Lecom-B Mini Pharm Ch 36 By Mac

Front 1

trxt of acute gout targets

Back 1

inflammation

Front 2

trxt of chronic gout targets

Back 2

both inflamm processes and prod/elim of uric acid

Front 3

what tissue type does inflamm primarily occur

Back 3

vascularized CT

Front 4

enzymes at the head of the enzymatic path for PG

Back 4

COX

Front 5

how fast is the onset of DMARDs

Back 5

slow (weeks to months)

Front 6

what differentiates NSAIDs from steroids

Back 6

NSAIDs inhibit COX, steroids mediate anti-inflamm effects via activation of glucocorticoid receptors

Front 7

rare syndrome of rapid liver degen and encephalitis in children treated w aspirin during a viral inf

Back 7

reye syndrome

Front 8

cytokine that plays central role in inflamm

Back 8

TNF-alpha

Front 9

drug that increases renal excretion of uric acid

Back 9

uricosuric agent

Front 10

key enzyme in purine metab pathway that ends w prod of uric acid

Back 10

xanthine oxidase

Front 11

prototype of salicylates

Back 11

aspirin

Front 12

older nonselective NSAIDs

Back 12

ibuprofen, indomethacin

Front 13

effectiveness of ibuprofen, naproxen, indomethacin and ketorolac

Back 13

ibuprofen and naproxen = moderate; indomethacin has greater anti-inflamm, ketorolac has greater analgesic

Front 14

celecoxib

Back 14

COX2 inhibitor

Front 15

COX2 decrease ____ but increase ____ side effects

Back 15

GI distress, CV thrombotic events

Front 16

COX converts

Back 16

arachidonic acid into the endoperoxide precursors of PG

Front 17

where is COX 1 and 2 expressed

Back 17

COX 1 = noninflamm cells, COX 2 = activated lymphocytes, PMNs and other inflamm cells

Front 18

aspririn and nonselective NSAIDs decrease synthesis of

Back 18

PG and thromboxane

Front 19

COX 2 inhibitors have less effect on what PG

Back 19

those involved in homeostatic fxn esp in GI tract

Front 20

diff in MOA between aspirin and other NSAIDs

Back 20

aspirin acetylates and thereby irrev inhibits COX

Front 21

irrev action of aspirin results in longer duration of

Back 21

antiplatelet effect

Front 22

antipyretic action of NSAIDs by inhibiting PG synth in

Back 22

CNS stimulated by pyrogens

Front 23

analgesic MOA of NSAIDs

Back 23

decreased PG prod = decreased activ of periph pain sensors

Front 24

COX inhibitors most importantly do what to GI and renal fxn

Back 24

decr PG mediated cytoprotection in GI tract and autoregul of kidney fxn

Front 25

3 therapeutic dosages of aspirin

Back 25

low (<300) = antiplatelet
intermed (300-2400)=antipyretic and analgesic
high (2400-4000)=anti-inflamm

Front 26

what is aspirin hydrolyzed to in blood and tissues

Back 26

acetate and salicylic acid

Front 27

salicylate is ____ inhibitor of COX

Back 27

reversible

Front 28

at low doses, elim of salicylate is what order

Back 28

first

Front 29

at high doses, elim of salicylate is what order

Back 29

zero

Front 30

site of excretion of NSAIDs

Back 30

kidney

Front 31

site of excretion of acetaminophen

Back 31

liver

Front 32

half life of ibuprofen

Back 32

2hrs

Front 33

naproxen and piroxican are notable because

Back 33

have longer half lives

Front 34

ketorolac is notable as drug used mainly as

Back 34

systemic analgesic

Front 35

only NSAID availabile in parenteral form

Back 35

ketorolac

Front 36

what reduce polyp formation in pts w primary familial adenomatous polyposis

Back 36

nonselective NSAIDs

Front 37

long term use of NSAIDS reduces risk of

Back 37

colon cancer

Front 38

most common adverse effect from therapeutic anti-inflamm doses of aspirin

Back 38

gastric upset

Front 39

chronic aspirin use can cause

Back 39

gastric ulcers, upper GI bleeding, renal effects

Front 40

aspriin hypersensitivity pts experience ___ due to increased leukotriene synth

Back 40

asthma

Front 41

SE at high doses of aspirin

Back 41

tinnitus, vertigo, hyperventil, resp alkalosis

Front 42

SE at very high doses of aspirin

Back 42

metab acidosis, dehydration, hyperthermia, collapse, coma, death

Front 43

NSAIDS should not be used in pts w exisiting

Back 43

renal disease

Front 44

use of ____is restricted to 72h due to risk of GI and renal damage

Back 44

parenteral ketorolac

Front 45

indomethacin can cause

Back 45

serious hematologic rxns

Front 46

celecoxib, rofecoxib, valdecoxib have reduced risk of

Back 46

GI effects

Front 47

rofecoxib and valdecoxib have increased risk of

Back 47

MI and stroke

Front 48

why is there an incr risk of thrombosis w COX 2 inhibitors

Back 48

they have greater inhib effects on endothelial PG (PGI2) than on platelet TXA2 formation

Front 49

prostacyclin promotes

Back 49

vasodil and inhibits platelet aggreg

Front 50

TXA2 promotes

Back 50

vasoconstrict and platelet aggreg

Front 51

only OTC NSAID avail in US

Back 51

acetaminophen

Front 52

toxic prodrug metabolized to acetaminophen

Back 52

phenacetin

Front 53

why does acetaminophen lack anti-inflamm effects

Back 53

weak COX1, COX2 inhibitor

Front 54

what agent is acetaminophen

Back 54

antipyretic, analgesic

Front 55

acetaminophen is effective for same indications as

Back 55

intermed dose aspiriin

Front 56

half life of acetaminophen

Back 56

2-3hr

Front 57

when is acetaminophen a dangerous hepatotoxin

Back 57

overdosed in pts w severe liver impairment

Front 58

mech of toxicity of acetaminophen

Back 58

oxid to cytotoxic intermed by phase I cyt P450 enzymes if substrates for phase II conj rxns (acetate and glucuronide) are lacking

Front 59

acetaminophen overdose antidote

Back 59

acetylcysteine

Front 60

who is at incr risk for acetaminophen induced hepatotoxicity

Back 60

those who drink 3+ alcoholic drinks per day

Front 61

considered anti-inflamm drugs w intermed rate of action

Back 61

corticosteroids

Front 62

MOA of methotrexate

Back 62

reducing # of immune cells avail to maintain inflamm response

Front 63

sulfasalazine, hydroxychloroquine, cyclosporine all interfere with activity of

Back 63

T lymphocytes

Front 64

what drug interferes w B lymphocytes

Back 64

rituximab

Front 65

what drugs inhibit TNF-alpha

Back 65

infliximab, adalimumab, etanercept

Front 66

anti TNF-alpha drugs are given via what route

Back 66

injection

Front 67

3 trxt strategies for gout and drugs that address each

Back 67

decr inflamm (colchicine, NSAIDs, glucocorticoids), incr uric acid excretion (probenecid), decr uric acid prod (allopurino, febuxostat)

Front 68

purines-->uric acid via

Back 68

xanthine oxidase

Front 69

NSAID that is effective at inhibiting inflamm of acute gouty arthritis

Back 69

indomethacin

Front 70

selective inhibitor of microtubule assembly that reduces leukocyte migration and phagocytosis

Back 70

colchicine

Front 71

reduces prod of LTB4 and free radical formation

Back 71

colchicine

Front 72

general mitotic poison

Back 72

colchicine

Front 73

preferred trxt for acute gouty arthritis

Back 73

NSAID or glucocorticoid

Front 74

lower doses of ___ used to prevent attacks of gout in pts w hx of multiple acute attacks

Back 74

colchicine

Front 75

drug used in management of familial mediterranean fever

Back 75

colchicine

Front 76

colchicine can be given by what routes

Back 76

oral, parenteral

Front 77

can cause bone marrow depression

Back 77

indomethacin

Front 78

can cause behavioral changes and impaired glucose control

Back 78

short courses of glucocorticoids

Front 79

colchicine can severly damage

Back 79

liver and kidney

Front 80

high doses of colchicine can cause

Back 80

severe GI disturbance esp diarrhea

Front 81

where is 90% of uric acid reabsorbed

Back 81

PCT

Front 82

weak acids that compete w uric acid for reabsorption in PCT

Back 82

probenecid, sulfinpyrazone

Front 83

when can serum uric acid conc be elevated by drug rather than reduced

Back 83

low doses of probenecid and sulfinpyrazone when they compete w uric acid for secretion...or with aspirin

Front 84

what do uricosuric drugs inhibit

Back 84

secretion of other weak acids and reabsorp of uric acid

Front 85

what drugs are of no value in acute episodes

Back 85

uricosuric drugs

Front 86

how can acute gout attack during early phase of action of uricosuric drugs be avoided

Back 86

simult admin of colchicine or indothemacin

Front 87

uricosuric share allergenicity w

Back 87

sulfonamid drugs

Front 88

enzyme that converts hypoxanthine to xanthine and xanthine to uric acid

Back 88

xanthine oxidase

Front 89

converts allopurinol to oxypurinol (alloxanthine)

Back 89

xanthine oxidase

Front 90

irrev suicide inhibitor of xanthine oxidase

Back 90

alloxanthine

Front 91

nonpurine inhibitor of xanthine oxidase

Back 91

febuxostat

Front 92

what is more effective than allopurinol in lowering serum uric acid

Back 92

febuxostat

Front 93

xanthine oxidase inhib and uricosuric drugs are withheld for ___ after acute attack of gouty arthritis

Back 93

1-2wks

Front 94

adjunct to cancer chemotherapy to slow formation of uric acid from purines released by death of large numbers of neoplastic cells

Back 94

allopurinol

Front 95

SE of allopurinol

Back 95

GI upset, rash, periph neuritis, vasculitis, BM dysfxn incl aplastic anemia

Front 96

SE of febuxostat

Back 96

liver fxn abnorm, h/a, GI upset