UNIT 12
Alterations in Gastrointestinal Function
Originally developed by:
Anne Mueller RN, MN
Revised (1993) by:
Dot Hughes RN, MSc, PhD
Revised (2000) by:
May Chow RN, MN
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 14 Alterations in Gastrointestinal Function1
Unit 12 Table of Contents
Overview
Aim
Objectives
Resources
Web Links
Section 1: Inflammatory Bowel Disease
Introduction
Pathophysiology
Clinical Manifestations
Evaluation and Treatment
Learning Activity #1
Section 2: Peptic Ulcer Disease
Introduction
Pathophysiology
Clinical Manifestations
Evaluation and Management
Learning Activity #2
Final Thoughts
References
Acronym List
Checklist of Requirements
Readings
Learning Activities
Answers to Learning Activities
Clinical Manifestations of Ulcerative Colitis
Effect of Prolonged Bleeding and Diarrhea
Clinical Manifestations of Crohn’s Disease
Mechanisms Underlying Differences Between Diseases
Outcome Differences of IBD Surgery
Answers to Learning Activity #1
Student Assessment Answers: Peptic Ulcer Disease
Answers to Learning Activity #2
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 14 Alterations in Gastrointestinal Function1
UNIT12
Alterations in Gastrointestinal Function
Disorders of the gastrointestinal tract represent some of the most challenging health care problems for both health care workers and their clients. Despite extensive research and the development of numerous theories, the etiology of many of these disorders remains unknown. Patients and their families are faced with diseases whose course and response to therapy is unpredictable, the severity may range from mild to life threatening, impacting every facet of life.
A sound understanding of the underlying pathophysiology of these disease conditions greatly enhances the nurse’s ability to plan comprehensive patient care. The knowledge gained in this unit will build upon knowledge you have acquired in earlier units, specifically wound healing and the inflammatory process, and the mechanism of immunity.
There are two main sections to this unit:
- Inflammatory Bowel Disease
- Peptic Ulcer Disease
Overview
Aim
The general aim of this unit is to facilitate your understanding of the pathophysiology underlying common gastrointestinal disorders such as Inflammatory Bowel Disease (IBD) and specific types of ulcers. Upon completing this unit you will be familiar with the development, manifestations, therapeutic interventions, and terminology of inflammatory bowel disease and peptic ulcer disease.
Objectives
Upon completing this unit you will be able to:
- Describe the pathogenesis, clinical manifestations, and principles of management of Inflammatory Bowel Disease (IBD).
- Compare the etiology, pathogenesis, and clinical features of gastric and duodenal ulcers.
- Discuss the surgical and medical management of peptic ulcer disease.
Resources
Required
In completing this unit you will be required to do the following readings:
Print Companion: Alterations in Gastrointestinal Function
Pardi, D.J., & Tremaine, W.J. (1998). Inflammatory bowel disease: Keys to diagnosis and treatment. Consultant, 38(1), 87-92, 96-98.
Porth, C. M. (2005). Pathophysiology-Concepts of Altered Health States (7th ed.). Philadelphia:Lippincott.
Please read Chapter 38 for an overview of GI Function and Chapter 39 for a discussion on Disorders of Gastrointestinal Function.
Supplemental Materials
Brozenec, J.A. (1996), Ulcer therapy update, RN, 59(9), 48-50, 52-54.
Cumbic, B. (1996). Bowel obstruction, Nursing 96, 26(1), 33.
Heslin, J.M. (1997). Peptic ulcer disease. Nursing 97, 27(1), 34-40.
Pullen, M. (1999). Nutrition in Crohn’s disease. Nursing Standard, 13(27), 48-52.
Web Links
All web links in this unit can be accessed through the Web CT system.
Section 1: Inflammatory Bowel Disease
Introduction
A disorder of inflammation occurs when defence mechanisms are inappropriate or when they become chronic as in Inflammatory Bowel Disease.
Definition
Inflammatory Bowel Disease (IBD) is a term used to describe disorders of chronic inflammation, primarily ulcerative colitis and Crohn’s disease (Cooke, 1991; Katz, 1994; Ogorek & Fisher, 1994). The term, IBD, is currently used due to the overlapping of clinical manifestations and therapeutic interventions in these diseases.
Prevalence
The development of an epidemiologic profile for IBD is difficult due to problems associated with accurate diagnosing and delayed reporting of the disease. In many countries, medical attention may not be sought or when sought, vague and overlapping signs and symptoms may not be easily recognized. Even in more advanced centres definitive diagnoses may take many months. Despite these uncertainties, statistical estimates and trends have been determined.
Worldwide, the highest prevalence of IBD occurs in Northern Europe and the United States, with low incidence in South Africa and Australia, and a relative rarity in South America, South African blacks, and Asia (Whelan, 1990).
In the United States, there is an estimated 200,000 to 500,000 persons with IBD, and an estimated 20,000 to 25,000 new cases diagnosed annually. Worldwide statistics suggest that the prevalence of ulcerative colitis has stabilized over the past two decades and that following a dramatic rise in the occurrence of Crohn’s disease, it may also be reaching a plateau (Whelan, 1990).
Population at Risk
Inflammatory bowel disease can effect any age group, but occurrence rates tend to peak in the third and sixth decade of life. IBD is evident in both sexes however, incidence rates of Crohn's disease are 20% higher and incidence rates for men are 20% higher in ulcerative colitis. These factors suggest a possible hormonal, occupational or dietary influence (Lashner, 1995). Both ulcerative colitis and Crohn's disease seem to be more common in descendants of Northern Europeans and less common among African-American and Orientals (Cooke, 1991). Studies suggest that migration from a location of low prevalence to one of high prevalence does not change the prevalence rates. This suggests that developing IBD may be related to genetics and early exposure to environmental factors (Lashner, 1995). There is a disproportionately high prevalence among Jewish people.
Higher socioeconomic groups with sedentary indoor jobs also appear to have a higher prevalence. Psychological factors such as stress and anxiety were once thought to contribute to the onset of this disease but it now seems evident that their role is more associated with "flare ups" in existing disease (Whelan, 1990).
Pathophysiology
Etiology
One of the most frustrating aspects of IBD, for both patients and health care workers, is the unknown etiology of the disease (Cooke, 1991; Frank, Ott & Shanahan, 1993; Katz, 1994). While many theories exist, there is no clearly identifiable cause.
At present, research into the cause of IBD seems to centre around three areas: genetics and the influence of the environment; immunology; and microbiology. These three areas will be discussed in more depth.
Genetics and Environmental Factors
Ten to twenty percent of patients with IBD have a positive family history, usually involving a first-degree relative (Frank, Ott, & Shanahan, 1993; Katz, 1994;). A patient with ulcerative colitis may have family members with ulcerative colitis or Crohn’s disease. The same holds true for patients with Crohn’s disease. Although no genetic markers have been identified, the familial association suggests the presence of a genetic factor. However, it also has been argued that familial aggregations simply reflect common environmental factors.
Some environmental factors implicated include: absence of breast feeding, toilet training practices, infections, pesticides, radiation, and a diet high in refined sugar. It is interesting to note that some studies suggest that smoking protects individuals against the development of ulcerative colitis; however, the opposite relationship holds true for Crohn’s disease (Heller & Bernell, 1990).
Although the exact relationship between genetics and the environment is uncertain, it appears that in some cases there is a genetic factor that predisposes an individual to the development of IBD if exposed to certain environmental factors (Sartor, 1995).
Immunology
In the field of immunology, researchers have attempted to determine if IBD is the result of an immune process damaging the intestine or a defective immunological defensive mechanism producing a susceptibility to the disease (Cooke, 1991; Katz, 1994; Ogorek & Fisher, 1994).
As you will recall the intestinal lumen is populated by bacteria, and other noxious agents such as viruses. Therefore, an effective defense system is necessary to identify and neutralize potentially harmful substances. In a normal intestinal immune system pro-inflammatory and anti-inflammatory cell activity is balanced to provide defense without causing damage. In patients with IBD, it is thought that cytokines, which play a role in inhibiting the inflammatory response, may be missing or malfunctioning. Therefore the inflammatory process is allowed to continue (MacDermott, 1994).
Microbiology
The inflammatory process seen in IBD is consistent with infection by a microbial pathogen, leading researchers to consider a bacterial explanation for the disease. Specific agents investigated include Chlamydia and Mycobacteria. However, no organism has been shown to be specific for either ulcerative colitis or Crohn’s disease. Salmonella, Shigella, Campylobacter, and Clostridium difficile have been implicated in “flare-ups” of existing IBD (Sacher, 1985).
Pathogenesis
Ulcerative colitis
Ulcerative colitis is a mucosal disease, meaning a disease of the mucous secreting cells (lamina propria) and the submucosa. The inflammatory process tends to originate in the rectum and spread proximally through the large intestine in a continuous manner. Ulcerative colitis is primarily limited to the colon and rectum (Katz, 1994; Ogorek & Fisher, 1994).
Early in the disease process the lamina propria become crowded with plasma cells, segmented leukocytes, and inflammatory cells. This dense cellular infiltrate is accompanied by thinning of surface epithelium and loss of mucin from goblet cells in the crypts (Ogorek & Fisher, 1994).
As the disease progresses the crypts become obstructed, filled with pus and eventually rupture, leaving an ulceration in the mucosa (Ogorek & Fisher, 1994).
The inflammatory process is limited to the mucosa and does not result in the edema and fibrosis noted in Crohn’s disease. Eventually, pseudopolyps may develop from the mucosal layer.
Endoscopic examination via colonoscopy shows a clear margin between the diseased portion of the bowel and healthy mucosal tissue. In chronic ulcerative colitis, muscular hypertrophy occurs accompanied by the deposition of fibrous tissue and fat. The colon eventually becomes thick, narrow, and short, resembling a lead pipe (Cooke, 1991).
Crohn’s disease
In contrast, Crohn’s disease (CD) is an IBD which is not limited to the colon and rectum but which occurs anywhere along the alimentary tract (Frank, Ott, & Shanahan, 1993). Crohn’s is commonly found near the terminal ileum and throughout the small intestine. CD also differs significantly from ulcerative colitis in that it is an inflammatory process involving all layers of the bowel wall, not only the mucosa and submucosa layers (Frank, Ott, & Shanahan, 1993; Katz, 1994; Ogorek & Fisher, 1994). The widespread distribution and transmural (involving all layers) nature are distinguishing features of CD (Frank, Ott, & Shanahan, 1993; Ogorek & Fisher, 1994).
Over time the inflammatory process in Crohn’s disease results in edema and thickening of the bowel wall. Layers of fat are deposited around the bowel and are known as “fat wrappings”. This does not occur in ulcerative colitis (Ogorek & Fisher, 1994). As well, the transmural inflammatory nature of Crohn’s disease commonly leads to the formation of fistulas and fissures, particularly in the perianal and perirectal regions (Thomson & Shaffer, 1997).
Endoscopic examination in Crohn’s disease reveals areas of diseased tissue interspersed with areas of healthy tissue. These are referred to as “skip” lesions and give the bowel a “cobblestone-like” appearance (Ogorek & Fisher, 1994).
In summary, ulcerative colitis is a continuous inflammatory process of the mucosal and submucosal layers of the bowel wall and primarily involves the colon and rectum, whereas Crohn’s disease is a discontinuous process in which healthy tissue is interspersed with diseased tissue. It involves all layers of the bowel wall and may occur along the entire alimentary tract (Frank, Ott, & Shanahan, 1993; Katz, 1994; Ogorek & Fisher, 1994).
Clinical Manifestations
In the pathogenesis section of this unit you became familiar with the underlying mechanisms of IBD. Based on this knowledge, answer the following questions on clinical manifestations of IBD. Compare your responses to those at the back of this unit.
- How would you expect ulcerative colitis to manifest itself?
- How would rectal bleeding and diarrhea affect the patient’s general health?
- How would the clinical manifestations of Crohn’s disease differ from ulcerative colitis? Include rationale.
- What accounts for the presence of these clinical features in Crohn’s disease and their absence in ulcerative colitis?
The skin lesions associated with IBD are erythema nodosum and pyoderma gangrenosum. Erythema nodosum appears as red, raised, tender nodules usually on the legs, and is more prevalent in Crohn’s disease. Pyoderma gangrenosum is a purplish-red lesion with a deep, necrotic centre, and occurs more commonly in ulcerative colitis.
Lesions also may occur in the mouth and eyes. Oral lesions occur as ulcerations similar to those of the intestinal mucosa. Ocular lesions are slightly more common in Crohn’s disease and manifest themselves as conjunctivitis, uveitis, and occasionally as corneal ulcerations. (Nord, 1987; Rankin, 1990).
As with ulcerative colitis, patients with Crohn’s disease are subject to malnutrition (Cooke, 1991). This is further complicated when large portions of ileum are resected, thereby decreasing the area of absorption, and when interenteric fistulae cause intestinal contents to bypass absorptive areas of the bowel.
Complications
There are approximately 100 system complications of IBD involving most organ systems of the body. The effect of IBD on other body systems is thought to have an immunological basis, perhaps as a result of an antigen-antibody mechanism. Extra-intestinal or extra-colonic manifestations, meaning disorders outside the bowel, involve the joints, skin, mouth, eyes, vascular system and hepatobiliary system. Studies have reported a 24 to 36% incidence of extra-intestinal manifestations with IBD (Swartz, 1989). Arthritis associated with IBD may be monoarticular, polyarticular, or spondylitic. Arthritis tends to parallel the severity of the disease and occurs in approximately 15-20% of patients with IBD. Hepatobiliary complications include fatty liver disease, gallstones, cholangitis, cirrhosis of the liver, and pancreatitis.
Evaluation and Treatment
Articles in the required readings deal specifically with the nursing of patients with IBD. The medical and nursing care of patients with IBD focuses on the treatment of acute flare- ups, the maintenance of remission, and the management of chronic illness. These are accomplished through drug therapy, surgery, dietary and lifestyle teaching, and psychosocial counselling. The following will focus only on drug therapy and surgery.
Drug Therapy
Drug therapy in IBD has focused traditionally on the use of sulfasalazine and corticosteroids. More recently, the antibiotic metronidazole (Flagyl) and the immunosuppressive agents 6-mercaptopurine and azathioprine have been added to the treatment protocol (Hanauer & Baert, 1994).
Sulfasalazine has proven effective in treating mild to moderate cases of ulcerative colitis, preventing recurrence in cases of ulcerative colitis in remission, and in active Crohn’s disease of the colon (Hanauer & Baert, 1994). Sulfasalazine is composed of 5 amino-salicylic acid (5-ASA) and sulfapyridine, a sulfonamide antibiotic.
Recent studies suggest the active agent in treating colonic inflammation is 5-ASA. As the second compound, sulfapyridine appears responsible for the majority of the drug’s side effects: anorexia, vomiting and oligospermia, current research is addressing methods of delivering 5-ASA to the colonic mucosa in the absence of sulfapyridine. These methods include topical 5-ASA in the form of enemas and suppositories, and new oral preparations of 5-ASA such asolsalazine (Dipentum), Salofalk, and Asacol (Hanauer & Baert, 1994; Ruderman, 1990).
Topical corticosteroids in the form of hydrocortisone enemas have been widely used in the treatment of distal ulcerative colitis and Crohn’s disease of the rectosigmoid area. As topical corticosteroids can give rise to the same side effects as systemic corticosteroids, newer preparations are being examined.
IBD may involve an immunoregulation disorder, therefore medications aimed at altering the immune response have been evaluated. In Crohn’s disease, immunosuppressive therapy is reserved for individuals whose disease has become steroid-dependent or steroid-resistant. One such agent, 6- mercaptopurine as been shown to have some effect in controlling the disease. Overall, the use of immunosuppressive agents have been unsuccessful in treating ulcreative colitis. Recently, research is being directed toward the role of cyclosporin A, levamisole, and methotrexate in ulcerative colitis and Crohn’s disease. The mechanism of action of these immune suppressors has not been established (Hanauer & Baert, 1994).
Research is also being heavily focused on the role of immunomodulators in the inflammatory process. Immunomodulatory agents such as interleukin-10 (IL-10) and anti tumour necrosis factor-alpha (anti-TNFa), currently under clinical trials for Crohn’s disease, have demonstrated marked improvement in the disease (Thomson & Shaffer, 1997).
Metronidazole (Flagyl), an antibiotic used in anaerobic infections has been shown to have some effect in treating Crohn’s disease of the colon and perianal complications of Crohn’s disease, but is ineffective in treating ulcerative colitis (Hanauer & Baert, 1994; Rankin, 1990).
Surgical Management
Despite the advances in medical therapy, an estimated one third of patients with ulcerative colitis and two thirds of patients with Crohn’s disease will require surgery.
The majority of surgery occurs within 5 years of diagnosis. Indications for surgery include bowel perforation, toxic megacolon, massive hemorrhage, growth and developmental retardation, carcinoma and chronic illness.
Owing to the high rate of recurrence of Crohn’s disease following resection of diseased bowel, surgery is reserved only for complications arising from the disease or when the disease become refractory to medical management. The recurrence rate of Crohn’s disease is 40% within 5 years, 60% within 10 years, and 85% within 15 years (Thomson & Shaffer, 1997).
Indications for surgery in ulcerative colitis may be acute or chronic in nature. Acute indications include illness resistant to therapy, toxic megacolon, and hemorrhage. The operation of choice for acute ulcerative colitis is a subtotal colectomy and ileostomy. In this procedure, the rectum is preserved, allowing for future surgery if re-anastomosis is desired.