Rheumatoid arthritis diagnosis


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Rheumatoid arthritis diagnosis

  1. 1. There is no singular test for diagnosing rheumatoid arthritis. Instead, rheumatoid arthritis is diagnosed based on :history & physical examination & investigations The Importance of Early Diagnosis RA is progressive, not benign. Structural damage/disability occurs within first 2 to 3 years of disease. Slower progression of disease linked to early treatment
  2. 2. 1. 2. 3. 4. 5. 6 weeks of morning stiffness > 1 hr . 6 weeks of swelling of three or more joints . 6 weeks of swelling of wrist, MCP, PIP. Symmetrical joint swelling. X-ray changes that must include erosions or unequivocal bony decalcification. 6. Rheumatoid nodules. 7. Positive serum rheumatoid factor.
  3. 3. Can do usual activity ,discomfort or limited mobility of 1-3 joints.
  4. 4. • Are made after a full medical and family history and physical and diagnostic testing. • Medical testing may include a wide variety of tests like:- • • • • • • ESR Inflammatory CRP markers RF ANA (Anti nuclear antibodies) Joint x-rays MRI (Magnetic resonance imaging) & US (ultra sound)
  5. 5. CONTD…. Anti cyclic citrullinated peptide (CCP): has been found to be more specific than rheumatoid factor in rheumatoid arthritis And high titer anti-CCP may predict aggressive erosive disease Antinuclear antibody: positive in systemic lupus erythematosus (SLE) and related conditions; also in up to 30% of rheumatoid arthritis patients and weakly positive in up to 10% of the normal population.
  6. 6. • C-Reactive protein – Correlates with disease activity and radiologic progression – One of the most responsive acute phase reactants – Can be elevated in many non-RA related diseases • Erythrocyte sedimentation rate – Influenced by non-acute phase response factors – Can be elevated in many non-RA related diseases
  7. 7. Is an autoantibody that is present in the blood of most people with RA (75-80%)  Directed against host immunoglobulin (is positive in no more than 5 percent of patients without rheumatoid arthritis). Repeat negative 6-12 months following disease onset if
  8. 8. Liver function tests… mild elevation of alkaline phosphatase and .Low serum albumin . CBC…normochromic normocytic or Microcytic anemia . Hemoglobin slightly decreased; hemoglobin averages around 10 g/dL .Platelets & WBCs Usually increased. Urinalysis … Microscopic hematuria or proteinuria may be present, indicat connective tissue diseases. Joint fluid … to rule out other diseases; 5,000 to 25,000 WBC with polymorphonuclear leukocytes . cultures are negative, there are no crystals, and fluid glucose level typically is low.
  9. 9. X-Ray of both hands and wrists and feet for suspected RA. MRI it is more sensitive to detect RA change.  X-ray change • • • • • Loss of joint space Soft tissue swelling Bony decalcification Erosions Peri-articular osteoporosis
  10. 10. • Social factors – Low socioeconomic status – Less education – Psychosocial stress – female sex • Physical factors – Extra-articular manifestations – Elevated CRP and ESR – High titers of RF – early Erosions on x-ray – Duration of disease
  11. 11. • • • • • Goals of Treatment Relieve pain Reduce inflammation Slow down or stop joint damage Maintaining the ability to function in daily activities, improving the quality of life. • Current Treatment • Non - pharmacological • pharmacological • Surgery • Routine monitoring and ongoing care.
  12. 12. • Physiotherapy is a vital part of treating RA may be useful in decreasing the symptoms of RA. • program of exercise strengthens joints & minimize deformity and increase the range of movement and functions. • Natural treatments include using massage with herbs, magneto therapy etc.. • Occupational therapy can give advice to do every day activities with less pain or advice on how to use splints, skills training. • Weight loss & Smoking cessation
  13. 13. • Analgesics used only for pain relief E.g.:- Oral Paracetamol Topical Capsaicin Diclofenac
  14. 14. •NSAID’s •used as an adjunct along with DMARD’s to reduce the inflammation and pain •Effective reduction in swelling. •Improves mobility, flexibility, range of motion Ineffective in Erosive disease NSAID’S act by inhibiting COX-1 &2 & thus reduces inflamation • - GI toxicity – ulcer - Hepatotoxicity -Aseptic meningitis -Nephrotoxicity -Bleeding
  15. 15. •DMARD,s (disease modifying anti-rheumatic drugs) • used to slow down the progression of disease. E.g. Methotrexate once weekly Oral or IM & Sulfasalazine Advantages of DMARDs •Slow disease progression •Improve functional disability •Decrease pain •Interfere with inflammatory processes •Retard development of joint erosions
  16. 16. Alkylating agent . -Alopecia -Nausea -Infertility -Infection -BM suppression (pancytopenia) -Renal: hemorrhagic cystitis, bladder malignancy
  17. 17. • Combination DMARD regimen -Does not increase toxicity levels -long-term outcome more favorable -Superior efficacy to single-DMARD regimen • Possible combinations – Methotrexate/sulfasalazine/hydroxychloroquine – Cyclosporine/methotrexate – Leflunomide/methotrexate
  18. 18. Biologic DMARD’s genetically engineered medications that reduce inflammation and structural damage to the joints. Include: TNFα antagonists: Adalimumab, Etanercept , Infliximab Interleukin-1 antagonist Anakinra Suppress T-Cell activation Abatacept Anti B-Cell monoclonal antibody Rituximab
  19. 19. Anti-inflammatory block TNF-α (proinflammatory cytokine) Improves Clinical Signs & Symptoms -Etanercept- 50mg SC weekly -Infliximab - 3mg/kg IV -Adalimumab - 40mg SC -Infection -Pancytopenia -Exacerbate CHF -Reactivated TB -Autoantibody/SLE-like -Malignancy- lymphoma
  20. 20.  Active Hepatitis B Infection  Multiple sclerosis, optic neuritis  Active serious infections  Chronic or recurrent infections  Current neoplasia  History of TB or positive PPD (untreated)  Congestive heart failure (Class III or IV)
  21. 21. Early appropriately aggressive intervention in patients with inflammatory arthritis: critical to best possible outcome. The combination of a biologic plus MTX is frequently more effective than either agent alone.
  22. 22. • Early and aggressive disease control – Rheumatologist Referral • Early/Undiagnosed: NSAIDs, short course Corticosteroids • Late/Uncontrolled: DMARD therapy – depends on the presence or absence of joint damage, functional limitation, presence of predictive factors for poorer prognosis
  23. 23. Diagnosis • Establish early diagnosis of RA • Document baseline disease activity and damage • Estimate prognosis of patient Initiate therapy • Patient education • Physical/occupational therapy • Consider NSAID and/or local or low-dose steroids • Start disease-modifying agent within 3 months Periodically assess disease activity Subjective criteria Physical exam Laboratory tests Radiography
  24. 24. Periodically assess disease activity Inadequate response (ongoing disease activity) Adequate response with disease activity Change or add disease-modifying drugs Methotrexate response Methotrexate Suboptimal methotrexate response Other Combination monotherapy therapy Biologics
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