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Rheumatoid Arthritis (Monitoring (Dependent on drug of choice, Baseline…
Rheumatoid Arthritis
Monitoring
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Baseline monitoring: LFTs, SCr, BUN, CBC, BP, TB skin test
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Symptoms of concern; myelosuppression, infection, blood in stool, severe GI effects
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Epidemiology
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T lymphocytes: HLA-DR4, HLA-DR1, or both
6x more common dizygotic twins, nontwin children of parents with rhematoid factor positive, erosive RA
one (monozygotic twin) affected, 30x greater risk of RA
1% prevalence, no racial predilections
Pathophysiology
Chronic inflammation of the synovial tissue lining the joint capsule results in the proliferation of the issue.
Pannus: inflammed, proliferating synovium characteristic of RA
Invades cartilage and eventually bone surface, thus producing erosion of both substances and ultimately destroys the joint
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This is due to the body of patients with RA attacking itself (i.e. synovial/other connective tissues). Reason why this is an autoimmune disease.
Risk factors
Genetic factors, environmental factors (i.e. smoking), pulmonary disease, infectious agents (I.e. Epstein-Barr virus, Escherichia coli), periodontal disease (Porphyromonas gingivalis)
Inflammation process
Antigen-presenting cells present antigens to T cells. This stimulates B cells to produce antibodies/osteoclasts that destroy/remove bone. Macrophages stimulated by the immune response to stimulate T cells/osteoclasts and promote inflammation. Both T cells and macrophages release factors that promote tissue destruction, increase blood flow, and result in cellular invasion of synovial tissue/joint fluid, which causes synovitis.
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Clinical Presentation
Signs and Symptoms
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may see fatigue, weakness, low-grade fever, loss of appetite, muscle pain, afternoon fatigue
tenderness with warmth and swelling over affected joints, usually involving hands and feet
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Labs
Anemia? : Stool Guaiac, Ferritin, Serum iron-to-iron binding, Mean Corpuscular volume
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