Ch 36 Pharm, Nsaids, Ra And Gout Meds

Front 1

What are the four actions of the non selective COX inhibitors?

Back 1

anit-inflammatory, Anti-platelet, Anti-pyretic, and analgesic

Front 2

Acetaminophen exhibits which two properties?

Back 2

anti-pyretic and analgesic

Front 3

MOA of the non selective COX inhibitors

Back 3

blocks cyclooxygenase COX pathway, limiting prostaglandin synthesis

Front 4

Difference between aspirin and other non selective COX inhibitors

Back 4

aspirin is irreversable

Front 5

Name the three oral, reversible non selective COX inhibitors

Back 5

Ibuprofin, Indomethacin, and naproxen

Front 6

Which NSAID is available in a parenternal formulation and is mainly used for its analgesic properties.

Back 6

Ketorlac

Front 7

Ketorlac use is restricted to 72 hours due to which side effects?

Back 7

GI and renal damage

Front 8

Which non selective, oral, COX inhibitor has the highest anti-inflammatory property, and is a 1st line treatment of a gouty attack?

Back 8

Indomethacin (reduces prostaglandin, and crystal phagocytosis by macrophages)

Front 9

Toxicity of Aspirin

Back 9

tinnitis, vertigo, GI bleeding, and increased bleeding time, risk of reyes syndrome in kids with viruses.

Front 10

Common side effects of all NSAIDS

Back 10

risk of renal damage, especially in preexisting renal disease, and GI upset.

Front 11

What is acetaminophen, what is it used for?

Back 11

is an OTC antipyretic/analgesic, used in patients with renal disease. metabolized by liver

Front 12

Toxicity of acetaminophen

Back 12

hepatic failure in cases of overdose due to toxic metabolite by phase II reactions. Alcohol predisposes to this toxicity

Front 13

Antidote for Acetaminophen poisoning

Back 13

N-acetylcysteine. used to regenerate glutathione, and continue degredation of toxic metabolite

Front 14

What are the COX 2 inhibitors, and why were they developed?

Back 14

Celecoxib, refecoxib, valdecoxib. developed to limit GI effects of non selective NSAIDs

Front 15

Toxicities of COX 2 selective inhibitors

Back 15

renal toxicity, as well as increased risk of myocardial infarction and stroke. this is due to the increased inhibition of prostacyclin (PGI2), than over TXA2. causes platelet aggregation and vasoconstriction

Front 16

What are DMARDS, and what is their clinical use?

Back 16

slow active disease modifying drugs, may take 6 weeks to 6 months to have effect. Limit or even reverse progression of Rheumatic disease

Front 17

What class of drugs have an intermediate effect on rheumatic disease, but are too toxic for long term, chronic use?

Back 17

corticosteroids, reduce inflammation, and other immune responses in rheumatic disease.

Front 18

Which cytotoxic drug acts by limiting the number of immune cells available to carry out inflammatory response?

Back 18

methotrexate, also used to treat cancer, inhibits dihydrofolate reductase (thereby stopping DNA synthesis)

Front 19

Toxicity of methotrexate

Back 19

nausea, mucosal ulcers, hematotoxicity, hepatotoxicity, teratogenicity

Front 20

Antidote used for methotrexate overdose

Back 20

Leucovorin

Front 21

DMARD drugs used that interfere with activity of T lymphocytes

Back 21

sulfasalazine, cyclosporin, hydroxychloroquine.

Front 22

Toxicity of T lymphocyte altering DMARDS

Back 22

hepatotoxicity, GI disturbance, rash, headache, leukopenia

Front 23

DMARD drugs that act by limiting activity of B lymphocytes and macrophages

Back 23

Rituximab for B lymphocytes Gold compounds for macrophages

Front 24

Other use for Rituximab and toxicities

Back 24

also used for Non-Hodgkins lymphoma, causes infusion reaction, rash, infection, and cardiac toxicity

Front 25

Other use for Hydroxychloroquine

Back 25

anti malarial

Front 26

Other use for Sulfasalazine

Back 26

Ulcerative colitis

Front 27

Other use for methotrexate

Back 27

cancer treatment

Front 28

Other use for cyclosporine

Back 28

tissue transplant

Front 29

What immunoglobulin based biologic agents work by inhibiting Tumor necrosis factor A, and have shown success in treating RA?

Back 29

Infliximimab, adalimumab, and entarecept.

Front 30

What is another major use for the tumor necrosis factor A drugs?

Back 30

Crohn's disease

Front 31

Which DMARD for RA works as an interleukin 1 receptor antagonist

Back 31

Anakinra, causes infection, worsening of COPD, and hypersensitivity reactions

Front 32

DMARDS have also shown to be of use in what other autoimmune diseases?

Back 32

SLE, sjogrens arthritis, JRA, and ankylosing Spondylitis,

Front 33

What are the 3 treatment strategies associated with gout?

Back 33

1) reduce inflammation during acute attacks 2) accelerating renal excretion of uric acid 3) reducing conversion of purines to uric acid

Front 34

Which treatment of acute gout works by inhibiting microtubule assembly, reducing leukocyte migration, and phagocytosis? also works with familial mediterranean fever

Back 34

colchicine. is a general mitotic poison, and is being phased out due to severe liver and kidney damage

Front 35

What is the standard 1st line treatment for acute gouty attacks, and is used in conjunction with other treatments to reduce risk of acute attack?

Back 35

indomethacin. (NSAID) anti-inflammatory. reduces protsaglandin formation, and phagocytosis of crystals by macrophages

Front 36

What are the uricosuric agents, and how do they work

Back 36

probenecid and sulfinpyrazone. these are weak acids that compete for reabsorption in in the proximal tubules. at low doses can compete for secretion (bad)

Front 37

When should these be used, and why should they be combined initially with indomethacin?

Back 37

they can precipitate an acute attack during early use, should not be used for treatment of initial attack. Indomethacin reduces chance of precipitating an attack

Front 38

What are the Xanthine Oxidase inhibitors? what are they used for?

Back 38

Allipurinol and febuxostat. these are used to reduce formation of uric acid in the body, by inhibit xanthane oxidase, which breaks down hypoxanthine and xanthine into uric acid. Allopurinol is a suicide inhibitor, and febuxostat is a non purine inhibitor, and is more selective

Front 39

When should these be used, and why are they combined with indomethacin?

Back 39

not for 1-2 weeks after acute attack. combined with indomethacin because they can induce an acute attack

Front 40

What other clinical use is there for Allopurinol?

Back 40

used as adjunct to cancer therapy to slow the formation of uric acid from purines released by the death of large numbers of neoplastic cells

Front 41

Toxicities of allopurinol

Back 41

GI upset, rash, peripheral neuritis, vasculitis, aplastic anemia. Also inhibits metabolism of mercaptopurine and azathioprine, drugs which need xanthine oxidase for metabolization

Front 42

Toxicities of Febuxostat

Back 42

liver function abnormalities, headaches, and GI upset