of catecholamine
tyrosine - tyrosine hydroxylase --> DOPA - DOPA decarboxylase --> dopamine --> dopamine b-hydroxylase --> noradrenaline - PNMT --> adrenaline
53
NET
noradrenaline transporter --> for reuptake of noradrenaline from synapse to presynaptic terminal
54
monoamine oxidase
catalysing conversion of noradrenaline to metabolites in presynpatic terminal
55
VMAT
vesicular monamine transporter --> reuptake noradrenaline from cytoplasm to vesicle in presynaptic terminal
56
reserpine !!!
inhibit VMAT --> more NA is metabolised by MAO --> deplete storage granules of NA
57
Guanethidine !!!
taken up into presynpatic terminal through NET --> inhibit exocytosis + displace NA from vesicle --> more NA being metabolized by MAO - weak local anaesthetic effect
58
a-methy-DOPA
enter the NA biosynthetic pathway as a false transmitter a-methyl-NA - activate a2 to inhibit further release of NA - do not activate adrenoreceptor at end organ
59
tyramine
sympathomimetics uptaken into presynaptic terminal through NET - reduce NA reuptake - displace NA from vesicle --> more release - competitive inhibition to MAO - weak adrenoreceptor agonist location
60
cocaine | !!!
noradrenaline reuptake inhibitor (NRI) --> local anaesthetics
61
phenoxybenzamine
Noradrenaline reuptake inhibitor and a a-blocker
62
imipramine | !!!
weak a1-blocker
63
effect of NRI
- block reuptake --> prolong action of NA and other agonist which are substrates for NET
64
Cheese-reaction
cheese is rich in tyramine --> substrate for MAO - should be properly metabolized in gut and liver when MAO inhibitor is present --> cannot be metabolised --> reach sympathetic terminal and show sympathomimetic effect --> provoke sudden and dangoerous rise in BP
65
anaphylactic shock / acute anaphylaxis | !!!
type I hypersensitivity reaction - second exposure to antigen cause release of inflammatory mediators from mast cells --> wide spread urticaria, edema, bronchospasm, hypotension --> laryngeal edema, bronchospasm, cardiovascular collapse
66
!!!treat acute anaphylaxis
intramuscular injection of adrenaline - a1 and b2 improve cardiovascular function - b2 dilate airway
67
phaeochromocytoma
tumour of adrenal cortex --> releasing large amount of catecholamine
68
premedication of surgical removal of phaeochromocytoma
phenoxybenzamine - irreversible a-blocker to reduce BP + atenolol (B1-blocker)
69
benign prostate hyperplasia treatment
tamsulosin (a1a antagonist) - prostatic / urethral smooth muscle relaxation to facilitate urination
70
treat nasal congestion
phenylephrine - a1 agonist to contract blood vessel in nasal cavity to exert nasal decongestant action
71
asthma treatment
salbutamol - b2-adrenoreceptor agonist relieve bronchospasm
72
premature labour treatment | !!!
ritodrine - B2- agonist given by IV to reduce uterine contraction
73
opthalmological exam | !!!
tropicamide to inhibit M3 receptor --> relax circular iris muscle phenylephrine to activate a1 receptor to contract radial iris muscle - produce mydriasis
74
parkinsonism !!!
clinical syndrome characterized by tremour, bradykinesia, rigidity, postural instability - due to increased Ach level and degeneration of dopaminergic nigrostriatal pathway
75
side effect of a-adrenoreceptor blocker
sexual dysfunction, dizziness, tachycardia, postural hypotension

ANS pharmacology (1 decks)

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