Short bowel syndrome pathophysiology: Difference between revisions
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**Reduced [[absorption]] capacity of the [[small intestine]] due to loss of surface area, leading to: | **Reduced [[absorption]] capacity of the [[small intestine]] due to loss of surface area, leading to: | ||
***Loss of [[fluid]] and [[dehydration]] | ***Loss of [[fluid]] and [[dehydration]] | ||
*** | ***[[Electrolyte disturbance|Electrolyte imbalance]] | ||
***Loss of Macronutrients including carbohydrates, lipids and proteins | ***Loss of Macronutrients including [[Carbohydrate|carbohydrates]], [[Lipid|lipids]] and [[Protein|proteins]] | ||
**Disturbance in production of enzymes and hormones, leading to: | **Disturbance in production of [[enzymes]] and [[Hormone|hormones]], leading to: | ||
***Diarrhea | ***[[Diarrhea]] | ||
***Steatorrhea | ***[[Steatorrhea]] | ||
***Loss of vitamins | ***Loss of [[Vitamin|vitamins]] | ||
**Resection of specific sites, leading to: | **Resection of specific sites, leading to: | ||
***Loss of absorption of vitamin B12 and bile salts | ***Loss of [[absorption]] of [[vitamin B12]] and [[Bile acid|bile salts]] | ||
***Reduced capacity of fluid retention | ***Reduced capacity of [[Water retention|fluid retention]] | ||
**Loss of ileocecal valve, leading to: | **Loss of [[ileocecal valve]], leading to: | ||
***Small | ***[[Small bowel bacterial overgrowth syndrome|Small bowel bacterial overgrowth]] | ||
***Increased gastric and intestinal transit | ***Increased [[Stomach|gastric]] and [[Intestine|intestinal]] transit | ||
**Compromised production of gastrointestinal regulators including cholecystokinin | **Compromised production of [[Gastrointestinal tract|gastrointestinal]] regulators including [[cholecystokinin]], [[secretin]], [[gastric inhibitory polypeptide]] and [[peptide YY]], leading to: | ||
***Increased gastric and intestinal transit | ***Increased [[Stomach|gastric]] and [[Intestine|intestinal]] transit | ||
***Hypergastrinemia | ***Hypergastrinemia | ||
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==Gross Pathology== | ==Gross Pathology== | ||
*On gross pathology, the resected bowel may show the underlying causes including Crohn's disease, malignancies or ischemia. | *On gross pathology, the resected [[Intestine|bowel]] may show the underlying causes including [[Crohn's disease]], [[Cancer|malignancies]] or [[ischemia]]. | ||
{| | {| | ||
|[[image:ResectedIleum.jpg|thumb|410px|center|Terminal ileum resected for Crohn's disease. | |[[image:ResectedIleum.jpg|thumb|410px|center|[[Terminal ileum]] resected for [[Crohn's disease]]. | ||
By PPSE15 - Own work, CC BY-SA 4.0<ref name="urlFile:ResectedIleum.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/w/index.php?curid=39360128 |title=File:ResectedIleum.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]] | By PPSE15 - Own work, CC BY-SA 4.0<ref name="urlFile:ResectedIleum.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/w/index.php?curid=39360128 |title=File:ResectedIleum.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]] | ||
|} | |} | ||
Revision as of 14:55, 6 December 2017
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Short bowel syndrome Microchapters |
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Short bowel syndrome pathophysiology On the Web |
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Risk calculators and risk factors for Short bowel syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
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The small intestine has an average length of 5.5-6 meter and is responsible for digestion and absorption of food and nutrients. Three portions of small intestine are duodenum, jejunum, and ileum. There is an anatomic gradient for absorption throughout the gastrointestinal tract.[2][3]
- The duodenum, first portion of small intestine, is responsible for the breakdown of food in the small intestine. Brunner's glands, which secrete mucus, are found in the duodenum.
- The jejunum, second portion of small intestine, is responsible to absorb nutrients. The inner surface of the jejunum is covered in villi, which increase the surface area of tissue available to absorb nutrients from the gut contents. The villi in the jejunum are much longer than in the duodenum or ileum. It has many large circular folds in its submucosa called plicae circulares, which increase the surface area for nutrient absorption.
- The ileum, third portion of small intestine, is responsible to absorb vitamin B12 and bile salts and whatever products of digestion that were not absorbed by the jejunum. Its surface is made up of folds, mainly villi and microvilli. Therefore the ileum has an extremely large surface area both for the adsorption of enzymes and for the absorption of products of digestion. The diffuse neuroendocrine system (DNES) cells that line the ileum contain the protease and carbohydrase enzymes (gastrin, secretin, cholecystokinin) responsible for the final stages of protein and carbohydrate digestion.
Pathogenesis
- Short bowel syndrome is the result of bowel resection following various causes including Crohn's disease, malignancies, ischemia, and trauma.
- The small intestine has a very good adaptation following bowel resection of up to half of the small bowel length. However, the small intestine less than 2 meters is considered as short bowel syndrome and requires nutritional therapy to prevent malnutrition.[4]
Post bowel resection adaptation
- Adaptation is the specific ability of the intestine to increase its capacity to absorb nutrients following loss of its surface and length.
- There will be structural, motility and functional changes in the remaining intestine to compensate its loss.
- Adaptation depends on multiple factors including individual, intestinal and therapeutic measurements.
- Adaptation is usually occurred during the first two years after the bowel resection.
- Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, early introduction of nutrition therapy.
- Following the bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases.
| Intestinal adaptation | |||
|---|---|---|---|
| Phase | Duration | Main features | |
| Acute phase | |||
| Adaptive phase | |||
| Maintenance phase |
Malabsorption
- The main reasons for malabsorption following bowel resection include:
- Reduced absorption capacity of the small intestine due to loss of surface area, leading to:
- Loss of fluid and dehydration
- Electrolyte imbalance
- Loss of Macronutrients including carbohydrates, lipids and proteins
- Disturbance in production of enzymes and hormones, leading to:
- Diarrhea
- Steatorrhea
- Loss of vitamins
- Resection of specific sites, leading to:
- Loss of absorption of vitamin B12 and bile salts
- Reduced capacity of fluid retention
- Loss of ileocecal valve, leading to:
- Small bowel bacterial overgrowth
- Increased gastric and intestinal transit
- Compromised production of gastrointestinal regulators including cholecystokinin, secretin, gastric inhibitory polypeptide and peptide YY, leading to:
- Increased gastric and intestinal transit
- Hypergastrinemia
- Reduced absorption capacity of the small intestine due to loss of surface area, leading to:
Associated Conditions
Gross Pathology
- On gross pathology, the resected bowel may show the underlying causes including Crohn's disease, malignancies or ischemia.
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Microscopic Pathology
- On microscopic histopathological analysis, the resected bowel may show the underlying causes including Crohn's disease, malignancies or ischemia.
References
- ↑ "File:Diagram of the small bowel 01 CRUK 045.svg - Wikimedia Commons".
- ↑ Tappenden KA (2014). "Pathophysiology of short bowel syndrome: considerations of resected and residual anatomy". JPEN J Parenter Enteral Nutr. 38 (1 Suppl): 14S–22S. doi:10.1177/0148607113520005. PMID 24500909.
- ↑ Thomson, Alan B.R.; Drozdowski, Laurie; Iordache, Claudiu; Thomson, Ben K.A.; Vermeire, Severine; Clandinin, M. Tom; Wild, Gary (2003). Digestive Diseases and Sciences. 48 (8): 1546–1564. doi:10.1023/A:1024719925058. ISSN 0163-2116. Missing or empty
|title=(help) - ↑ Eça, Rosário; Barbosa, Elisabete (2016). "Short bowel syndrome: treatment options". Journal of Coloproctology. 36 (4): 262–272. doi:10.1016/j.jcol.2016.07.002. ISSN 2237-9363.
- ↑ "File:ResectedIleum.jpg - Wikimedia Commons". External link in
|title=(help) - ↑ "File:Crohn Jejunum.PNG - Wikimedia Commons".