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PMCOL 343 > NSAID 2 > Flashcards

NSAID 2 Flashcards

1
Q

what does analgesic mean

A

stops pain

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2
Q

what does antipyretic mean

A

stops fever

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3
Q

what does of aspirin is the only effective antiplatelet NSAID

A

low dose

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4
Q

what do prostaglandins do to mucous secretion

A

secretion is promoted

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5
Q

what do prostaglandins do to peptic ulcers

A

prevent

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6
Q

what do prostaglandins do to uterine

A

causes contrations

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7
Q

are prostaglandins vasoconstrictors or vasodilatiors

A

usually vasodilation but some are vasoconstrictors

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8
Q

what kind of blood flow are prostaglandins important for

A

regulation of renal blood flow

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9
Q

what do prostaglandins do to fever and where does this occur

A

promote it by actions in the hypothalamus

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10
Q

what do prostaglandins do to inflammation

A

cause it

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11
Q

why may prostaglandins be given to induce labour

A

because it promotes uterine contraction

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12
Q

what are 6 things that prostaglandins cause

A
  • inflammation
  • gastric mucous secretion
  • uterine contraction
  • vasoconstrict + dilate
  • renal blood flow
  • fever (hypothalamus)
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13
Q

what is misoprostol

A

synthetic PGE1

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14
Q

what is the role of misoprotol

A

induce labour and treat peptide ulcers

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15
Q

how do glucocorticoids work

A

induce lipocortin which inhibits phospholipase A2

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16
Q

what is a problem with corticosteroids / glucocorticoids (1 word)

A

toxicity

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17
Q

what kind of syndrome do glucocorticoids cause the appearance of

A

cushing’s syndrome

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18
Q

what are a few signs of cushing’s syndrome

A

-abnormal fat deposition, hair growth, acne, developmental disorders. breakdown of protein to glucose, muscle wasting. peptic ulcers, hypokalemia, immunosuppression

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19
Q

what does glucocorticoids do to fat deposition

A

makes it abnormal

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20
Q

what does glucocorticoids do to hair growth

A

increase

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21
Q

what does glucocorticoids do to skin

A

acne

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22
Q

what does glucocorticoids do to development

A

may cause development disorders

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23
Q

what does glucocorticoids do to protein

A

breaks it down into glucose

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24
Q

what does glucocorticoids do to muscle

A

causes wasting

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25
Q

what does glucocorticoids do to would healing

A

impairs it

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26
Q

what does glucocorticoids do to stomach

A

causes peptic ulcers

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27
Q

what does glucocorticoids do to blood K+ levels

A

hypokalemia

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28
Q

what does glucocorticoids do to immune system

A

suppress

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29
Q

what are 3 things that NSAIDS do

A

analgesia
antipyretic
anti-inflammatory

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30
Q

what are 4 things that NSAIDs are used for

A

mild - moderate pain
fever
arthritis + other inflammatory disorders
grout + hyperuricemia

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31
Q

what is myalgia

A

muscle pain

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32
Q

what is arthralgia

A

bone pain

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33
Q

what is hyperuricemia

A

lots of urea in blood

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34
Q

what are 2 ways that NSAIDS reduce pain

A

they act at the site of origin of pain and interfere with the perception of pain by CNS

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35
Q

what is the mechanism of action of NSAIDS

A

inhibit fatty acid cyclo-oxygenase (COX)

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36
Q

what do NSAIDS do to prostaglandins

A

inhibit their synthesis

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37
Q

what do NSAIDS do to thromboxanes

A

inhibit their synthesis

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38
Q

what do NSAIDS do to prostacyclin

A

inhibit their synthesis

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39
Q

what are 3 things that NSAIDS inhibit the synthesis of

A

prostaglandins
thromboxanes
prostacyclin

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40
Q

how do NSAIDS cause the antipyretic effects

A

inhibition of prostaglandin E2 biosynthesis in the preoptic region of the hypothalamus

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41
Q

what do NSAIDS do to GI

A

ulceration and intolerance

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42
Q

what do NSAIDS do to to platelet aggregation

A

block (but not COX2 selective NSAIDS)

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43
Q

which NSAIDS dont block platelet aggregation

A

COX2

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44
Q

what do NSAIDS do to uterine motility

A

inhibit

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45
Q

what do NSAIDS do to renal function

A

inhibit prostaglandin-mediated renal function

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46
Q

what do NSAIDS do to blood pressure

A

may cause hypertension

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47
Q

what kind of reactions can happen with NSAIDS

A

hypersensitivity

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48
Q

what are 6 common untoward effects of all NSAIDS

A
  • GI ulcers
  • block platelet aggregation
  • inhibit uterine motility
  • inhibit prostaglanding mediated renal function
  • hypersensitivity reactions
  • may cause hypertension
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49
Q

what kind of compounds are All NSAIDS

A

organic acids

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50
Q

where do NSAIDS bind

A

arachidonic acid site on COX 1 or 2

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51
Q

which is the standard NSAID with which all others are compared

A

aspirin

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52
Q

what is the mechanism of action of aspirin

A

inhibition of both COX isoforms (1 and 2)

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53
Q

what does aspirin do to inflammation

A

interferes with adhesion and migration of granulocytes, leukocytes and macrophages to the site of inflammation

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54
Q

can aspirin be used for rheumatoid arthritis, which dose

A

yes at high doses

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55
Q

does aspirin affect fevers

A

yes it is antipyretic

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56
Q

what does aspirin do to body temperature (normal temp and fever temp)

A

reduces elevated temp without affecting normal temp

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57
Q

how does aspirin stop fever

A

reduces prostaglandin release in hypothalamus

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58
Q

what are 2 autonomic effects of aspirin as an anti-pyretic

A

vasodilation and sweating

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59
Q

how does aspirin do the analgesic effect

A

peripheral action at site of injury and perhaps within CNS

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60
Q

what compound is involved in platelet aggregation

A

thromboxane A2

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61
Q

why can’t platelets just make more COX when inhibited by apsirin

A

because it has no nucleus

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62
Q

what is special about COX inhibition by aspirin

A

it is irreversible

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63
Q

how does aspirin do its antiplatelet effect

A

blocks synthesis of thromboxane A2 in platelets

64
Q

how does aspirin effect the heart and how

A

reduces risk of myocardial infarction and transient ischemic episodes by stopping blot formation in coronary vessels

65
Q

what does aspirin do to bleeding time

A

doubles

66
Q

what does high doses of aspirin do and how

A

overcomes beneficial anti-platelet effect by stopping prostacyclin synthesis and thereby increasing chance of vasoconstriction

67
Q

what does prostacyclin do to platelet aggregation

A

helps stop it

68
Q

what is inhibited with high doses vs low dose of aspirin (general)

A

low: thromboxane (bad guy)
high: prostacyclin (good guy that stops aggregation

69
Q

what are 3 main undesirable effects of aspirin

A
  • gastric irritation and bleeding
  • salicylism
  • renal and hepatic effects
70
Q

what does aspirin do to gastric

A

irritate, bleed

71
Q

how does aspirin cause GI irritation and bleeding

A

inhibition of production of protecting prostaglandins which normally enhance mucous secretion

72
Q

what dose causes salicylism from aspirin

A

high doses

73
Q

what are 4 things that happen in salicylism

A

vomiting, tinnitus, deafness, vertigo

74
Q

what can aspirin do to renal and hepatic system

A

rare but cause hepatic damage or reduction of renal function

75
Q

whos renal and hepatic system is most effected by aspirin and why

A

in heart failure because prostaglandin mechanisms become important in renal function

76
Q

who gets reyes syndrome

A

kids with viral infections who are treated with aspirin

77
Q

what is reye’s syndrome associated with (what happens)

A

encephalopathy and hepatitis

78
Q

what does salicylate poisoning produce

A

uncoupling of oxidative phosphorylation

79
Q

what is uncoupling of oxidative phosphorylation

A

electron transport and generation of pH gradient across mitochondrion inner membrane still occurs but ATP is not made

80
Q

what happens to body temp in salicylate poisoning and why

A

hyperthermia : e transport is exothermic, ATP production is endothermic

81
Q

is e transport exo or endo thermic

A

exothermic

82
Q

is ATP production exo or endo thermic

A

endothermic

83
Q

what happens to O2 consumption in salicylate poisoning

A

increased

84
Q

what happens to CO2 production in salicylate poisoning

A

increased

85
Q

how does aspirin cause the uncoupling

A

they mess up the H gradient (reduces it) so that they diffuse back in and dont make ATP

86
Q

what does aspirin do to H gradient

what does it cause

A

reduces it

less ATP can be made

87
Q

why are most NSAIDS other than aspirin not used for antiplatelet

A

because they dont block COX irreversibly so they would need high doses (compared to aspirin)

88
Q

compare diclofenac and aspirin in terms of side effects

A

really similar, diclofenac is not much better

89
Q

what is sulindac

A

a prodrug that needs to be converted into an active metabolite to work

90
Q

what is the duration of action of sulindac

A

long

91
Q

where is sulindac absorbed

A

intestine

92
Q

where is sulindac excreted

A

bile

93
Q

what is the potency of ibuprofen compared to aspirin

A

more potent

94
Q

does ibuprofen do analgesia

A

yes

95
Q

what is the analgesia effects of ibuprofen compared to aspirin

A

does it at a lower dose than aspirin

96
Q

what is the GI effects of ibuprofen compared to aspirin

A

less because ibuprofen more potent and needs a smaller dose

97
Q

what does ibuprofen do to blood pressure

A

hypertension

98
Q

how does ibuprofen cause hypertension

A

stops PGE1 synthesis in kidney and/or altering balance of thromboxane (vasoconstrictor) / prostacyclin (vasodilator) synthesis

99
Q

is thromboxane a vasodilator or constrictor

A

vasoconstrictor

100
Q

is prostacyclin a vasodilator or constrictor

A

vasodilator

101
Q

what is naproxen

A

a non selective COX inhibitor

102
Q

what is naproxen typically used for

A

osteoarthritis

103
Q

what is unique about naproxen

A

it is the only NSAID that is a single isomer (others are racemates)

104
Q

what is the duration of action of naproxen

A

12h hours - long time

105
Q

what are the side effects of naproxen like

A

less cardio effects than COX 2 inhibitors

106
Q

how does indomethacin work

A

inhibits COX and phospholipase A2

107
Q

what does indomethacin do (immune)

A

impedes migration and proliferation of immune cells

108
Q

what are conditions that indomethacin is used for

A 
extreme things (really strong)
rheumatic conditions (gout, ankylosing spondylitis) patent ductus arteriosus
109
Q

how strong is indomethacin

A

very

110
Q

what are the side effects of indomethacin

A

lots because its so strong

111
Q

what are some side effects of indomethacin

A

GI upset, pancreatitis, headache, dizziness, confusion, thrombocytopenia, aplastic anemia

112
Q

what is ductus arteiosis

A

a short circuit vessel in fetal circulation that bypasses the lugns

113
Q

why is ductus arteiosis used

A

because the fetus doesny need to send blood to lungs

114
Q

what drug do you use to treat ductus arteiosis that persists after birth

A

indomethacin

115
Q

what maintains ductus arteiosis in fetus

A

cyclo-oxygenase products

116
Q

what is the role of COX 1 (2 main + one side role)

A

generating prostaglandins (which produce mucous in stomach) and cause platelet aggregation

117
Q

what is the role of COX 2 (3)

A

inflammation pain and fever

118
Q

which COX is consititutive

A

COX1

119
Q

which COX is inducible

A

COX2

120
Q

do COX2 inhibitors (selective) cause platelet effects

A

no

121
Q

do COX2 inhibitors (selective) cause gastric irritation

A

no

122
Q

do COX1 inhibitors (selective) cause anti-platelet

A

yes

123
Q

do COX1 inhibitors (selective) cause gastric irritation

A

yes

124
Q

what are 3 drugs that are COX 2 selective

A

meloxicam
etodolac
celecoxib

125
Q

what is the mechanism of action of meloxicam

A

COX 2 selective

126
Q

what is the mechanism of action of etodolac

A

COX 2 selective

127
Q

how much more selective is celecoxib for the different COX forms

A

10X more for COX2 than COX1

128
Q

what is celecoxib often used for

A

rheumatoid arthritis and osteoartritis

129
Q

does celecoxib cause GI upset

A

no

130
Q

what are some cardiovascular effects of celecoxib

A

possibly hypertension

131
Q

why does celecoxib cause hypertension

A

due to altered ratio of thromboxane (constrict) to prostacyclin (dilate)

132
Q

what are 4 types of prostaglandin receptors

A

EP1 EP2 EP3 EP4

133
Q

what does EP1 do

A

potentiation of responses to painful stimulus

134
Q

what does EP2 do

A

vasodilation, bronchoconstriction

135
Q

what does EP4 do

A

vasodilation, bronchoconstriction

136
Q

what does EP3 do

A

gastric mucous secretion

137
Q

which prostaglandins receptor have the same function and what do they do

A

EP2 and EP4

vasodilation, bronchoconstriction

138
Q

what is the interest in trying to do along with a prostaglandin receptor antagonist (what are they trying to avoid when designing prostaglandins antagonists)

A

not disturbing balance between thromboxanes and prostacyclin that use different receptors

139
Q

what do drugs want to do to prostaglandins receptors

A

antagonize

140
Q

is acetaminophen an NSAID

A

no

141
Q

what does acetaminophen do

A

analgesia, antipyretic

142
Q

does acetaminophen do pain

A

analgesia

143
Q

does acetaminophen do fever

A

antipyretic

144
Q

does acetaminophen do inflammation

A

nothing

145
Q

does acetaminophen do platelets

A

nothing

146
Q

what does acetaminophen do GI

A

doesnt cause bleeding

147
Q

does acetaminophen affect COX1

A

no

148
Q

does acetaminophen affect COX2

A

no

149
Q

which COX does acetaminophen affect

A

COX 3

150
Q

what are 2 uses of tylenol / acetaminophen

A

mild pain, fever in children (no reye’s sendrom)

151
Q

is tylenol good for arthritis

A

no not alone

152
Q

what are 5 effects of tylenol / acetaminophen

A

dizziness, excitement, disorientation, hepatic damage, renal damage

153
Q

what does tylenol do to hepatic system + symptoms

A

cause damage : nausea vomiting diarrhea abdominal pain

154
Q

how much tylenol is fatal

A

15g

155
Q

can renal damage from tylenol happen with hepatic damage

A

yes

156
Q

can renal damage from tylenol happen without hepatic damage

A

yes

PMCOL 343 (31 decks)

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