RA tx Flashcards
1
Q
What are the current treatment options for RA?
A
- NSAIDS
- Corticosteroids
- Syntheitc DMARDs
- Biologic DMARDS
- Combination therapy
2
Q
NSAIDS
A
- still in use, high ulcer risk, higher cardiovascular risk
- Pros: control pain/inflamm, dec swelling, improve function, improve QOL, cheap
Cons: doesn’t affect progression, GI toxicity, hepatic dysfunction, renal complications, CNS toxicity
3
Q
Corticosteriods
A
-IV or oral
-may have disease modifying effect
bridge while awaiting DMARD effect
-used for major flares
-low does alternative to NSAIDS
-use lowest does possible
4
Q
Methotresate- Rhematrex
A
- 1st line agent, start 7.5mg/wk inc to 15-25mg over 6-8 wks
- Purine antagonist, document to decrease erosion of bone
- reduction of T-cell proliferation –> inc adenosine release –> alter expression of cytokines
- slows course of diseas, anchor in combos
- liver/lung/GI toxicity
- Can be used aggressively: greater improvement in tender joint count and swollen joint count. 20 mg vs 10 mg
- Before using: ask about alcohol, pregnancy, chrck renal/liver function
5
Q
Leflunomide- Arava
A
- Pyrimidine antagonist; long half life
- liver toxicity, diarrhea, HTN,
- dec jount damage, slows progression
- blocks T cell clonal expansion
- avoid getting pregnant–> teratogenic
6
Q
Sulfasalazine- Azulfidine
A
- disease modification
- can induce leukopenia–> greater risk for infrection
- used in combo regimens
7
Q
Hydroxychloroquine- Plaquenil
A
- used for milder cases; part of combo
- diarrhea/skin rash are side effects
8
Q
Biologic Response Modifiers
A
- very effective/expensive
- can be toxic
9
Q
Monoclonal Antibodies
A
- Large molecules, synthesized by animals or cells
- directed at cytokine or cell receptor
- neutralize the action of cytokine or cell or kill cell
- very expensive
- end in “MAB”
10
Q
What does TNF do?
A
- stimulates cytokine production including IL-6 and TNF
- inhibits bone formation and stimulates resportion
11
Q
What is Etanercept- Enbrel
A
- Soluble TNF-receptor from fusion of TNF-aplha to human Fc portion of IgG
- BINDS AND INACTIVATES FREE TNF-aplha
- biologic response modifier
12
Q
What is Infliximab- Remicade (I.V.)
A
- Chimeric mouse/human Monoclonal Antibody
- anti- TNF–> binds soluble and cell surface TNF
- 3mg/kg, administered by IV
- used with MTX or Arava
-bio-modify
13
Q
Adalimumab- Humira
A
- Human monoclonal anti-TNF antibody
- bio-modify
14
Q
Golimumab- Simponi
A
- recombinant fully human monoclonal anti-TNF antibody
- bio-modify
15
Q
Certolizumab pegol - Cimza
A
- PEGylated Fab fragment of humanized anti TNF antibody
- lacks FC fragment so it does not activate complement or antibody dependent cytotoxicity
- benefit may be seen as early as 1 wk
