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ANS pharmacology > ANS pharmacology > Flashcards

ANS pharmacology Flashcards

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
Q

edrophonium

A

short-duration antiAchE - form readily reversible ionic bond with esteratic site

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26
Q

neostigmine

A

medium duration antiAchE

forming carbamate ester - slowly hydrolysed from esteratic site

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27
Q

dyflos

A

long duration antiAchE

phosphate ester is very stable

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28
Q

pralidoxime

A

AchE reactivator given in case of moderate to severe antiAchE poisoning –> only effective before aging occur

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29
Q

Benzodiazepine

A

diazepam, lorazepam, midazolam prevent convulsion

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30
Q

myasthenia gravis

A

weakness and fatigue of muscle caused by reduction of nicotinic receptor at skeletal neuromuscular junction

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31
Q

diagnosis of myasthenia gravis

A

short-acting edrophonium produce improvement on muscle strength

32
Q

treatment of myasthenia gravis

A

medium-duration neostigmine

33
Q

reverse non-depolarising neuromuscular block e.g. tubocurarine

A

neostigmine - medium acting

34
Q

long acting insecticides and nerve gases

A

dyflos –> severe poisoning

35
Q

anticholinesterase poisoning

!!

A

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
Q

a1-adrenoreceptor mechanism

A

Gq protein –> activate phospholipase C –> increase intracellular Ca2+ –> vasoconstriction

37
Q

a2-adrenoreceptor mechanism

A

Gi protein –> lower cAMP –> lower [Ca2+]i –> lower [K+] –> inhibit noradrenaline release (autoreceptor)

38
Q

b1/2/3-adrenoreceptor mechanism

A

Gs protein –> increase cAMP –> increase heart rate and contractility / bronchodilation + vasodilation / lipolysis

39
Q

a1-adrenoreceptor agonist

A

phenylephrine

40
Q

a2-adrenoreceptor agonist

A

clonidine –> reduce further release of NA

41
Q

b1-adrenoreceptor agonist

A

dobutamine

42
Q

b2-adrenoreceptor agonist

A

salbutamol

43
Q

terbutaline

A

b2-adrenoreceptor agonist

44
Q

competitive reversible a1 antagonist

A

phentolamine

45
Q

irreversible a1 antagonist

A

phenoxybenzamine

46
Q

long acting a1 antagonist

A

terazosin

47
Q

selective a1a antagonist

A

tamsulosin

48
Q

a2 antagonist

A

yohimbine

49
Q

propanolol

A

block b1 and b2 adrenoreceptor

50
Q

cardioselective b-blockers

A

metoprolol and atenolol - higher affinity for b1 than b2

51
Q

3rd generation b-blocker

A

carvedilol - block b1,b2 and a1 blocking leading to vasodilation –> extra effect on reducing BP

52
Q

biosynthesis of catecholamine

A

tyrosine - tyrosine hydroxylase –> DOPA - DOPA decarboxylase –> dopamine –> dopamine b-hydroxylase –> noradrenaline - PNMT –> adrenaline

53
Q

NET

A

noradrenaline transporter –> for reuptake of noradrenaline from synapse to presynaptic terminal

54
Q

monoamine oxidase

A

catalysing conversion of noradrenaline to metabolites in presynpatic terminal

55
Q

VMAT

A

vesicular monamine transporter –> reuptake noradrenaline from cytoplasm to vesicle in presynaptic terminal

56
Q

reserpine

!!!

A

inhibit VMAT –> more NA is metabolised by MAO –> deplete storage granules of NA

57
Q

Guanethidine

!!!

A

taken up into presynpatic terminal through NET –> inhibit exocytosis + displace NA from vesicle –> more NA being metabolized by MAO
- weak local anaesthetic effect

58
Q

a-methy-DOPA

A

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
Q

tyramine

A

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
Q

cocaine

!!!

A

noradrenaline reuptake inhibitor (NRI) –> local anaesthetics

61
Q

phenoxybenzamine

A

Noradrenaline reuptake inhibitor and a a-blocker

62
Q

imipramine

!!!

A

weak a1-blocker

63
Q

effect of NRI

A
  • block reuptake –> prolong action of NA and other agonist which are substrates for NET
64
Q

Cheese-reaction

A

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
Q

anaphylactic shock / acute anaphylaxis

!!!

A

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
Q

!!!treat acute anaphylaxis

A

intramuscular injection of adrenaline

  • a1 and b2 improve cardiovascular function
  • b2 dilate airway
67
Q

phaeochromocytoma

A

tumour of adrenal cortex –> releasing large amount of catecholamine

68
Q

premedication of surgical removal of phaeochromocytoma

A

phenoxybenzamine - irreversible a-blocker to reduce BP + atenolol (B1-blocker)

69
Q

benign prostate hyperplasia treatment

A

tamsulosin (a1a antagonist) - prostatic / urethral smooth muscle relaxation to facilitate urination

70
Q

treat nasal congestion

A

phenylephrine - a1 agonist to contract blood vessel in nasal cavity to exert nasal decongestant action

71
Q

asthma treatment

A

salbutamol - b2-adrenoreceptor agonist relieve bronchospasm

72
Q

premature labour treatment

!!!

A

ritodrine - B2- agonist given by IV to reduce uterine contraction

73
Q

opthalmological exam

!!!

A

tropicamide to inhibit M3 receptor –> relax circular iris muscle
phenylephrine to activate a1 receptor to contract radial iris muscle
- produce mydriasis

74
Q

parkinsonism

!!!

A

clinical syndrome characterized by tremour, bradykinesia, rigidity, postural instability
- due to increased Ach level and degeneration of dopaminergic nigrostriatal pathway

75
Q

side effect of a-adrenoreceptor blocker

A

sexual dysfunction, dizziness, tachycardia, postural hypotension

ANS pharmacology (1 decks)

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