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Rheumatoid arthritis (RA) is a chronic inflammatory disease which affects about 0.5 to 2% of the population worldwide. It is the most common form of arthritis among adults and is a common cause of serious disability. The characteristic feature of RA is inflammation of synovial joints, usually symmetrical, and subsequent damage to joint integrity. It affects women more than men by a ratio of 3:1. It is equally common among all races and affects all age groups, but is seen most frequently in the age group of 40 to 60 years (Scott, Kingsley & Gabrielle, 2007). RA was first described by Landre- Beauvais in the year 1800 in Paris, and the term “rheumatoid arthritis” was coined invented by Garrod in 1859, though the disease itself is much older. In fact, it is one of the oldest known diseases of humans, and it currently afflicts about three million people in the US (Stanich, Carter, Whittum-Hudson & Hudson, 2009). This paper researches the etiology, clinical presentation, diagnosis, treatment and prognosis of rheumatoid arthritis.
Etiology and Pathophysiology
The etiology of RA remains unclear even after many decades of intensive research. Various studies indicate an infectious agent, autoimmune response or genetic predisposition as the cause. RA is rather common within families; therefore, people with a positive family history are more likely to develop the disease. A specific genetic marker, called the HLA-DR gene, is found more frequently in people with RA, and this finding supports the genetic basis of disease. Rheumatoid arthritis has also been described as an autoimmune disease where the body’s own immune system starts attacking the joints. Rheumatoid factor, an auto antibody, can be detected in the blood of most RA patients. It binds with antibodies to form an antigen-antibody complex; furthermore, the formation of this complex is thought to trigger chronic inflammatory response in joints. Bacterial or viral infections have also been held responsible for precipitating RA in genetically predisposed individuals as infections usually coincide with flare-ups of RA (Cush, Weinblatt & Kavanaugh, 2010)
RA affects the synovial lining of joints. Synovial membrane lines the joint cavity and is normally one to three cells thick. With the onset of RA, it undergoes proliferation, and there is an increase in the number of synovial lining cells. There is the formation of new blood vessels, and the normally flat synovial membrane becomes villous and edematous. This is followed by activation and accumulation of T cells in the joint which leads to a cascade of inflammatory responses. Consequently, there is a panus formation, further accumulation of inflammatory cells, destruction of periarticular tissue, bone erosions and localized osteoporosis. Inflammation of synovium results in accumulation of inflammatory joint fluid (Cush, Weinblatt & Kavanaugh, 2010).
Most patients experience a gradual onset of symptoms like fatigue, weakness, malaise, fever and weight loss. After weeks or months, the classic symptoms of joint pain and swelling appear. Involvement of joints is classically symmetrical, and the initial joints to be affected are usually the small joints of hands and feet – the metacarpophalangeal, the metatarsophalangeal and the proximal interphalangeal joints. The second most commonly involved joints are the wrist joints. Patients experience stiffness of joints after inactivity periods, most prominent in the morning, which typically lasts for about 1 hour. During this time, they are unable to bend their fingers. Synovial inflammation causes pain, tenderness, swelling and limitation of motion. Pain occurs primarily because of distension of the joint capsule; it is extremely sensitive to stretching due to abundance of pain fibers. Swelling of joints results from synovial fluid amassing, joint capsule thickening and synovial hypertrophy. Motion limitation occurs due to pain, as the patient tries not to bend the joint in order to minimize distension of the joint capsule. In later stages of the disease, soft tissue contractures or bony or fibrous ankylosis are observed which result in fixed deformities (Fauci & Langford, 2010)
Persistent chronic inflammation causes the rise of a number of characteristic joint changes, including weakening or damage of ligaments, tendons and joint capsule, degradation of cartilage and muscular imbalance. Unopposed physical forces result in distinctive changes in hands and feet, some of which are –
1. “Z” deformity – Radial deviation of wrist and ulnar digit deviation.
2. Swan- neck deformity – hyperextension of proximal interphalangeal joints and flection of distal interphalangeal joints.
3. Boutonniere deformity – Extension of distal interphalangeal joints with flexion contracture of proximal interphalangeal joints (Fauci & Langford, 2010).
RA is a systemic disease with a number of extra-articular manifestations. These include the development of rheumatoid nodules. The subcutaneous granulomatous lesions usually develop in areas that are subjected to mechanical pressure. They are generally asymptomatic but can become infected. RA also causes weakness and atrophy of skeletal muscles, especially those approximating the affected joints, parenchymal lung disease, Sjogren’s syndrome, pericarditis and rheumatoid vasculitis (Fauci & Langford, 2010)
A definitive diagnosis of RA depends generally on observation of clinical characteristics and exclusion of other inflammatory diseases of joints. In addition to patient’s history and physical examination, laboratory tests and imaging studies are used as diagnostic aids. Even though no tests are specific for RA, certain blood tests are used to support the diagnosis. Among the abovementioned tests there are tests for rheumatoid factor, ESR, C-reactive protein and complete blood count. ESR and C-reactive protein are general markers of inflammation, not specific to RA. Patients in early stages of the disease have a slightly increased white blood cell (WBC) count, but remarkably increased level of platelets in the blood. Imaging studies are unable to detect the earliest changes caused by RA. Sensitive imaging techniques can only detect such changes as joint erosion about 4 months after the onset of disease. Radiographic evidence of joint destruction can be seen only after 1-2 years of active disease. Therefore, imaging techniques are more useful in evaluating the progression of the disease (Fauci & Langford, 2010).
The diagnostic criteria for definitive diagnosis of rheumatoid arthritis have been laid down by the American College of Rheumatology. Four of the seven criteria are required to diagnose a case as RA. These are, arthritis of at least three joints, symmetric arthritis, hand joints arthritis, rheumatoid nodules, the presence of serum rheumatoid factor, morning stiffness, and radiographic evidence of erosion or bone decalcification of the involved joint (Fauci & Langford, 2010).
Since etiology of rheumatoid arthritis is unknown, all treatment is only palliative, aimed at relieving the signs and symptoms, rather than being curative. The goals of therapy are the relief of pain and inflammation, protection of articular structures, maintenance of function and minimizing systemic involvement. Management of RA requires an interdisciplinary approach with many physical therapy modalities combined with pharmacological management. Splinting of joints is done in order to reduce the unwanted movement; and specific exercises are prescribed to maintain muscle strength and joint mobility without aggravating the inflammation. Adequate rest is an essential part of the therapy as it relieves many symptoms. A number of assistive devices are available to improve function. Pharmacologic management of RA involves five approaches. The first one is the use of NSAIDS (Non Steroidal Anti inflammatory Drugs) to mitigate inflammation and reduce pain, but they do not reduce the progression of the disease. The second approach is the use of oral glucocorticoids. In addition to relieving pain and inflammation, they also retard the development and progression of bone erosions. The third line agents are DMARDS (Disease Modifying Anti-rheumatic Drugs). These drugs reduce the destructive potential of RA by modifying its inflammatory component. DMARDs include methotrexate, sulfasalazine and hydroxychloroquine. A combination of these drugs is more effective than single agents. The fourth group of drugs is the biologics which includes TNF-neutralizing agents, IL-1 neutralizing agents and drugs that interfere with B cells and T cells (rituximab and abatacept). The fifth group of drugs includes immunosuppressive and cytotoxic drugs. Severely damaged joints may require surgical intervention such as arthroplasty or joint replacement (Fauci & Langford, 2010)
RA is a progressive and debilitating disease which reduces the quality of life and shortens the life expectancy of a patient due to involvement of vital organ systems. The course of the disease varies from patient to patient, and remission is the best possible outcome. In general, the course of rheumatoid inflammation depends on numerous factors, including age of the patient at onset, time lapse between the onset and diagnosis and between diagnosis and treatment initiation, genetic background, radiographic erosions, degree of disability, co-morbidities and socioeconomic status of thepatient.
Many of these factors, such as age of onset, socioeconomic status and other, are unavoidable. Hence, the physician needs to focus on those aspects which can be modified to produce a better outcome. The most significant of these factors is early diagnosis along with a prompt initiation of DMARD treatment (Cush, Weinblatt & Kavanaugh, 2010)
Rheumatoid arthritis is one of the oldest diseases known to mankind and one of the most debilitating. It incurs an enormous cost to the nation in terms of loss of productivity and healthcare costs. There has been a lot of new research in the last two decades, resulting in development of better imaging techniques and more effective and safer drugs. The ongoing studies in gene therapy, stem cell transplantation and role of T cells may lead to the development of targeted therapies in the near future that could result in hampering the progression of inflammation or even inventing a vaccine to prevent rheumatoid arthritis.
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