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- QUESTION
RESPONSE TO JESSICA BANWELL PAPER ON INFLAMMATORY BOWEL DISEASE
Jessica Banwell
Initial Post - Week 8
COLLAPSE
Initial PostInflammatory Bowel Disease
Ulcerative colitis and Crohn disease are different types of inflammatory bowel disease (IBD) (Huether & McCance, 2014). IBD is differentiated from other types of bowel disorders by the exclusion of infectious process, episodes of mucopurulent bloody diarrhea, failure to respond to antibiotic treatment, and exacerbations followed by times of remission (Hammer & McPhee, 2014).
Ulcerative Colitis
Ulcerative colitis (UC) causes lesions to appear in the colon, most commonly in the sigmoid colon and rectum (Huether & McCance, 2014). The affected mucosa of the colon has increased blood flow, appears dark red, and is continuous in nature (Huether & McCance, 2014). Abscess formation occurs followed by edema and thickening of the muscularis mucosae; as the destruction of the colon occurs bleeding, cramping pain and diarrhea (Huether & McCance, 2014). Dehydration, weight loss, and anemia can be seen from loss of the absorptive surface of the intestinal mucosa and rapid colonic transit time which causes large numbers of watery stools (Hammer & McPhee, 2014). In people with UC, lymphocytes may have cytotoxic effects on epithelial cells in the colon which causes the associated lesions and symptoms (Huether & McCance, 2014). UC may be seen more often in patients with other autoimmune disorders (Huether & McCance, 2014).
Treatment. Treatment of UC depends on the severity of the disease (Huether & McCance, 2014). Treatments to suppress the inflammatory response are often helpful such as steroids and aminosalicylates (Huether & McCance, 2014). More aggressive treatment may include immunosuppressants may assist in inducing remission, however, due to the nature of the disease, it is often difficult to discern whether treatment or the natural progression of the disease has caused an episode of remission (Hammer & McPhee, 2014).
Crohn Disease
Chrohn Disease (CD) also causes inflammation of the colon but can affect both the large and small intestine (Huether & McCance, 2014). The inflammatory process is thought to be caused by increased levels of interferon-gamma and tumor necrosis factor (Huether & McCance, 2014). The inflammatory lesions in CD often affect the intestines in segments causing “skip lesions” to be seen (Huether & McCance, 2104). These lesions may cause fissures that can extend between loops of intestine, into the bladder, rectum or vagina (Huether & McCance, 2014). Symptoms of CD may be different based on the area of intestine involved; diarrhea, weight loss, rectal bleeding, and anemia caused by malabsorption of vitamin B12 (Huether & McCance, 2014).
Treatment. Treatment of CD is similar to that of UC. Smoking cessation is an important component to control CD and surgery may be needed to treat fistulas associated with the disease (Huether & McCance, 2014).
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is characterized by recurrent abdominal pain accompanied by either constipation, diarrhea or both (Huether & McCance, 2014). IBS is a complex disorder that is diagnosed with no other detectable pathological processes or structural abnormalities are found to cause symptoms (Hammer & McPhee, 2014). Several proposed pathophysiological mechanisms have been thought to be the cause of IBS including, abnormal gastrointestinal motility, overgrowth of intestinal flora, food allergy or food intolerance, or emotional stress (Huether & McCance, 2014).
Treatment. Treatment of IBS includes the use of laxatives or fiber, antidiarrheals, antidepressants, and analgesics (Huether & McCance, 2014). Alternative therapies that have shown to provide relief include probiotics, hypnosis, and acupuncture (Huether & McCance, 2014).
The Role of Genetics
Genetics have been shown to play a role in the development of both IBD and IBS. Recent studies have found that patients with IBD have abnormalities in several categories of genes, including genes that affect immune function, autophagy and epithelial function (Hammer & McPhee, 2014). However, only about 20-30% of persons with these genetic changes actually develop the disease (Hammer & McPhee, 2014). With regards to IBS, a specific gene has not been found to be associated with the condition, although recent studies suggest that genetics may play a role (Henstrom & D’Amanto, 2016). A Swedish survey with more than 50,000 participants was able to show an increased risk of IBS among first, second, and third-degree relatives; showing a genetic connection exists (Henstrom & D’Amanto, 2016).
Hammer, G.D. & McPhee, S.J. (2014). Pathophysiology of Disease: An Introduction to Clinical Medicine. (7th ed.). McGraw-Hill Education. New York, New York.
Henström, M. & D’Amato M. (2016). Genetics of irritable bowel syndrome. Molecular and Cellular Pediatrics. 3(7). doi: 10.1186/s40348-016-0038-6
Huether, S.E. & McCance, K.L. Understanding Pathophysiology. (5th ed.) Elsevier-Mosby. St. Louis, Missouri.
| Subject | Nursing | Pages | 6 | Style | APA |
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Answer
Response to Jessica Banwell Paper on Inflammatory Bowel Disease
Inflammatory Bowel Disease refers to a group of inflammatory conditions which affect the digestive system (Ananthakrishnan, 2015). Like you mentioned, Ulcerative Colitis and Crohn disease are types of IBD. They are just the more common ones however; there are other types. Did you know that approximately 1.6 million people in America suffer from IBD according to the Crohn’s & Colitis Foundation of America? In Europe at least 2.5 million suffer from IBD (Kaplan, 2015).
It is true that Crohn Disease may affect both the small and large intestines (Huether & McCance, 2014). However, it is important to note that it is more common in the small intestines particularly in the tail end. You also mentioned that “the inflammatory process is thought to be caused by increased levels of interferon-gamma and tumor necrosis factor” but I found that the exact course of inflammatory bowel disease is actually unknown and is attributed more to immunity and genetics.
Finally, while I agree with your discussion about the treatment of IBM I feel that you left out important information about the diagnosis of IBM. IBM can be diagnosed using a stool sample and a blood test, flexible sigmoidoscopy and colonoscopy, CT Scans and MRIs, and X-Rays. Each of these tests has its own pros and cons therefore the doctor will decide the best method to use in a particular case. Since IBM is linked to genetics (like you stated) the doctor will ask the patient questions about his/her family’s medical history. It is also important to note that despite the available medications and therapies, IBM cannot be cured. Treatment is only meant to help manage the inflammation.
References
Kaplan, G. G. (2015). The global burden of IBD: from 2015 to 2025. Nature reviews Gastroenterology & hepatology, 12(12), 720.
Ananthakrishnan, A. N. (2015). Epidemiology and risk factors for IBD. Nature reviews Gastroenterology & hepatology, 12(4), 205.
Huether, S.E. & McCance, K.L. (2014). Understanding Pathophysiology. (5th ed.) Elsevier-Mosby. St. Louis, Missouri.