AstraZeneca has delivered this text only version of the course to serve those users who have difficulty accessing the interactive version.
You can access it here: Demo Interactive Version
Further information can be found at: "Inflammatory Bowel Disease (IBD)" main page
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Welcome to the “Inflammatory Bowel Disease” course.
Before beginning, please take a moment to read the course details.
Click on the Course Notes button to download a PDF version of the course. The course notes contain all the text associated with the course, including objectives, transcripts, and progress checks.
Course Details
Course Length: Approximately 2 hours. Your time may vary based on modem speed, prerequisite knowledge and other factors.
Prerequisites: Anatomy & Physiology of the Gastrointestinal (GI) System.
Date Published: December 2005
Inflammatory bowel disease or IBD is comprised of two conditions, ulcerative colitis, which occurs only in the large intestine, and Crohn's disease, which may occur anywhere in the alimentary canal. Throughout the course, we will be comparing and contrasting ulcerative colitis and Crohn’s disease in the context of each section.
This course, “Inflammatory bowel disease,” presents basic medical background information about the immune and inflammatory systems in health and disease, types of disease states associated with IBD, and the currently available treatments.
The first section, AETIOLOGY, introduces the causes of IBD and the pathophysiology behind both ulcerative colitis and Crohn's disease. It begins with a description of the causes of IBD and then gives an overview of the pathophysiology of the inflammatory reaction and immune response associated with IBD.
The second section, EPIDEMIOLOGY, summarises some of the epidemiological data relating to IBD.
The third section, PROGNOSIS, details the outcomes of the initial attack of the disease and discusses long-term prognosis. It also lists the complications of both ulcerative colitis and Crohn's disease.
The fourth section, DIAGNOSIS, covers the clinical features of IBD. It also reviews the differential diagnosis of the disease and explains the laboratory, imaging, and pathology findings associated with the disease.
The fifth section, TREATMENT, covers the various non-pharmacological and pharmacological treatments that are currently utilised to treat IBD.
The underlying disease process in IBD is chronic inflammation, characterised by persistent infiltration of the wall of the alimentary canal by immune cells, including including monocytes and macrophages, and polymorphonuclear leukocytes such as neutrophils and mast cells. In Crohn’s disease there is specific histological picture that includes granuloma formation, and aggregates of epitheliod cells with a rim of lymphocytes.
These cells release inflammatory mediators, which damage the tissues of the alimentary canal. The cause of this chronic inflammation is unclear. This section introduces the suggested causes of IBD. It then reviews the inflammatory reaction and immune response associated with the disease.
These are the objectives for this section. You will be tested on these objectives in the final assessment.
After you finish this section, you should be able to:
The specific cause of IBD is unknown. Some of the causes that have been suggested include infective agents and diet, genetic, and psychological factors. These are described in detail in this lesson.
An infectious hypothesis for IBD is attractive for several reasons. To begin with, the colon contains many microorganisms.
Several infectious diseases of the colon cause inflammation and the tissue changes in IBD resemble those seen in infection. The intestinal microflora is also abnormal in many IBD patients.
However, no single organism has been consistently observed in IBD patients, and the geographical pattern of IBD does not resemble the transmission of an infection. The infectious hypothesis for IBD is, therefore, unproven.
It has been reported that patients with Crohn's disease eat more refined sugar and less dietary fibre than healthy people. These differences have not been observed in all studies and their significance is unclear.
Several studies have indicated that IBD is less common in people who were breast fed as infants than in those who were given formula feeding. However, the number of people fed on formulas is far greater than the number of individuals with IBD, which indicates that formula feeding cannot be more than a contributory factor.
Ulcerative colitis is more prevalent among non-smokers or ex-smokers than among continuing smokers. By contrast, patients with Crohn's disease have the same or higher frequencies of cigarette smoking as control groups. The links between IBD and smoking are thus unclear.
Crohn's disease is more prevalent among users of oral contraceptives than among non-users, and a number of investigators have reported remission of symptoms after discontinuation of oral contraceptives. This indicates that there may be a link between female hormones and Crohn's disease.
Extensive studies have not shown any consistent psychological differences between IBD patients and control groups. However, many clinicians believe that once IBD is established, the pattern of relapse and remission is significantly influenced by stressful life events.
There is an increased incidence of IBD in families of patients with the disease. Compared with the general population, brothers or sisters of patients with Crohn's disease are approximately 30 times more likely to develop the disease.
From 10 to 40% of patients with ulcerative colitis have first-degree relatives with the disease. Some researchers believe that the HLA system, a series of genes involved in the regulation of the immune system, may be implicated.
In Crohn's disease a genetic defect in the NOD 2 receptor gene on chromosome 16 has been found in about 25% of the patients.
Roll your cursor over this summary table to review the information for each section.
The characteristic feature of IBD is inflammation. This lesson gives a general introduction to inflammation.
The inflammatory reaction involves two major components, the activation of immune cells, and the responses of the tissues to mediators.
Antigens derived from pro-inflammatory protein or from infectious agents in the damaged region stimulate B lymphocytes to produce antibodies.
These antigens can also be presented to T cells via antigen processing cells such as macrophages.
Some antibodies can activate the complement cascade and indirectly cause degranulation of tissue bound mast cells, while IgE antibodies can do so directly.
The mediators released from mast cells lead to the recruitment of circulating granulocyles such as neutrophils, basphils and eosinophils. These also produce mediators such as histamine, and leukotrienes, which elicit a range of responses.
Normally, inflammation subsides gradually and is followed by repair and healing. However, if the infection cannot be destroyed or if the control of inflammatory responses is impaired, inflammation may become greatly prolonged, leading to chronic inflammation. Chronic inflammation is the principal feature of IBD.
Rollover Text: More Information
Many of the events shown here are coordinated by cytokines, which are proteins that enable communication between cells of the immune system. Cytokines are secreted by macrophages, and T cells. Some examples of pro-inflammatory cytokines are interleukin-1 (IL-1), interleukin-6 (IL-6) and Tumour necrosis factor- alpha (TNF-α).
Many observations indicate that the immune system is intimately involved in IBD. The evidence for this is summarised in this lesson. Different models for the involvement of the immune system are also described.
In IBD, many types of immune cells infiltrate the mucosa: B cells that produce IgA, lgM, lgE, and IgG, T cells that produce a variety of cytokines, neutrophils containing lysosomal enzymes, mast cells, some of which are degranulating, and eosinophils.
The release of inflammatory mediators by these cells probably causes much of the tissue damage in IBD.
The distribution of immune cells in ulcerative colitis and Crohn's disease corresponds to the depth to which the inflammation penetrates the alimentary canal.
Thus, in ulcerative colitis, in which the inflammation is confined mainly to the mucosa, immune cells are found in the mucosa and upper submucosa.
In Crohn's disease, which affects the entire wall, immune cells can be seen in the mucosa, submucosa and deeper layers.
Two hypotheses that are shown in this table have been put forward to explain the role of the immune system in IBD. The infectious hypothesis proposes that an as yet undiscovered pathogen causes the disease, and the immune system is responding appropriately to it.
The immunological hypothesis proposes that the immune system is acting abnormally against a common antigen to which everyone is commonly exposed, such as a dietary factor, or that IBD is an autoimmune disease - a condition in which the body is attacked by its own immune system. This idea is supported by the observation of colon autoantibodies in IBD patients.
This “drag and drop” progress check will test your knowledge of the information presented in this section. Because your score will not be recorded, you may take the progress check as many times as you would like.
Please feel free to review the lessons as often as required to successfully complete the progress check.
Determine if the statements are “true” or “false.” Use the “rewind” button to reset.