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Rheumatoid arthritis dr.abdallah

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Rheumatoid arthritis dr.abdallah

  1. 1. RHEUMATOID ARTHRITIS (RA) By: DR.ABDALLAH FAHEL 1
  2. 2. RHEUMATOID ARTHRITIS (RA) Gergely Péter dr Definition: Chronic destructive of joint inflammation with pain and swelling,mainly characterized by inflammation of the lining( synovium) of the joints .In a considerable proportion of patients, the arthritis is progressive, resulting in joint destruction and ultimately incapacitation and increased mortality. Relatively common, prevalence: 0.3-1.5 % , the male:female ratio cca. 1:3. Typical case: woman aged 30-40 years with polyarthritis and early joint deformities. 2
  3. 3. History of Rheumatoid Arthritis 1858 – Dr Alfred Baring Garrod, named the condition Rheumatoid Arthritis. 1895 – X-Ray was discovered. 1912 – Dr. Frank Billings introduced the concept of focal infection. In the 1920’s, physicians suspected the cause of RA was bacterial infection, they used gold and malaria drugs. 3
  4. 4. RA in European Art Dutch Priest 1631 4
  5. 5. Renoit in 1911 Wheelchair bound w/ classic RA in his hands 5
  6. 6. Etiology : 1-gentic factor : may be involved because it is usually associated with HLA-DR4 In white people and DR1 in indo-pak. 2-autoimmunity: RA is considered to be an autoimmune disease for the following reasons: *autoantibodies are present . *immune comlex are common in synovial Fluid. There is defect in cell mediated immunity . 3-female gender: is a risk factor and this susceptibility is increased post-partum and by breast feeding 4-cigarette smoking : is also a risk factor 6
  7. 7. Pathogenesis :. Is a disease of the synovium. *inflammation :the synovium shows signs of chronic inflammation .there swilling and congestion of synovial membrane , and the underlying connective tissue which becomes infilterated with lymphocyte,plasma cells and macrophages . *proliferation : the synovial membrane then proliferates and grows out over the surface of the cartilage, which causes erosion and destruction of the cartilage . 7
  8. 8. Cytokine Cytokinek interactions interakciói 8
  9. 9. Rheumatoid Synovium Normal Synovium Rheumatoid Synovium 9
  10. 10. 10
  11. 11. Symptoms of Rheumatoid Arthritis: • Symptoms first begin in the small joints of the fingers, wrists and feet, with warm, swollen and tender joints that are painful and difficult to move. • Joints of both sides of the body (symmetrical) are typically affected. • People with RA often experience fatigue, loss of appetite and low-grade fever. • There is often stiffness in the morning that lasts for several hours or more. • Nodules may form under the skin, often over the bony areas exposed to pressure (such as the elbows). • Over time, damage to the cartilage and bone of the joints may lead to joint deformities. 11
  12. 12. Classification criteria of RA (ARA, 1987) 1. Morning stiffness – for at least 1 hr and present for at least 6 weeks 2. Swelling of 3 or more joints for at least 6 weeks 3. Swelling of wrist, metacarpophalangeal (MCP) or proximal interphalangeal (PIP) joints for at least 6 weeks 4. Symmetric joint swelling 5. Typical radiologic changes in hands (erosions or unequivocal bony decalcification) 6. Rheumatoid nodules 7. Serum rheumatoid factor (RF) positivity Diagnosis is made by the presence of 4 or more criteria 12
  13. 13. Differential diagnosis of polyarthritis RA should be differentiated from: - Other autoimmune diseases (SLE, primary Sjögren’s syndrome, MCTD, PM/DM, PSS, PAN, gian cell vasculitis, polymyalgia rheumatica, adult onset Still’s disease) - Viral diseases (parvovirus B19 infection, rubella, hepatitis B & C infection) - Bacterial infections (tbc, rheumatic fever, Jaccoud’s arthritis, septic endocarditis, mycoplasma arthritis) - Seronegative spondylarthritides (erosive psoriatic arthitis, reactive arthritis, enteropathic arthritis) - Paraneoplastic arthritis - Other diseases (e.g. hyperthrophic osteoarthropathy, erythema nodosum, agammaglobulinemia, acromegaly, diabetes mellitus) - Other rheumatic diseases (chronic gout, inflamed erosive osteoarthritis) 13
  14. 14. Signs of early RA (=undifferentiated arthritis) In the early stage (within the first 3-6 months) (ARA) classification criteria cannot be used. The patient should be referred to a rheumatologist, if • • the patient has 3 or more swollen joints the metacarpophalangeal (MCP) and/or metatarsophalangeal (MTP) joints are involved; the squeeze test is positive • morning stiffness is 30 min or more. 14
  15. 15. How to diagnose a case of RA? HISTORY: Insidious onset Slow development of sign & symptoms Stiffness Polyarticular Most common: PIP & MCP of hands Morning stiffness > 1hr Fatigue, malaise, depression 15
  16. 16. Squeeze test 16
  17. 17. Joint involvement in RA The most specific sign of RA is arthritis. It is progressive and deforming in the majority (2/3) of cases (= erosive polyarthritis) 17
  18. 18. RA early stage 18
  19. 19. Early assymmetric RA 19
  20. 20. PIP joint involvement in RA 20
  21. 21. RA: swan neck deformity 21
  22. 22. RA: ulnar deviation 22
  23. 23. Ulnar deviation in RA with severe atrophy of interosseal muscles 23
  24. 24. RA: Boutonnière deformity 24
  25. 25. RA: arthritis mutilans 25
  26. 26. Involvement of joints of feet in RA 26
  27. 27. Severe destruction of ankles in RA 27
  28. 28. Baker’s cyst 28
  29. 29. Bursitis in the shoulder 29
  30. 30. Bursitis and rheumatoid nodule 30
  31. 31. Rheumatoid nodules 31
  32. 32. RA – end stage 32
  33. 33. Laboratory Tests Initial work-up CBC, Metabolic panel, Urinalysis, Rheumatoid factor, Anti-nuclear antibody. Chem: nl, slight decr albumin, incr total protein. Hema:hemocrit- ACD, wbc- mildly up, platelet- rare thrombocytosis ESR: elevated 33
  34. 34. Radiology: X-Ray MRI Bone Scan Symmetrical 1-Early: no sig changes 2-Late: -Juxta-articular osteoporosis w/ decr bone density *Uniform jt narrowing. *Marginal erosions. *Marginal cortical erosions *Juxtaarticular osteoporosis of lesser mets Ill-defined ersosion of posteroanterior aspect of calcaneus Resiters, PA, AS, hyperparathyroidism 34
  35. 35. Periarticular osteoporosis (decalcification) 35
  36. 36. Erosions and sclerosis (in late stage) 36
  37. 37. Erosion in RA 37
  38. 38. Early erosions (MRI) 38
  39. 39. Scintigraphy of the hands 39
  40. 40. Atlantoaxial subluxation 40
  41. 41. Extraarticular manifestations of RA • rheumatoid nodules • • • • • – subcutaneous - in internal organs (lung, aortic valve) pleuritis/pericarditis fibrotizing alveolitis Felty’s syndrome vasculitis amyloidosis 41
  42. 42. Systemic manifestations of RA: pulmonary fibrosis 42
  43. 43. Interstitial pneumonitis in RA 43
  44. 44. Systemic manifestations of RA: Caplan’s syndrome 44
  45. 45. Rheumatoid nodules in the lungs 45
  46. 46. Episcleritis in RA 46
  47. 47. Scleritis in RA 47
  48. 48. Scleromalacia perforans 48
  49. 49. Vasculitis in RA 49
  50. 50. Vasculitis in RA 50
  51. 51. Leg ulcers in Felty’s syndrome 51
  52. 52. Large granular lymphocytes in Felty’s syndrome 52
  53. 53. What is “Quality of Life”? • Ability to – Work – Be a parent – Socialize with others – Exercise and be mobile 53
  54. 54. Management of Rheumatoid Arthritis: • The goals of treatment of RA are to reduce joint pain and swelling, relieve stiffness and prevent joint damage. • Evaluation by a rheumatologist for the development and monitoring of a treatment plan is required in most people with RA. • Treatment plans often include a combination of rest, physical activity, joint protection, use of heat or cold to reduce pain, and physical or occupational therapy. • Maintain a healthy body weight and maintain a physical activity plan (i.e. Arthritis . 54
  55. 55. • Drugs play a very important role in the treatment of RA. • Many people with RA take nonsteroidal anti-inflammatory drugs (NSAIDs) to help reduce joint pain, stiffness and swelling. • Low doses of corticosteroids such as prednisone may also be used to relieve joint pain, stiffness and swelling and to reduce the risk of joint swelling. • People with RA are often treated with disease-modifying antirheumatic drugs (DMARDs), such as methotrexate or leflunomide 55
  56. 56. Disease modifying antirheumatic drugs (DMARD): Drug gold (i.m.) Adverse effects Dose dermatitis, stomatitis, 25-50 mg /2-4 proteinuria, enterocolitis, weeks thrombocytopenia gold (p.o.) less frequently used, brecause of lower tolerability chloroquine (hydroxy- retinopathia, pigment250 mg/day chloroquine) anomalies Regular ophthalmology check is required d-penicillamine proteinuria, myasthenia, 125-750 mg/day stomatitis Owing to low tolerability it is not used any more azathioprine hepatitis, bone marrow depression 50-150 mg/day Scarcely given in RA methotrexate hepatotoxicity, pulmonary fibrosis, 7,5-25 (MTX) bone marrow depression mg/week most frequently used therapy 56
  57. 57. sulfasalazine cyclosporine A leflunomide TNF-α blockers: (etanercept, infliximab, and abatacept) nausea, vomiting 1,5-2 g/day diarrhea, bone marrow depression nephrotoxicity, tremor 1,5-4 mg/kg/day creatinine and blood pressure should be checked regularly hepatotoxicity, GI 10-20 mg/day complaints local reaction, autoimmune disease (SLE, SM) infection (tbc) etanercept: 25 mg 2x weekly s.c. infliximab: 3 mg/kg every 8 week i.v. Other: anakinra (IL-1 blocker) rituximab (anti-CD20 antibody) abatacept (T cell activation blocker antibody) 57
  58. 58. THANK YOU DR.ABDALLAH FAHEL 58

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