Intro to Pharm Sci Flashcards
1
Q
A
2
Q
alpha 1 agonists function / use
A
vasoconstriction topical decongestants vasoconstriction of cornea = treat red eye
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
4
Q
beta 1 agonist function / use
A
increase FOC and HR preserve CO racemic mixture used for decompensated heart failure
5
Q
beta 2 agonist function / use
A
bronchodilation can be SA or LA
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)
7
Q
phenylephrine
A
alpha1 agonist
8
Q
clonidine
A
alpha2 agonist
9
Q
dobutamine
A
beta1 agonist
10
Q
albuterol
A
SA beta 2 agonist
11
Q
fenoldopam
A
D1 agonist
12
Q
oxymetazoline
A
alpha1 agonist
13
Q
methyldopa
A
alpha2 agonist
14
Q
terbutaline
A
beta2 agonist
15
Q
tetrahydrozoline
A
alpha1 agonist
16
Q
guanfacine
A
alpha2 agonist
17
Q
salmeterol
A
beta2 agonist LA
18
Q
naphazoline
A
alpha1 agonist
19
Q
dexmedetomodine****
A
alpha2 agonist induction and sedation of patients on ventilator
20
Q
formoterol
A
beta 2 agonist LA
21
Q
olodaterol****
A
beta 2 agonist LA COPD treatment
22
Q
vilanterol****
A
beta 2 agonist LA COPD treatment
23
Q
isoproterenol
A
beta 1 and beta 2 agonist
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
25
metoprolol
cardioselective B blocker
26
atenolol
cardioselective B blocker
27
osmolol
cardioselective B blocker
28
bisoprolol
cardioselective B blocker
29
acebutolol
cardioselective B blocker
30
which 3 have intrinsic sympathomimetic activity
pindolol acebutolol labetalol
31
labetalol
specifically a beta 2 with ISA
32
carvedilol
block alpha 1 = vasoconstriction block L type CC = decrease HR and cause vasodilation anti oxidation = limit oxidative damage seen in HF
33
nebivolol
increase NO production in vasculature not sure why maybe B3 causes vasodilation
34
labetalol
B1 antagonist, B2 ISA alpha1 block eliminated through glucronidation gives vasodilation, blocks RAA on B1
35
which 3 are eliminated by the kidney
bisoprolol (50%) Nadalol (really long half life) Atenolol good for patients with decreased liver function
36
esmolol
half life = 10 minutes bc of plasma esterase in gut
37
prazosin
first selective alpha 1 antagonist subtype=non selective
38
terazosin
alpha 1 antagonist subtype=non selective
39
doxazosin
alpha 1 antagonist subtype=non selective
40
alfuzosin
alpha 1 antagonist
41
tamsulosin
alpha 1 antagonist type A
42
silodosin
alpha 1 antagonist type A
43
phentolamine
alpha 1 antagonist and alpha 2 antagonist
44
phenoxybenzamine
IRREVERSIBLE! alpha 1 antagonist and alpha 2 antagonist
45
alpha 1 antagonist are effective in treating
benign prostatic hypertrophy BPH in females kidney stones = by decrease vasoconstriction leading to decreased pressure on urethra allowing stone to pass
46
Methacholine
M\>\>N slower metabolism with methyl on B carbon
47
Carbachol
non selective M = N decreases hydrolysis due to presence of the carbamate less likely to be broken down with AChE longer circulation time
48
Bethanechol
longer half life due to presence of the carbamate and methyl on B carbon
49
pilocarpine
plant derived M agonist lactone ring with ester = selective
50
Cevimeline
muscarinic agonist
51
post op or postpartum non obstructive urinary retention
bethanechol
52
disabling anticholinergic side effects from medications such as tricyclic antidepressants
bethanechol
53
diagonsis of bronchial airway hyper reactivity in subjects that do not have asthma
methacholine
54
miosis induction after ophthalmoscopic examination
pilocarpine
55
treatment of dry mouth (xerostomia) caused by radiation from cancer treatments / or Sjogren's syndrome
pilocarpine
56
atropine
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
57
tropicamide
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
58
cyclopentolate
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
59
Tiotropium
muscarinic antagonists COPD
60
Ipratropium
muscarinic antagonists COPD
61
Glycopyrrolate
muscarinic antagonists COPD
62
Aclidinium
muscarinic antagonists COPD
63
Umeclidinium
muscarinic antagonists COPD
64
Benztropine
muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS
65
Trihexyphenydil
muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS
66
Dicyclomine
muscarinic antagonists IBS - d
67
Scopolamine
patch given to help with motion sickness muscarinic antagonist blocks M1 effects which causes vestibular nausea and vomiting
68
Oxybutynin IR / XL / patch
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
Detrol LA / Tolterodine
muscarinic antagonists OAB
70
Vesicare / solifenacin
muscarinic antagonists OAB functional tissue selectivity for bladder M3 lower ADE such as dry mouth
71
Enablex / darifenacin
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
Sanctura / Trospium
muscarinic antagonists OAB has a quat ammonium = limit CNS effects has an ester = can be metabolized by plasma esterases with CYP450
73
Toviaz / Fesoterodine
muscarinic antagonist OAB
74
tolterodine
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
Fesoterodine
muscarinic antagonist prodrug of 5-HMT ester prodrug abundance of esterases in plasma has a higher affinity for muscarinic
76
neostigmine
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
physostigmine
AChE inhibitor
78
pyridostigmine
AChE inhibitor charged = less CNS effects
79
Rivastigmine
AChE inhibitor
80
carbamate esters
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
Edrophenium
reversible AChE inhibitor
82
Galantamine
reversible AChE inhibitor
83
donepezil
reversible AChE inhibitor
84
organophosphates
extremely toxic phosphorylated enzyme is extremely resistant to hydrolysis delay or even prevention of a functional enzyme
85
organophosphates
extremely toxic phosphorylated enzyme is extremely resistant to hydrolysis delay or even prevention of a functional enzyme
86
donepezil
reversible AChE inhibitor
87
Galantamine
reversible AChE inhibitor
88
Edrophenium
reversible AChE inhibitor
89
carbamate esters
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
Rivastigmine
AChE inhibitor
91
pyridostigmine
AChE inhibitor charged = less CNS effects
92
physostigmine
AChE inhibitor
93
neostigmine
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
Fesoterodine
muscarinic antagonist prodrug of 5-HMT ester prodrug abundance of esterases in plasma has a higher affinity for muscarinic
95
tolterodine
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
Toviaz / Fesoterodine
muscarinic antagonist OAB
97
Sanctura / Trospium
muscarinic antagonists OAB has a quat ammonium = limit CNS effects has an ester = can be metabolized by plasma esterases with CYP450
98
Enablex / darifenacin
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
Vesicare / solifenacin
muscarinic antagonists OAB functional tissue selectivity for bladder M3 lower ADE such as dry mouth
100
Detrol LA / Tolterodine
muscarinic antagonists OAB
101
Oxybutynin IR / XL / patch
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
Scopolamine
patch given to help with motion sickness muscarinic antagonist blocks M1 effects which causes vestibular nausea and vomiting
103
Dicyclomine
muscarinic antagonists IBS - d
104
Trihexyphenydil
muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS
105
Benztropine
muscarinic antagonists Parkinsons disease tertiary amine = increases ability to reach the CNS
106
Umeclidinium
muscarinic antagonists COPD
107
Aclidinium
muscarinic antagonists COPD
108
Glycopyrrolate
muscarinic antagonists COPD
109
Ipratropium
muscarinic antagonists COPD
110
Tiotropium
muscarinic antagonists COPD
111
cyclopentolate
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
112
tropicamide
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
113
atropine
muscarinic antagonists ophthalmic = causing midrasis and relaxation of ciliary muscle
114
treatment of dry mouth (xerostomia) caused by radiation from cancer treatments / or Sjogren's syndrome
pilocarpine
115
miosis induction after ophthalmoscopic examination
pilocarpine
116
diagonsis of bronchial airway hyper reactivity in subjects that do not have asthma
methacholine
117
disabling anticholinergic side effects from medications such as tricyclic antidepressants
bethanechol
118
post op or postpartum non obstructive urinary retention
bethanechol
119
Cevimeline
muscarinic agonist
120
pilocarpine
plant derived M agonist lactone ring with ester = selective
121
Bethanechol
longer half life due to presence of the carbamate and methyl on B carbon
122
Carbachol
non selective M = N decreases hydrolysis due to presence of the carbamate less likely to be broken down with AChE longer circulation time
123
Methacholine
M\>\>N slower metabolism with methyl on B carbon
