3 learning resources available for this topic
Rheumatoid arthritis (RA) is a chronic systemic autoimmune inflammatory disorder that primarily affects synovial joints, causing progressive joint destruction and disability. It typically presents with symmetric polyarthritis involving small joints of the hands and feet, along with morning stiffness lasting more than one hour. RA affects approximately 1% of the population worldwide, with a 3:1 female predominance and peak onset between ages 30-50.
RA develops when environmental triggers activate the immune system in genetically susceptible individuals, leading to loss of self-tolerance and autoantibody production including rheumatoid factor and anti-citrullinated protein antibodies. Chronic synovial inflammation results from infiltration of activated T cells, B cells, and macrophages, which release pro-inflammatory cytokines like TNF-α, IL-1, and IL-6. This inflammatory cascade leads to synovial hyperplasia, pannus formation, and release of proteolytic enzymes that destroy cartilage and erode bone.
Diagnosis relies on clinical presentation of symmetric joint swelling, tenderness, and morning stiffness, supported by elevated inflammatory markers (ESR, CRP) and positive autoantibodies (RF, anti-CCP). Early recognition is crucial as irreversible joint damage can occur within the first two years, making prompt initiation of disease-modifying antirheumatic drugs (DMARDs) essential. The treat-to-target approach aims for clinical remission or low disease activity to prevent joint destruction and preserve function.