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RHEUMATOID ARTHRITIS

RHEUMATOID ARTHRITIS. Rheumatoid Arthritis. “A chronic autoimmune disease characterized by the inflammation of the synovial joints”. (The Arthritis Society, 2012; Gulanick & Myers, 2011; Firth, 2011). Def.

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RHEUMATOID ARTHRITIS

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  1. RHEUMATOID ARTHRITIS

  2. Rheumatoid Arthritis “A chronic autoimmune disease characterized by the inflammation of the synovial joints” (The Arthritis Society, 2012; Gulanick & Myers, 2011; Firth, 2011)

  3. Def • Rheumatoid arthritis is an autoimmune disease in which the normal immune response is directed against an individual's own tissue, including the synovial joints, tendons, and bones, resulting in inflammation and destruction of these tissues.

  4. Causes • Exact cause Is unknown • AUTOIMMUNITY – abnormal IgG is being developed due to some reasons. Antibodies will produce against this abnormal IgG. This antibody is termed as rhemuatoid factors (RF). RF combine with IgG and deposits in the joints, blood vessels • Smoking • Infection -helicobacter pylori, epstein-bar virus, parvovirus and mycobacteria can trigger the process • Vitamin D deficiency, Genetic predisposition

  5. Pathophysiology • Etiological factors (infectious microorganism) • Antigen –antibody response (production of normal immunoglobulins against the antigen) • Transformation of IgG and IgM into rheumatoid factors (RF) -{prolonged exposure to the antigen causes normal antibodies to become autoantibodies and attack host tissues }

  6. Formation of immune complexes in blood and synovial membrane (Normally synovial tissue secretes synovial fluid that both lubricate the joint and is the medium through which nutrients are supplied to articular cartilage) • Due to inflammation -Edema, vascular congestion, fibrin exudate and cellular infiltration occurs • Activated macrophages release cytokines and interleukins and tumor necrosis factor

  7. PANNUS (inflammatory granular tissues) forms at junctions of synovial tissues and articular cartilage, it interfere with nutrition transport • Articular cartilage becomes necrotic • Pannus invades subchondral bone and supporting soft tissues (ligaments, tendons) and destroys it

  8. Fibrous tissues replace pannus leads to occluding the joint movements • As fibrous tissues calcifies, total bone joint immobilization occurs

  9. Signs and Symptoms Joint involvements • Begin with small joints in hands, wrists and feet • Palpation of joints reveals spongy tissue • Progressively involves knees, shoulders, hips, elbows, ankles etc • Symptoms usually acute in onset, bilateral and symmetric • Joints may be hot, swollen and painful (not relieved by rest), morning stiffness lasts more than 30 min • Deformities of hands and feet.

  10. Deformities due to RA – boutonniere deformity, swan neck deformity, ulnar deviation and hallux valgus

  11. Extra articular features • pallor • Paresthesias • Contractures • Atrophy • Color changes of digits (bluish, rubor) • Rheumatoid nodules (nontender and movable, found in subcutaneous tissues over bony prominences) • Fever • Weight loss • Fatigue • Anemia • Lymph node enlargement

  12. Rhematoid Nodules

  13. Systemic manifestations • Cardiovascular – pericarditis, valvular lesions, myocarditis, vasculitis, raynauds phenomenon • Pulmonary – pleurisy, rheumatoid nodules on lungs, pul. fibrosis, pul.hypertension • Neurologic – neuropathy, myelopathy • Hematologic – anemia, leukopenia

  14. Renal – rheumatoid nodules on kidney • Dermatologic – rheumatoid nodules, brown lesions, ulcers and fistulas • Ophthalmologic – scleritis, keratoconjuncitivitis (sjogren’s syndrome), glaucoma • Other – fever, malaise, weakness

  15. Diagnosis • CBC • Radiographs of involved joints • CT/MRI scans • Direct arthroscopy • Synovial Fluid aspirate/ Arthrocentesis - cloudy, milky, or dark yellow containing leukocytes • Synovial membrane biopsy

  16. ESR and C-reactive protein will be elevated • Antinuclear Antibody test to find out rheumatoid factor

  17. X-Ray

  18. Diagnostic criteria –ARA(american rheumatism association) • Morning stiffness lasting more than 1 hour for atleast 6 weeks duration • Swelling of wrist, metacarpophalangeal, or interphalangeal joints for atleast 6 weeks • Symmetric soft tissue swelling • Rheumatoid nodules • Positive serum rheumatoid factor test • Radiographic changes • Elevated ESR, c reactive protein

  19. Management • The major goal is to relieve pain and inflammation and prevent further joint damage • To reduce Anxiety, depression, and maintain self esteem because these factors commonly accompanies Rheumatoid Arthritis

  20. Medications • There are four types of medications used to treat RA: • Non-steroidal anti-inflammatory drugs (NSAIDs) • Disease-modifying anti-rheumatic drugs(DMARDs). • Corticosteroids • Biologic Response Modifiers (“Biologics”)

  21. Non-steroidal anti-inflammatory drugs (NSAIDs)

  22. Corticosteroids

  23. Disease-modifying anti-rheumatic drugs(DMARD)

  24. Biologic Response Modifiers (“Bioligics”)

  25. Bracescastssplintswalkerscrutches Supportive devices • Support injured joints and weak muscles • Improve joint mobility and stability • Help to alleviate pain, swelling and muscle spasm • May prevent further damage and deformity

  26. Spring – loaded braces • Resting splints • Functional splints • Dynamic splints

  27. Application of heat and cold packs Application of HEAT may be applied by means of • Hydrocollator packs (retains heat ) • Paraffin baths • Electric heating pads • Warm soaks or showers Application of cold packs and ice packs (15 to 20min) will reduce swelling, pain and stiffness.

  28. Exercise 4 times a week for 30 minutes • Walking • Light jogging • Water aerobics • Cycling • Yoga • Tai chi • stretching

  29. Nutrition • The most commonly observed vitamin and mineral deficiencies in patients with RA are: • folic acid • vitamin C • vitamin D • vitamin B6 • vitamin B12 • vitamin E • calcium • magnesium • zinc

  30. Alternative Medicine Olive leaf extract Aloe Vera Green Tea Omega 3 Ginger Root Extract

  31. Surgical management Goals • Prevention or correction of deformity • Relief from pain • To relieve symptoms • Prevent joint destruction • Maintain joint and muscle function • Promote quality of life

  32. Increases function of the joint, Decreases pain and inflammation

  33. Nursing management • Pain r/d inflammation, tissue damage • Fatigue related to pain , emotional stress • Impaired physical mobility related to weakness, lack of improper use of ambulatory devices • Deficient self care related to contractures • Disturbed sleep pattern • Disturbed body image • Ineffective coping

  34. Interventions • Relieving pain and discomfort • Reducing fatigue • Increasing mobility • Self care • Improving sleep • Improving body image and coping skills • Monitoring and managing complications • Increasing knowledge of disease management • Follow up care

  35. Osteoarthritis (OA) Osteoarthritis is defined as “a degenerative joint disease characterized by destruction of the articular cartilage, inflammation of joints and overgrowth of bone”

  36. CAUSES or risk factors • Idiopathic – primary OA • Resulted from previous joint injury or inflammation – secondary OA • Age – elderly, Usually seen in the 50-70 years • Obesity • Excessive weight • Family history

  37. Congenital structural defects – (leg clave perthes disease – osteochondritis of head of the femur in children) • Metabolic disturbances (diabetes mellitus, acromegaly, pagets disease) • Repeated intra articular hemorrhage (hemophilia) • Neuropathic arthropathy (charcot’s joints) • Excessive use of stress on joints (knees of football players)

  38. Pathophysiology OA affects the articular cartilage and leads to chondrocyte response , subchondral bone (bony plate that supports the articular cartilage) and synovium

  39. Pathologic changes • Erosion of articular cartilage • Thickening of subchondral bone • Formation of osteophytes or bone spurs

  40. Due to etiological factors • Degenerative changes cause the normally smooth, white joint cartilage to become yellow and opaque with rough surfaces • Chondrocyte response – release of cytokines and proteolytic enzymes due to inflammation • As cartilage become thinner the bony surfaces are drawn closer together • Cartilage break down and fissures may develop • As cartilage is thinned, the subchondral bone increases in density and become sclerotic • New bone outgrowth (osteophytes) will forms at joint margins

  41. Signs & Symptoms of OA • Joint pain – sharp pain is caused by inflamed joint, stretching of the joint or irritation of nerve endings • Crackling noise - crepitus • Spasms and contractions • Stiff joints in the morning • Joint swelling • Loss of joint flexibility or strength

  42. Heberdens nodes – hard bony enlargements on distal interphalangeal joints • Bouchards nodes – hard bony enlargements on proximal interphalangeal joints • Stiffness is most common – morning and lasts about 30 min • Coxarthrosis – pain in the hip on weight bearings progressing to groin and knee

  43. Diagnosis Physical examination History collection X-rays - osteophytes MRIs Joint Aspirate Lab tests- ESR

  44. Management Aim Symptomatic relief and control of pain Prevention of progression and disability and restoration of joint function

  45. Non-Pharmacological Management Exercise (isometric and aerobic exercise) Weight reduction Heat & Cold Therapy Use of assistive devices Prevention of injuries Perinatal screening

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