Br Pharmacology: Nsaids, Drugs Used In Ra And Gout

Front 1

Does Ibuprofen, naproxen or indomethacin have greater anti-inflammatory effects?

Back 1

indomethacin

Front 2

Does ketorolac, ibprofen or indomethacin have greater analgesic effect?

Back 2

ketorolac

Front 3

What is an example of a COX2 inhibitor? What are the side effects with these drugs?

Back 3

celecoxib... lead to cardiovascular thrombotic events

Front 4

Where is COX1 primarily expressed? COX2?

Back 4

non-inflammatory cells

activated lymphocytes, polymorphonuclear cells and others

Front 5

Aspirin and nonselective NSAIDS decrease synthesis of what molecules?

Back 5

prostaglandins and thromboxanes

Front 6

Do NSAIDs or aspirin have a stronger antiplatlet effect?

Back 6

aspirin

Front 7

Is salicylate as effective as aspirin?

Back 7

no it does not acetylate COX

Front 8

COX inhibitors have an effect on inflammation. What is their effect on tissue damage and immunologic reactions?

Back 8

They have no effect on these other processes

Front 9

What are the effects of COX inhibitors in the GI tract and kidney?

Back 9

1) in GI they reduce prostaglandin cytoprotection
2) in kidney they reduce autoregulation via prostaglandins

Front 10

What is the low range dose of ASA and what is used for?

Back 10

<300mg/day good for reducing platlet aggregation

Front 11

What is the mid range dose of ASA and what is used for?

Back 11

300-2400mg/day good for antipyretic and analgesic effects

Front 12

What is the high range dose of ASA and what is used for?

Back 12

2400-4000mg/day good for anti-inflammatory effects

Front 13

What is ASA broken down into and where does this occur?

Back 13

in blood and tissues ASA is hydrolyzed to acetate and salicylate

Front 14

Which NSAIDs are known for their long half-life?

Back 14

naproxen and piroxicam

Front 15

What is a potent NSAID with increased toxicity?

Back 15

indomethacin

Front 16

What conditions can non-selective NSAIDs be used to treat?

Back 16

decrease polyp formation in FAP, decrease colon CA, treat dysmenorrhea, headache, PATENT DUCTUS ARTERIOSUS

Front 17

What are side effects of ASA with chronic use?

Back 17

chronic use: gastric ulcer, upper GI bleed, ARF, interstitial nephritis

Front 18

Someone with ASA hypersensitivity may experience what? Why?

Back 18

asthma from increased leukotriene synthesis... Note that this would occur with any NSAID

Front 19

What can happen when someone takes high doses of ASA? At very high doses?

Back 19

tinnitus, vertigo, hyperventilation, respiratory alkalosis

metabolic acidosis, dehydration, hyperthermia, coma, death

Front 20

children treated with ASA are at risk for developing what?

Back 20

Reyes syndrome.... rapid liver failure with encephalopathy

Front 21

What are soem of the side effects of nonselective NSAIDs?

Back 21

renal damage

Front 22

What are the COX2 inhibitors?

Back 22

celecoxib, rofecoxib, valdecoxib

Front 23

What are the side effects of COX2 inhibitors compared to compared with other NSAIDS?

Back 23

1) reduced risk of GI effects
2) same risk of renal damage
3) increased risk of MI, stroke, arterial thrombosis. Thrombus formation is from less effect on reducing TA2

Front 24

What is the only over the counter analgesic in US?

Back 24

tylenol

Front 25

What is the MOA of tylenol?

Back 25

weak inhibitor of COX1 and 2 in peripheral tissues making it not as effective as an anti-inflammatory. works mostly in CNS

Front 26

What is tylenol given for? what does it lack?

Back 26

analgesic and antipyretic

lacks anti-inflammatory and antiplatelet effects

Front 27

What strength ASA is equivalent to taking tylenol?

Back 27

intermediate dose (300-2400mg/day ASA)

Front 28

What are the toxic effects of tylenol?

Back 28

hepatoxicity via lack of phase II conjugation reactions

Front 29

How can tylenol overdose be corrected?

Back 29

administration of acetylcysteine

Front 30

What is the goal of giving someone DMARDS? What are they also known as? Why?

Back 30

1) slow or reverse joint damage
2) SAARDs because they take 6 weeks to 6 months to begin working

Front 31

in comparison to NSAIDS and DMARDS where do corticosteroids fit in when treating RA?

Back 31

In the middle (intermediate)

Front 32

When are corticosteriods given to someone with RA?

Back 32

when they have a severe act or for long term use in patients in which NSAIDs and DMARDs are not effective

Front 33

What is the MOA of methotrexate in RA?

Back 33

1) reduces number of immune cells by competitively inhibiting dihydrofolate reductase

Front 34

What drugs are used to reduce T cells in RA?

Back 34

1) sulfasalazine
2) hydroxychloroquine
3) cyclosporine
4) lefunomide
5) mycophenolate
6) abatacept

Front 35

What drugs are used to reduce B cell in RA?

Back 35

rituximab

Front 36

What drug reduces macrophages in RA?

Back 36

gold

Front 37

What drugs are used in RA that inhibit TNF-alpha?

Back 37

etanercept, infliximab and adalimunab

Front 38

What DMARDs is given early to help with RA?

Back 38

low dose methotrexate

Front 39

What are the toxicities of methotrexate?

Back 39

nausea, mucosal ulcers, HEMATOXICITY, TERATOGEN

Front 40

What are the toxicities of cyclosporine? What is its MOA?

Back 40

1) nephrotoxicity, HTN, hepatoxicity
2) cyclophilin inhibits calcineurin which prevents the dephosphorlyation of NF-AT which prevents cytokine (IL2) release

Front 41

What are the adverse effects of chloroquine?

Back 41

Rash, ocular toxicity, GI disturbances

Front 42

What are the adverse effects of sulfasalazine? What else is it used for?

Back 42

1) leukopenia and rash
2) inflammatory bowel disease (UC)

Front 43

What are toxicities of anti-TNF-alpha drugs? What else are they used in?

Back 43

1) macrophage dependent infections, formation of antibodies to dsDNA, antinuclear antibodies and vasculitis
2) Inflammatory bowel disease

Front 44

What are the side effects of leflunomide? What is its MOA?

Back 44

teratogen, hepatoxicity, GI disturbances, skin reactions

inhibits dihydroorotate dehydrogenase (an enzyme involved in de novo pyrimidine synthesis)

Front 45

What are the toxicities of gold compounds?

Back 45

dermatitis, aplastic anemia

Front 46

What are the adverse effects of penicillamine? What is it used for? What is its MOA?

Back 46

1) proteinuria, dermatitis, aplastic anemia
2) RA and as a chelating agent
3) It works by reducing numbers of T-lymphocytes, inhibiting macrophage function, decreasing IL-1, decreasing rheumatoid factor, and preventing collagen from cross-linking.

Front 47

What are the treatment strategies for treating gout?

Back 47

1) reduce inflammation
2) increase uric acid excretion
3) reduce purine metabolism

Front 48

What NSAIDs are effective in treating gout? What other drugs have a similar effect?

Back 48

1) indomethacin
2) colchicine (mitotic poison)

Front 49

What is the MOA of colchicine? what molecule does it reduce?

Back 49

1) inhibit microtubules polymerization
2) reduce leukocyte migration and phagocytosis and degranulation
3) decrease LTB4 and free radical formation

Front 50

What is the preferred treatment in acute gouty arthritis?

Back 50

indomethacin or colchicine or glucocorticoid

Front 51

When is colchicine given?

Back 51

1) low doses to prevent acute attacks in someone with a history of gout.
2) used in mediterranean fever

Front 52

What is mediteranean fever? What is used to treat it?

Back 52

1) idopathic fever, hepatitis, peritonitis, pleuritis, arthritis, amyloidosis
2) colchicine

Front 53

What toxicities are associated with indomethacin? What neonatal condition is it used for?

Back 53

renal damage and bone marrow suppression

closure of a PDA

Front 54

What are side effects of colchicine?

Back 54

hepato and renal toxic, fatal in overdose

Front 55

What are the urocosuric agents?

Back 55

probenecid and sulfinpyrazone

Front 56

How much uric acid is normally reabsorbed by kidney?

Back 56

90% reabsorbed in PCT

Front 57

How do urocosuric agents work?

Back 57

they are weak acids that compete with uric acid reabsorption

Front 58

In low doses how can urocosuric agents enhance a gout attack?

Back 58

they can compete with uric acid secretion and therefore increase its blood concentration

Front 59

How does ASA effect uric acid levels?

Back 59

it elevates them by impairing secretion of uric acid

Front 60

What other drugs do urocosuric drugs inhibit the secretion of?

Back 60

methotrexate and penicillin

Front 61

Are urocosuric drugs effective in an acute gout episode?

Back 61

no

Front 62

What should uricosuric agents be given with to avoid acute flare-ups?

Back 62

colchicine or indomethacin

Front 63

What other drugs do urocosuric agents resemble and share the same side effects as? Which COX inhibitor has same side effect?

Back 63

1) allergies of sulfonamides
2) celecoxib

Front 64

what are the xanthine oxidase inhibitors?

Back 64

allopurinol

Front 65

What does xanthine oxidase do?

Back 65

converts hypoxanthine to xanthine to uric acid

Front 66

What drug is a nonpurine that works like allopurinol? Why might it be better?

Back 66

febuxostat does not inhibit other enzymes involved in purine and pyrimidine metabolism

Front 67

When are xanthine oxidase inhibitors given?

Back 67

like uricosuric acid they are given 1-2 weeks after an acute episode of gouty arthritis and are administered with colchicine or NSAIDs to avoid acute attacks

Front 68

What are the toxicities of allopurinol/

Back 68

peripheral neuritis, vasculitis, aplastic anemia

Front 69

What drugs are not metabolized when xanthine oxidase is inhibited?

Back 69

mercaptopurine and azathioprine

Front 70

NSAIDS availble for opthalmic solution

Back 70

Diclofenac, ketoralac

Front 71

NSAID available orally, IM and ophthalmically?

Back 71

ketoralec

Front 72

NSAID that is used for acute condition, such as pre-op anesthesia and has limited duration (<5 days) of
use due to nephrotoxicity?

Back 72

ketoralec

Front 73

Drug often used in combination with TNF - alpha inhitors for RA

Back 73

methotrexate

Front 74

DMARD that Causes bone marrow suppression

Back 74

methotrexate

Front 75

DMARDS that interferes with T cells? What is the SE?

Back 75

hydroxychloroquine

Retinal destruction and dermatitis

Front 76

Anti-rheumatic agent also used for Chron's disease?

Back 76

infliximab