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pharm sci > final material > Flashcards

final material Flashcards

1
Q

what causes catecholamines to be released

A

sympathetic stimulus - usually a fight or flight response

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2
Q

what is a catecholamine

A

2 OH + amine on a aromatic ring

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3
Q

epinephrine low concentration

A

best B1 agonist
Beta > alpha
B1, B2
not much B3 bc NE

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4
Q

beta 1

A

increases heart rate and force of contraction (positive chronotropic and positive inotropic effects, renin release

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5
Q

Beta 2

A

bronchodilation, relaxes the smooth muscles (uterine and bronchus), increases vasculature, increases renin

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6
Q

Alpha 1

A

acts on more than sympathetic activity, vasoconstriction, contraction of smooth muscles (ureter, uterus, ciliary body), glycolysis/gluconeogenesis

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7
Q

alpha 2

A

auto-receptor, negative synaptic loop, decreases synaptic activity, decreases heart rate, vasodilation, inhibits NE, inhibit insulin, stimulates glucagon release

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8
Q

epinephrine response at the heart

A

inc heart rate, increase SV, increase CO, increase force of contraction, increase blood pressure

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9
Q

epinepherine response at lungs

A

bronchodilation can enhance epi for asthma, BUT high heart rate

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10
Q

epi response at vasculature

A

high conc: alpha 1 predominates, vasoconstrict, increases TPR
low conc: B2, decreases TPR, vasodilation

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11
Q

epi therapeutic uses

A

not as much vasoconstriction as NE

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12
Q

epi in asthma

A

dilates airways

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13
Q

epi in conjunction with local anesthetic

A

prolongs action of anesthetic, hangs out longer, vasoconstrictor can be removed from site

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14
Q

MOA of epi-pen

A

activates the alpha 1 receptors, lessens the vasodilation and lessens the increased vascular permeability that occurs during anaphylaxis - leads to a loss of intravascular fluid volume and hypotension

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15
Q

NE

A

best at increases BP, synthesized and stored in the terminal of the sympathetic post-ganglionic neuron, targets alpha 1, alpha 2, b1, b2

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16
Q

NE effect on the heart

A

increases the heart rate and increases the force of contraction and increases the CO

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17
Q

NE on lungs

A

no effect, no B2

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18
Q

NE on vasculature

A

vasoconstrict - alpha 1

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19
Q

NE administered for shock

A

dangerously low blood pressure - admin levophed, dec BP, not enough BV, vasoconstrict because not enough BP, increases peripheral resistance

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20
Q

isoproterenol

A

B1 and B2 agonist, decreases peripheral resistance, increases pulse rate, decreases blood pressure

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21
Q

dopamine

A

synthesized and stored in the terminal of the SNS postganglionic neuron, concentration dependent

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22
Q

low concentration dopamine

A

D1

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23
Q

high conc dopamine

A

alpha 1, lowest kd affinity

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24
Q

mild conc dopamine

A

B1

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25
Q

D1

A

vasodilator, prominent in mediatic vasculature, renal vasculature, helps regulate renal flow, highest affinity

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26
Q

renal dose dopamine

A

low dose, keeps the renal flow going to preserve kidney function

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27
Q

dopamine at the kidney

A

increases RPF, increases GFR at low and mild dose, starts going away at higher dose

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28
Q

dopamine at the heart

A

increases heart rate, force of contraction

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29
Q

dopamine at vasculature

A

TPR decreases in low conc, TPR increases at high conc

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30
Q

therapeutic uses for dopamine

A

shock, hypotension, poor tissue perfusion, low cardiac output

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31
Q

sympathommetics

A

mimic endogenous catecholamines so they are called sympathomemetics

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32
Q

phenylephrine

A

alpha 1 receptor agonist, opthalmic (dilates), visine (gets red out), constricts vessels

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33
Q

naphazoline

A

alpha 1 receptor agonist

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34
Q

oxymetazoline

A

alpha 1 receptor agonist

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35
Q

tetrahydrozoline

A

alpha 1 receptor agonist

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36
Q

alpha 2 receptor agonist

A

centrally, decreases SNS, decreases HR, TPR, BP

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37
Q

clonidine

A

alpha 2 receptor agonist

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38
Q

guanfacine

A

alpha 2 receptor agonist

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39
Q

methyldopa

A

alpha 2 receptor agonist

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40
Q

Dexmedetomidine

A

alpha 2 receptor agonist

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41
Q

upregulation

A

alpha/b receptors upregulate because not normal stimulation, cause tachycardia because receptors not activated alpha 2 agonist and need more alpha 2 regulation in the frontal cortex

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42
Q

dobutamine

A

B1 receptor agonist, increases heart rate and force of contraction, IV only, can have down regulation and loose effect over time, opposing alpha 1 effect (R,S) eantiomer

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43
Q

B2 receptor agonist

A

bronchodialation

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44
Q

(lev)albuterol

A

SABA - short acting beta agonist, asthmatic episode, not an every day drug

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45
Q

terbutaline

A

B2 receptor agonist

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46
Q

salmeterol

A

long acting beta 2 agonist

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47
Q

(Ar)Formoterol

A

Beta 2 receptor agonist

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48
Q

indacterol

A

long acting beta 2 agonist

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49
Q

olodaterol

A

long acting beta 2 agonist, inhalation administration

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50
Q

D1 receptor agonist

A

selective, fenoldopam

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51
Q

alpha 2 receptor dopamine

A

possible to increase the symp and decrease the para symp - alpha 2 hetero receptor when symp neuron is activated, activity decreases

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52
Q

beta adrenergic receptor antagonists

A

used in CV disorders (hypertension), chronic angina, heart failure, anxiety, migraine headaches, glaucoma, hypertension, angina

53
Q

hypertension and angina - NE

A

block effect of NE on the heart

decrease HR, decrease FOC, decrease CO

54
Q

beta blockers therapeutic uses

A

CV disorders, hypertension, chronic angina, heart failure, anxiety, migraine headaches, glaucoma

55
Q

hypertension and angina- bblockers

A

block effects of NE on the heart. decreases the HR, decreases FOC, decreases the CO

56
Q

bblocker - RAA system

A

JG cells secrete renin- B1 receptors

B2 very powerful vasoconstrictor through Ang 2, can cause vasodilation through blocking of ang 2!

57
Q

heart failure - BBlocker

A

patients have high levels of catecholamines and excess sympathetic activity - leads to acute coronary syndromes and altered contractility - bblockers very effective!`

58
Q

BBlockers cardioselectivity

A

B1 over B2, lower kd for B1 over B2

59
Q

BBlockers are great for

A

COPD (want to avoid B2), diabetes (glucose/glycogen regulation), decrease insulin secretion, tissue sensitivity to insulin

60
Q

Intrinisic Sympathomimetic Activity

A

partial agonist

61
Q

pindolol

A

ISA bblocker

62
Q

acebutolol

A

ISA bblocker

63
Q

labetolol

A

ISA bblocker, has B2 receptors, causes vasodilation- causes TPR to decrease, B1 antagonist, B2 ISA, alpha 1 block

64
Q

nimidane

A

normalizes pressure

65
Q

advantages of B1 with ISA

A

reduce the degree of brady cardia, limits the effects of lipid profile

66
Q

carvedilol

A

blocks alpha, blocks L-type CC, anti-oxidant

67
Q

elimination of b-blockers

A

nearly all eliminated in the liver

68
Q

bblockers excreted in the kidney

A

nadolol, atenolol - used in patients with liver issues who require a bblocker

69
Q

nadalol half life

A

24 hours. most of all bblockers

70
Q

atenolol half life

A

12 hours

71
Q

esmolol half life

A

10 minutes

72
Q

most hepatically cleared bblockers half life

A

4-6 hours

73
Q

lipids and bblockers

A

inc LDL and VLDL

dec HDL

74
Q

CNS and bblocker

A

drowsiness, fatique, nightmares

75
Q

sexual dysfunction and bblockers

A

dec libido, erectile dysfunction

76
Q

hypoglycemia and bblockers

A

masks symptoms of hypoglycemia (which are inc heart rate, shakiness, sweating, SNS increased)

77
Q

bblocker effects on the EKG

A

dec heart rate, prolonged PR interval, conduction time increase, abrupt discontinuation of bblocker, 2x receptor upregulation (hypertension, tachycardia)

78
Q

glaucoma and bblocker

A

aqueous humor production

79
Q

thyrotoxicosis bblocker

A

thyroid hormone increases the expression of beta receptors

80
Q

tremor bblocker

A

activation of beta 2 receptors cause tremor

81
Q

migraine bblocker

A

bblocker effective at preventing migraines

82
Q

alpha-adrenergic antagonists (alpha blocker) treatment for

A

BPH (benign prostatic hyperplasia) and hypertension (last resort)

83
Q

have alpha 1 antagonists demonstrated superiority over other drug classes?

A

no they have not demonstrated superiority over other drug classes such as ACE inhibitors, B blockers, or thiazide diuretics

84
Q

doxazosin

A

alpha 1 agonist - discontinued because its inferiority in reducing coronary events

85
Q

prazosin

A

alpha 1 subtype non-selective reversible competitive antagonist

86
Q

terazosin

A

alpha 1 subtype non-selective reversible competitive antagonist

87
Q

doxazosin

A

alpha 1 subtype non-selective reversible competitive antagonist

88
Q

alfuzosin

A

alpha 1 urinary tract reversible competitive antagonist

89
Q

tamulosin

A

alpha 1 A reversible competitive antagonist

90
Q

silodosin

A

alpha 1 A reversible competitive antagonist

91
Q

phentolamine

A

alpha 1 / alpha 2

92
Q

phenoxybenzamine

A

irreversible competitive antagonist

93
Q

zosin

A

non-selective alpha 1 antagonist

94
Q

osin

A

selective

95
Q

amine

A

alpha 1/ alpha 2

96
Q

B2 adrenergic agonists and binding sites

A

affinity- if you want a highly potent agent (low dose)

activation: full agonist or partial agonist
lipophilicity: does play a role in b2 selectivity,

97
Q

B2 adrenergic agonist SAR

A

NE- B1, alpha 1/2

Epi- addition of a methyl B2 > b1, alpha 1

98
Q

drawbacks to isoproterenol

A

short duration of action, increases the heart rate and the force of contraction

99
Q

isoproterenol structure

A

isopropyl, bulky

100
Q

metaproterenol structure

A

phenolic groups not a substitute for COMT, more selective than tertbutyl, like isoproterenonol but OH instead of ortho they are meta

101
Q

albuterol

A

B2» B1, active eantiomer of albuterol, short acting b2 agonist, t-butyl group, 3 hydroxy methyl, OH on a methyl makes it more selective

102
Q

tertbutyl

A

B2>b1, like metaproterenol but with a t-butyl group instead of an isopropyl group

103
Q

long acting beta2 agonists

A

B2&raquo_space;> B1

104
Q

salmeterol

A

long acting beta2 agonists, has the 3-hydroxymethyl group that makes it more selective

105
Q

vilanterol

A

looks like salmeterol but has 2 Cl- on the ring, partial agonist, binds to exo-site, long chain is like hinges of a door bound to the exo site - long acting beta2 agonists

106
Q

formoterol

A

long acting beta2 agonists- formic acid attached, lipophillic side chain that fits inside the receptor

107
Q

indacaterol

A

tautomer, looks like 3-hydroxymethyl, full agonist, either tautomer or could bind to the receptor long acting beta2 agonists

108
Q

olodaterol

A

bind with the receptor at the active site, has formic acid- long acting beta2 agonists

109
Q

formoterol, indacaterol, olodacterol

A

QD daily, effecient agonist, fast onset of action 15-45 seconds

110
Q

structure- activity relationship: Long acting B2 agonists

A
  1. aromatic ring: 4-hydroxy group required unless there is a 3,5 biphenolic substitution, better affinity for the b2 receptor- long acting beta agonist
  2. 3-hydroxymethyl aromatic substituents
  3. ethanol-amine side chain absolute requirement- R configuration for the hydroxyl group is required for receptor activation
  4. 3-formidioo - not substrates for COMT
  5. basic nitrogen alkyl substitutes-
111
Q

carostyril

A

has 4 phenol, 3-formamido, hydroxymethyl like, indacaterol - long acting beta agonist

112
Q

beta blocker SAR

A

aromatic ring containing system and not specific variable, either bridge (beta 1 selective), aromatic side chain

113
Q

non specific beta blockers

A

ether bridge connectts side chain

114
Q

nadolol

A

not aromatic, single aromatic ring, nonspecific bblocker

115
Q

pindolol

A

indole, ISA, nonspecific bblocker

116
Q

metoprolol

A

H bond acceptor ether b1 selective bblocker

117
Q

atenolol

A

H bond acceptor carbonyl - b1 selective bblocker

118
Q

bisprolol

A

b1 selective bblocker H bond acceptor ether

119
Q

esmolol

A

H bond acceptor ester DOA short, soft drug, fine control of BP

120
Q

structure activity on bblocker SAR

A
  • bulky substituent on nitrogen beta adrenergic side chain
  • ether group between aromatic ring and beta adrenergic side chain (contributes to antagonist properties)
  • aromatic ring system- non-selective antagonists have a non-specific aromatic system containing group, beta-1 selective agents have the following: single benzene ring, para substituent (H bond acceptor, 1 to 3 atoms from the benzene ring, meta substitution is out)
121
Q

alpha 2 agonists structure

A

ortho attachments with bridge and cl-

122
Q

structure-activity relationships for alpha 2 agents

A
  • Aromatic ring with 2,6-ortho substituents- all seen with 2,6 Cl- structure
  • Bridge- Ch2 or NH
  • Basic nitrogen grouping:
  • Perpendicular relationship between:
    Aromatic ring and basic functional group - not in the same plane
123
Q

yohimbine

A

alpha 2 antagonist, increases blood pressure on alpha 2

124
Q

hydroxylation is decreased or inhibited by

A

strong electron withdrawing groups: § CN, SO2R, NO2, CF3, Cl, C=OR (ester, amide)

125
Q

hydroxylation will occur on rings that have ___

A

electron donating groups attached

126
Q

steric hinderence - what substitutions are favored

A

meta electronically not favored, ortho may not happen because it can;t get to the site easily, para is the most favored.

127
Q

phase 1 dealkylation via CYP 450 enzymes

A

carvedilol undergoes dalkylation (removal of a methyl ether), drug is initially oxidized to drug- O-Ch2-OH t

128
Q

side chain oxidation

A

secondary oxidized over primary - free radical reactions, where oxidation occurs it is governed by the following:

  • free radical stability Benzylic > tertiary > secondary > primary
  • sterics

pharm sci (12 decks)

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