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Rheumatoid arthritis dr.abdallah
 

Rheumatoid arthritis dr.abdallah

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  • PHYSICAL EXAMINATION IS VERY IMPORTANT <br />

Rheumatoid arthritis dr.abdallah Rheumatoid arthritis dr.abdallah Presentation Transcript

  • RHEUMATOID ARTHRITIS (RA) By: DR.ABDALLAH FAHEL 1
  • 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
  • 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
  • RA in European Art Dutch Priest 1631 4
  • Renoit in 1911 Wheelchair bound w/ classic RA in his hands 5
  • 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
  • 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
  • Cytokine Cytokinek interactions interakciói 8
  • Rheumatoid Synovium Normal Synovium Rheumatoid Synovium 9
  • 10
  • 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
  • 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
  • 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
  • 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
  • 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
  • Squeeze test 16
  • 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
  • RA early stage 18
  • Early assymmetric RA 19
  • PIP joint involvement in RA 20
  • RA: swan neck deformity 21
  • RA: ulnar deviation 22
  • Ulnar deviation in RA with severe atrophy of interosseal muscles 23
  • RA: Boutonnière deformity 24
  • RA: arthritis mutilans 25
  • Involvement of joints of feet in RA 26
  • Severe destruction of ankles in RA 27
  • Baker’s cyst 28
  • Bursitis in the shoulder 29
  • Bursitis and rheumatoid nodule 30
  • Rheumatoid nodules 31
  • RA – end stage 32
  • 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
  • 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
  • Periarticular osteoporosis (decalcification) 35
  • Erosions and sclerosis (in late stage) 36
  • Erosion in RA 37
  • Early erosions (MRI) 38
  • Scintigraphy of the hands 39
  • Atlantoaxial subluxation 40
  • Extraarticular manifestations of RA • rheumatoid nodules • • • • • – subcutaneous - in internal organs (lung, aortic valve) pleuritis/pericarditis fibrotizing alveolitis Felty’s syndrome vasculitis amyloidosis 41
  • Systemic manifestations of RA: pulmonary fibrosis 42
  • Interstitial pneumonitis in RA 43
  • Systemic manifestations of RA: Caplan’s syndrome 44
  • Rheumatoid nodules in the lungs 45
  • Episcleritis in RA 46
  • Scleritis in RA 47
  • Scleromalacia perforans 48
  • Vasculitis in RA 49
  • Vasculitis in RA 50
  • Leg ulcers in Felty’s syndrome 51
  • Large granular lymphocytes in Felty’s syndrome 52
  • What is “Quality of Life”? • Ability to – Work – Be a parent – Socialize with others – Exercise and be mobile 53
  • 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
  • • 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
  • 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
  • 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
  • THANK YOU DR.ABDALLAH FAHEL 58