Overview
Introduction
RA often begins with genetic susceptibility and environmental or mucosal immune triggers.
RA often begins with genetic susceptibility and environmental or mucosal immune triggers. Smoking, periodontal disease, respiratory mucosal inflammation, microbiome changes, and other immune exposures are associated with risk in susceptible people. Many clients develop autoantibodies such as rheumatoid factor or anti-cyclic citrullinated peptide antibodies before or during clinical disease. The central joint process is persistent synovitis. Inflamed synovium becomes thick, vascular, and invasive. Pannus damages cartilage and erodes bone. Cytokines activate osteoclasts, which break down bone at joint margins. Tendon sheaths can become inflamed, causing tenosynovitis, tendon rupture, trigger symptoms, carpal tunnel syndrome, and deformity. Disease progression can produce ulnar deviation, swan-neck deformity, boutonniere deformity, subluxation, loss of grip, reduced mobility, cervical spine instability, and severe disability. However, modern treat-to-target care aims for remission or low disease activity before irreversible damage occurs. RA is systemic. Chronic inflammation contributes to fatigue, low-grade fever, anemia of inflammation, osteoporosis, accelerated cardiovascular risk, interstitial lung disease, pleural disease, nodules, vasculitis, ocular inflammation, depression, and reduced quality of life. Nursing assessment must therefore look beyond the painful joint. For REx-PN (Canada), items rarely announce the...
