Ch 16 1 Pharm

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  1. 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
  2. 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
  3. Drug Therapy in RA Goals
    • Decrease joint inflammation
    • Arrest progression of the disease
  4. Three drug categories used in RA
    • NSAIDs
    • ----Decrease inflammation
    • Glucocorticoids
    • ----Decrease inflammation
    • DMARDs (disease modifying anti-rheumatic drugs)
    • ----Prevent progression of disease
  5. 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
  6. 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
  7. 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
  8. 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
  9. Glucacorticoids adverse effects
    • Catabolic effects
    • ----On muscle, tendon, bone: osteoporosis
    • Muscle wasting
    • HTN
    • Aggravation of DM
  10. 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
  11. Antimalarial drugs
    Chloroquine (Aralen) and hydroxychoroquine (Plaquenil)
  12. Antimalarial drugs Adverse effects
    Retinal damage
  13. 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
  14. Azathioprine (Imuran)
    • DMARD
    • Immunosuppressant drug normally used to prevent organ transplant rejection
    • Relatively toxic
Card Set:
Ch 16 1 Pharm
2015-06-10 16:31:59
16 Pharm

Ch 16 1 Pharm
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