Rheumatoid Arthritis (RA) PDF

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lec...

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams &Wilkins  Rheumatoid Arthritis (RA) Clinical Pathophysiology Diagnosis Treatment manifestations  Arthritis Arthritis Inflammatory disorders that damage articular cartilages of synovial joints Acute forms: caused by bacteria via traumatic wound, surgery, contamination & treated with antibiotics Chronic forms: rheumatoid arthritis, gouty arthritis Marieb EN, Hoehn KN. Human Anatomy & Physiology. 9th ed. Boston, Pearson Education; 2013  RA Pathophysiology RA is systemic autoimmune disease Chronic inflammation and hyperplasia of synovial membranes Increased synovial exudate Swelling and thickening of synovial membrane Joint erosion Pain Onset between 36-50 years RA affects 0.8% of adults worldwide! Females affected 3x more  RA Pathophysiology Etiology combines Genetic susceptibility Immune triggering event Subsequent autoimmunity against synovial cells Lack of identifiable trigger Kumar, Robbins & Cotran: Pathophysiological basis of disease. 8th ed. Philadelphia: Saunders;2010  RA Pathophysiology Kumar, Robbins & Cotran: Pathophysiological basis of disease. 8th ed. Philadelphia: Saunders;2010 Lymphocytes and plasma cells form antibodies in the synovial membrane and cartilage Antibodies against other antibodies Antibodies and antigens form immune complexes in the synovium These immune complexes trigger the complement system and exaggerate the inflammatory response  RA Pathophysiology Initial synovial changes cause minimal damage to joints Exacerbations of the disease progressively damage joints through pannus formation, cartilage erosion, fibrosis, and joint fixation (ankylosis) and deformity (muscle atrophy and spasm) Kumar, Robbins & Cotran: Pathophysiological basis of disease. 8th ed. Philadelphia: Saunders;2010  RA Clinical Manifestations Most RA onset is insidious Severity: mild to debilitating Joint swelling is symmetric and widespread involve any number of joints Pain, stiffness most notable upon rising Redness, heat, swelling Decreased mobility Malalignment/deviation is common for long-standing RA Combination of cartilage, bone erosion, fibrosis Systemic manifestations during exacerbations Low-grade fever, fatigue, anorexia, weight loss, weakness Granulomas (nodules) can form on blood vessels  RA Diagnostic Criteria No definitive test History and physical examination Several diagnostic tests Morning joint stiffness lasting at least 1 hour Increased likelihood with positive findings: Arthritis of 3 or more joint areas Erythrocyte sedimentation rate (ESR): elevated Arthritis of the hand joints C-reactive protein (CRP): elevated Symmetric arthritis Presence of Rheumatoid factor (IgG) Rheumatoid nodules Presence of Antinuclear antibodies (ANA) Presence of inflammatory products in synovial fluid Radiographic visualization of joint damage Many of these tests are not specific False positive (indicate disease without the disease) False negative (does not indicate disease with disease present)  RA Treatment Balance between pharmacologic and non-pharmacologic approach Pharmacologic: Drugs that induce remission Anti-inflammatory drugs Immunosuppressant drugs Non-pharmacologic: Rest/activity balance Physical therapy exercises to promote joint mobility, physiotherapy Splints to allow joint to rest and prevent deformities Heat/cold therapy Surgery: synovial membrane removal, joint replacement