Rheumatoid arthritis

71 Rheumatoid arthritis




Overview/pathophysiology


Rheumatoid arthritis (RA) is a chronic systemic disease associated with severe morbidity and functional decline caused by inflammation of connective tissue, primarily in the synovial joints. Mortality rates of persons with RA are double that of the general population, particularly if the disease is not well controlled. Individuals with RA are at increased risk for cardiovascular events. Women are affected two to three times more often than men. Although no single known cause exists for RA, theory suggests that it occurs in a susceptible host who initially experiences an immune response to an antigen. Because complex genetic factors appear to be involved, the antigen is probably not the same in all patients. Autoimmunity has been suggested as a cause because of association of RA with occurrence of rheumatoid factor (RF), the antibody against an abnormal immunoglobulin G (IgG). Support for a genetic predisposition has come from studies of disease clusters in families, and formal genetic studies have confirmed this familial aggregation. No microorganism has been cultured from blood and synovial tissue or fluid with enough reproducibility to determine an infectious etiology for RA. In addition, no environmental factors have been identified as disease precipitators.


The immune response appears to center on synovial tissue, where disease changes are first seen. Synovitis develops when immune complexes are deposited onto the synovial membrane or superficial articular cartilage. As hypertrophied synovium invades surrounding tissues, highly vascularized fibrous exudate (pannus) forms to cover the entire articular cartilage. Pannus also scars and shortens adjacent tendons and ligaments to create the laxity, subluxation, and contractures characteristic of RA.





Diagnostic tests


Diagnosis of RA is based primarily on physical findings and patient history. Radiographic studies are not usually needed to make a diagnosis. Laboratory results are helpful in confirming diagnosis and monitoring disease progression.










Arthroscopy:


Reveals pale, hypertrophic synovium with destruction of cartilage and formation of fibrous scar tissue.





Nursing diagnosis:


Deficient knowledge

related to unfamiliarity with drugs used in RA treatment


Desired Outcome: Immediately following teaching, patient verbalizes accurate information about prescribed RA drugs.






























































ASSESSMENT/INTERVENTIONS RATIONALES
Teach patient about all drugs prescribed for treatment of arthritis: indications for use, possible side effects, administration time and method, and need for follow-up laboratory tests. Drug therapy remains the cornerstone of an interdisciplinary approach to care for RA.
A knowledgeable patient is likely to comply with the drug therapy and report necessary signs and symptoms to ensure prompt treatment of untoward side effects.
Disease-Modifying Antirheumatic Drugs (DMARDs)
  Accurate, timely diagnosis is critical to initiation of DMARDs, which have been shown to control active synovitis and prevent joint erosions and damage. Early use is critical because they have been shown to slow the erosive course of RA and are now considered to be a first-line therapy in disease treatment. Nonsteroidal antiinflammatory drugs (NSAIDs) are often prescribed along with DMARDs to allow optimal management of pain and swelling until the slower acting disease-modifying agent begins to exert its effect.

Most frequently prescribed by rheumatologists in the United States in doses of 7.5-25 mg weekly by mouth (PO) or intramuscular (IM).

Include sulfasalazine (2000-3000 mg daily), hydroxychloroquine (200-400 mg daily), cyclosporin (1.5-2.5 mg/kg daily), cyclophosphamide (1-2 mg/kg daily), and leflunomide (10-20 mg daily).
Teach patient that laboratory monitoring of renal and liver function is necessary with all DMARDs. Because the potential is great for renal and hepatic toxicity with DMARDs, patient should be instructed to complete all follow-up laboratory tests as prescribed.
Biologic Response Modifiers (BRMs)  
  BRMs interfere with cell surface antigens of modulating cytokines to manage RA symptoms in patients with moderate to severe disease who have not responded to DMARDs. Adalimumab, etanercept, infliximab, and golimumab block a cytokine known as tumor necrosis factor alpha (TNF-α), while anakinra blocks interleukin-1 (IL-1). Abatacept is the first approved T-cell co-stimulation modulator. The cancer drug rituximab selectively targets CD20-positive B cells. BRMs are frequently given with a DMARD.
Explain that because most BRMS are given subcutaneous by self-injection, they may not be appropriate for all RA patients. Self-administration by RA patients may be problematic because of muscle weakness and joint deformity. If patient does not have a family member/significant other who can be taught the injection technique, a home health care provider may need to determine patient’s ability to return to an outpatient clinic for medication administration. Infliximab is given intravenously, often in the physician’s office, and offers an alternative to subcutaneous administration.
Teach patient to minimize exposure to ill individuals and immediately report personal illness to the physician. Both DMARDs and BRMs cause immunosuppression, and can increase patient’s risk for illness. Illness, particularly if resistant to conventional treatment (e.g., common cold), should be reported immediately to the physician for more aggressive treatment.
NSAIDs
  A number of NSAIDs provide largely equal analgesic and antiinflammatory effects in the treatment of RA. They do not affect disease progression and their use in alleviating RA symptoms may in fact delay initiation of DMARD therapy or referral to a rheumatologist.
Teach patient that NSAIDs are linked to increased risk for gastrointestinal (GI) toxicity, and patient should recognize signs and symptoms of internal bleeding or GI ulceration. The patient must be able to seek prompt medical attention for any suspected bleeding or ulceration.
Corticosteroids
  Injection of corticosteroids directly into affected joints can temporarily relieve the pain and inflammation of RA exacerbations. Low-dose oral prednisone may be useful in selected patients to minimize disease activity until the prescribed DMARD becomes therapeutic.
Explain that caution is necessary in long-term use of oral corticosteroids. Corticosteroids have been associated with development of avascular necrosis or osteoporosis and therefore should not be a mainstay of treatment for the patient with RA. Patients who take corticosteroids should receive additional instruction on risks associated with long-term use.
Antibiotics
  Minocycline is the only antibiotic to be studied carefully for use in treatment of RA. It can improve mild-to-moderate symptoms but has no disease-modifying properties. Side effects such as skin discoloration, dizziness, GI upset, and autoimmune phenomenon (including hepatitis) frequently lead to discontinuation of therapy.
Future Drug Therapies
  Research on underlying causes of inflammation associated with RA may lead to development of new medications or new uses for previously marketed medications. The nurse should listen carefully to patient’s stated interest in any other pharmacologic therapies and inform health care provider of patient’s willingness to try additional treatments.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Rheumatoid arthritis

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