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Drug categories for RA
- NSAIDs
- ----Used initially
- Disease-modifying antirheumatic drugs (DMARDs)
- ----Antimalarial drugs : 3 names
- Gold compounds
- ----Not used frequently bc other biologic medications on market
- ----still used frequently in RA
- Biological DMARDs
- ----Tumor necrosis factor
- --------Humaria, embral
- --------abetacet
- Osteoarthritis
- ----Complementary and alternative medications
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Rheumatoid arthritis
- Chronic, progressive, Systemic disorder
- ----Synovitis
- ----Destruction of articular tissue
- ----Criteria for classification of RA
- Autoimmune response
- Marked by periods of exacerbation and remission
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Drug Therapy in RA Goals
- Decrease joint inflammation
- Arrest progression of the disease
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Three drug categories used in RA
- NSAIDs
- ----Decrease inflammation
- Glucocorticoids
- ----Decrease inflammation
- DMARDs (disease modifying anti-rheumatic drugs)
- ----Prevent progression of disease
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NSAIDs
- First line of defense
- Not as powerful as glucocorticoids but less side effects and added analgesic effect
- Decrease inflammation
- Relieve mild-to-moderate pain
- Decrease elevated body temperature
- Decrease blood clotting
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NSAIDs mechanism of action
- Potent inhibitor of cyclooxygenase (COX enzyme)
- ----Prevent produce of prostaglandins by inhibiting COX enzymes that initiates synthesis
- Blocks production of prostaglandins and thromboxanes
- ----Anti inflammatory/ Anti analgesic
- COX-1 and COX-2 enzymes
- ----Inhibit both COX1 and 2 preventing production of protective prostaglandins and prostaglandins produced in painful inflamed tissue
- COX-2 inhibitors
- ----Stop production of inflammatory prostaglandins, keeping protective prostaglandins from COX 1
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Glucocorticoids (corticosteroids)
- Prednisone
- Decrease inflammatory response
- Treat acute exacerbations of RA but do not arrest disease (short term effects lost with prolonged use)
- Oral and intra-articular
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Mechanism of Action
- binds to receptor in cytoplasm of macrophages and leukocytes forming glucocorticoid receptor complex
- Complex moves to cell nucleus and binds to genes that regulate inflammatory process increasing the production of anti-inflammatory proteins (annexins) and inhibiting production of inflammatory substances (IL-10, IL-1 receptor agonist, and neutral endopeptidase)
- Regulate activity
- ----Macrophages
- ----Eosinophils
- ----T lymphocytes
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Glucacorticoids adverse effects
- Catabolic effects
- ----On muscle, tendon, bone: osteoporosis
- Muscle wasting
- HTN
- Aggravation of DM
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DMARDs
- Retard the progression or rheumatic disease
- Essential in early treatment of RA
- Attempt to induce remission
- ----Control Synovitis and erosive changes of RA
- Inhibit function of monocytes and T and B lymphocytes
- ----Normally cause joint inflammation and destruction
- DMARDs Adverse effects
- Hepatic and renal toxicity
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Antimalarial drugs
Chloroquine (Aralen) and hydroxychoroquine (Plaquenil)
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Antimalarial drugs Adverse effects
Retinal damage
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Anti malarial drugs Mechanism of Action
- Increase pH in intracellular macrophage vacuoles
- Progress antigenic proteins and present antigens to T cells
- ----Decreased T-cell stimulation results in immunosuppression of arthritic response
- Stabilize lysosomal membranes and impair DNA/RNA synthesis
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Azathioprine (Imuran)
- DMARD
- Immunosuppressant drug normally used to prevent organ transplant rejection
- Relatively toxic
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