Frank MacDonald RN, MN - ucalgary.ca€¦ · Web viewTen to twenty percent of patients with IBD...

UNIT 12Alterations 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 Function 1

Unit 12 Table of ContentsOverview..................................................................................................................... 3

Aim.......................................................................................................................... 3Objectives................................................................................................................. 3Resources................................................................................................................. 3Web Links................................................................................................................ 4

Section 1: Inflammatory Bowel Disease....................................................................5Introduction.............................................................................................................. 5Pathophysiology....................................................................................................... 6Clinical Manifestations............................................................................................. 9Evaluation and Treatment.......................................................................................11Learning Activity #1..............................................................................................15

Section 2: Peptic Ulcer Disease................................................................................19Introduction............................................................................................................ 19Pathophysiology..................................................................................................... 21Clinical Manifestations........................................................................................... 24Evaluation and Management................................................................................... 25Learning Activity #2..............................................................................................31

Final Thoughts......................................................................................................... 33

References................................................................................................................. 34

Acronym List............................................................................................................ 36

Checklist of Requirements.......................................................................................36Readings................................................................................................................. 36Learning Activities................................................................................................. 36

Answers to Learning Activities................................................................................37Clinical Manifestations of Ulcerative Colitis..........................................................37Effect of Prolonged Bleeding and Diarrhea............................................................37Clinical Manifestations of Crohn’s Disease............................................................37Mechanisms Underlying Differences Between Diseases.........................................37Outcome Differences of IBD Surgery.....................................................................38Answers to Learning Activity #1............................................................................39Student Assessment Answers: Peptic Ulcer Disease...............................................40Answers to Learning Activity #2............................................................................40


2 Unit 14 Alterations in Gastrointestinal Function

UNIT 12Alterations 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:

1. Inflammatory Bowel Disease2. Peptic Ulcer Disease



OverviewAim

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.

ObjectivesUpon completing this unit you will be able to:

1. Describe the pathogenesis, clinical manifestations, and principles of management of Inflammatory Bowel Disease (IBD).

2. Compare the etiology, pathogenesis, and clinical features of gastric and duodenal ulcers.

3. Discuss the surgical and medical management of peptic ulcer disease.

ResourcesRequiredIn 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 MaterialsBrozenec, 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 LinksAll web links in this unit can be accessed through the Web CT system.



Section 1: Inflammatory Bowel DiseaseIntroduction

A disorder of inflammation occurs when defence mechanisms are inappropriate or when they become chronic as in Inflammatory Bowel Disease.

DefinitionInflammatory 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.

PrevalenceThe 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 RiskInflammatory 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).

PathophysiologyEtiologyOne 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 FactorsTen 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).

ImmunologyIn 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).

MicrobiologyThe 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).

PathogenesisUlcerative colitisUlcerative 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 diseaseIn 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 ManifestationsIn 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.

1. How would you expect ulcerative colitis to manifest itself?

2. How would rectal bleeding and diarrhea affect the patient’s general health?

3. How would the clinical manifestations of Crohn’s disease differ from ulcerative colitis? Include rationale.

4. 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.

ComplicationsThere 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 TreatmentArticles 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 TherapyDrug 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 ManagementDespite 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.

Individuals with long term ulcerative colitis may elect surgery because they are frustrated with poor disease control, medication side effects, or concern over developing colon cancer. Surgical procedures for these individuals include proctocolectomy and ileostomy, an ileoanal pouch procedure, a continent ileostomy (see Figure 14.1 in this unit), or a colectomy and ileorectal anastomosis.



Figure 14.1 Continent ileostomy

A proctocolectomy and ileostomy removes the colon and rectum, and necessitates that the patient wear an ileostomy pouch or appliance to collect fecal output. A continent ileostomy eliminates the necessity of wearing an appliance by creating a pouch from the ileum into which feces collects. Leakage is prevented by the creation of a “nipple” valve in the skin. The pouch is emptied via catheterization (see Figure 14.2 in this unit) as necessary throughout the day. Unfortunately, there is a 15% incidence of slippage of the nipple valve, requiring corrective surgery.



Figure 14.2 Catheterization of an ileal pouch (Koch pouch).

An ileoanal pouch or reservoir operates under the same principle except the pouch is created near the rectum and the rectal sphincter maintains continence. The rectal mucosa is usually resected to prevent future risk of cancer.

These three procedures eliminate the disease and the risk of future colonic cancer. The fourth procedure, a colectomy and ileorectal anastomosis involves removing the colon and anatomosing the ileum to the rectum. In this case the rectum remains intact requiring further surveillance for cancer (Jagelman, 1990).

How would you expect the outcome of surgery to significantly differ between ulcerative colitis and Crohn’s disease? (Answers in at the back of this unit).

SurveillanceInflammatory bowel disease is a chronic disease made up of acute illness and remission (Cooke, 1991; Katz, 1994). Successful management of IBD requires coordinated monitoring by many individuals: family members, general practitioners, gastroenterologists, pharmacists, nutritionists, and nurses. In addition to monitoring the patient’s status and response to treatment, surveillance for colon cancer is necessary.



There does not appear to be a generally accepted protocol for monitoring IBD. In addition to general physical assessments, surveillance procedures generally include colonoscopies, sigmoidoscopies, rectal biopsies, and barium enemas at spaced intervals.

Prognosis/Trajectory of DiseasePatients newly diagnosed with ulcerative colitis indicated there were four main questions to which they wanted answers:

Is my condition dangerous? Will I develop cancer? Will I need an operation? Will my condition spread?

Use the knowledge you have gained throughout this unit to develop answers to these patients’ questions regarding their course of illness and prognosis. Consider how your answers would differ for the patient with Crohn’s disease.

Learning Activity #1Now that you have completed this section on IBD, see if you can use knowledge you have acquired in solving the following crossword puzzles. Good Luck!

The answers are at the end of this unit.



Crossword #1

Clues:Across2. a formerly perceived cause of IBD3. group of drugs used in treating

IBD6. ulcerative colitis involves the

whole bowel wall, y or n?8. dietary roughage should be

__________10. physician for which an IBD was

named11. a complication of IBD12. body system thought to be

involved in IBD etiology13. suffix referring to bowel opening

through skin14. helper: suppressor ratios involve

Down1. prefix signifying rectum3. “descriptive” appearance of bowel in

Crohn’s4. diagnostic test5. extracolonic complication7. possible consequence of resecting

large portions of bowel8. ulcerative colitis is usually confined

to the __________9. general physical characteristic

affected by IBD



these15. alternate source of nutrition

(abbrev.)



Crossword #2

Clues:

Across1. drug used in treating Crohn’s4. most common symptom of ulcerative

colitis8. common complication of ileorectal

anastomosis9. surgical creation of an opening into

ileum11.therapeutic diet recommends low

_______12.term used to describe fatty stool

Down2. symptom of Crohn’s affecting weight3. organism implicated in IBD5. cure for ulcerative colitis6. section has described disorders of

__________7. eroded intestinal mucosa may

resemble these10. lamina propria __________ mucous



Crossword #3

Clues:Across1. term used to describe “fatty stool”4. a serious complication of ulcerative

colitis5. one etiological factor under study7. surgical removal of colon9. common intestinal feature of Crohn’s10.continent with high incidence of IBD

(abbrev.)12.surgical creation of an opening into

ileum

Down1. lamina propria __________ mucous2. risk of cancer increases after _____

years3. one of the IB diseases5. integral department in patient

education6. ulcerative colitis involves the whole

bowel wall, y or n?8. site of surgical procedures9. antibiotic used in IBD11. suffix signifying inflammation12. this section is on __________ (abbrev.)

(get this wrong and you’re in trouble)



Section 2: Peptic Ulcer DiseaseIntroduction

A primary function of the gastrointestinal (GI) tract is secretion of such substances as saliva, mucus, HCl acid, pancreatic enzymes, and bicarbonate. The GI tract is normally protected against potentially damaging secretions by defensive mechanisms such as mucus and bicarbonate secretion. When the balance of these two substances is upset, disorders of secretion develop. This section will examine one such disorder, peptic ulcer disease.

DefinitionPeptic ulcer disease (PUD) is generally a chronic, recurring disorder of the alimentary tract and encompasses gastric and duodenal ulcer disease. Please begin this section by defining the following terms. (Check your definitions at the back of this chapter)

erosion

ulcer

peptic ulcer

gastric ulcer

duodenal ulcer



PrevalenceDetermining the exact incidence of PUD is difficult, however an increase has occurred recently (Katz, 1991). Factors affecting accurate statistics include the availability and quality of medical help, utilization of health care, diagnostic standards, and means of disease classification. Ulcers may be diagnosed through symptomatology, radiography, or endoscopy, with varying degrees of accuracy. Having acknowledged these limitations, some general trends appear evident.

Peptic ulcer disease is evident worldwide although the ratio of duodenal ulcers to gastric ulcers may vary. In North America, an estimated 3.5 million people are affected annually, with a 4:1 ratio of duodenal to gastric ulcers. An estimated 1 in 10 men, and 1 in 25 women will develop a peptic ulcer in their lifetime.

Ulcer related deaths are ranked as the thirteenth most common cause of death among white males and are usually related to age and complications such as hemorrhage or perforation (Katz, 1991). The economic impact of PUD is illustrated by the fact that its associated loss of productivity and medical costs account for an economic loss of over $3 billion in the United States.

Population at RiskPrior to your readings on PUD, how would you have described the average “sufferer”? Most people would likely say that HE is a middle aged executive in a highly stressful job, with a type-A personality. He smokes, consumes large amounts of coffee and alcohol, eats spicy food, and regularly takes aspirin for headaches. Keep this stereotypic profile in mind as you examine the risk factors and etiology of PUD. The risk factors associated with diet, alcohol and drug consumption will be discussed in more depth under etiology.

Men are twice as likely to develop duodenal ulcers as women and equally likely to develop gastric ulcers. There tends to be a one year delay between developing symptoms and diagnosing the disease in gastric ulcers and a two-year delay in duodenal ulcers.

The prevalence of duodenal ulcers steadily increases between 25 and 70 years of age, whereas the prevalence of gastric ulcers increases between 40 and 70 years of age. There appears to be a higher prevalence of PUD among males in lower social classes, which is in contrast to the often held belief that it is a disease of the upper and middle classes.



PathophysiologyEtiologyDespite extensive research, etiology of PUD remains unclear (Katz, 1991; Mertz & Walsh, 1991; Partipilo & Woster, 1993). Research into the etiology of PUD primarily centres around four areas: genetics, environment, drugs, psychosomatic factors, and infection.

GeneticsA number of research findings have led to the conclusion that a genetic factor is present in PUD. Studies show first-degree relatives of patients with PUD to be two to three times more likely to develop ulcers than relatives in control subjects (Katz, 1991). Monozygotic twins have a higher concordance for ulcers than dyzygotic twins. Finally, genetic differences in relation to ABO blood grouping have been noted between patients with PUD and those without PUD. Individuals with blood group O have a 30% higher incidence of duodenal ulcers than individuals with other blood groups. Another finding within the ABO blood grouping system is that individuals who do not secrete ABO antigens in their saliva have an increased risk of duodenal ulcers.

EnvironmentEnvironmental factors under study include diet, smoking, alcohol and drug consumption. Research has not supported the role of specific dietary factors responsible for ulcer formation; however, a low protein, low fiber, high refined carbohydrate diet may be a predisposing factor (Katz, 1991; Mertz & Walsh, 1991). Hot, spicy foods are not a contributing factor, but may produce dyspepsia in individuals who already have gastric disturbances.

In contrast, some studies attempt to implicate smoking as a contributing factor (Katz, 1991; Mertz & Walsh, 1991). Peptic ulcers are twice as likely to develop in smokers versus nonsmokers, and existing ulcers are less likely to heal. Cigarette smoking is thought to alter the individual’s defence mechanism by reducing pancreatic secretion, thereby reducing neutralization of gastric acid; by reducing pyloric sphincter pressure allowing duodenogastric reflex; inhibiting synthesis of prostaglandins and reducing mucosal blood flow (Katz, 1994).

DrugsGenerally speaking the role of drugs in the development of PUD is controversial. Aspirin consumption of four times weekly over a period of three months increases an individual’s risk of developing gastric ulcers. The mechanism responsible seems to be aspirin’s inhibitory effect on prostaglandin synthesis. Mucosal resistance is partially dependent on mucosal prostaglandins to stimulate mucus and bicarbonate production and to maintain mucosal blood flow. Nonsteroidal anti-inflammatory (NSAIDS) agents such as



indomethacin and naprosyn also cause gastric mucosal erosion and may cause ulceration with long term use (Katz, 1991; Mertz & Walsh, 1991).

The role of steroid ingestion in ulcer formation is controversial, but studies indicate that prednisone therapy is associated with an increased incidence of PUD. Again, it is believed that steroids alter prostaglandin production.

Coffee, regular or decaffeinated, stimulates gastric acid secretion but has not been found to be an immediate cause of ulcer formation.

Psychosomatic FactorsDespite the fact that many emotions are felt at a “gut” level, psychological stress is not a definitive cause of PUD (Katz, 1991; Mertz & Walsh, 1991). Individuals in highly stressful occupations have not been found to have a higher incidence of PUD but may demonstrate ulcer-like symptoms due to dyspepsia. In contrast, however, some studies suggest a link between ulcer formation and dependency versus self-sufficiency conflict. A psychosomatic theory suggests that a psychic conflict and a stressful event may decrease mucosal resistance and increase acid production.

InfectionMore recently infection has been proposed as a cause of certain peptic ulcers. Helicobacter pylori infection is now recognized as a leading cause of gastric and duodenal ulcer disease. Eradication of the bacteria with antibiotic therapy has been highly successful in healing peptic ulcers, with a resultant low rate of recurrence.

PathogenesisThe development of a peptic ulcer is the result of an imbalance of HCl acid secretion and mucosal resistance factorsIncreased acid secretion may result from an increased number of parietal cells, an increased capacity to secrete acid and pepsin, or an increased basal rate of secretion.

Factors influencing impaired defence mechanisms include:

breakdown of the gastric mucosal barrier failure of normal cellular metabolism in buffering hydrogen (H+) local mucosal ischemia decreased secretion of bicarbonate mucus accelerated shedding of cells or reduced rates of cell renewal



Not all of these factors need be present for an individual to develop a peptic ulcer. For this reason, peptic ulcer disease is referred to as a heterogeneous disease, meaning not of uniform composition.

Patients diagnosed with the same type of ulcer may demonstrate different underlying pathophysiology. Helicobacter pylori (H. pylori), formerly campylobacter pylori, has been found to infect gastric mucosa, and it is strongly associated with antral gastritis and duodenal ulcers, and to a lesser degree, with gastric ulcers (Gilbert, Chan, & Thomas, 1991). H. pylori infection is confirmed by C-urea breath test, enzyme-linked immunosorbent assay (ELISA) for IgG antibodies, or direct culture of biopsy specimens (Feldman, Maton, McCallum, & McCarthy, 1992; Partipilo & Woster, 1993).

Gastric UlcersThe development of a gastric ulcer is not well understood and may depend upon a number of factors (Katz, 1991; Mertz & Walsh, 1991). Many patients with gastric ulcers have a normal or reduced rate of gastric acid secretion, therefore ulcer formation likely results from impaired mucosal resistance. Gastric ulcers usually occur in nonacid-secreting mucosa, commonly on the lesser curvature of the stomach. Why these cells are more prone to ulceration is unknown.

Gastric ulcer development is thought to be related to defective defence mechanisms likely in the area of gastric motility and pyloric sphincter function (Katz, 1991; Mertz & Walsh, 1991). A deficit in the pyloric sphincter may allow reflex of duodenal contents (bile acids, pancreatic juices, and lysolecithin) into the stomach. Delayed gastric emptying then increases the time the stomach mucosa is exposed to damaging duodenal contents. The exact mechanism of damage is not known but may possibly be related to an alteration in the mucus layer and the mucosal back-diffusion barrier which then allows H+ to diffuse back into the gastric mucosa. Frequent repetition of this back-diffusion results in chronic atrophic gastritis which is frequently associated with gastric ulcers. The direct relationship between gastric ulcers and chronic atrophic gastritis is unknown. Gastric ulcers also may result from hypersecretion of HCl acid.

Duodenal UlcersDuodenal ulcers (DU) commonly occur in the first portion of the duodenum or the duodenal bulb. DU pathophysiology differs somewhat from gastric ulcers in that patients with duodenal ulcers tend to be hypersecretors of HCl acid, both in the basal state and after stimulation.

Hypersecretion in the stimulated state seems to be the result of an increased number of parietal cells, whereas hypersecretion in the basal state may be the result of increased vagal nerve tone. You



will recall that the vagus nerve (CN X) controls gastric secretion. Many of these patients also have been noted to be hypersecretors of pepsinogen 1.

Altered defence mechanisms in the form of rapid gastric emptying contribute to ulcer formation. This rapid emptying delivers highly acidic gastric contents to the duodenum thereby lowering duodenal pH. The role of mucosal resistance in duodenal ulcers is not fully understood but cigarette smoking is thought to impair bicarbonate secretion into the duodenum thereby further lowering duodenal pH (Katz, 1991; Mertz & Walsh, 1991). As with gastric ulcers, the formation of duodenal ulcers depends upon an imbalance between aggressive and defensive factors in the presence of interacting factors such as genetics, the environment, and personal physiology.

Stress UlcersAs noted earlier, stress ulcers do not refer to ulcers brought about by psychological stress, but are the result of severe physiological stressors such as burns, head injuries, sepsis, multiple trauma, adult respiratory distress syndrome, and major surgery. These ulcers, which initially appear as gastric erosions, have been found to develop within hours of a severe stress. As gastric acid production tends to be initially normal or lowered, their development is thought to result from decreased defence mechanisms such as decreased mucosal blood flow, decreased mucosal cell renewal, and altered mucosal back-diffusion barrier. These ulcers are painless and are usually detected via endoscopy or by the presence of gastrointestinal bleeding. Treatment of these patients focuses on preventive therapy in the form of antacids and H2 receptor antagonists, and supportive therapy to decrease the physiological stress (Konopad & Noseworthy, 1988).

Clinical ManifestationsThe most common clinical manifestation of PUD is “heartburn” or epigastric pain which sometimes radiates to the lower abdomen or back (Katz, 1991). It may be sharp or burning and may fluctuate with eating patterns. Typically food relieves the pain by buffering Hydrochloric (HCl) acid during acute episodes of PUD. Pain often occurs 1 to 3 hours following a meal and again at night time, but is unusual in the morning as HCl production is low. Patients often have symptoms lasting a few days or weeks followed by long pain free periods. It is interesting to note that the patient’s symptomatology does not always correlate with detectable disease (Katz, 1991). Similarly, patients may be pain free but have active disease upon endoscopy (Feickert, 1987).

PUD also may be manifested by acute gastrointestinal bleeding as a result of the ulcer’s perforation of a blood vessel. Patient presentation depends upon the rate and amount of blood loss and



therefore symptoms range from melena, anemia, and fatigue to hypotension, hematemesis, and shock. Treatment is indicated by the degree of bleeding.

ComplicationsA serious and potentially life-threatening complication of PUD is perforation of the ulcer through the gastric or duodenal wall. This is accompanied by sudden, severe pain, leakage of intestinal contents, and the signs and symptoms of shock. As the intestinal contents frequently spill into the peritoneal space, peritonitis results. Surgery is indicated to repair the perforation or resect the ulcer.

Gastric outlet obstruction is a complication resulting from stenosis of the pyloric sphincter due to inflammation, edema, and scarring (Mertz & Walsh, 1991). Obstructions which do not correct themselves with conservative medical management require surgery.

Evaluation and ManagementThe diagnostic procedures for identifying PUD include radiography (barium swallows, upper GI series) and endoscopy. While radiography will detect craters along the mucosal wall, endoscopy is required to accurately identify the type of lesion and its severity. Biopsies may be performed during endoscopy to rule out gastric cancer. Laboratory tests which reflect blood loss such as CBC and stool for occult blood provide some insight into the patient’s condition but are not too reliable diagnostically as they also may reflect other disease processes.

Nursing ManagementThe nursing care of the patient with PUD focuses on alleviating acute manifestations of the disease, promoting healing, and patient education. Promoting comfort through rest, antacids, and possibly antisecretory drugs is of primary importance.

The patient’s nutritional status may be compromised from long standing dyspepsia. Traditionally, patients with PUD consumed frequent small meals of bland foods and plenty of milk. As eating stimulates acid secretion, frequent meals are no longer thought to be sensible. Today, patients are taught to avoid foods which have proven troublesome for them, commonly coffee, alcohol, spicy foods, and to eat normal sized meals. Milk is not promoted as it has been shown to have no effect on gastric pH.

If the patient has had a gastric resection, counselling regarding “dumping syndrome,” in which gastric contents rapidly empty into the duodenum causing pain, nausea, and dizziness, is necessary. This syndrome may be avoided by eating smaller, more frequent



meals, avoiding high carbohydrate meals, and drinking between meals rather than with meals. Dumping syndrome usually corrects itself in 6 to 12 months.

Medical TherapyThe goal of drug therapy in PUD is to address one or more of the aggressive or defensive factors inherent in ulcer formation; thus, medications are aimed at inhibiting acid secretion, coating the base of the ulcer to protect it from acid and pepsin, and neutralizing secreted acid. Just as there is no uniform cause of PUD, there is no uniform therapeutic protocol or response. Treatment is tailored to individual response.

Acid Secretion InhibitorsAcid secretion inhibitors act by competing with histamine at the H2 receptor sites on the parietal cells, and are thus referred to as H2 receptor antagonists. These medications inhibit the action of histamine which is a gastric acid secretion stimulator.

There are a number of inhibitors available, cimetidine, (Tagamet) ranitidine (Zantac), famotidine, nizatidine, and roxatidine acetate. The most commonly used H2-receptor antagonists are cimetidine and ranitidine . Both have proven effective in healing acute ulcers and in reducing recurrence of healed ulcers. Ranitidine may be slightly more popular at present because its higher potency allows for smaller, less frequent doses and therefore produces fewer side effects. The development of the H2 receptor antagonists has largely eliminated the use of anticholinergic drugs which also decrease acid secretion but which produce numerous side effects (Feldman et al., 1992).

Prostaglandins also have been found to inhibit acid secretion in addition to promoting mucosal defence. Misoprostol (Cytotec) has been found to be effective in healing duodenal and gastric ulcers, and in preventing gastric ulcers caused by NSAIDS. However, Cytotec can cause diarrhea, but more importantly it is uterotonic and therefore causes increased uterine contractions, bleeding, and spontaneous abortions. For this reason, it is approved in the United States only for gastric ulcer prevention with NSAIDS, and is contraindicated in women with child bearing capacity (Freston, 1990).

A third group of acid secretion inhibitors are proton pump inhibitors which bind H+/K+-ATPase and thereby block acid secretion. Omeprazole is one such inhibitor. Again, side effects including enteric infections and hypergastrinemia have limited its approval (Freston, 1990).



Mucosal Protective DrugsAntacidsAntacids have been used for hundreds of years and still remain effective in neutralizing secreted acid and relieving peptic ulcer symptoms; however, their effect on ulcer healing is unknown. Antacids have a relatively short action time, therefore dosage and administration time in relation to meals is important. Some physicians use antacids concurrently with H2-receptor antagonists whereas others recommend single agent therapy (Feldman et al., 1992).

Ulcer CoatersThe ulcer coaters act by forming a protective barrier which binds to the ulcer crater thereby protecting it from damage. These medications do not reduce acid secretion or neutralize existing acid. The commonly used medications in this group are sucralfate and bismuth compounds. Both may be taken in tablet form (Feldman et al., 1992). Healing rates are comparable to those achieved with H2-blockers for duodenal ulcer.

Bismuth Compounds and AntibioticsTriple therapy with two antibiotics -- e.g. tetracycline, amoxycillin, and metronidazole (Flagyl), plus bismuth subsalicylate (Pepto-Bismol) to eradicate H.pylori is a treatment still under study. Bismuth triple therapy was an early regimen of choice for H pylori eradication. But over the last decade or so, the therapy has evolved considerably. Bismuth triple therapy works well in part with Flagyl-sensitive H.pylori infection, but not in those individuals with Flagyl-resistant strains. In addition, the success of using bismuth compounds has been limited by its large volume dosing frequency and by its taste. Currently, the therapy of choice is the combination of a proton pump inhibitor and two antibiotics (usually clarithromycin and flagyl). This combination has a success rate of 88-94% for H.pylori eradication (Thomas & Shaffer, 1997).

Maintenance TherapyUlcer recurrence is common but ulcers usually respond to standard therapeutic regimens. Cigarette smoking, the presence of H. pylori and gastric acid hypersecretion affect recurrence rates. Low doses of H2 antagonists are effective for maintenance therapy (about 12 months) as well as sucralfate.

Surgical TherapySurgical intervention is indicated in PUD when ulcers are unresponsive to medical therapy, when life threatening complications arise such as perforation and hemorrhage, or when a malignancy is expected. There are two common types of gastric surgery: gastrectomy and vagotomy and pyloroplasty.



An antrectomy or subtotal gastrectomy involves the removal of a portion of the stomach in order to resect the ulcer and a portion of acid secreting cells. The section of stomach removed is usually the distal one half to two thirds. The gastric stump is then attached to the duodenum (a Billroth I procedure) or to the jejunum (a Billroth II procedure) (see Figures 14.3 and 14.4 respectively in this unit).

Figure 14.3 Billroth I procedure



Figure 14.4 Billroth II procedure

In a Billroth II (see Figure 14.4 in this unit) procedure the duodenal stump is left attached to the jejunum. Why is this necessary?

The duodenal stump is necessary to maintain a normal route for pancreatic secretions and bile to reach the chyme in the small intestine. This procedure is preferred for treatment of duodenal ulcers. These two procedures decrease acid secretion by removing acid secreting cells. Based on your understanding of gastric physiology, what other procedure would reduce acid secretion?

Point of Interest: Did you know that Dr. Billroth

used to operate using his bare hands?

was the first to demonstrate that, just as a person could have an arm or a leg cut off and still live, so could a person have part of his stomach or bowel removed and the severed ends could be sewn back together?

was a contemporary and friend of Brahms, the famous musician?

Stone, I. (1971). The passions of the mind. Bergenfield, New Jersey: New American Library Co. (pp. 65-68).



As you recall the vagus nerve (CN X) controls stimulation of the gastric cells, therefore severing of the vagus nerve eliminates its acid secreting stimulus. This procedure is termed a vagotomy. Three forms of a vagotomy exist: a truncal, selective, and highly selective or proximal. In the first, the posterior and anterior trunks are severed resulting in innervation to the stomach, bile ducts, liver, pancreas, and small intestine. A selective vagotomy affects innervation to the stomach alone and a highly selective only affects innervation to the acid secreting cells of the stomach. A stomach innervation is affected in the first two procedures, gastric motility and emptying is reduced, therefore necessitating a pyloroplasty to enhance gastric emptying (Bader, 1985; Feikert, 1987).



Figure 14.5 Vagal innervation of the stomach

Proximal

Selective

Truncal

SurveillanceSurveillance in PUD is largely dependent upon the patient’s response to therapy, as it is a disease of healing and relapses (Katz, 1991). One recommended format for monitoring patient response for duodenal ulcers is effectiveness of 6 week course of medication, such as Cimetidine or Ranitidine. If the patient is asymptomatic after six weeks the treatment is stopped. If a relapse occurs the treatment is repeated but the patient is not “rediagnosed” by x-ray or endoscopy unless the relapse is atypical. If relapses occur more frequently than every four to six months, maintenance drug therapy is considered. If initial therapy fails, an alternate drug therapy is tried, possibly followed by surgery.

Gastric UlcersSurveillance in gastric ulcers may require the need to document ulcer healing radiographically or endoscopically. Following a six to eight week course of medication, the patient is re-tested and if the



ulcer is unhealed follow-up examinations are scheduled in 12 weeks. Surgical intervention is considered if healing has still not occurred. If the ulcer reveals any malignant features during the initial endoscopy, regardless of biopsy results, the patient is examined endoscopically again in three weeks and at regular intervals until the ulcer heals.

Prognosis/TrajectoryPUD is a chronic disease highlighted by periods of healing and recurrence. The trajectory of the disease depends upon the patient’s response to treatment and therefore is individualistic. PUD requires life style adjustments for the patient and family.

Learning Activity #2You have now completed part two. Please complete the post-test to see how well you understood it.

Post-Test—Peptic Ulcer Disease(Note: Some of these questions have been adapted from Olsen and Barton (1987). Check your answers with those in at the back of this unit.)

1. Which of the following have been implicated as causing PUD?a. dietb. heredityc. corticosteroidsd. all of the above

2. The most common symptom of PUD is:a. mid-epigastric painb. nauseac. dysphagiad. vomiting

3. Possible complications of PUD include:a. perforationb. hemorrhagec. obstructiond. all of the above

4. The relapse rate of ulcers in smokers is:a. increasedb. decreasedc. equald. none of the above



5. Reported advantages of ranitidine over cimetidine include:a. longer half-lifeb. fewer side effectsc. fewer drug reactionsd. all of the above

6. The ratio of duodenal ulcers to gastric ulcers is:a. 1:4b. 1:1c. 4:1d. 2:1

7. Prostaglandins:a. are ulcerogenicb. exert a cytoprotective effectc. inhibit H2 receptorsd. none of the above

8. The ulcerogenic effect of aspirin vs. buffered aspirin is:a. increasedb. decreasedc. unchangedd. unknown

9. Which of the following may be used to diagnose PUD?a. physical examb. barium x-rayc. endoscopyd. all of the above

10.Which of the following affect acid production?a. number of parietal cellsb. capacity to secrete acid and pepsinc. basal cell secretion rated. all of the above



Final ThoughtsThe pathophysiology underlying selected disorders of the gastrointestinal system has been examined. These disorders have been found to be complex, multi-faceted mechanisms which require significant adaptation by the patient and family. The knowledge you have gained will help you face the challenge of providing comprehensive care to patients with disorders of the gastrointestinal system.

If you wish to examine any of the content covered in this unit in further detail, refer to any of the references. You may want to check out the following website too:

The Canadian Association of Gastroenterologywww.cag.ucalgary.ca.

This features a weekly endoscopy quiz which showcases all types of GI pathology as found by endoscopic means. This quiz section is maintained by the U of C GI group. A great learning resource and fun! (but very graphic).

If you have successfully completed the post-tests you are ready to proceed to the next unit. If not, review selected portions of the readings.

Good Luck!


http://www.cag.ucalgary.ca/


ReferencesAteshkadi, A., Lam, N. P., & Johnson, C. A. (1993).

Helicobacter pylori and peptic ulcer disease. Journal of Clinical Pharmacology, 12(1), 34-38.

Brozenec, J.A. (1996), Ulcer therapy update, RN 59 (9), 48-50, 52-54.

Choi, P.M., & Kimm W.H. (1995). Colon cancer surveillance. 671-787.

Cooke, D. M. (1991). Inflammatory bowel disease: Primary health care management of ulcerative colitis and Crohn’s disease. Nurse Practitioner, 16(8), 27-39.

Cumbic, B. (1996), Bowel obstruction, Nursing 96, 26 (1), 33.

Feldman, M., Maton, P., McCallum, R., & McCarthy, D. (1992, August). Treating ulcers and reflux: What’s new? Patient Care, 53-72.

Frank, M. S., Ott, D. J., & Shanahan, F. (1993). How to tell it’s Crohn’s disease. Patient Care, 27(16), 30-51.

Freston, J. W. (1990). Overview of medical therapy for peptic ulcer disease. Gastroenterology Clinics of North America, 19(1), 121-140.

Gilbert, G. Chan, C., & Thomas, E. (1991). Peptic ulcer disease: How to treat it now. Postgraduate Medicine, 89(4), 91-96.

Glotzer, D.J. (1995). Surgical therapy for Crohn's disease, Gastroenterology Clinics of North America, 24 (3). 577-596.

Griffin, M.G., & Miner, P.B. (1995). Conventional drug therapy in inflammatory bowel disease, Gastroenterology Clinics of North America, 24 (3), 509-533.

Hanauer, S. B., & Baert, F. (1994). Medical therapy of inflammatory bowel disease. Medical Clinics of North America, 78(6), 1413-1426.

Heller, G. H., & Bernell, O. (1990). Genetic aspects of inflammatory bowel disease. Medical Clinics of North America, 74(1), 13-20.

Jagelman, D. G. (1990). Surgical alternatives for ulcera-tive colitis. Medical Clinics of North America, 74(1), 155-167.



Katz, J. (1991). The course of peptic ulcer disease. Medical Clinics of North America, 75(4), 831-840.

Katz, J. (1994). The course of inflammatory bowel disease. Medical Clinics of North America, 78(6), 1275-1280.

Lashner, B.A. (1995). Epidemiology of inflammatory bowel disease. Gasroenterology Clinics of North America, 24(3), 467-474.

MacDermott, R.P. (1994). Alterations in mucosal immune system in ulcerative colitis and Crohn's disease. Medical Clinic of North America, 78(6), 1207-1232.

Mertz, H. R., & Walsh, J. H. (1991). Peptic ulcer pathophysiology. Medical Clinics of North America, 75(4), 799-814.

Muller-Lissner, S. (1993). The hypersensitive gut: Adequate approach or further confusion? Digestion, 54(6), 331-336.

NIH Consensus Development Panel on Helicobacter pylori in peptic ulcer disease: Helicobacter pylori in peptic ulcer disease. (1994). Journal of the American Medical Association, 272(1), 65-69.

Ogorek, C. P., & Fisher, R. S. (1994). Differentiation between Crohn’s disease and ulcerative colitis. Medical Clinics of North America, 78(6), 1249-1258.

Pardi, D.J., & Tremaine, W.J. (1998). Inflammatory bowel disease: Keys to diagnosis and treatment. Consultant, 38(1), 87-92, 96-98.

Partipilo, M. L., & Woster, P. S. (1993). The role of helicobacter pylori in peptic ulcer disease. Pharmacotherapy, 13(4), 330-339.

Porth, C. M. (2005). Pathophysiology-Concepts of Altered Health States (7th ed). Philadelphia: Lippincott.

Prevost, S., & Oberle, A. (1993). Stress ulceration in the critically ill patient. Critical Care Nursing Clinics of North America, 5(1), 163-169.

Rankin, G. B. (1990). Extraintestinal and systemic manifestations of inflammatory bowel disease. Medical Clinics of North America, 74(1), 39-50.

Ruderman, W. (1990). Newer pharmacologic agents for the therapy of inflammatory bowel disease. Medical Clinics of North America, 74(1), 133-153.

Sartor, R.B. (1995). Current concepts of the etiology and pathogenesis of ulcerative colitis and Crohn's disease. 475-507.



Swartz, M. (1989, Summer). Beyond the scope: A nursing view of the extraintestinal manifestations of inflammatory bowel disease. Society of Gastroenterology Nurses and Associates, 3-9.

Thomson, A.B.R., & Shaffer, E.A. (Eds.) (1997). First principles of gastroenterology: The basis of disease and an approach to management (3rd Ed.). Toronto: CAG.

Weiss, E.G., & Wexer, S.D. (1995). Surgical therapy for ulcerative colitis. Gastroenterology Clinics of North America, 24(3), 559-577.

Whelan, G. (1990). Epidemiology of inflammatory bowel disease. Medical Clinics of North America, 74(1), 1-12.

Acronym ListGI: gastrointestinal

IBD: inflammatory bowel disease

PUD: peptic ulcer disease

Checklist of RequirementsReadings

Print Companion: Alterations in Gastrointestinal Function

Read McCance & Huether, pp. 1322-1345, pp. 1261-1281

Learning Activities Clinical Manifestations of IBD (short answer questions)

Crossword Puzzles re: IBD

Definitions re Peptic Ulcer

Post-Test – Peptic Ulcer Disease



Answers to Learning ActivitiesClinical Manifestations of Ulcerative Colitis

Ulcerative colitis is an ulcerative disease of the mucosa of the large intestine resulting in the breakdown and sloughing of the lining of the intestine. Thus, it can be seen that rectal bleeding is the predominant symptom of ulcerative colitis. Severe diarrhea, up to 10 to 20 liquid stools daily, is also characteristic of this disease.

One less frequent clinical manifestation of ulcerative colitis is toxic megacolon. This is a life-threatening complication in which a portion of the bowel, usually the transverse colon, becomes dilated, paralyzed, and filled with fluid. It is associated with fever, leukocytosis, hypoalbuminemia, and abdominal distension. As bowel perforation may result, surgery is indicated in the majority of cases.

All patients with IBD have a higher risk of developing colon cancer than the general population, but the incidence in ulcerative colitis after 10 years is greatly more significant.

Effect of Prolonged Bleeding and DiarrheaProlonged rectal bleeding predisposes the patient to anemia which further results in generalized fatigue and pallor. Patients experiencing severe episodes of diarrhea will suffer weight loss, malnutrition, and anorexia. Caloric requirements for these patients are increased due to the inflammatory process, fever, and catabolic effects of steroid therapy, further complicating malnutrition.

Clinical Manifestations of Crohn’s DiseaseAlthough there is some overlap in the signs and symptoms of ulcerative colitis and Crohn’s disease, there are a number of differing features. In contrast to ulcerative colitis,

Crohn’s disease does not frequently present with rectal bleeding. If bleeding does occur it is usually the result of a perforated blood vessel rather than mucosal ulceration. The majority of cases of Crohn’s disease present with diarrhea, abdominal cramping, and weight loss. Additional clinical features include internal fistulae, abscesses, and perianal disease.

Mechanisms Underlying Differences Between Diseases

Crohn’s disease involves an inflammation of all layers of the bowel wall, thereby making it susceptible to sinus, fissure, and fistula formation through the weakened intestinal wall. Internal fistulae



may develop from small bowel to small bowel, small bowel to colon, small bowel to bladder, small bowel to skin, or from the colon to adjacent structures such as the vagina. This process also occurs in the perianal region resulting in fissures, fistulae, and abscesses around the rectum.

The “skip lesion” nature of Crohn’s disease results in a significantly higher number of bowel obstructions among these patients in comparison to patients with ulcerative colitis.

Outcome Differences of IBD SurgerySurgical resection of the colon in ulcerative colitis cures the disease whereas resection in Crohn’s disease is followed by recurrences. Since virtually all patients with Crohn’s disease having surgery will suffer a recurrence, surgery is postponed as long as possible. Patients are managed medically until specific indicators necessitate surgical intervention. These include bowel perforation, massive hemorrhage, possible appendicitis, carcinoma of the colon or rectum, and irreversible bowel obstruction. The surgical procedure again depends on the indication for surgery and may involve a resection of a diseased portion of bowel followed by a re-anastomosis of the proximal and distal segments, the formation of an ileostomy, or a strictureplasty (repair of a stricture).



Answers to Learning Activity #1Crossword #1 Word Listanemia

cobblestone

corticosteroids

colonoscopy

Crohn

erythemanodosum

immune

large intestine

low

malabsorption

no

ostomy

proct

stress

tcells

TPN

weight

Crossword #2 Word List anorexia

bleeding

Chlamydia

diarrhea

granulomas

ileostomy

polyps

residue

secrete

steatorrhea

sulfasalazine

surgery

Crossword #3 Word Listcolectomy

dietary

diet

fissures

flagyl

IBD

ileostomy

itis

NA

no

OR

secrete

steatorrhea

ten

toxicmegacolon

ulcerativecolitis



Student Assessment Answers: Peptic Ulcer Disease

Definitionserosion: a defect that does not extend through the entire thickness of the mucosal lining

ulcer: a hole in the tissue covering one of the surfaces of the body. Involves entire thickness of mucosa and extends at least into the submucosa.

peptic ulcer: ulcer occurring in areas of the digestive tract that are exposed to acid and pepsin secreted by the stomach

gastric ulcer: a peptic ulcer of the stomach or lower esophagus

duodenal ulcer: a peptic ulcer of the duodenal bulb or duodenum

Answers to Learning Activity #2Post-test Answers: Peptic Ulcer Disease

1. d / 2. a / 3. d / 4. a / 5. d / 6. c / 7. b / 8. c / 9. d / 10. d


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