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Rheumatoid arthritis.pptx

  1. Rheumatoid Arthritis Ghadeer Ismail Eideh Supervised by Dr. Amjad Alnatsheh References: step up to medicine.
  2. Introduction Treatment Uworld questions 01. Clinical features Diagnosis 02. 03. 04. 05. Outlines
  3. Introduction 01.
  4. Definition RA is a chronic inflammatory autoimmune disease involving the synovium of joints. The inflamed synovium can cause damage to cartilage and bone.
  5. General charactristics Age The usual age of onset is 20 to 40 years; Gender It is more common in women than in men (3:1). Etilogy Etiology is uncertain. It may be caused by an infection or a series of infections (most likely viral), but genetic predisposition is necessary.
  6. Clinical features 02.
  7. 1. Inflammatory polyarthritis (joint swelling is the most common sign)— can involve every joint in the body except the DIP joints Morning stiffness lasting >1 hour improves as the day progresses. Joints commonly involved include joints of the hands (PIP, MCP) and wrists, knees, ankles, elbows, hips, and shoulders.
  8. Characteristic hand deformities.
  9. A. Ulnar deviation of the MCP joints
  10. B. Boutonnière deformities of the PIP joints (PIP flexed, DIP hyperextended)
  11. C. Swan-neck contractures of the fingers (MCP flexed, PIP hyperextended, DIP flexed)
  12. 3. Cervical spine involvement is common at C1-C2 (subluxation and instability), but it is less common in the lower cervical spine. a. Instability of the cervical spine is a potentially life-threatening complication of RA. Most patients do not have neurologic involvement, but if they do, it can be progressive and fatal if not treated surgically. b. This is seen in 30% to 40% of patients. All patients with RA should have cervical spine radiographs before undergoing any surgery (due to risk of neurologic injury during intubation).
  13. However, disease- modifying antirheumatic drugs (DMARDs) have dramatically reduced the need for cervical spine surgery in RA patients.
  14. 4. Cardiac involvement may include pericarditis, pericardial effusions, conduction abnormalities, and Valvular incompetence.
  15. 5. Pulmonary involvement—usually pleural effusions; interstitial fibrosis may occur.
  16. 6. Ocular involvement—episcleritis or scleritis.
  17. 7. Soft tissue swelling (rather than bony enlargement).
  18. 8. Drying of mucous membranes: Sjögren xerostomia.
  19. 9. Subcutaneous rheumatoid nodules over extensor surfaces may also occur in visceral structures—for example, lungs, pleura, pericardium. a. Pathognomonic for RA. b. Nearly always occurs in seropositive patients (i.e., those with RF).
  20. Diagnosis 03.
  21. 1. Laboratory findings
  22. a. High titers of RF are associated with more severe disease and are generally nonspecific. RF is eventually present in 80% of patients with RA (may be absent early in the disease), but is also present in up to 3% of the healthy population. RF titers rarely change with disease activity and are not useful for following patients. Helpful in determining prognosis. High titers → more severe disease.
  23. b. Anticitrullinated peptide/protein antibodies (ACPA)—sensitivity is 50% to 75%, specificity is over 90%. c. Elevated ESR, C- reactive protein. d. Anemia of chronic disease.
  24. 2. Radiographs . Not required for a diagnosis of RA but may have the following characteristic findings. a. Loss of juxta- articular bone mass (periarticular osteoporosis) near the finger joints. b. Narrowing of the joint space (due to thinning of the articular cartilage) is usually seen late in the disease. c. Bony erosions at the margins of the joint.
  25. Radiographs .
  26. 3. Synovial fluid analysis (see Table 6-5) is nonspecific.
  27. Diagnosis of RA
  28. Treatment 04.
  29. Treatment Goal is to minimize pain and swelling, prevent disease progression, and help patient remain as functional as possible.
  30. 2. Symptomatic treatment. a. NSAIDs are the drugs of choice for pain control b. Corticosteroids (low dose)— use these if NSAIDs do not provide adequate relief. Short-term treatment may be appropriate but avoid long- term use.
  31. 3. DMARDs
  32. a. General principles Can reduce morbidity and mortality (by nearly 30%)—by limiting complications, slowing progression of disease, and preserving joint function Should be initiated early (at the time of diagnosis) They have a slow onset of action (6 weeks or longer for effect to be seen), so begin treating RA while waiting for the disease-modifying therapy to take effect. Gradually taper and discontinue NSAIDs and corticosteroids once effects are evident
  33. b. Methotrexate—best initial DMARD _ Initial improvement is seen in 4 to 6 weeks. _ Supplement with folate. Closely monitor liver and renal function Side effects include GI upset, oral ulcers (stomatitis), mild alopecia, bone marrow suppression (coadminister with folinic acid), hepatocellular injury, and idiosyncratic interstitial pneumonitis, which may lead to pulmonary fibrosis. It increases liver enzymes in some patients.
  34. c. Alternatives: leflunomide, sulfasalazine, hydroxychloroquine d. Antitumor necrosis factor (anti-TNF) inhibiting agents (etanercept, infliximab, etc.)—used if methotrexate does not fully control the disease. Requires PPD screening because of risk of reactivation of TB. e. Non-TNF biologics (abatacept, rituximab, tofacitinib) are also options if disease activity remains high despite methotrexate
  35. 5. Surgery (in severe cases) a. Synovectomy (arthroscopic) decreases joint pain and swelling but does not prevent x-ray progression and does not improve joint range of motion b. Joint replacement surgery for severe pain unresponsive to conservative measures
  36. Uworld question 05.
  37. Thank you