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Human Large Intestines- Inflammatory Bowel Disease

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Human large intestines

The large intestine is composed of the colon, cecum, appendix, rectum and the anal canal.  The main functions of the colon are the reabsorption of electrolytes and water and the removal of undigested food and waste. The cecum is a blind pouch which is positioned at the distal position to the ileocecal valve which has a histology that is similar to that of the colon. The appendix is a thin extension of the cecum that looks like a finger. The rectum is the enlarged distal portion of the large intestines. It has a histology that is similar to that of the colon although it is well-known by its transverse rectal folds found in its submucosa and the lack of tenia coli in its muscularis externa (Gasche et al, 2000).

The mucosa of the large intestines appears smooth due to lack of villi. Instead there are very many straight, tubular glands which extend as far as the muscular mucosae. The glands are lined with simpler columnar epithelium. The muscular externa is composed of an inner circular and outer longitudinal layer. The inner circular layer is distinctive, but the outer longitudinal layer of the colon is very slim save for three extremely thick longitudinal bands referred to as teniae coli (Vasiliauskas et al, 2000).

Inflammatory Bowel Disease

Inflammatory Bowel Disease is a tern used to describe two chronic diseases that result to inflammation of the intestines: ulcerative colitis and Crohn’s disease.

Ulcerative colitis is an inflammatory disease that affects the large intestines. In ulcerative colitis, the internal lining that is, the mucosa of the intestine is inflamed implying that the lining of the intestine wall gets red and swell and develops ulcers. Ulcerative colitis is regularly the most severe in the colon which can often cause diarrhea. Mucus and blood often found in the stool when the lining of the colon is damaged.

Crohn’s disease varies from ulcerative colitis in the in the particular areas it affects. It commonly affects the final part of the small intestine as well some parts of the large intestine. Crohn’s disease can attack both the small as well as the large intestines. Crohn’s disease leads to inflammation that progress much deeper into the layers of the intestinal wall.

Causes of inflammatory bowel disease

Several factors are associated with inflammatory bowel disease. Environment, diet and genetic could be some causes of the disease although the exact cause is not been determined. Current evidence shows that there is a possible genetic defect affects the manner in which the immune system operates and the way the inflammation is switched on and off in those individuals with inflammatory bowel disease due to unsuitable agents such bacteria, viruses or a protein food (Vasiliauskas et al, 2000).

Sighs and symptoms

The most regular symptoms of both ulcerative colitis and Crohn’s disease are diarrhea and pain in the abdomen. Diarrhea can either be severe or mild. If the diarrhea persists, then it can lead to dehydration, rapid heartbeat and a fall in blood pressure. Continued loss of significant loss of blood in the stool can result to anemia. At other times, people with inflammatory bowel disease may suffer from constipation.  Constipation due to Crohn’s disease results from a partial obstruction in the intestines which are described as stricture. In ulcerative colitis, constipation may be an indication of inflammation of the rectum- a condition referred to as proctitis. Due to loss of fluid as well as nutrients from diarrhea and severe inflammation of the bowel, individuals with inflammatory bowel may experience fever, exhaustion, weight loss, dryness and underfeeding. Pain normally results from the abdominal cramping which results from irritation of the nerves and muscles that control intestinal narrowing (Louis et al, 2001).

Diagnosis and treatment

Inflammatory bowel disease is difficult to diagnose since there are no clear symptoms. Once symptoms appear, they may be similar those of other conditions. The disease is normally diagnosed based on previous history. The doctor usually suggests certain tests to confirm the condition. In children the colon is tested using an instrument called endoscope (Louis et al, 2001).

The disease is treated using a method for alleviating the symptoms of both ulcerative colitis and Crohn’s disease. Great progress has been made in the development of medications for the disease. Some of the medications that may be prescribed are anti-inflammatory drugs to minimize the inflammation resulting from the disease or immunosuppressive agents to restrain the immune system (Louis et al, 2001).

Conclusion

Latest research findings

There has been latest research finding in regard to Inflammation bowel disease especially in relation to its treatment.  Depending on the intensity of severity, IBD may call for immunosuppression to control the symptom like prednisone, TNF inhibition, azathioprine, methotrexate or 6-mercaptopurine. Mesalamine has also been developed to control the symptoms of the disease. Steroids are now being used to control conditional flares after being accepted as maintenance drug. It is interesting that some forms of Inflammatory Bowel Disease result from overactive immune system attacking some tissues of the large intestines due to lack of traditional targets like parasites and worms (Ho et al, 2005).

Bibliography

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Gasche C, Scholmerich J, Brynskov J, et al. A simple classification of Crohn’s disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998. Inflamm Bowel Dis2000;6:8–15.

Brant SR, Panhuysen CI, Bailey-Wilson JE, et al. Linkage heterogeneity for the IBD1 locus in Crohn’s disease pedigrees by disease onset and severity. Gastroenterology2000;119:1483–90.

Rioux JD, Silverberg MS, Daly MJ, et al. Genomewide search in Canadian families with inflammatory bowel disease reveals two novel susceptibility loci. Am J Hum Genet2000;66:1863–70.

Russell RK, Drummond HE, Nimmo EE, et al. Genotype-phenotype analysis in childhood-onset Crohn’s disease: NOD2/CARD15 variants consistently predict phenotypic characteristics of severe disease. Inflamm Bowel Dis2005;11:955–64.

Vasiliauskas EA, Kam LY, Karp LC, et al. Marker antibody expression stratifies Crohn’s disease into immunologically homogeneous subgroups with distinct clinical characteristics. Gut2000;47:487–96.

Louis E, Collard A, Oger AF, et al. Behaviour of Crohn’s disease according to the Vienna classification: changing pattern over the course of the disease. Gut2001;49:777–82.

Abreu MT, Taylor KD, Lin YC, et al. Mutations in NOD2 are associated with fibrostenosing disease in patients with Crohn’s disease. Gastroenterology2002;123:679–88.

Ahmad T, Armuzzi A, Bunce M, et al. The molecular classification of the clinical manifestations of Crohn’s disease. Gastroenterology2002;122:854–66.

Mow WS, Vasiliauskas EA, Lin YC, et al. Association of antibody responses to microbial antigens and complications of small bowel Crohn’s disease. Gastroenterology2004;126:414–24.

Arnott ID, Landers CJ, Nimmo EJ, et al. Sero-reactivity to microbial components in Crohn’s disease is associated with disease severity and progression, but not NOD2/CARD15 genotype. Am J Gastroenterol2004;99:2376–84.

Ho GT, Nimmo ER, Tenesa A, et al. Allelic variations of the multidrug resistance gene determine susceptibility and disease behavior in ulcerative colitis. Gastroenterology2005;128:288–96.

Joossens S, Reinisch W, Vermeire S, et al. The value of serologic markers in indeterminate colitis: a prospective follow-up study. Gastroenterology2002;122:1242–7.

Langholz E, Munkholm P, Davidsen M, et al. Course of ulcerative colitis: analyses of changes in disease activity over years. Gastroenterology2004;107:3

Price AB. Overlap in the spectrum of non-specific inflammatory bowel disease—‘colitis indeterminate’. J Clin Pathol2000;31:567–77.

Targan SR, Landers CJ, Yang H, et al. Antibodies to CBir1 flagellin define a unique response that is associated independently with complicated Crohn’s disease. Gastroenterology2005;128:2020–8.

Economou M, Trikalinos TA, Loizou KT, et al. Differential effects of NOD2 variants on Crohn’s disease risk and phenotype in diverse populations: a metaanalysis. Am J Gastroenterol2004;99:2393–404.

Inoue N, Tamura K, Kinouchi Y, et al. Lack of common NOD2 variants in Japanese patients with Crohn’s disease. Gastroenterology2002;123:86–91.

Arnott ID, Nimmo ER, Drummond HE, et al. NOD2/CARD15, TLR4 and CD14 mutations in Scottish and Irish Crohn’s disease patients: evidence for genetic heterogeneity within Europe? Genes Immun2004;5:417–25.

Bairead E, Harmon DL, Curtis AM, et al. Association of NOD2 with Crohn’s disease in a homogenous Irish population. Eur J Hum Genet2003;11:237–44

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