Rheumatoid Arthritis Christine Aranyi and Rebecca Boon State university of new york institute of technology Pathophysiolog y Rheumatoid Arthritis (RA)

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Rheumatoid Arthritis Christine Aranyi and Rebecca Boon State university of new york institute of technology Pathophysiolog y Rheumatoid Arthritis (RA) is a symmetric, inflammatory, peripheral polyarthritis of multifactorial etiology. Inflammatory pathways -> proliferation of synovial cells in joints -> pannus formation -> cartilage destruction and periarticular bony erosions If left untreated or unresponsive to therapy, inflammation and joint destruction lead to joint deformities, loss of physical function, inability to carry out daily tasks of living or employment. Etiology Cause is multifactorial, autoimmune Second most common connective tissue disease and is the most destructive to the joints. Occurs more in women than men with an incidence of 3:1 Incidence increases with age, with a peak of cases occurring between No racial or ethnic groups determined to have increased incidence. Increased incidence for smokers. Follows a familial pattern, and genetics studies are ongoing. Typical Presentation Arthralgias Fatigue, fever, weight-loss Pain and stiffness in multiple joints, often symmetrically Morning stiffness lasting more than one hour Boggy swelling/synovial thickening, typically wrist and interphalangeal joints Diagnosis The diagnosis of RA can be made when the following clinical features are present Inflammatory arthritis involving 3 or more joints. Positive Rheumatoid Factor (RF) and/or anti-citrullinated peptide /protein testing. Increased levels of CRP or ESR. Diseases with similar clinical features have been excluded. Duration of the symptoms is at least 6 weeks. Treatment Goals: Minimize joint pain, swelling, deformity, and radiographic damage,Maintain quality of life Educate on infection prevention Prevent/Minimize extraarticular manifestations (Cardiac, Ophthalmologic, Hematologic, Neurological Pulmonary, Integument) Prevent cardiac disease (main cause of mortality in RA) Regularly test for lymphoma (risk doubled in RA) Medications DMARDs – Disease modifying antirheumatic drugs,Mainstay of treatment Biologic: Infliximab (Remicade) IV q6-8 weeks, Adalimumab (Humira) SQ weekly, Abatcept (Orencia) Nonbiologic: Methotrexate – first line treatment Leflunomide (Arava) Sulfasalazine (Azulfudine) Hydroxychloroquine (Plaquenil) Short term: NSAIDS, corticosteroids Herbals, Exercise Possible benefits from/inconclusive or new studies: Gamma-linoleic acid (from evening primrose or black currant seed oil) Tripterygium wilfordi (thunder god vine) Physical exercise Tai Chi Iyengar yoga References Dunphy, L. B. (2011). Primary Care: The art and science of advanced practice nursing (3rd ed.). Philadelphia: F.A. Davis Company. Venables, P. (2013). Diagnosis and differential diagnosis of rheumatoid arthritis. Retrieved from differential-diagnosis-of-rheumatoid-arthritis Wasserman, A. (2011). Diagnosis and management of rheumatoid arthritis. American Family Physician 84(11)