NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease

NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease

NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease

• Identify the pathophysiological mechanisms of inflammatory bowel disease and irritable bowel syndrome. Think about similarities and differences between the disorders.
• Consider common treatments for inflammatory bowel disease and irritable bowel syndrome. Reflect on whether treatments for one disorder would work for the other disorder.
• Select one of the following patient factors: genetics, gender, ethnicity, age, or behavior. NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease. Reflect on how the factor you selected might impact the pathophysiology of and treatments for each disorder.

Solution – NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease

Inflammatory Bowel Disease

Inflammatory bowel disease is an idiopathic disease caused by dysregulated immune response to host intestinal microflora (Rowe, 2017).  The two major types of inflammatory bowel diseases are ulcerative colitis, which is limited to the colonic mucosa, and Crohn disease, which can affect any segment of the gastrointestinal tract from the mouth to the anus and is transmural.

Pathophysiology

The common end pathway of ulcerative colitis is inflammation of the mucosa of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss (Thoreson, 2007).  In several studies, genetic factors appeared to influence the risk of inflammatory bowel disease (IBD) by causing a disruption of epithelial barrier integrity, deficits in autophagy, deficiencies in innate pattern recognition receptors, and problems with lymphocyte differentiation, especially in Crohn disease (Tslanos, Katesanos, Tslanos, 2012).

Inflammatory mediators have been identified in IBD, and considerable evidence suggests that these mediators play an important role in the pathologic and clinical characteristics of these disorders. Cytokines, which are released by macrophages in response to various antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine effects. Cytokines differentiate lymphocytes into different types of T cells. Helper T cells, type 1 (Th-1), are associated principally with Crohn disease, whereas Th-2 cells are associated principally with ulcerative colitis. The immune response disrupts the intestinal mucosa and leads to a chronic inflammatory process (Lashner, 2009).

NURS 6521N Pathophysiological Mechanisms of Inflammatory Bowel Disease

Etiology

Three characteristics define the etiology of inflammatory bowel disease (IBD): (1) genetic predisposition; (2) an altered, dysregulated immune response; and (3) an altered response to gut microorganisms. However, the triggering event for the activation of the immune response in IBD has yet to be identified. Possible factors related to this event include a pathogenic organism or an inappropriate response (Lashner, 2009).

References:

Chumpitazi, BP, Shulman RJ. Underlying molecular and cellular mechanisms in childhood irritable bowel syndrome. Moi Cell Pediatri. 2016 Dec 3 (1):11.

Lacy BE. The science, evidence, and practice of dietary interventions in irritable bowel syndrome. Clinic Gastroenterology. 2015 Nov. 13(11):1899-906

Lashner B. Inflammatory bowel disease. Carey WD. Ed. Cleveland Clinic: Current Clinical Medicine- 2009. Philadelphia, PA: Saunders; 2009

Lehrer, J. (2018). Irritable Bowel Syndrome. Medscape. Retrieved October 15, 2018.
Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel disease; an overview. Surgical Clinic North America 2007 Jun 87(3):575-85

Tslanos EV, Katesanos KH, Tslanos VE. Role of genetics in the diagnosis and prognosis of Crohn’s disease. World J Gastroenterology 2012 Jan 14. 18(2): 105-18

Quigley, EMM. The gut-brain axis and the microbiome: clues to pathophysiology and opportunities for novel management strategies in irritable bowel syndrome (IBS). J Cin Med. 2018 Jan 3. 7(1)

Schirbel A, Fiocchi C. Inflammatory bowel disease: Established and evolving considerations on its etiopathogenesis and therapy. J Dig Dis. 2010;11(5):266–276.

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NURS 6521N Advanced Pharmacology – IBD Prevalence

IBD is most common among people of Northern European and Anglo-Saxon origin and is 2 to 4 times more common among Ashkenazi Jews than non-Jewish whites from the same geographic location. The incidence is lower in central and southern Europe and lower still in South America, Asia, and Africa. However, the incidence is increasing among blacks and Latin Americans living in North America. Both sexes are equally affected. First-degree relatives of patients with IBD have a 4- to 20-fold increased risk; their absolute risk may be as high as 7%. Familial tendency is much higher in Crohn disease than in UC. Several gene mutations conferring a higher risk of Crohn disease (and some possibly related to UC) have been identified.

Cigarette smoking seems to contribute to development or exacerbation of Crohn disease but decreases risk of UC. Appendectomy done to treat appendicitis also appears to lower the risk of UC. NSAIDs may exacerbate IBD. Oral contraceptives may increase the risk of Crohn disease. Some data suggest that perinatal illness and the use of antibiotics in childhood may be associated with an increased risk of IBD.

For unclear reasons, people who have a higher socioeconomic status may have an increased risk of Crohn disease.

There is a genetic predisposition for IBD, and patients with this condition are more prone to the development of malignancy.

Assignment Details – NURS 6521N Advanced Pharmacology – IBD Prevalence

For this Assignment, you are going to write a paper explaining how you developed your theory through the four stages (theorizing, syntax, theory testing, and evaluation). Your paper must be 3 to 5 pages, not including the title and reference pages.

To view the Grading Rubric for this Assignment, please visit the Grading Rubrics section of the Course Resources.

Assignment Requirements

Before finalizing your work, you should:

• Minimum requirement of at least 5 sources of support
• be sure to read the Assignment description carefully (as displayed above);
• consult the Grading Rubric (under the Course Resources) to make sure you have included everything necessary; and
• utilize spelling and grammar check to minimize errors.

NURS 6521N Advanced Pharmacology – IBD and IBS Differences

Although both ulcerative colitis and Crohn disease have distinct pathologic findings, approximately 10%-15% of patients cannot be classified definitively into either type; in such patients, the disease is labeled as indeterminate colitis. Systemic symptoms are common in IBD and include fever, sweats, malaise, and arthralgias.

The rectum is always involved in ulcerative colitis, and the disease primarily involves continuous lesions of the mucosa and the submucosa. Both ulcerative colitis and Crohn disease usually have waxing and waning intensity and severity. When the patient is symptomatic due to active inflammation, the disease is considered to be in an active stage (the patient is having a flare of the IBD). (See Presentation.)

In many cases, symptoms correspond well to the degree of inflammation present for either disease, although this is not universally true. In some patients, objective evidence linking active disease to ongoing inflammation should be sought before administering medications with significant adverse effects (see Medication), because patients with IBD can have other reasons for their gastrointestinal symptoms unrelated to their IBD, including coexisting irritable bowel syndrome (IBS), celiac disease, or other confounding diagnoses, such as nonsteroidal anti-inflammatory drug (NSAID) effects and ischemic or infectious colitis.

Although ulcerative colitis and Crohn disease have significant differences, many, but not all, of the treatments available for one condition are also effective for the other. Surgical intervention for ulcerative colitis is curative for colonic disease and potential colonic malignancy, but it is not curative for Crohn disease.

NURS 6521N Advanced Pharmacology – IBD and IBS Differences

References:

Chumpitazi, BP, Shulman RJ. Underlying molecular and cellular mechanisms in childhood irritable bowel syndrome. Moi Cell Pediatri. 2016 Dec 3 (1):11.

Lacy BE. The science, evidence, and practice of dietary interventions in irritable bowel syndrome. Clinic Gastroenterology. 2015 Nov. 13(11):1899-906

Lashner B. Inflammatory bowel disease. Carey WD. Ed. Cleveland Clinic: Current Clinical Medicine- 2009. Philadelphia, PA: Saunders; 2009

Lehrer, J. (2018). Irritable Bowel Syndrome. Medscape. Retrieved October 15, 2018.

Thoreson R, Cullen JJ. Pathophysiology of inflammatory bowel disease; an overview. Surgical Clinic North America 2007 Jun 87(3):575-85

Tslanos EV, Katesanos KH, Tslanos VE. Role of genetics in the diagnosis and prognosis of Crohn’s disease.  World J Gastroenterology 2012 Jan 14. 18(2): 105-18

Quigley, EMM. The gut-brain axis and the microbiome: clues to pathophysiology and opportunities for novel management strategies in irritable bowel syndrome (IBS). J Cin Med. 2018 Jan 3. 7(1)

Schirbel A, Fiocchi C. Inflammatory bowel disease: Established and evolving considerations on its etiopathogenesis and therapy. J Dig Dis. 2010;11(5):266–276.

Kindly Order Now for a complete and more resourceful answer.

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