Chapter 59 - Rheumatic Disorders

• joint inflammation is the underlying common symptom that unites the multiple forms of arthritis
• primary arthritis affects body systems in addition to the musculoskeletal system resulting from an immune response
• secondary arthritis results from a degenerative process and the resulting joint irregularities that occur as the bone attempts to remodel itself
• systemic autoimmune rheumatoid diseases are chronic disorders characterized by diffuse inflammatory lesions and degenerative changes in connective tissue
• systemic autoimmune rheumatoid disorders share similar clinical features and may affect many of the same organs
• systemic autoimmune rheumatoid diseases include:

  • rheumatoid arthritis
  • systemic lupus erythematosis
  • systemic sclerosis/scleroderma
  • polymyositis
  • dermatomyositis
• in rheumatoid arthritis, immune complexes are created from rheumatoid factor and circulating IgG deposit in the synovial membrane that surrounds the joint
• complement activation in the joint initiates processes associated with inflammation, known as synovitis (redness, swelling, and pain)
• pannus releases enzymes and proinflammatory mediators that cause damage to the cartilage of articulating surfaces
• pannus blocks the supply of nutrients to cartilage which further erodes the cartilage
• over time, pannus becomes fibrotic and calcified as scar tissue in the joint fills the joint cavity and impairs joint mobility
• as RA progresses, the joint undergoes ankylosis with joint stiffness or fixation and deformity
• RA is progressive where subsequent exacerbations further damage the already joints and new joints become involved
• complications of RA:

  • muscle atrophy leading to further joint destabilization
  • bone misalignment (due to cartilage damage and muscle imbalances)
  • muscle spasm (due to inflammation and pain)
  • contractures and deformities
• signs and symptoms of RA:

  • initially, may experience aching and stiffness in joints (often in fingers and wrists)
  • redness and swelling of joints
  • stiffness after rest improved by activity
  • loss of joint mobility
  • fatigue, weakness, anorexia, weight loss
  • low-grade fever
  • anemia
• diagnosis of RA depends upon evidence of at least 3 affected joints for at least 6 weeks
• diagnostic criteria for RA:

  • morning stiffness at least 1 hour for at least 6 weeks
  • swelling of 3 or more joints for at least 6 weeks
  • swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for 6 or more weeks
  • systemic joint swelling
  • hand roenterogram changes typical of RA
  • rheumatoid nodules
  • serum rheumatoid factor
• anti-cyclic cirtullinated peptide antibodies tend to have higher specificity for RA
• treatment for RA:

  • reduce pain (ASA, NSAIDs, COX-2 inhibitors)
  • minimize stiffness and swelling (glucocorticoids)
  • maintain mobility
  • establish pacing of activity
  • balance, rest, and exercise
  • specialized therapies (gold particle injections)
• individuals that are genetically predisposed to RA experience an activated T cell mediated response to a trigger such as a microbe which resulting in an immune response leading to synovial inflammation and joint destruction
• IgRF and IgG immune complexes and complement components are present in the pathogenesis of RA
• angiogenesis at the synovial membrane contributes to synovitis in RA
• pannus is a distinguishing feature of RA
• inflammatory cells in the pannus destroy adjacent cartilage and bone, eventually developing between joint margins, decreasing motion
• general RA progression results in joint instability, muscle atrophy, ligament stretching, and tendon/muscle alterations
• the cause of SLE is unknown, but is thought to involve the formation of autoantibodies and immune complexes due to B cell hyper-reactivity
• autoantibodies in SLE can directly damage tissues or combine with corresponding antigens to form tissue-damaging immune complexes
• rheumatoid factor is foind in SLE, making it seropositive
• examples of autoantibodies in SLE:

  • antinuclear (DNA, phospholipid)
  • cytoplasmic (microtubules, ribosomes)
  • blood elements (cells)
  • plasma proteins (e.g., coagulation factors and complement)
• 90% of SLE cases report joint pain, which may confuse it for RA; however, joint destruction is rarely found but varies deformities from ligament and tendon alterations exist
• dermatologic manifestations of SLE include a "butterfly" rash on the nose and cheeks
• cardiovascular manifestations of SLE include anemia
• 40-50% of SLE cases have pulmonary manifestations
• renal manifestations are present in 50% of SLE cases and include glomerulonephritis and nephrotic syndrome
• neuropsychiatric manifestations of SLE include seizures, depression, confusion, and altered consciousness
• seronegative spondyloarthropathies are an interrelated group of inflammatory disorders (multi-system) primarily affecting the axial skeletal
• signs and symptoms of seronegative spondyloarthropathies overlap with other inflammatory types of arthritis
• the cause of inflammation in seronegative spondyloarthropathies is unknow, but symptomatology is the same
• ankylosing spondylitis is an inflammatory erosion of the sites where tendons and ligaments attach to bone manifested by pain and progressive stiffening of the spine
• reactive arthritis is distant in time and place from the initial infection