Multiple Sclerosis and Crohns Disease - Term Paper Example

MULTIPLE SCLEROSIS AND CROHN’S DISEASE MULTIPLE SCLEROSIS 1. Normal structure and function of the tissues involved in this disorder Multiple sclerosis is an autoimmune disorder in which the immune system of the body produces antibodies that act against the myelin sheath. This causes inflammation of the myelin sheath as well as its destruction (Cichoke, 1999, p. 27). Myelin is a fatty material that offers cover and protection to the nerve fibbers. Thus, when a scar tissue (referred to as sclera) develops on the myelin, it hinders nerve communication. As such, this distorts messages that are transmitted to and from the brain, and may as well impair sight, speech or movement. Multiple sclerosis is usually chronic and sometimes progressive, featured by one or multiple areas of inflammation as well as scarring of the myelin sheath (Cichoke, 1999, p. 28). Although it is commonly perceived that multiple sclerosis occurs when a scar tissue develops on the myelin sheath, it is not exactly known why this happens. It is highly likely that the condition occurs due to an autoimmune reaction, but again, is not understood why this happens (Cohen & Rudick 2003, p. 541). Under normal conditions, the myelin sheath is essential for the normal working of the nerves. This is includes delivery of oxygen to body sites where it is required. However, with an inflammation occurring due to multiple sclerosis, the affected area becomes depleted of oxygen, thus limiting the capability to reduce further inflammation and inhibit further plaque or scar formation (Kesselring, 1997, p.15). 2. Pathogenesis of the disease/dysfunction Multiple sclerosis has been identified to develop when self reacting T-cells in combination with monocytes facilitate inflammation of the nervous system’s white matter as well as demyelination of the axons. The disease is clinically categorized either as primary progressive multiple sclerosis (PPMS) or relapsing-remitting multiple sclerosis (RRMS) that can further develop into the more advanced secondary progressive multiple sclerosis (SPMS) (Cohen & Rudick 2003, p. 541). The disease is widely believed to arise in genetically vulnerable hosts, when common microbes that have protein sequences that are cross-reactive with myelin-based antigens trigger antigen presenting cells or APCs in blood. The activated APCs stimulate myelin-reactive Th1 cells in the circulation. It has been observed that immunoregulatory defects such as low activity levels of the regulatory T-cells (that is Th2, Tr1 and Th3) in patients suffering from multiple sclerosis allow the myelin-reactive cells to extravasate, move through the brain barriers, and finally end up in the central nervous system. Within the central nervous system, the myelin-reactive cells interact with localized APCs referred to as microglia, resulting in the secretion of inflammatory cytokines such as TNFalpha, IFNgamma, and IL-2. These cytokines are understood to instigate the inflammatory cascade (Columbus, 2004). It is believed that viruses are involved in the myelin disturbance as a result of multiple sclerosis. Some types of viruses can remain dormant for many years in an organism after a bout of measles or other viral infection. This causes multiple sclerosis months to even years after the viral infection has disappeared. The blood serum of patients suffering from multiple sclerosis contains higher levels of circulating immune complexes in comparison to that of healthy individuals. This serves as proof of the autoimmune nature of the multiple sclerosis. It is also possible that predisposing factors such as selenium deficiency, genetic predisposition, viruses, and fat imbalance lead to a failure of the immune system, resulting in an uncontrolled reaction against the body (Porth, 2007, p. 281; Cichoke, 1999, p.28). 3. Signs and symptoms of multiple sclerosis and how they relate to the pathophysiology The common initial signs and symptoms of multiple sclerosis include difficulty in walking, abnormal feelings such as numbness, loss of vision as a result of optic neuritis, and pain. There are also less common initial symptoms of the disease including tremor, incoordination, slurred speech or other speech disabilities, and a decline in cognitive function, characterized by inability to think, remember and reason (Columbus, 2004, p.157). Due to the nature of the various signs and symptoms, they are categorized in various categorized into various categories i.e. primary, secondary and tertiary symptoms. This depends on the nature the condition. Primary symptoms occur as a result of demyelination, i.e. the obliteration of the fatty myelin sheath that insulates or surrounds the nerve fibres of the central nervous system. The effect hampers transmission of nerve impulses from the brain to muscles as well as other organs. This is reflected through numbness, weakness, tremor, paralysis, loss of vision, loss of balance, and dysfunction of the kidney and bowel as a result of poor coordination between the brain and the various organs (Kesselring, 1997, p.15). Secondary symptoms are the disorders that occur due to the primary symptoms. For instance, dysfunction of the bladder can lead to recurring urinary tract infections. In addition, inactivity may result in weakness due disuse of the muscle (though not related to demyelination). Inactivity also causes poor trunk control and postural alignment and muscle imbalances (i.e. stretch weakness and /or adaptive shortening). There also occurs decreased bone density due to poor build up of tissues, and shallow, ineffective breathing. Tertiary symptoms are associated with both primary and secondary symptoms (Kesselring, 1997, p.17). As a person becomes weak due to severe inflammation, he or she loses the drive to livelihood and social life. The strain of dealing with multiple sclerosis may lead to depression. 4. Contributing causes/risk factors and how they might lead to the disease It is not known exactly what causes multiple sclerosis but most researchers are of the opinion that the disease is caused by the immune system acting against the body. In particular, the T-cells attack cells in the spinal cord and brain, thus damaging the myelin sheath. The damage caused affects how well nerves function (Columbus, 2004, p.158). It has been observed that multiple sclerosis affects women about twice as frequently as it occurs in men. Moreover, it has been established that the disease affects Caucasians about twice as it is likely to affect Hispanics or African-Americans. Its prevalence is about 20 times lower among the Inuit people of Canada and it is also rare in the native people of North America, Australian Aboriginal people and the Maori of New Zealand; and among people of Asian descent (Holland, Murray & Reingold, 2007, p. 28). These differences show that the disease has a link to genetic composition. The disease occurs more frequently in people living in temperate climates such as the United States, Europe and Canada than in people living in the tropics. Nevertheless, even though the disease is known to occur more frequently in temperate regions, no particular link has been established between it and the environment (Goldberg, Trivieri, Anderson, 2002, p.34). There are many other risk factors part from the environment. Dietary and nutritional disorders, toxins, allergies, stress and other infections are known to contribute significantly to the worsening of the multiple sclerosis condition. As such, demyelination can be treated as a factor of secondary importance. It is also likely that multiple sclerosis is frequent in western countries such as the United States because people consume large amount of meat, processed foods and dairy products. All these foods are low in essential fatty acids. On the other hand, the disease is less common in countries where diets are in unsaturated fats such as olive oil, seed oils, fresh fruits, oily fish and vegetables (Goldberg, Trivieri, Anderson, 2002, p.23). These foods have high essential fatty acid content. It has also been noted that a predominantly meat versus vegetarian diet is a likely risk factor. This analysis shows that foods that have high saturated fat content can raise one’s susceptibility to multiple sclerosis. 5. Treatment of the condition and its complications Treatment of multiple sclerosis is achieved through approaches grouped under the following categories: Managing the cute attack Treating the underlying disease Managing the various symptoms Use intervention programmes related to emotional and social issues (this is fundamentally suited to the tertiary symptoms of the disease) (Holland, Murray & Reingold, 2007, p. 28). When a change occurs in symptoms over some days or weeks, leading to development of new signs or worsening of the initial condition, this may be an indication of a new attack of the disease. It indicates that new inflammation and demyelination are occurring. Such needs to be reversed by use of high dose intravenous steroids such as methylprednisolone that hinders further inflammation (Cook, 2006, p.448). Conditions such as dizziness, numbness in a limb, or other symptoms need to be observed as the first treatment is given. Attacks that have been slowed down by the initial treatment should be allowed to clear on their own under the observation of a neurologist. In addition treatment is given on an individual basis since some steroids are known to cause cataracts and osteoporosis if applied for a long time. Some conditions are serious and need specialized intervention. Such include avascular necrosis of the hip, which may require hip replacement because the hip tissues are severely damaged (Holland, Murray & Reingold, 2007, p. 29). Hip replacement thus replenishes the tissues. Tertiary interventions such as counselling provide patients with emotional support that enables them to deal with the condition as other forms of treatment are applied (Holland, Murray & Reingold, 2007, p. 29). CROHN’S DISEASE 1. Normal structure and function of the tissues involved in this disorder Crohn’s disease is a chronic inflammatory condition of the intestines. Its symptoms include diarrhoea and abdominal pain that is caused by inflammation of the terminal ileum (small intestines) but is also observed in the colon (large intestines). The intestinal epithelium comprises a single layer of epithelial cells that line the gastrointestinal tract. During normal functioning, intestinal epithelium plays conflicting functions; one being a major role in digestion and absorption of nutrients. At the same time, the lining plays a role in limiting the uncontrolled uptake of nutrients from the lumen of the digestive tract (Johnson, 2006, p. 1917). Being in constant contact with the luminal contents and various immune cells, the epithelium plays an important role in being a barrier between the body proper of the organism and the external environment. The epithelium also prevents excessive passage of antigens or other toxic substances that may cause inflammatory response. Crohn’s disease causes inflammatory cells such as neutrophils lymphocytes and macrophages that produce cytokines which damage the intestinal mucosa (Kierszenbaum, 2002). The initial damage of the intestinal mucosa involves infiltration of neutrophils into the crypts of Lieberkuhn. This process results in the damage of intestinal glands due to the formation of crypt abscesses and the progressive ulceration and atrophy of the mucosa. Inflammation of the mucosa occurs as the lymphocytes accumulate into aggregates of cells that are also referred to as granulomas, a typical feature of Crohn’s disease (Kierszenbaum, 2002, p. 437). 2. Pathogenesis of the disease/dysfunction Crohn’s disease is an inflammatory condition which, in about 60 percent of reported cases, shows a granulomatous orientation. The gut wall becomes unable to control its immune response, resulting in inflammation (Marshall Cavendish Corporation, 2007, p.57). In regard to the sites affected by the disease, it is confers the following features: It can occur anywhere in the gastrointestinal tract i.e. from the mouth to the anus. The lesions caused as a result of the disease are characteristically discontinuous, with segments of unaffected bowel between affected areas. It involves the entire thickness of the gut wall i.e. the inflammation is considered transmural in distribution. The disease may involve sites outside the gut, including the skin, vulva, bone, joints, and particularly round ileostomy or colostomy. The clear cause of Crohn’s disease is still unknown, but a theoretical model can be used to construct a number of rubrics, such as: An exogenous injurious agent, for instance a microorganism. Genetic factors that might modify the host’s response to injury arising from the microorganism. Environmental factors, especially those related to lifestyle, which contribute to the host response. Nature of the response, in particular the inflammatory response to immune-mediated mechanisms. There many possible infectious agents that can be linked to Crohn’s disease. These are discussed below. Mycobacteria Mycobacteria can be linked to the granulomatous response in about two thirds of Crohn’s disease cases. Mycobacterial species such as Mycobacterium kansasii, M. paratuberculosis and M. avium intracellulare are particularly identified with this (Prantera & Korelitz, 1996, p.12). Other pathogens Ultrafiltrates of affected gut have been noted to cause granulomatous inflammation when infused into small animals and also have a cytopathic impact on cultured mucosal epithelial cells. There is however no evidence that the ultrafiltrates exacerbate the Crohn’s condition. Genetic factors It has been observed that Crohn’s disease may be conferred by the existence of a recessive gene with partial penetrance. Since the disease is usually noted in families with patients Crohn’s disease and ulcerative colitis, there is a likelihood that it is linked to genes (Marshall Cavendish Corporation, 2007, p.58). Additional exogenous factors Research studies have indicated that cigarette smoking doubles the risk of Crohn’s disease irrespective of dose (Woolf, 1998). 3. Signs and symptoms of Crohn’s disease and how they relate to the pathophysiology The symptoms of Crohn’s disease include loss of appetite, abdominal pain, diarrhoea, emaciation, rectal pain, fever, and bleeding (in about 80 percent of reported cases). This paper will describe some to the symptoms and their causes. Diarrhoea occurs when Crohn’s disease patients experience frequent watery or loose bowel movements. In addition, the stool is infrequently accompanied by thick dark blood. This blood results from a bleeding haemorrhoid. However, there occurs less pus or mucus for Crohn’s disease in comparison to ulcerative colitis (Roach & Zorko, 2005). Pain is associated with crampy or achy or sensation in the affected area. In many patients, the pain is felt on the lower right position of the abdomen and below the bellybutton. This occurs because many cases of Crohn’s disease are associated with terminal ileum as mentioned earlier. The kind of pain felt due to Crohn’s disease depends on the part of the gastrointestinal tract that is affected. The terminal ileum area is usually associated with sharp pain while the colon experiences crampy pain (Marshall Cavendish Corporation, 2007, p. 58). Fever is one of the key features of inflammation due to Crohn’s disease. As the tissues undergo atrophy, affected individuals suffer a high fever and this is particularly worse during the acute stage of a flare-up. Some fevers occur at night and are therefore associated with night sweats (Woolf, 1998, p. 13). 4. Contributing causes/risk factors and how they might lead to the disease According to Balch (2002), there is no known cause of Crohn’s disease. However, because the disorder has been commonly since the 1950s, there is a belief among researchers that it is linked to the use of antibiotics. The disease occurs when the bacteria that reside in the intestines are partially, but not completely, wiped out. The other bacteria, which are normally friendly, produce toxins as a self-defence mechanism, which causes ulceration and inflammation. Crohn’s disease has also been associated with food allergies (Balch, 2002). Research on the relationship between Crohn’s disease and the environment has established that some environmental factors cause relapses of episodes of the disease. The disease occurs primarily in people living in the western world, and could therefore be linked to the type of diets in these countries. However no direct link has been established. Apart from where one lives, the other risk factors that have been identified include ethnicity, family history, cigarette smoking and use of isotretinoin. As mentioned earlier, the disease considered heritable, and 1 in 5 Crohn’s disease patients has a family member with the disease (Michetti, 2005). Cigarette smoking is the most significant controllable risk factor associated with Crohn’s disease. It has been observed that smoking lead to severity of the disease and a danger of surgery. Isotretinoin or Accutane is a strong medication that is sometimes used to treat acne that does not respond to other types of treatment (scarring cystic acne). Its use has been linked to Crohn’s disease although not substantially proved (Michetti, 2005). 6. Treatment of the condition and its complications Many drugs have been developed for short term and long term treatment of Crohn’s disease. However, only a limited number have been studied meticulously in wide groups of patients showing similar symptoms of the disease. The widely used drugs include 5-ASA compounds; antibiotics such as metronidazole and ciprofloxacine; corticosteroids such as budesonide and prednisone and their equivalents; thiopurine (such as azathiopurine and 6-mercaptopurine); methotrexate; tacrolimus; cyclosporine; and mycophenolate mofetil (Michetti, 2005). Anti-inflammation drugs such as 5-ASA function by significantly suppressing inflammation. Corticosteroids are very effective at the onset of the disease. They function in regulating hormonal balance thus reducing instances of conditions such as inflammatory bowel disorder that are key features of Crohn’s disease (Kierszenbaum, 2002). Immune system suppressors such as 6-mercaptopurine work by suppressing the immune system such that the body does not attack itself. They have also been noted to improve the effectiveness of corticosteroids in preventing inflammation of the gastrointestinal tract (Kierszenbaum, 2002, p. 437). Nutritional therapy is also phenomenal in dealing with Crohn’s disease. There are nutritional supplements for children whose growth has been slowed by the disease. As well, some patients may need intravenous supplements to replenish inflamed tissues (Michetti, 2005). Such treatment is appropriate for patients whose patients are severely damaged that they cannot absorb nutrients and those who need to rest. However, there are no foods specifically known to cause Crohn’s disease. References Balch, P.A. (2002). Prescription for Herbal Healing. New York: Avery. Cichoke, A.J. (1999). The Complete Book of Enzyme Therapy. London: Avery Cohen, J. A. & Rudick, R.A. (2003). Multiple Sclerosis Therapeutics. New York: Informa Health Care. Columbus, F. H. (2004). Treatment and Management of Multiple Sclerosis. New York: Nova Publishers. 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Philadelphia: Lippincott Williams & Wilkins. Prantera, C & Korelitz, B.I. (1996). Crohn's Disease. New York: Informa Health Care. Roach, S. S. & Zorko, J. (2005). Study Guide for Pharmacology for Health Professionals. Philadelphia: Lippincott Williams & Wilkins. Woolf, N. (1998). Pathology: Basic and Systemic. Sydney: Elsevier Health Sciences. Read More