Describe common locations, signs, symptoms, and onset of rheumatoid arthritis (RA). 3.
Given clinical characteristics, differentiate between RA and osteoarthritis. 4.
Describe extraarticular manifestations of RA and recommend preventative measures. 5.
List laboratory and radiology tests useful in evaluating and/or diagnosing RA. 6.
Describe pharmacological and non-pharmacological approaches to treating RA. 7.
Counsel on indication, SE, CI, MOA, black box warnings, monitoring, drug interactions, dose, and special precautions for pharmacological products used in managing osteoarthritis.
* Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder characterized by potentially deforming symmetric polyarthritis and a wide spectrum of extra-articular manifestations. * The exact cause of RA is unknown.
* The prevalence of RA is estimated to be about 1% worldwide. * It is 2 to 3 times more common in women than in men
* Disease is usually more severe in men
* Onset typically occurs between the 3rd and 4th decades of life * Prevalence increases with age up to the 7th decade
* In the US, RA affects as many as 2 million people.
* The inflammatory process leading to RA is believed to begin with abnormal propagation and activation of immune cells (T-cells, B-cells, and Macrophages). * It is unknown what initiates this process of abnormal propagation. * Immune cells promote the secretion of cytokines and other mediators (TNF-α, IL1, and IL6) which activate additional macrophages and rheumatoid arthritis synovial fibroblasts (RASFs), a more aggressive phenotype of synovial fibroblasts than found in non-RA patients. * Activated macrophages and RASFs release additional pro-inflammatory cytokines and mediators of vascular growth (VEGF). * VEGF cells promote angiogenesis and contribute to the growth of pannus, the proliferation of the tissue lining the joint capsule. * As the pannus grows, inflammatory processes continue. * RASFs and macrophages degrade the cartilage matrix resulting in irreversible cartridge damage and narrowing of the joint space. * Excessive TNF-α, IL-1, and IL-6 facilitate the expression of RANKL which activates osteoclasts leading to an imbalance in bone remodeling and bone destruction. * This is a continuous cycle of inflammation, and irreversible cartilage and bone destruction. Etiology: Unknown, Likely Multifactorial
* Genetic susceptibility
* Effects of aging
* Environmental influence
A. Local Involvement
* Symptoms of RA usually develop over the course of several weeks to months.
* Joint pain and stiffness, fatigue and muscle pain precede the development of joint swelling and deformity. * Acute phase: pain, swelling, tenderness, decreased strength/range of motion * Chronic phase: Joint dislocation, instability, deformity, muscle atrophy * Joint involvement may be non-symmetrical early in the disease but will become symmetrical quickly. Patient may present initially with symmetrical symptoms (common). * The most common joints involved are the small joints of the hands, feet, and wrists, but the knees, elbows, ankles, hips, jaw, and spine may be involved.
| Laboratory Tests
Joint pain and stiffness worse in the AM or after sitting for long periods. (Lasting > 6 weeks)
| Tenderness with warmth
| Rheumatoid factor (RF) detectible in 60-70%
| Fatigue (worse in the afternoon and accompanied by muscle pain)
| Swelling over joint (may be visible; feels soft and spongy upon palpitation)
| Anticyclic citrullinated peptide (anti-CCP) antibodies detectible in 50-85%
| Symmetrical joint involvement
| Elevated erythrocyte sedimentation rate
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