NSAIDS and non-opioid Flashcards

1
Q

what inflammatory substance is most involved in the inflammatory response

A

prostaglandins

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2
Q

chronic inflammation we see the release of what

A

interleukins, GM-CSF, TNF, interfeurons, PDGF

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3
Q

two different inflammatory pathways

A

COX and LO

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4
Q

LOI inhibitors block what

A

arachidonic acid creating leukotrienes

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5
Q

cox isoforms

A

cox 1 and cox 2

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6
Q

cox 1 is ___ and ___ distributed

A

constitutive and wide

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7
Q

COX 2 expression is dependant on what

A

stimulus

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8
Q

COX2 facilitates what

A

inflammatory

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9
Q

how many carbons in arachidonic acid

A

20 carbons

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10
Q

NSAIDs relieve __ and ___ pain

A

acute and chronic

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11
Q

glucocorticoids with chronic use produce what

A

toxicities

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12
Q

DMARDs mean what?

A

disease modifying anti-rheumatic drugs

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13
Q

NSAIDS inhibit the synthesis of what

A

PG

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14
Q

NSAIDs are weak acids or bases

A

acids

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15
Q

metabolism of NSAIDS

A

highly metabolized and removed in urine and bile

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16
Q

NSaids are inhibitors of ___

A

COX

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17
Q

do they decrease sensitivity of vessels to bradykinin and histmaine

A

yes

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18
Q

reverse or excite vasodilation

A

reverse

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19
Q

inhibit or excite plt aggregation with COX1

A

inihibt

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20
Q

plts only have cox __

A

1

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21
Q

aspirin is an ___ block for COX

A

irreversible

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22
Q

aspirin is equivalent to ___ for cox 1 and cox 2

A

ibuprofen

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23
Q

cox 1 and cox2 inhibitors

A

ibu, meclofenamate, toradol

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24
Q

cox 1 more than cox2

A

apsirin, sulindac, piroxicam

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25
Q

cox 2 more than cox 1

A

celebrex, vioxx, bextra

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26
Q

inhibits cox and lox

A

indomethacin, diclofenac

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27
Q

nsaids do what to the gastric

A

irritate the fuck out of it

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28
Q

all nsaids can cause __ and __

A

nephrotoxicity and heptotoxicity

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29
Q

aspirin drug name is

A

acetylsaylicylic acid

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30
Q

willow bark extracts made

A

aspirin

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31
Q

aspirin has what anti effects

A

analgesic and antipyretics

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32
Q

antipyretics are mediated by __ and ___-1 inhibition

A

COX and IL

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33
Q

antipyretics dissipation of heat caused by ____ of peripheral vessels

A

vasodilation

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34
Q

aspirin peripherally causes

A

vasodilation

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35
Q

aspirin in the CNS causes

A

vasoconstriction

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36
Q

aspirin causes slight ___ of bleeding time

A

prolongation

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37
Q

is asp a concern pre surgery?

A

yes

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38
Q

aspirin is taken for what (4)

A

RA, Rheumatoid fever, fever, clot prevention

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39
Q

other effects of aspirin

A

decreases transient ischemic heart attack, angina, coronry artery thrombosis, can cause work on colon cancer

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40
Q

adverse effects of aspirin

A

GI upset, stomach ulcers

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41
Q

aspirin has what kind of coating

A

enteric coated

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42
Q

enteric coating allows from what?

A

adequate absorbing in the small intestine

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43
Q

Aspirin toxicity can cause what

A

reye syndrome

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44
Q

what is reye syndrome

A

hepatic injury and encephalopathy in kids that were treated with aspirin after a viral illness

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45
Q

aspirin causes what poisoning

A

salicylate poisoning

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46
Q

acetaminophen cause what

A

liver failure

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47
Q

NSAID black box warning

A

pregnancy, fetal kidney development decreased, decreased amniotic fluid

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48
Q

aspirin overdose mild

A

N/v/d

49
Q

moderate side effects of aspirin

A

n/v/ ringing in ears, confusion, headache, hyperventilation, tachycardia, fever

50
Q

severe effects of aspirin

A

delirium, hallucinations, seziures, coma, respiratory arrest

51
Q

severe amt

A

100

52
Q

moderate asp

A

70

53
Q

mild aspirin amt in blood

A

50

54
Q

treatment for asp overdose

A

activated charcoal > fluids> dialysis

55
Q

any effect of COX 1 on taking care of COX 2

A

no

56
Q

COX 2 inhibitors have what effects

A

analgeis, antipyretics, anti-inflammatory

57
Q

celecoxib works on what

A

COX2

58
Q

pharmacokinetics of celecoxib

A

absorption increased by food, fewer GI effects, no impact on plts

59
Q

celecoxib allergies

A

sulfa allergies

60
Q

use of celecoxib

A

RA, osteoarthritis, decrease ulcer incidence

61
Q

black box warning of celecoxib

A

increased inhibition of PGI2 production

62
Q

Meloxicam inhibits COX-2 over COX1 causing what

A

fewer GI effects

63
Q

if celebrix is contraindicated what could be given

A

meloxicam

64
Q

nonselectives

A

diclonefac, ibuprofen, indomethacin

65
Q

___% of patients have adverse GI effects when taking diclofenac

A

20

66
Q

diclofenac overall effects

A

antiinflamm, analgesis, antipyr

67
Q

ibuprofen has less ____ than aspirin

A

GI upset

68
Q

equivalent what to aspirin

A

antiinflamm, analgesic

69
Q

rare adverse effects of ibuprofen

A

agranulocytosis and aplastic anemia

70
Q

indomethacin is a potent ___ inhibitor

A

COX

71
Q

what also might indometh ingibit

A

phospholpiase A and C

72
Q

indo can ___ T &B cel proliferation

A

decrease

73
Q

indo is used to treat

A

rheumatism, gout, patent ductus arteriosus

74
Q

toradol is used for (3)

A

post op, ER, sports meds

75
Q

toradol long term or short term

A

short term

76
Q

toradol is an NSAID but primary use if for ___

A

pain

77
Q

toradol decreases the need for ___

A

opioids

78
Q

Tyleno;l treats ___ to ___ pain

A

mild to moderate

79
Q

tylenol use when _____ effect not required

A

anti-inflammatory

80
Q

acetaminophen isn’t an NSAID bc its central vs ____

A

peripheral

81
Q

what is tylenol metabolized by

A

hepatic enzymes

82
Q

indications for tylenol

A

analgesic, antipyretic, no effect on plt aggregation

83
Q

adverse effects of tylenol

A

mild increase in hepatic enzymes, larger doses: dizzy, fatal >15 g,hepatotoxicity

84
Q

most toxic NSAIDS

A

indomethacin, tolmetin, meclofenamate

85
Q

least toxic NSAIDS

A

asp and ibu

86
Q

renal insufficieny will have a problem with

A

nonacetylated salicylates

87
Q

COX2 ihnhibitors are safest for pts at high rish for ___

A

stomach bleeding

88
Q

acute effects of glucocorticoids

A

suppress inflammation, mobilize energy stores, improve cognitive function, salt and water retention

89
Q

chronic effects of glucort

A

immunosuppression, diabetes, depression, HTN

90
Q

glucocorticoids transcription pathway

A

annexin 1, secretory leukoprotease inhibitor, IL10, inh-NFkB

91
Q

annexin suppresses and inhibits what

A

suppresses phospho A2 and inhibits leukocytes

92
Q

glucort drugs

A

hydrocortisone, prednisone, dexamethasone

93
Q

indications for gluco

A

suppression of infla, addisons diseases, cushings disease, fetal lung maturation

94
Q

DMARDS reduce inflammation and decrease ___ to bones and joints

A

damage

95
Q

DMARDS are often given with ___

A

NSAIDS

96
Q

cushings disease we remove what

A

adrenal gland tumor

97
Q

how do DMARDS reduce inflammation

A

reduced sedation rate, CRP, RF

98
Q

nonbiologic DMARDS

A

methotrexate, cyclophosphamide, cyclosporine

99
Q

biologic DMARDS

A

abatacept, rituximad, adalimumab

100
Q

chronic inflamm is a risk factor for developing __

A

cancer

101
Q

methotrextae works on

A

antimetabolite

102
Q

cyclophosphamide suppresses what

A

B&T Cell

103
Q

cyclosporine inhibits what

A

interleukins

104
Q

abatacept block whst

A

tcell activation

105
Q

rituximab depletes

A

b lymphocytes

106
Q

adalimumab is an

A

anti-TNF-a

107
Q

chronic exposure to inflammatory mediators leads to (4)

A

cell proliferation, mutagenesis, oncogene activation, angiogenesis

108
Q

ROS means

A

reactive oxygen species

109
Q

RNi means

A

reactive nitrogen intermediates

110
Q

ROS and RNI from inflammatory cells cause ____ in neighboring epithelial cells

A

mutations

111
Q

inflammatory response ____ mutational rates

A

increases

112
Q

nF-kB induces

A

production of cyclins, cdks

113
Q

NF-kB and stat3 induce ___ of chemokined

A

production

114
Q

cancers may see an increased ___ when taking low dose ___ for a long time

A

effects NSAIDs

115
Q

does tylenol have any effect on inflammation

A

no

116
Q

anti-inflammatories decrease

A

colon cancer, breast cancer, prostate cancer

117
Q

immune cells supply ____ to the tumor micorenvironment

A

bioactive molecules

118
Q

aspirin binds to ____ to block ___ from binding to the active site in the COx-1 plt

A

serine 529, Arachidonic acid