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17 Cards in this Set
- Front
- Back
Name the 6 DMARDS:
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Hydroxychloroquine
Methotrexate Gold Salts Sulfasalazine Leflunomide Cyclosporine |
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Name the 6 biologic DMARDS:
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Etanercept
Infliximab Adalimumab Anakinra Abatacepty Rituximab |
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Define the criteria for mild disease with respect to RA:
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• Elevations in ESR or serum C-reactive protein concentration
• at least 3 simultaneously inflamed joints • Arthralgias • No extra-articular disease • Negative RF test • No evidence of erosions or cartilage loss on plain radiographs |
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Define the criteria moderate disease with respect to RA:
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Between 6 and 20 inflamed joints
Absence of extraarticular disease Elevated ESR/CRP concentration Positive RF Evidence of inflammation via plain radiography such as osteopenia and periarticular swelling usually no erosions observed |
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Define the criteria severe disease with respect to RA:
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• More than 20 persistently inflamed joints
• A rapidly declining functional capacity • Elevated levels of ESR or CRP • Anemia of chronic disease • Hypoalbuminemia • High titer of RF Extra-articular diseases: rheumatoid nodules, eye or lung inflammation |
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Outline the treatment protocol for mild RA:
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• Recent onset: (<6wks)
o NSAIDS at full dose - naproxen - ibuprofen - diclofenac Patients with history of peptic ulcer • Selective Cox-2 Inhibitor - celecoxib Pain relieve and counsel for nonpharmcological treatments |
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Outline the treatment protocol for moderate RA:
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• Start on NSAID and a DMARD (methotrexate the usual choice, except in women in child baring age)
• If remain active or NSAID toxicity: - another NSAID and or intra-articular steroids • Addition of Prednisone: - usually for short period to treatment regimen while awaiting response to DMARD If long term oral corticosteroids used ant-resorptive bone therapy needed (bisphosphonate) |
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Outline the treatment protocol for severe RA:
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Goal: suppress synovitis
• NSAID full dose • One of the more effective DMARDS such as methotrexate • if MTX ineffective after 6-8 wks dose should be increased (stepwise) • Addition of prednisone: or selectively inject several joints with DepoMedrol Addition of further DMARDS: combo - Methotrexate and hydroxycholoroquine - Methotrexate, intramuscular gold, sulfasalazine (good for short term) - Methotrexate is a drug that’s used long term |
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What is the target for Abatacept therapy, and what cellular process does it interfere with?
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A B7-binding molecule, which inhibits the co-stimulatory signal required for RA pathogenesis.
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What are the four main classes of pharmalogical therapy for RA?
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1. Analgesics: acetaminophen, opiods
2. NSAID’s 3. Glucocorticoids 4. DMARDS |
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What would you monitor in your patients that are on Methotrextae therapy for RA?
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Watch for:
-Myelosupression Sx: fever, infection, bruising, bleeding -shortness of breath -nausea/ vomiting -lymph node swelling Every 4-8 weeks: -CBC, diff -liver function test (AST, albumin) -creatinine |
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What is the benefit of prescribing Leflunomide over Methotrexate?
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Leflunomide does not cause pneumoitis.
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Define Methotrexate’s mechanism of action.
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Methotrexate is a chemotherapeutic agent that is a folic acid antagonist. It is structurally similar to folic acid and acts by reversibly inhibiting dihydrofolate reductase, the enzyme that reduces folic acid to tetrahydrofolic acid. This inhibition ultimately interferes with the synthesis of DNA and cell reproduction.
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List the types of non-pharmacologic therapy used in treating RA:
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-Nutrition
-Exercise -Smoking cessation -Rest: joints -Physiotherapy -Occupational Therapy: -Prevention of Osteoporosis |
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What is the benefit of DMARD therapy?
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Potentially can reduce or prevent joint damage, preserve joint integrity and function.
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What mechanisms of action does biologic DMRD therapy employ?
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-Anticytokine therapies
-Anti-tumor necrosis factor agents (anti-TNF) Etanercept, Adalimumab, Infliximab -Interleukin 1 receptor antagonist (IL-1Ra) Anakinra -Newest (2006) Abatacept:, Rituximab |
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What is the general strategy in the pharmacological management of RA?
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Patients with established disease should be treated aggressively at the earliest point possible, this is based on the fact that destruction of diseased joints due to active inflammation occurs early on in the disease.
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