Effects of Rumatoid Arthritis on the Human Body - Term Paper Example

?Effects of Rheumatoid Arthritis on the Human Body and Section Number Introduction People of all ages, male and female, are susceptible to inflammatory diseases. These disorders such as rheumatoid arthritis are catabolic conditions that lead to loss of lean tissue and related functional abnormalities that alters energy and protein metabolism and that lead to changes in body composition (Heymsfield, Lohman and Wang, 2005, pg. 341). Rheumatoid Arthritis (RA) is a progressive inflammatory disorder characterized by proliferation of the synovial membrane and persistent uncontrolled inflammation resulting in a chronic destructive polyarthritis (Kavanaugh, Weinblatt and Cush, 2010, pg. 15). Typically, RA manifests itself as a symmetric arthritis involving numerous small and large joints. Articular symptoms may be accompanied by systemic inflammatory symptoms such as fatigue, articular stiffness, anorexia and fever. Rheumatoid Arthritis (RA) is a worldwide affliction with remarkably consistent prevalence, affecting approximately 1 percent of the population. It is most prevalent in highly developed countries, such as the United States, England and Scandinavia. The prevalence of the disease varies in some population, for example, it may exceed 5 percent in several Native American tribes (Yakima, Chippewa and Pima). In contrast, RA is less common in Japan and Hong Kong and relatively rare in Indonesia and sub Saharan Africa (Kavanaugh, Weinblatt and Cush, 2010, pg. 29). The average age of persons with RA is 66.8 yeasrs. According to CDC (2007), arthritis and related conditions such as RA, cost the U.S economy nearly $128 billion annually in medical care and indirect expenses including lost wages and productivity. It accounts for 22 percent of all deaths from athritis and other rheumatic conditions. Persons with RA are two times more likely to die than persons of the same age without RA in the general population (Wolfe, Mitchell and Siblety, 1994, pg. 483). Rheumatoid Arthritis RA is a chronic inflammatory disorder of the movable joints. It differs from osteoarthritis in that it is not caused by wear and tear, instead, it appears to be an autoimmune disorder. That is, the body’s own immune system produces antibodies against its tissues causing inflammation and pain. Though it can be controlled, it can be progressive if left untreated. Most important, it is not a terminal illness, if diagnosed early and treated appropriately. The human body consists of about 300 individual bones, connected by more than 140 joints. To function, a joint also requires ligaments, tendons and muscle tissue. It was once believed that bones were relatively inert once they were formed. Today it is known that bone is constantly turned over. Two special types of cells carry out remodeling and repair work; the osteoclasts which remove bone and the osteoblasts which are responsible for forming new born. Both of the two cells participate in mending of broken bones. Arthritis works by impacting on the balance between the osteoclasts and osteoblasts. The body consists of only three types of joints the synarthroid or fibrous joints, these are the ones separating the plates that form the skull, there is the amphiarthroidal or cartilaginous joints, which are responsible for the limited movement in the intervertebral bones and finally the diarthroidal or synovial joints which are highly mobile. The first two due to their level of movement are not affected by rheumatoid arthritis (RA), however, the highly mobile diarthroidal or synovial joints are the target of RA (Loebl, Lockshin and Paget, 2002, pgs. 39-40). This is especially so in the small joints of the hands and feet, the hips, knees, elbows and shoulder. As the disease progresses more and more joints get affected. RA is a degenerative disease of the joints. It is more serious and debilitating than osteoarthritis. The symptoms include swollen, painful and stiff joints. These symptoms can occur at any stage even in young children, although they usually develop later in life. This disease causes inflammation of the synovial membrane and disruption of the cartilage surface of joints. As it progresses, the cartilage surface of the joint may be completely destroyed, causing friction, pain and immobility. Bones may even fuse together. The small bones of the hands and the feet are the most often involve, but it is common for the disease to progress to larger joints. RA is an autoimmune disease in which the body’s antibodies mistakenly attack one’s own tissues, causing their inflammation. Heredity may play a part, but it is still unclear (Mahendra, 2000, pg. 1392). Prevalence Rheumatoid arthritis is one of the common forms of athritis.among the inflammatory forms of arthritis it is the most common form in this group. It is a chronic disease. Its incidences or pravalence varies among racial and ethnic groups. However, it does not seem to correlate with the geogarphical area of where one lives (Lahita, 2001, pg. 4). More than two million people in the United States suffer from rheumatoid arthritis, that’s about 2 out of every 100 adults. Researchers do not believe that gender might play some role in how rheumatoid arthritis develops and progresses. However, rheumatoid arthritis affects nearly twice as many women than men, usually between the ages of 25 and 50, although any age including children can be affected. Lahita (2001, pg. 5), states that women are affected by rheumatoid arthritis three to four times more commonly than men. A major American study conducted in 1964 indicated that the prevalence was 3.8 percent among women and 1.3 percent among men. Researchers are trying to understand what role female hormones might play. Interestingly, women with arthritis usually go into remission, that is, a period of time where symptoms of a disease are not present, this usually happens especially when they are pregnant. Moreover, there is a tendency although not confirmed that women tend to develop rheumatoid arthritis in the year after pregnancy and the symptoms of rheumatoid arthritis can increase the year after giving birth (Matzko and Newman, 2007, pg. 26). Rheumatoid is not an inherited disease, although the genes that are responsible for rheumatoid arthritis can be inherited and they make or tend to make a person be more predisposed to develop it (Matzko and Newman, 2007, pg. 8). Signs and Symptoms The causes of RA are yet to be known. Signs and symptoms of rheumatoid arthritis include stiffness, fatigue, pain, limited joint motion, joint swelling and warm and red joints. People with rheumatoid arthritis experience a great deal of stiffness and difficulty moving, this is especially so, in the morning and after sitting for a long time. Joints may ache with nagging pain causing one to be uncomfortable. The disease can cause enough joint pain and damage which can make one unable to perform routine daily activities. A feeling of tiredness can also be overpowering (Matzko and Newman 2007, pg. 4). Rheumatoid arthritis can affect other parts of the body. There could be nodules or lumps that form around the joint areas, dry eyes and a dry mouth from certain inflammatory “fighting” cells that clog the saliva and tear ducts. There might also have inflamation of the lung tissues called pulmonary fibrosis, lumps in the lungs (pulmonary nodules) and fluid around the lungs (pleural effusion). Additionally, inflammtion of the sac that sorrounds the heart (pericarditis) may occur (Matzko and Newman, 200, pg. 6). Diagnosis Merely having the signs and symptoms of RA does not mean one has the disease. There is need to see a doctor for a true diagnosis. Blood tests can be used to help diagnose RA. Blood often shows mild anemia and increased platelet count. These symptoms are a result of the body’s reaction to inflammation. Other ways of diagnosis of RA is the anti-cyclic citrullinated peptide. Risk Factors Several risk factors for the development of RA have been suggested, the mains ones include increasing age, female sex, RF and anti CCP antibody positivity. Smoking has also been shown to increase the risk of disease severity and extra-articular disease. Management RA is the most common form of inflammatory arthritis in adults. Its prevalence and destructive potential exact a considerable toll from affected patients in terms of substantial morbidity, progressive disability and accelerated mortality. This has profound economic implications for the affected patients, their families and the society. Without effective treatment, the expected course of RA is one of progressive disability (Kavanaugh, Weinblatt and Cush, 2010, pg. 15). Comprehensive studies from diverse countries have consistently shown progressive work disability in patients with RA. A systematic review of the literature reveals a consistent relationship between disease duration and work disability (Verstappen, Bijlsma and Verkleij, 2004, pg. 15). Many studies have clearly shown that RA is a costly disease. The treatment of RA has changed considerably in the past decade, moving from a conservative approach designed to control clinical symptoms to a more progressive designed to limit joint destruction. The goals of treatment of RA are to reduce joint pains and swelling, relieve stiffness and prevent joint damage. This mainly involves using drugs such as methotrexate, leflunomide or Biologic response modifiers (BRMs). These are a class of drugs that inhibit proteins called cytokines which contribute to inflammation and joint damage in RA. The more recent treatment option is surgery which comprise of arthroscopic surgery and joint replacement surgery. Conclusion There is a great deal of research being undertaken on arthritis, most of these have predominantly focused on the study of the cells of the immune system that create inflammation. However, still a lot more needs to be known about RA. There is a need to research more on the role that genetic predisposition plays in RA. Weyand and Goronzy ( 2001, pg. 2) had claimed that the prevalence of the disease is increased in the first degree relatives of RA patients, with a sibling occurrence risk estated at between 2.8 and 12.1 percent, however, no actual evidence has been released to proove the familial aggregation of RA. Another aspect that needs research on is the causes and treatment of RA. Research conducted has been inconclusive about what is the real cause of RA and the treatment of RA mainly comprises of manageent steps as well as pain reduction pills. Clearly this demonstrates the scope of RA that is yet to be shed light on. The good news is that scientists are making rapid progress in understanding the complexities of rheumatoid arthritis: how and why it develops, why some people get it and others do not, why some people get it ore severely than others. Results fro research are having a positive impact today, enabling people with rheumatoid anthritis to remain active in life, family and work for longer than was possible several years ago. Cited Works Heymsfield, Steven B, et al. Human body composition. 2, illustrated, revised. Vol. 918. Illinois: Human Kinetics, 2005. Kavanaugh, Arthur , Michael E Weinblatt and John J Cush. Rheumatoid Arthritis: Early Diagnosis and Treatment. 3, revised. New York: Professional Communications, 2010. Lahita, Robert G. Rheumatoid Arthritis: Everything You Need to Know. New York: Penguin, 2001. Loebl, Suzanne , Michael Lockshin and Stephen A Paget. The hospital for special surgery rheumatoid arthritis handbook. illustrated. New York: John Wiley and Sons, 2002. Mahendra, Jain. "Human Musculoskeletal System." Competition Science Vision 3.34 (2000): 1383-1393. Matzko, Cynthia K and Eric D Newman. Rheumatoid Arthritis. illustrated. Ontario: PMPH-USA, 2007. Verstappen, S M, J W Bijlsma and H Verkleij. "Overview of Work Disability in Rheumatoid Arthritis Patients as Observed in Cross-sectional and Longitudinal Surveys." Arthritis Rheum 51 (2004): 488- 497. Weyand, Cornelia M and J J Goronzy. Rheumatoid arthritis. Vol. Volume 3 of Chemical Immunology. Karger Publishers, 2001. Wolfe, F, D M Mitchell and J T Siblety. "The Mortality of Rheumatoid Arthritis." Arthritis Rheum 37.4 (1994): 481-494. Read More