Rheumatoid Arthritis
Introduction
Rheumatoid Arthritis (RA) refers to an autoimmune illness resulting from chronic and systemic inflammatory, which might affect various organs and tissues, though it primarily attacks synovial or flexible joints. Rheumatoid arthritis can be a painful and disabling condition that can result in significant loss of mobility and function if not treated adequately. The condition involves the inflammatory reaction of the capsules around the synovium due to the swelling of the synovial cells or turgenscence, development of fibrous tissue in the synovium and excess synovial fluid. The pathology of AR frequently results in fusion of the joints and destruction of articular cartilage. According to Cush, Weinblatt, & Kavanaugh (2010), rheumatoid arthritis can also produce inflammation in the membrane around the heart, lungs and white of the eye. Despite the cause of the illness not well-know, autoimmunity seems to play a crucial role in its progression and chronicity. RA is a clinical diagnosis made based on the symptoms, radiographs, physical exams and labs. In this regard, this paper discusses the RA by paying attention to the following: incidence, etiology, risk factors, clinical manifestations, and medical treatments.
Incidence
Rheumatoid Arthritis affects about 0.5 to 1 per cent of adults in developed countries. About 50 individuals in every 100000 people develop the disease annually. The onset of AR is not common for individuals aged below 15 years. However, the incidence of AR increases with the age f an individual until the age of 80 years. Women are the most affected as compared to men. They are affected about three to five times as frequently as men are.
Some groups of Native Americans seem to have higher rates of prevalence of about 5 to 6 per cent. On the other hand, people from the Caribbean have lower prevalence rates. In women, the disorder usually starts at the age between 40 and 50 years. In men, the disorder starts later than in women.
Etiology
Rheumatoid Arthritis is one of autoimmunity. Its causes are still not known. According to Goronzy & Weyand (2001), it is a disorder that affects the whole body, that is why it is referred to as systemic illness. There is no evidence indicating that emotional and physical effects could cause the disorder. The various negative findings argue that either the causes varies among individuals, or that it might be a an event inherent in the immune response. About half of the Rheumatoid Arthritis is believed to be genetic. The disorder is significantly linked to the inherited tissue type major histocompatibility complex (MHC) antigen. It is also associated with genes PAD14 and PTPN22. As a result, the history of the family is a significant factor. The inheritance of the PTPN22 gene has been said to increase the vulnerability of the disease. PAD14 has been detected to be a primary risk factor in individuals of Asian descent, and not in people of European descent. The prevalence rate of disease in first-degree relative is estimated to be about 2-3 per cent.
Risk Factors
Smoking is one of the most significant risk factor among the non-genetic risks. Rheumatoid arthritis is three times more popular in smokers than in non-smokers. Male smokers, especially heavy smokers, have been claimed to be at the highest risk of developing rheumatoid arthritis. Individuals who are rheumatoid factor positive and are smokers are also at the highest risk of developing the disease. According to Hochberg, Silman, Smolen, Weinblatt, & Weisman (2008), modest consumption of alcohol might be protective against the disease.
Epidemiological researches have affirmed a possible link between the two herpes virus that are Human Herpes Virus 6 (HHV-6) and Epstein-Barr virus (EBV) and rheumatoid arthritis. Individuals suffering from rheumatoid arthritis are most likely to show an abnormal unnube reaction to EBV. In addition, they have high levels of anti-Epstein-Barr virus antibodies. According to Goronzy & Weyand (2001), the deficiency of vitamin D is popular in individuals with rheumatoid arthritis and might causally be linked to the disorder. Some studies have revealed that there is reduced risk with supplemental, whereas others have not.
Clinical Manifestations
The disease usually affects joints, though problems involving other tissues and organs might also occur. According to Goronzy & Weyand (2001), these other manifestations are apparent in approximately 15 to 25 per cent of people. It can be extremely difficult to detect whether rheumatoid process directly causes the disease manifestations or side effects from the medications cause these manifestations.
The first sign in the swelling of the joint, which is also known as arthritis of the joints. The joints become warm and tender. The stiffness at the joints limits their movement. The most common affected joints are the joints of feet, hand, and cervical spine. However, larger joints, such as the knee and the shoulder can also be affected. RA frequently manifests with symptoms of inflammation, with the affected joints being painful and stiff. Gentle movements might relieve the symptoms during the early phases of the disease.
RA can also manifest itself through the skin. The rheumatoid nodule is one of the typical features of the disease. Rheumatoid nodule or necrotizing granuloma refers to a form of inflammatory response. According to Goronzy & Weyand (2001), the nodule has an area of frbrinoid necrosis, which might be fissured. A layer of palisading fibroblasts and macrophages surround the necrosis. Nodules are linked to positive rheumatoid factor (RF) titer and severe arthritis. These can rarely occur in internal tissues or organs (Cush, Weinblatt, & Kavanaugh, 2010).
The fibrosis of the lungs is another clinical manifestation of the disease. Lung fibrosis is rare, though it is a well-recognized effect of therapy. Pleural effusions are also linked to rheumatoid arthritis. The Rheumatoid Lung Disease is also a complication associated with the disorder.
Individuals suffering from RA are prone to heart attack, stroke and atherosclerosis. Other possible clinical indications include endorcarditis, pericarditis, fibrosis, valvulitis and left ventricular failure. Many individuals suffering from RA do not experience similar chest pains that other experience when having myocardial and angina infarction (Hochberg, Silman, Smolen, Weinblatt, & Weisman, 2008).
Diagnosis
The disease can be diagnosed through various techniques: imaging and blood tests among others. X-rays of feet and hand are usually performed in people suffering from polyarthritis. In Rheumatoid Arthritis, there might be no changes in the early phases of the disease. The X-ray might show loss of joint space, swelling of soft tissue and juxta-articular osteopenia. Other imaging techniques such as ultrasound and magnetic resonance imaging (MRI) are also used in diagnosing the disease (Cush, Weinblatt, & Kavanaugh, 2010).
Blood tests are necessary in testing for the presence of rheumatoid factor (RF). A negative RF does not imply that the individual is not suffering from RA; instead, individuals with negative RF are said to be seronegative. This is usually the case in approximately 15 per cent of the patients.
Medical Treatment
There is no recognized treatment for contraction of RA. Reducing the factors increasing the susceptibility to the disease is the most recommended action. Some of the available medications aim at relieving the symptoms, whereas others help I slowing the progression of the disease. Patients suffering this disease, experience it differently from each other. As a result, it is difficult to have best combination f medicine that suitably meets the needs of a patient. Some of the available medications include painkillers, non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids among others. Painkillers such as codeine and paracetamol reduce the pain and not the inflammation (Hochberg, Silman, Smolen, Weinblatt, & Weisman, 2008).
NSAIDs relieve both pain and the swelling at joints. There are two types of NSAIDs, which includes the traditional NSAIDs and COX-2 inhibitors. The traditional NSAIDs comprise of naproxen, diclofenac and ibuprofen. The COX-2 inhibitors comprise of etoricoxib and celecoxib. In addition, NSAIDs relieve stiffness while also reducing inflammation. However, they do not slow the progression of the disease (Cush, Weinblatt, & Kavanaugh, 2010).
Post-traumatic arthritis can be treated by losing weight, exercising to strengthen the muscles, and using NSAIDs. In addition, arthritic joints can also be injected with hylamers or cortisone that act as artificial fluid for the joint. Surgical treatment might be used where the above medications are not effective in relieving the pain and maintain the function. Surgical treatment might include debriding, replacing or reconstructing the joint surfaces (Cush, Weinblatt, & Kavanaugh, 2010).
Prognosis
The course of RA varies significantly. Some individuals might have mild short-term signs and symptoms. However, in many people the disease is progressive for life. Approximately 20 to 30 per cent of the patients have rheumatoid nodules, which is linked to poor prognosis. Some of the prognostic factors include positive serum RF findings, early erosive disease, persistent synovitis, family history, socioeconomic factors, poor functional status, C-reactive protein (CRP) and positive serum anti-CCP autoantibodies, The disease is known to reduce the lifespan by about 3 to 12 years. However, the use of biologic drug therapies extends the lifespan of people suffering from the disease (Cush, Weinblatt, & Kavanaugh, 2010).
Conclusion
Rheumatoid arthritis can be a painful and disabling condition that can result in significant loss of mobility and function if not treated adequately. Its causes are still not known. There is no evidence indicating that emotional and physical effects could cause the disorder. Smoking is one of the most significant risk factor among the non-genetic risks. The disease can be diagnosed through various techniques: imaging and blood tests among others.
References
Cush, J., Weinblatt, M., & Kavanaugh, A. (2010). Rheumatoid arthritis: early diagnosis and treatment. New York: Professional Communications.
Goronzy, J., & Weyand, C. (2001). Rheumatoid arthritis. London: Karger Publishers.
Hochberg, M., Silman, A., Smolen, J., Weinblatt, M., & Weisman, M. ( 2008). Rheumatoid Arthritis. New York: Elsevier Health Sciences.
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