NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays

NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays
Pathophysiology of Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a term given to chronic and recurring conditions that affect the gastrointestinal tract (Centers for Disease Control & Prevention (CDC), 2017). Irritable bowel syndrome (IBS) is a condition that affects the movement of the intestine (CDC, 2017). Ulcerative colitis and Crohn’s disease are the two most common IBD. In ulcerative colitis lesions are mostly contained in the large intestine especially on the left side. With ulcerative colitis, the crypt of Lieberkuhn in the large bowel becomes infiltrated with T cells that damage the epithelium.  Immunoglublin E and G, along with B cells and plasma cells increase at the site of inflammation and goblet cells release mucus (Basson, 2017). Ulceration occurs in the mucosa with rare narrowing of the lumen of the large intestine; polyps form throughout the large intestine (Dudley-Brown & Huether, 2012).  Crohn disease lesions may range from the mouth to the anus called skip lesions. The inflammation of Crohn disease is thought to be triggered by cell-mediated response and increased levels of interferon-gamma and tumor necrosis factor alpha.    In IBD, Crohn disease, the increase in interferon-gamma and tumor necrosis factor-alpha, along with stimulation of Th1 cells, produces inflammation throughout the small and large intestine mucosa and serosa layers. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays. Injury to bowel tissue occurs as neutrophils and macrophages infiltrate the site of inflammation.  Granuloma ulcerations occur in some areas of the bowel and skip other areas (Dudley-Brown & Huether, 2012).
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Pathophysiology of Irritable Bowel Syndrome
Irritable bowel syndrome is a functional gastrointestinal bowel disorder causing increased contractions of the colon.  IBS is diagnosed by characteristic cluster of symptoms without detectable structural abnormalities. The pathophysiology of IBS is complex and involves a number of factors.  Hypersensitivity to pain in the visceral gut occurs by either malfunctioning of the central nervous system or receptors in the wall of the gut; known as the brain-gut axis.  Malfunction of the brain-gut axis can increase gastrointestinal motility causing diarrhea or decease gastrointestinal motility causing constipation.  A decreased transit time is, also, associated with normal intestinal flora overgrowth.  Individuals with IBS have minimal intestinal inflammation, permeability alterations, and decreased immune response in the gut.  Intolerance or allergy to certain foods stimulate an immune response in the mucosa, change the normal gut flora and increase visceral hypersensitivity.  Furthermore, changes in the brain-gut axis and pain perception increase with psychosocial issues such as stress (Dudley-Brown & Huether, 2012).
 
Similarities/Differences with Inflammatory Bowel Disorder and Irritable Bowel Syndrome
Similarities and differences between IBS and IBD can be addressed by the interactions of the gut immune system and the central nervous system. Both inflammatory bowel diseases (IBD) and irritable bowel syndrome (IBS) have similar symptoms of altered bowel patterns associated with abdominal pain or discomfort. Both diseases share pathophysiologic mechanisms include altered mucosal permeability; the mucosal immune system alters the interaction of luminal flora, mucosal immune triggering, gut motility alterations, and severe, prolonged life stressors in symptom alteration.  IBD is characterized by inflammation or ulcerations in the small or large intestine; thus these changes are not linked with IBS. Classic signs and symptoms of the inflammatory process in the gastrointestinal tract are diarrhea, rectal bleeding, weight loss, and fever, sometimes related with extra intestinal signs.  Usually, abdominal pain is not the most obvious symptom in IBD, whereas, the main symptom in IBS is abdominal pain.  Unlike IBS, the cause of IBD is caused by genetic predisposition, environmental factors, infectious agents, altered gut epithelial permeability, and impaired immune responses. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays.
Treatments for Inflammatory Bowel Disorder and Irritable Bowel Syndrome
Diagnosis and treatment of Irritable Bowel Disease is based on clinical presentation, history, physical and exclusion of other causes of symptoms (Huether & McCance, 2017). To rule out other causes of the symptoms, endoscopies, CT scans, blood tests, abdominal ultrasounds and tests to rule out illnesses such as lactose intolerance and celiac disease could be done (Huether & McCance, 2017). The patient is diagnosed using the Rome III criteria which basically says that the patient has abdominal pain or discomfort for at least 3 days per month for the past 3 months with at least two incidences if improvement with bowel movement, change in frequency of stool or change in appearance of stool (Huether & McCance, 2017). Mesalamine products are often prescribed; steroids and aminosalicylates are used to suppress the inflammatory response and help to alleviate cramping pain. Immunosuppressants and immunomodulatory agents may induce and maintain remission. For severe cases, hospital admission for the administration of intravenous fluids and steroids may be needed. Surgical intervention to manage complications may also be necessary. There is no cure for IBS and the treatment is not specific, but based on each patient symptoms and is often started with incorporation of fiber in the diet. Laxatives, anti-diarrheals, antispasmodics and analgesics are often a part of the treatment plan (Huether & McCance, 2017). Evaluations for food allergies, parasites, and bacterial infections are also performed. Alternative therapies may include: probiotics, hypnosis, acupuncture, and psychotherapy. The treatment of IBD and IBS are very different and cannot be used interchangeably.
 
Genetics Impact on Inflammatory Bowel Disorder and Irritable Bowel Syndrome
There is a strong genetic factor with IBD with a positive family history. UC is more predominate in the white population and is associated with other auto immune disorders. CD includes genetic factor with positive family history and altered immune responses (Huether & McCance, 2017). According to McPhee & Hammer (2014), “a combination of genetic risk and environmental factors are recognized key elements in the pathogenesis of inflammatory bowel disease. There are many newly recognizable genes that are susceptible for both Crohn’s disease and ulcerative colitis. It is postulated that the stigma associated with IBS led to relatives not sharing information with others, resulting in underestimates of familial aggregation of IBS (Saito, et al., 2008).  An estimated 33 percent of individuals with IBS have a positive family history of the disorder (p. 790).  A positive family history of any of these disorders can alarm the examining practitioner and can lead to early diagnosis and treatment.
References
Basson, M. (2017). Ulcerative colitis. Retrieved from http://emedicine.medscape.com/ article/183084-overview# aw2aab6b2b4aa.
Centers for Disease Control and Prevention. (2017). Inflammatory bowel disease. Retrieved from www.cdc.gov/ibd/
 
Dudley-Brown, S. & Huether, S. (2012). Alterations of digestive function. In S.J. Huether & K.L. McCance (Eds.). Understanding pathophysiology (5th ed, p. 894-937). St. Louis, MO: Mosby.
Heitkemper, M., Kohen, R., Jun, S., & Jarrett, M. (2011). Genetics and gastrointestinal symptoms. Annual Review Of Nursing Research, 29261-280. doi:10.1891/0739-6686.29.261
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Saito, Y., Zimmerman, J., Harmsen, W., De Andrade, M., Locke, G., Petersen, G., & Talley, N. (2008). Irritable bowel syndrome aggregates strongly in families: a family-based case-control study. Neurogastroenterology And Motility, 20, 790-797. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays.
 
Pathophysiology of Inflammatory Bowel Disease (IBD) and Irritable Bowel Syndrome (IBS)
WEEK 8 DISCUSSION
As we know all know, our gastrointestinal tract which extends from the mouth to anus is a hallow organ (Huether &Re McCance, 2017, p. 906).  Sometimes, it may often be challenging to come up with a diagnosis of irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) due to the presence of overlapping mechanism which still makes both as separate conditions. IBD is divided into two types of condition namely ulcerative colitis and Crohn disease. NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays. According to rectum (Dudley-Brown and Huether, ulcerative colitis is a chronic inflammatory disease that causes an ulceration of the colon and rectum. It is characterized with a period of remission followed with relapse.  According to (Hammer & McPhee, 2014, p. 372).  It is unknown what triggers inflammatory bowel disease. Ulcerative colitis is superficial and most likely developed in the colonic mucosa While crohn diseases granulomatous and is located throughout the gastrointestinal tract (Hammer & McPhee, 2014). Patient with crohn disease may exhibit symptoms such as diarrhea, rectal bleeding, weight loss and abdominal pain along with vitamin b12 and vitamin D malabsorption, while those patients with ulcerative colitis may present with fever, tachycardia, dehydration, weight loss, bleeding and inflammation (Huether & McCance, 2017).
Pathophysiology of IBD
(Huether & McCance, 2017).
Pathophysiological Mechanisms of Inflammatory Bowel Disorder and Irritable Bowel Syndrome
It is unclear what the triggers are for inflammatory bowel disease (IBD), but what we do know is that there are two forms; Crohn disease and ulcerative colitis (Hammer & McPhee, 2014, p. 372).  Crohn disease (CD) is transmural and granulomatous which can be found throughout the GI track, whereas ulcerative colitis (UC) is superficial and limited to the colonic mucosa (Hammer & McPhee, 2014).  CD symptoms include diarrhea, rectal bleeding, weight loss and abdominal pain along with vitamin b12 and vitamin D malabsorption (Huether & McCance, 2017).  In UC a patient may experience fever, tachycardia, dehydration, weight loss, bleeding and inflammation (Huether & McCance, 2017) NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays.
Pathophysiology of IBD
            There are two forms of IBD.  Crohn disease “is transmural and granulomatous in character, occurring anywhere along the GI tract while ulcerative colitis is superficial and limited to the colonic mucosa” (Hammer & McPhee, 2014, p. 372).  Under normal circumstances, the intestine is able to control mucosal epithelieum inflammatory responses to dietary and microbial antigens.  In IBD, this process is defective, resulting in uncontrolled inflammation.  Common symptoms for both CD and UC are diarrhea and abdominal pain though it is important to note that constipation may associated with UC.  The diarrhea can be quite severe, resulting in dehydration, malnutrition, and weight loss.  Diarrheal blood loss can result in anemia.
 
Pathophysiology of Inflammatory Bowel Disease (IBD) and Irritable Bowel Syndrome (IBS)
IBD is categorized into two sections: ulcerative colitis and Crohn disease. Ulcerative colitis is a chronic inflammatory disease that causes an ulceration of the colon and rectum (Dudley-Brown and Huether, 2017). Ulcerative colitis is characterized by remition and relapse. According to Stratton (2017), ulcerative colitis results from aberrant immune response to gut luminal antigen in a genetically susceptible individual. Phagocyte’s response to gut flora and secretion of proinflammatory cytokines activates the T cells, causing mucosal inflammation and damage NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays. It is also believed that an abnormal or deficient interleukin (IL)-25 that controls some T helper cell responses is involved in the mechanism of ulcerative colitis. In Crohn disease, the inflammation results from the activation of cell-mediated responses, elevated interferon-gamma, and tumor necrosis factor-alpha. The inflammation originates from the intestinal submucosa and proliferates to the mucosa and serosa. The inflammation and tissue injury seen in this disorder is associated with the activation of neutrophils and marcophages (Dudley-Brown and Huether, 2017) NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays.
 
References
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Dudley-Brown, S., & Huether, S. E. (2017). Alterations of digestive function. In Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby NURS 6501 – Pathophysiology of Inflammatory Bowel Disease sample essays
 

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