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P1 Spring - Pharm Sci > Intro to Pharm Sci > Flashcards

Intro to Pharm Sci Flashcards

1
Q
A
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2
Q

alpha 1 agonists function / use

A

vasoconstriction topical decongestants vasoconstriction of cornea = treat red eye

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3
Q

alpha 2 agonist function / use

A

decrease SNS activity ADHD, decrease TPR, HR, BP lead to up-regulation of alpha 1 and 2

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4
Q

beta 1 agonist function / use

A

increase FOC and HR preserve CO racemic mixture used for decompensated heart failure

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5
Q

beta 2 agonist function / use

A

bronchodilation can be SA or LA

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6
Q

D1 agonist function / use

A

get DA effects without alpha 1 or beta 1 very low TPR due to mesenteric (renal/gut network)

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7
Q

phenylephrine

A

alpha1 agonist

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8
Q

clonidine

A

alpha2 agonist

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9
Q

dobutamine

A

beta1 agonist

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10
Q

albuterol

A

SA beta 2 agonist

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11
Q

fenoldopam

A

D1 agonist

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12
Q

oxymetazoline

A

alpha1 agonist

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13
Q

methyldopa

A

alpha2 agonist

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14
Q

terbutaline

A

beta2 agonist

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15
Q

tetrahydrozoline

A

alpha1 agonist

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16
Q

guanfacine

A

alpha2 agonist

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17
Q

salmeterol

A

beta2 agonist LA

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18
Q

naphazoline

A

alpha1 agonist

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19
Q

dexmedetomodine****

A

alpha2 agonist induction and sedation of patients on ventilator

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20
Q

formoterol

A

beta 2 agonist LA

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21
Q

olodaterol****

A

beta 2 agonist LA COPD treatment

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22
Q

vilanterol****

A

beta 2 agonist LA COPD treatment

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23
Q

isoproterenol

A

beta 1 and beta 2 agonist

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24
Q

beta blockers used in the treatment of

A

hypertension, angina, heart failure, performance anxiety, migraine headaches, glaucoma are capable of lowering HR, FOC, CO, also are effective in blocking RAA system

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25
Q

metoprolol

A

cardioselective B blocker

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26
Q

atenolol

A

cardioselective B blocker

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27
Q

osmolol

A

cardioselective B blocker

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28
Q

bisoprolol

A

cardioselective B blocker

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29
Q

acebutolol

A

cardioselective B blocker

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30
Q

which 3 have intrinsic sympathomimetic activity

A

pindolol acebutolol labetalol

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31
Q

labetalol

A

specifically a beta 2 with ISA

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32
Q

carvedilol

A

block alpha 1 = vasoconstriction block L type CC = decrease HR and cause vasodilation anti oxidation = limit oxidative damage seen in HF

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33
Q

nebivolol

A

increase NO production in vasculature not sure why maybe B3 causes vasodilation

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34
Q

labetalol

A

B1 antagonist, B2 ISA alpha1 block eliminated through glucronidation gives vasodilation, blocks RAA on B1

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35
Q

which 3 are eliminated by the kidney

A

bisoprolol (50%) Nadalol (really long half life) Atenolol good for patients with decreased liver function

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36
Q

esmolol

A

half life = 10 minutes bc of plasma esterase in gut

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37
Q

prazosin

A

first selective alpha 1 antagonist subtype=non selective

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38
Q

terazosin

A

alpha 1 antagonist subtype=non selective

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39
Q

doxazosin

A

alpha 1 antagonist subtype=non selective

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40
Q

alfuzosin

A

alpha 1 antagonist

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41
Q

tamsulosin

A

alpha 1 antagonist type A

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42
Q

silodosin

A

alpha 1 antagonist type A

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43
Q

phentolamine

A

alpha 1 antagonist and alpha 2 antagonist

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44
Q

phenoxybenzamine

A

IRREVERSIBLE! alpha 1 antagonist and alpha 2 antagonist

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45
Q

alpha 1 antagonist are effective in treating

A

benign prostatic hypertrophy BPH in females kidney stones = by decrease vasoconstriction leading to decreased pressure on urethra allowing stone to pass

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46
Q

Methacholine

A

M>>N slower metabolism with methyl on B carbon

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47
Q

Carbachol

A

non selective M = N decreases hydrolysis due to presence of the carbamate less likely to be broken down with AChE longer circulation time

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48
Q

Bethanechol

A

longer half life due to presence of the carbamate and methyl on B carbon

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49
Q

pilocarpine

A

plant derived M agonist lactone ring with ester = selective

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50
Q

Cevimeline

A

muscarinic agonist

51
Q

post op or postpartum non obstructive urinary retention

A

bethanechol

52
Q

disabling anticholinergic side effects from medications such as tricyclic antidepressants

A

bethanechol

53
Q

diagonsis of bronchial airway hyper reactivity in subjects that do not have asthma

A

methacholine

54
Q

miosis induction after ophthalmoscopic examination

A

pilocarpine

55
Q

treatment of dry mouth (xerostomia) caused by radiation from cancer treatments / or Sjogren’s syndrome

A

pilocarpine

56
Q

atropine

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

57
Q

tropicamide

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

58
Q

cyclopentolate

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

59
Q

Tiotropium

A

muscarinic antagonists COPD

60
Q

Ipratropium

A

muscarinic antagonists COPD

61
Q

Glycopyrrolate

A

muscarinic antagonists COPD

62
Q

Aclidinium

A

muscarinic antagonists COPD

63
Q

Umeclidinium

A

muscarinic antagonists COPD

64
Q

Benztropine

A

muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS

65
Q

Trihexyphenydil

A

muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS

66
Q

Dicyclomine

A

muscarinic antagonists IBS - d

67
Q

Scopolamine

A

patch given to help with motion sickness muscarinic antagonist blocks M1 effects which causes vestibular nausea and vomiting

68
Q

Oxybutynin IR / XL / patch

A

OAB muscarinic antagonists Cmax is related to adverse effects adverse effects decrease as dosing interval becomes smaller lipophilic active metabolite = desethyloxybutynin tert amine = easily gets into CNS most likely to cause ADR do not use IR in elderly patients most likely metabolized by CYP enzymes - remove an ethyl group and replace with a H

69
Q

Detrol LA / Tolterodine

A

muscarinic antagonists OAB

70
Q

Vesicare / solifenacin

A

muscarinic antagonists OAB functional tissue selectivity for bladder M3 lower ADE such as dry mouth

71
Q

Enablex / darifenacin

A

muscarinic antagonists OAB pharmacologically selective for M3 causes dry mouth metabolized by 3A4 and 2D6 check for genetic polymorphisms and watch if they are on another drug that inhibits these enzymes

72
Q

Sanctura / Trospium

A

muscarinic antagonists OAB has a quat ammonium = limit CNS effects has an ester = can be metabolized by plasma esterases with CYP450

73
Q

Toviaz / Fesoterodine

A

muscarinic antagonist OAB

74
Q

tolterodine

A

muscarinic antagonist active metabolite = 5-hydroxymethyltolterodine both are pharmacologically active in a patient that is a poor metabolizer or rapid metabolizer = same pharmacological effect

75
Q

Fesoterodine

A

muscarinic antagonist prodrug of 5-HMT ester prodrug abundance of esterases in plasma has a higher affinity for muscarinic

76
Q

neostigmine

A

AChE inhibitor carbamate / 2 methyl groups looks similar enough to get into AChE binding site takes significantly longer to regenerate charge regulation at all cholinergic synapses drug must be metabolized in order to be activated plasma conc would be decreased charged = less CNS effects

77
Q

physostigmine

A

AChE inhibitor

78
Q

pyridostigmine

A

AChE inhibitor charged = less CNS effects

79
Q

Rivastigmine

A

AChE inhibitor

80
Q

carbamate esters

A

very long processes plasma conc of these drugs would decrease as AChE is breaking it down work through temporary covalent modification of enzyme active site

81
Q

Edrophenium

A

reversible AChE inhibitor

82
Q

Galantamine

A

reversible AChE inhibitor

83
Q

donepezil

A

reversible AChE inhibitor

84
Q

organophosphates

A

extremely toxic phosphorylated enzyme is extremely resistant to hydrolysis delay or even prevention of a functional enzyme

85
Q

organophosphates

A

extremely toxic phosphorylated enzyme is extremely resistant to hydrolysis delay or even prevention of a functional enzyme

86
Q

donepezil

A

reversible AChE inhibitor

87
Q

Galantamine

A

reversible AChE inhibitor

88
Q

Edrophenium

A

reversible AChE inhibitor

89
Q

carbamate esters

A

very long processes plasma conc of these drugs would decrease as AChE is breaking it down work through temporary covalent modification of enzyme active site

90
Q

Rivastigmine

A

AChE inhibitor

91
Q

pyridostigmine

A

AChE inhibitor charged = less CNS effects

92
Q

physostigmine

A

AChE inhibitor

93
Q

neostigmine

A

AChE inhibitor carbamate / 2 methyl groups looks similar enough to get into AChE binding site takes significantly longer to regenerate charge regulation at all cholinergic synapses drug must be metabolized in order to be activated plasma conc would be decreased charged = less CNS effects

94
Q

Fesoterodine

A

muscarinic antagonist prodrug of 5-HMT ester prodrug abundance of esterases in plasma has a higher affinity for muscarinic

95
Q

tolterodine

A

muscarinic antagonist active metabolite = 5-hydroxymethyltolterodine both are pharmacologically active in a patient that is a poor metabolizer or rapid metabolizer = same pharmacological effect

96
Q

Toviaz / Fesoterodine

A

muscarinic antagonist OAB

97
Q

Sanctura / Trospium

A

muscarinic antagonists OAB has a quat ammonium = limit CNS effects has an ester = can be metabolized by plasma esterases with CYP450

98
Q

Enablex / darifenacin

A

muscarinic antagonists OAB pharmacologically selective for M3 causes dry mouth metabolized by 3A4 and 2D6 check for genetic polymorphisms and watch if they are on another drug that inhibits these enzymes

99
Q

Vesicare / solifenacin

A

muscarinic antagonists OAB functional tissue selectivity for bladder M3 lower ADE such as dry mouth

100
Q

Detrol LA / Tolterodine

A

muscarinic antagonists OAB

101
Q

Oxybutynin IR / XL / patch

A

OAB muscarinic antagonists Cmax is related to adverse effects adverse effects decrease as dosing interval becomes smaller lipophilic active metabolite = desethyloxybutynin tert amine = easily gets into CNS most likely to cause ADR do not use IR in elderly patients most likely metabolized by CYP enzymes - remove an ethyl group and replace with a H

102
Q

Scopolamine

A

patch given to help with motion sickness muscarinic antagonist blocks M1 effects which causes vestibular nausea and vomiting

103
Q

Dicyclomine

A

muscarinic antagonists IBS - d

104
Q

Trihexyphenydil

A

muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS

105
Q

Benztropine

A

muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS

106
Q

Umeclidinium

A

muscarinic antagonists COPD

107
Q

Aclidinium

A

muscarinic antagonists COPD

108
Q

Glycopyrrolate

A

muscarinic antagonists COPD

109
Q

Ipratropium

A

muscarinic antagonists COPD

110
Q

Tiotropium

A

muscarinic antagonists COPD

111
Q

cyclopentolate

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

112
Q

tropicamide

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

113
Q

atropine

A

muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle

114
Q

treatment of dry mouth (xerostomia) caused by radiation from cancer treatments / or Sjogren’s syndrome

A

pilocarpine

115
Q

miosis induction after ophthalmoscopic examination

A

pilocarpine

116
Q

diagonsis of bronchial airway hyper reactivity in subjects that do not have asthma

A

methacholine

117
Q

disabling anticholinergic side effects from medications such as tricyclic antidepressants

A

bethanechol

118
Q

post op or postpartum non obstructive urinary retention

A

bethanechol

119
Q

Cevimeline

A

muscarinic agonist

120
Q

pilocarpine

A

plant derived M agonist lactone ring with ester = selective

121
Q

Bethanechol

A

longer half life due to presence of the carbamate and methyl on B carbon

122
Q

Carbachol

A

non selective M = N decreases hydrolysis due to presence of the carbamate less likely to be broken down with AChE longer circulation time

123
Q

Methacholine

A

M>>N slower metabolism with methyl on B carbon

P1 Spring - Pharm Sci (9 decks)

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