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Pharmacology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

diagnosis of rheumatoid arthritis

A

at least 4 of these: morning stiffness for >1hr, arthritis of >=3 joints for >6wks, arthritis of hand joints, symmetric arthritis for >6wks, rheumatoid nodules, serum rh factor positive, radiographic changes typical of RA; FOGGY to diagnose

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2
Q

treatment modalities for rheumatoid arthritis

A

rest, motion exercise, physiotherapy, diet, heat, cold; symptomatic tx w/nsaid; dz modifying drugs (dmard); immunosuppressant drugs (w/fair up); corticosteroids, surgery, novel/experimental

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3
Q

arichidonic acid pathway

A

http://o.quizlet.com/5bUb3BmmAwqT3O4S76h2Vg.png

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4
Q

NSAIDs clinical effects in rheumatoid arthritis

A

anti-inflammatory; analgesic

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5
Q

risk for NSAID-induced GI bleeding

A

low: acetaminophen (not used in RA), ibuprofen; intermediate: aspirin, diclofenac, diflunisal; high: piroxicam, indomethacin, ketoprofen

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6
Q

clinical effects of the arichidonic acid pathway

A

http://o.quizlet.com/91-u88uHatI7uxBV7RGEkQ.png

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7
Q

disease modifying anti-rheumatic drugs (DMARDs) uses

A

to reduce/prevent joint damage (nsaids relieve symptoms, no real effect on destruction)

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8
Q

DMARDs features

A

poorly understood mech’s; none effective in >60% pt’s -> unpredictable efficacy; therapeutic effects take 2-4 mths; if ineffective in pt once, not considered in future for same pt

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9
Q

important DMARDs

A

methotrexate (MTX), gold compounds, cytotoxic agents

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10
Q

methotrexate characteristics

A

aminopterin analogue; cytostatic drug

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11
Q

methotrexate pk

A

oral, subQ, im, iv

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12
Q

methotrexate pd in rheumatoid arthritis

A

low doses DMARD -> module immune system; inhibit AICAR transformylase, thymidilate synthetase pathway (higher conc) -> dec PMN chemotaxis; inhibit DHFR -> dec lymphocyte, macrophage gxn

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13
Q

methotrexate moa1

A

-> inc AICAR -> AICAR inhibits ADA, AMP deaminase -> AMP, adenosine inc, AMP -> adenosine -> inc inc adenosine -> act on A2b receptors -> suppress NF-kappaB activation induced by TNF, other inflammatory mediators

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14
Q

methotrexate moa2

A

http://o.quizlet.com/6qxx-VwnznZgu.kP5hMW6g.png

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15
Q

methotrexate interactions

A

nsaid reduce Cl; combo w/sulfonamides potentiates bone marrow toxicity

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16
Q

methotrexate adverse effects

A

GI, stomatitis, hair loss, mild inc liver enzymes; RARE: leukopenia, thrombopenia, severe inc liver enzymes, cns disturbances

17
Q

methotrexate contraindications

A

teratogen in pregnancy

18
Q

combine methotrexate with:

A

folic acid daily (stomatitis)

19
Q

methotrexate effects at (time)

A

6-8 weeks

20
Q

methotrexate advantages vs DMARDs

A

best response rate; less ae’s; well-tolerated longterm; well tolerated in dmard combo tx

21
Q

gold compounds moa

A

taken up by macrophages -> suppress phagocytosis, enzyme activity -> slows bone/articular destruction in ra

22
Q

gold compounds effects at (time)

A

after 4-6mths of tx, with ae’s acting immediately

23
Q

gold compounds toxicity

A

dermatology, hematology, kidneys -> infrequently used

24
Q

cytotoxic agents

A

alkylating agents; antimetabolites; others

25
Q

alkylating agents

A

chlorambucil, cyclophosphamide

26
Q

chlorambucil, cyclosphosphamide moa

A

cross-link dna -> prevent replication

27
Q

chlorambucil, cyclophosphamide toxicities

A

bone marrow suppression; infertility; carcinogenic risk (most cytostatics); hemorrhagic cystitis (characteristic)

28
Q

chlorambucil, cyclophosphamide contraindications

A

teratogen - pregnancy

29
Q

antimetabolites

A

azathioprine (azt)

30
Q

azathioprine characteristics

A

purine metabolite; prodrug of 6-mercaptourine

31
Q

azathioprine pd

A

converted to 6-mercaptourine -> convert to additional metabolites -> inhibit de novo purine synth -> suppress B, T cell fxn, Ig synth, IL-2 secretion

32
Q

azathioprine interactions with allopurinol

A

xanthine oxidase metabolizes active material of azt b4 excretion in urine -> pt’s on allopurinol need to reduce azt dose

33
Q

azathioprine toxicities

A

bone marrow suppression; GI disturbances; inc infections/malignancies

34
Q

leflunomide pd

A

arrest cells in G1 phase -> inhibit autoimmune T cell prolif, autoantibody synth by B cells; other cells not affected -> use salvage pathway whereas activated lymphocytes need de novo since need is 8x

35
Q

biological response modifiers

A

anti-cytokine (anti-TNF); anti-IL1; others (abatacept, rituximab)

36
Q

anti-cytokines (anti-TNF)

A

adalimumab; etanercept; infliximab

37
Q

anti-IL1

A

anakinra

38
Q

biological response modifiers uses

A

in combo with low dose mtx; in earlier tx

39
Q

biological response modifiers contraindications

A

when pt has history of immunosuppression i.e. TB

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