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NURS 6521N – Pathophysiological Mechanisms of Irritable Bowel Syndrome
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is a functional gastrointestinal (GI) disorder characterized by abdominal pain and altered bowel habits in the absence of a specific and unique organic pathology, although microscopic inflammation has been documented in some patients. Population-based studies estimate the prevalence of irritable bowel syndrome at 10-20% and the incidence of irritable bowel syndrome at 1%-2% per year (Lehrer, 2018).
Pathophysiology
Traditional theories regarding the pathophysiology of irritable bowel syndrome (IBS)Â may be visualized as a three-part complex of altered gastrointestinal (GI) motility, visceral hyperalgesia, and psychopathology (Chumpitazi & Shulman, 2016). More recently, it is believed that components of the gut microbiota potentially influence brain morphology and function, behavior, and cognition, which expands the paradigm of the gut-brain axis (Quigley, 2018).
Etiology
The causes of irritable bowel syndrome remain poorly defined, but they are being avidly researched. Abnormal transit profiles and an enhanced perception of normal motility may exist. Delayed colonic motility may be more common in patients with constipation-predominant irritable bowel syndrome than in healthy controls. Similarly, accelerated colonic transit may be more common in patients with diarrhea-predominant disease than in healthy controls. NURS 6521N – Pathophysiological Mechanisms of Irritable Bowel Syndrome. Infection with Giardia lamblia has been shown to lead to an increased prevalence of irritable bowel syndrome, as well as chronic fatigue syndrome. Intestinal permeability appears to be increased, especially in diarrhea-predominant irritable bowel syndrome (Lacey, 2015).
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.
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. NURS 6521N Advanced Pharmacology – IBD Prevalence. 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.
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.
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Assignment Requirements
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• 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.
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
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.