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Rheumatoid Arthritis PowerPoint Presentation

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RHEUMATOID ARTHRITIS
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DEFINITION Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammatory polyarthritis, which affects peripheral joints, especially the small joints of the hands and feet. Chronic untreated inflammation may lead to joint erosions and joint destruction.
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Epidemiology Prevalence of 1% More common in women than men (female:male ratio of 3:1) Peak onset is in the fourth or fifth decade for women and the sixth to eighth decades for men 40% of RA patients are registered as disabled within 3 years of onset, and around 80% are moderately to severely disabled within 20 years
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Pathophysiology Genetic, epigenetic and environmental factors The MHC class II gene, HLA-DR4, is the major susceptibility haplotype in 50–75% of Caucasian patients with RA DR1 is more important in Indians and Israelis, and DW15 in Japanese Porphyromonas gingivalis, present in the mouths of people with periodontal disease, appears to stimulate the production of ACPA linked to rheumatoid arthritis7
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Pathophysiology The clinical onset – infiltration of the synovial membrane with Lymphocytes Plasma cells Dendritic cells Macrophages. CD4+ T lymphocytes, including Th1 cells and Th17 cells play a central role by interacting with other cells in the synovium.
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Pathophysiology Lymphoid follicles form within the synovial membrane in which T cell–B cell interactions lead B cells to produce cytokines and autoantibodies, including RF and ACPA. Synovial macrophages - activated by immune complexes - produce proinflammatory cytokines, including TNF, IL-1, IL-6 and IL-15.
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Pathophysiology Proinflammatory cytokines act on synovial fibroblasts, to promote swelling of the synovial membrane and damage to soft tissues and cartilage. Activation of osteoclasts and chondrocytes drives destruction of bone and cartilage The RA joint is hypoxic and this promotes new blood vessel formation (neoangiogenesis).
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Pathophysiology The inflammatory granulation tissue (pannus) formed by the above sequence of events spreads over and under the articular cartilage, which is progressively eroded and destroyed. Later, fibrous or bony ankylosis may occur. Muscles adjacent to inflamed joints atrophy and may be infiltrated with lymphocytes
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Clinical Findings Symptoms and Signs Highly variable Symmetric swelling of multiple joints with tenderness and pain is characteristic >6 wk of pain, swelling, warmth in one or more peripheral joints, frequently with symmetric joint involvement involving wrists, hands, and/or feet, and often associated with >1 hr of morning stiffness.
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Most common joints involved include MCP, PIP, wrists, MTP, ankles, elbows, shoulders, hips, and knees. DIP joints, Sacroiliac and vertebral joints are spared except for C1 to C2. Atlantoaxial (C1–C2) subluxation can lead to myelopathy.
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Subluxation of cervical spine. Flexion, showing widening of the space (arrow) between the odontoid peg of the axis (behind) and the anterior arch of the atlas (in front).
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Characteristic deformities in hands with long- standing uncontrolled disease, including ‘swan neck’ deformity the boutonnière or ‘button hole’ deformity Z deformity of the thumb Dorsal subluxation of the ulna at the distal radio- ulnar joint is common and may contribute to rupture of the fourth and fifth extensor tendons. Triggering of fingers may occur because of nodules in the flexor tendon sheaths.
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‘Swan neck’ deformity of the fingers.
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Ulnar deviation of the fingers with wasting of the small muscles of the hands and synovial swelling at the wrists, the extensor tendon sheaths, the metacarpophalangeal and proximal interphalangeal joints.
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Dorsal subluxation of the MTP joints - ‘cock- up’ toe deformities leading to secondary adventitious bursae and callosities. In the hindfoot, calcaneovalgus (eversion) - damage to the ankle and subtalar joint. Associated with loss of the longitudinal arch (flat foot) due to rupture of the tibialis posterior tendon.
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Cock Up Toe Deformity
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EXTRA-ARTICULAR MANIFESTATIONS Systemic Fever Weight loss Fatigue Susceptibility to infection Musculoskeletal Muscle-wasting Tenosynovitis Bursitis Osteoporosis Haematological Anaemia Thrombocytosis Eosinophilia Lymphatic Felty’s syndrome Splenomegaly Nodules Sinuses Fistulae Ocular Episcleritis Scleritis Scleromalacia Keratoconjunctivitis sicca
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EXTRA-ARTICULAR MANIFESTATIONS Vasculitis Digital arteritis Ulcers Pyoderma gangrenosum Visceral arteritis Cardiac Pericarditis Myocarditis Endocarditis Conduction defects Coronary vasculitis Granulomatous aortitis Pulmonary Nodules Pleural effusions Fibrosing alveolitis Bronchiolitis Neurological Cervical cord compression Compression neuropathies Peripheral neuropathy Mononeuritis multiplex
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Rheumatoid nodules and olecranon bursitis. Nodules were palpable within as well as outside the bursa.
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INVESTIGATIONS Establish Diagnosis Clinical criteria E S R and C R P Ultrasound or MRI anti-citrullinated peptide antibodies Rheumatoid factor and Monitor Drug Safety Monitor Disease Damage X-rays Functional assessment Urinalysis Full blood count Urea, creatinine and liver function tests
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*Criteria for Diagnosis of Rheumatoid Arthritis Criterion Score Serology Negative RF and ACPA Low positive RF or ACPA (<3 times ULN) High positive RF or ACPA (>3 times ULN) 0 2 3
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Duration of symptoms < 6 wks 0 1 > 6 wks Acute phase reactants Normal CRP and ESR Abnormal CRP or ESR 0 1 Patients with a score ≥ 6 are considered to have definite RA. *European League Against Rheumatism/American College of Rheumatology 2010 Criteria.
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IMAGING STUDIES Plain radiography: Radiographic changes are the most specific for rheumatoid arthritis. Earlier changes include soft tissue swelling, joint space narrowing, and periarticular osteopenia. Later changes include periarticular erosions, especially in MCPs, PIPs, MTPs, and wrist. This reflects cartilage and bone destruction secondary to pannus. MRI and musculoskeletal ultrasound are more sensitive for detecting erosive disease and joint effusion / synovitis.
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Periarticular osteopenia and marginal erosions in MCP and a PIP joint (arrows).
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Marginal erosions at metatarsal heads
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MANAGEMENT Primary Objectives Target is low disease activity or remission Reduction of inflammation and pain Preservation of function Prevention of deformity DRUGS USED NSAIDs CORTICOSTEROIDS DMARDs SYNTETIC BIOLOGICAL
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NSAIDs Some symptomatic relief in RA - do not prevent erosions or alter disease progression. They are not appropriate for monotherapy Used in conjunction with DMARDs. A large number of NSAIDs are available; all appear equivalent in terms of efficacy
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Corticosteroids Prompt anti-inflammatory effect in RA and slow the rate of articular erosion. Multiple side effects limit their long term use. Low-dose corticosteroids - a “bridge” to reduce disease activity until the slower acting DMARDs take effect Adjunctive therapy for active disease that persists despite treatment with DMARDs. 10 mg of prednisone or equivalent per day is appropriate for articular disease.
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Corticosteroids Higher doses are used to manage serious extra-articular manifestations (eg, pericarditis, necrotizing scleritis). Intra-articular corticosteroids may be helpful if one or two joints are the chief source of difficulty. Intra-articular triamcinolone, 10–40 mg depending on the size of the joint Not more than four times a year.
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Synthetic DMARDs Methotrexate is usually the initial synthetic DMARD of choice. Beneficial effect in 2–6 weeks. The usual initial dose is 7.5 mg of methotrexate orally once weekly. Gastric irritation, stomatitis, cytopenias, and hepatotoxicity Either daily folate (1 mg orally) or weekly leucovorin calcium (2.5–5 mg taken orally 24 hours after the dose of methotrexate)
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Biological DMARDs
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*Which Drugs and When???4 Early RA - RA disease duration <6 months Established RA - RA disease duration >6 months or meeting the classification criteria Disease activity - Categorized as low, moderate, and high as per validated common scales Poor prognosis - Presence of 1 or more of the following features: functional limitation extraarticular disease (e.g., presence of rheumatoid nodules, RA vasculitis, Felty’s syndrome) positive rheumatoid factor or anti–cyclic citrullinated peptide antibodies bony erosions by radiograph *2012 Update of the 2008 American College of Rheumatology Recommendations for the Use of Disease-Modifying Antirheumatic Drugs and Biologic Agents in the Treatment of Rheumatoid Arthritis
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Other Treatments2 Surgery Synovectomy of the wrist or finger tendon sheaths of the hands may be required for pain relief or to prevent tendon rupture when medical interventions have failed. In later stages when joint damage has occurred, osteotomy, arthrodesis or arthroplasty may be required
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Bibliography Ferri's Clinical Advisor 2014 Davidsons Principles and Practice of Medicine 22ed Current Medical Diagnosis and Treatment 2014 2012 Update of the 2008 American College of Rheumatology Recommendations for the Use of Disease-Modifying Antirheumatic Drugs and Biologic Agents in the Treatment of Rheumatoid Arthritis Arthritis Care & Research Vol. 64, No. 5, May 2012, pp 625–639 DOI 10.1002/acr.21641 © 2012, American College of Rheumatology www.4s-dawn.com/DAS28 http://www.medscape.com/viewarticle/834584 2010 Rheumatoid Arthritis Classification Criteria ARTHRITIS & RHEUMATISM Vol. 62, No. 9, September 2010, pp 2569– 2581 DOI 10.1002/art.27584 © 2010, American College of Rheumatology