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Inflammatory bowel disease (Crohn disease and ulcerative colitis): Difference between revisions
Inflammatory bowel disease (Crohn disease and ulcerative colitis) (view source)
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(Created page with "Inflammatory bowel disease (IBD) is an umbrella term for two idiopathic conditions; Crohn disease (CD) and ulcerative colitis (UC). Both are chronic diseases of the gastrointestinal tract that involve some inappropriate immune activation of the mucosa. Luckily for us the two diseases have different features that can be used to differentiate them. We’ll give a summary of the differences at the end of this topic. IBD is a chronic disease, but it isn’t always active. T...") |
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Inflammatory bowel disease (IBD) is an umbrella term for two idiopathic conditions; Crohn disease (CD) and ulcerative colitis (UC). Both are chronic diseases of the gastrointestinal tract that involve some inappropriate immune activation of the mucosa. Luckily for | '''Inflammatory bowel disease''' (IBD) is an umbrella term for two idiopathic conditions; '''Crohn disease''' (CD) and '''ulcerative colitis''' (UC). Both are chronic diseases of the gastrointestinal tract that involve some inappropriate immune activation of the mucosa. Luckily for medical students the two diseases have different features that can be used to differentiate them. We’ll give a summary of the differences at the end of this article. | ||
IBD is a chronic disease, but it isn’t always active. There are usually periods of active disease with weeks or months of asymptomatic periods between them. The asymptomatic periods are called ''remission'' while the symptomatic periods are called ''flares''. Several factors may provoke a flare-up, like stress, specific types of food, or cigarette smoking. However, most flares occur without an apparent trigger. | IBD is a chronic disease, but it isn’t always active. There are usually periods of active disease with weeks or months of asymptomatic periods between them. The asymptomatic periods are called ''remission'' while the symptomatic periods are called ''flares''. Several factors may provoke a flare-up, like stress, specific types of food, or cigarette smoking. However, most flares occur without an apparent trigger. | ||
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* Diet poor in fibre and rich in total fat and animal fat | * Diet poor in fibre and rich in total fat and animal fat | ||
* White or Jewish ethnicity | * White or Jewish ethnicity | ||
* Absence of breastfeeding | * Absence of [[breastfeeding]] | ||
* NSAID use | * [[NSAID]] use | ||
* Previous <abbr>GI</abbr> infection | * Previous <abbr>GI</abbr> infection | ||
Interestingly enough, the risk of UC is ''decreased'' in people who smoke. The risk for CD is increased however, so don’t start smoking 🚬. | Interestingly enough, the risk of UC is ''decreased'' in people who smoke. The risk for CD is increased however, so don’t start [[smoking]] 🚬. | ||
== Pathomechanism == | == Pathomechanism == | ||
The causes of IBD are not known. We know that there are multiple factors, both genetic and environmental. The pathogenesis involves defects in the mucosal immunity, epithelium, and the intestinal microbiota, leading to chronic inflammation. | The causes of IBD are not known. We know that there are multiple factors, both genetic and environmental. The pathogenesis involves defects in the mucosal immunity, epithelium, and the intestinal microbiota, leading to chronic inflammation. | ||
One model states that epithelial defects in people with IBD allow bacterial components to transverse the epithelial barrier and enter the mucosa. This activates adaptive and innate immune responses, causing immune cells to release <abbr>TNF</abbr>. Here the genetic defects enter the picture, as people with these defects respond to the TNF by further increasing epithelial permeability, allowing even more bacterial components to enter. This is the beginning of a self-amplifying cycle. | One model states that epithelial defects in people with IBD allow bacterial components to transverse the epithelial barrier and enter the mucosa. This activates adaptive and innate immune responses, causing immune cells to release <abbr>[[TNF]]</abbr>. Here the genetic defects enter the picture, as people with these defects respond to the TNF by further increasing epithelial permeability, allowing even more bacterial components to enter. This is the beginning of a self-amplifying cycle. | ||
== Extraintestinal manifestations == | == Extraintestinal manifestations == | ||
Both types of IBD carry the risk for many extraintestinal manifestations of the disease. People with IBD have increased risk for: | Both types of IBD carry the risk for many extraintestinal manifestations of the disease. People with IBD have increased risk for: | ||
* Uveitis | * [[Uveitis]] | ||
* Primary sclerosing cholangitis | * [[Primary sclerosing cholangitis]] | ||
* Arthritis | * [[Arthritis]] | ||
* Erythema nodosum | * [[Erythema nodosum]] | ||
* Pyoderma gangrenosum | * [[Pyoderma gangrenosum]] | ||
* Ankylosing spondylitis | * [[Ankylosing spondylitis]] | ||
* Aphthous stomatitis | * Aphthous stomatitis | ||
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== Diagnosis and evaluation == | == Diagnosis and evaluation == | ||
Diagnosis of CD is histological, requiring biopsy. The workup of CD involves MR enterography (to visualise the small bowels) and colonoscopy. Biopsies should be taken from any lesions visible, as well as the terminal ileum. If there are oesophageal or gastric symptoms, upper endoscopy should be performed as well. Laboratory tests should check for anaemia and vitamin deficiencies. | Diagnosis of CD is histological, requiring biopsy. The workup of CD involves [[MR enterography]] (to visualise the small bowels) and [[colonoscopy]]. Biopsies should be taken from any lesions visible, as well as the terminal ileum. If there are oesophageal or gastric symptoms, [[upper endoscopy]] should be performed as well. Laboratory tests should check for [[anaemia]] and vitamin deficiencies. | ||
Non-infectious intestinal inflammation correlates directly with the amount of ''calprotectin'' in the faeces. Measurement of this marker is useful both for excluding the diagnosis (if negative) and for follow-up. | Non-infectious intestinal inflammation correlates directly with the amount of ''[[calprotectin]]'' in the faeces. Measurement of this marker is useful both for excluding the diagnosis (if negative) and for follow-up. | ||
== Treatment == | == Treatment == | ||
Early treatment is necessary to achieve remission and to maintain it, and to prevent complications. Unfortunately, many patients with CD require surgery due to complications in their lifetime. | Early treatment is necessary to achieve remission and to maintain it, and to prevent complications. Unfortunately, many patients with CD require surgery due to complications in their lifetime. | ||
Many drugs are used in the treatment of CD, including 5-ASA, | Many drugs are used in the treatment of CD, including [[5-ASA]], [[corticosteroids]], immunosuppressants ([[azathioprine]], [[6-MP]]), and biological therapies, like [[anti-TNF]], anti-integrin, and so on. Choice of treatment depends on the severity. 5-ASA is only effective in colonic Crohn disease. Steroids are often used for induction of remission, rather than for maintenance. | ||
In CD, surgery is used in cases where conservative therapy is insufficient. Surgical resection of inflamed bowels is avoided as much as possible, as inflammation will later recur at the area of the anastomosis. Surgery may treat the acute episode, but possible perioperative complications and long-term complications of losing bowel lengths (short bowel syndrome) means that radical resections must be avoided. | In CD, surgery is used in cases where conservative therapy is insufficient. Surgical resection of inflamed bowels is avoided as much as possible, as inflammation will later recur at the area of the anastomosis. Surgery may treat the acute episode, but possible perioperative complications and long-term complications of losing bowel lengths (short bowel syndrome) means that radical resections must be avoided. | ||
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The histology of UC is similar to that of CD, except that there are no granulomas in ulcerative colitis. | The histology of UC is similar to that of CD, except that there are no granulomas in ulcerative colitis. | ||
UC carries a higher risk for colonic adenocarcinoma than CD because it always affects the colon. | UC carries a higher risk for [[Colorectal cancer|colonic adenocarcinoma]] than CD because it always affects the colon. | ||
== Clinical features == | == Clinical features == | ||
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Many drugs are used in the treatment of UC, including 5-ASA, glucocorticoids, immunosuppressants (azathioprine, 6-MP), and biological therapies, like anti-TNF. Choice of treatment depends on the severity. 5-ASA is very effective for UC. Steroids are often used for induction of remission, rather than for maintenance. | Many drugs are used in the treatment of UC, including 5-ASA, glucocorticoids, immunosuppressants (azathioprine, 6-MP), and biological therapies, like anti-TNF. Choice of treatment depends on the severity. 5-ASA is very effective for UC. Steroids are often used for induction of remission, rather than for maintenance. | ||
UC carries an elevated risk for <abbr>CRC</abbr>. Patients should undergo regular (every 1 – 3 years) colonoscopy to assess for dysplasia and malignancy. | UC carries an elevated risk for <abbr>[[Colorectal cancer|CRC]]</abbr>. Patients should undergo regular (every 1 – 3 years) colonoscopy to assess for dysplasia and malignancy. | ||
Surgery plays a bigger role in UC than in CD. Total colectomy cures the disease and is therefore a valid option in severe cases. | Surgery plays a bigger role in UC than in CD. Total colectomy cures the disease and is therefore a valid option in severe cases. | ||