Acute diarrhea pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
The exact pathogenesis of acute diarrhea is different for infectious and non-infectious causes. [[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The pathophysiology of acute [[diarrhea]] include [[osmotic]], secretory, [[inflammatory]], altered motility, and [[iatrogenic]] mechanisms.<ref name="pmid22677080">{{cite journal| author=Sweetser S| title=Evaluating the patient with diarrhea: a case-based approach. | journal=Mayo Clin Proc | year= 2012 | volume= 87 | issue= 6 | pages= 596-602 | pmid=22677080 | doi=10.1016/j.mayocp.2012.02.015 | pmc=3538472 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22677080 }} </ref> | |||
[[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The | |||
===Osmotic | ===Osmotic diarrhea=== | ||
Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gap >125 mOsm/kg. In case of osmotic diarrhea, fasting leads to cessation of diarrhea. | |||
* | *Acute [[diarrhea]] due to an [[osmotic]] cause includes [[osmotic]] [[laxatives]] such as [[lactose intolerance]] [[Antacid|antacids]], [[fructose]], [[lactulose]], [[laxatives]] [[magnesium]], [[phosphate]], and [[sorbitol]], which induce a secretory state.<ref name="pmid7776987">{{cite journal| author=Suarez FL, Savaiano DA, Levitt MD| title=A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance. | journal=N Engl J Med | year= 1995 | volume= 333 | issue= 1 | pages= 1-4 | pmid=7776987 | doi=10.1056/NEJM199507063330101 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7776987 }} </ref><ref name="pmid467934">{{cite journal| author=Morris AI, Turnberg LA| title=Surreptitious laxative abuse. | journal=Gastroenterology | year= 1979 | volume= 77 | issue= 4 Pt 1 | pages= 780-6 | pmid=467934 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=467934 }} </ref> | ||
*[[Maldigestion]] [[syndromes]] such as [[disaccharidase]] deficiency may also result in [[osmotic]] chronic [[diarrhea]]. | |||
===Secretory | ===Secretory diarrhea=== | ||
Secretory | Secretory [[diarrhea]] results from disordered [[electrolyte]] transport and is the result of alteration of the absorptive role of the gut to a secretory one. In secretory diarrheas, stool osmotic gap is <50 mOsm/kg and fasting does not lead to diarrhea cessation. | ||
*Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions. | |||
* | *Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling. | ||
* | *Cytokines activate release of inflammatory mediators such as platelet activating factor and prostaglandins which stimulate secretion. | ||
* | |||
===Inflammatory | ===Inflammatory diarrhea=== | ||
Disruption of the normal colonic [[epithelial]] barrier by microorganisms is mainly responsible for [[inflammatory]] chronic [[diarrhea]]. This disruption can lead to exudative, secretory, or malabsorptive components of inflammatory chronic [[diarrhea]]. | Disruption of the normal colonic [[epithelial]] barrier by microorganisms is mainly responsible for [[inflammatory]] chronic [[diarrhea]]. This disruption can lead to exudative, secretory, or malabsorptive components of inflammatory chronic [[diarrhea]]. | ||
*[[Inflammatory]] causes of chronic [[diarrhea]] might present with features that suggest [[malabsorption]] or [[rectal bleeding]]. | *[[Inflammatory]] causes of chronic [[diarrhea]] might present with features that suggest [[malabsorption]] or [[rectal bleeding]]. | ||
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==== Osmotic diarrhea ==== | ==== Osmotic diarrhea ==== | ||
* | * | ||
* Diarrhea induced by enterotoxins generate a secretory state by increasing secretion of anions. | * Diarrhea induced by enterotoxins generate a secretory state by increasing secretion of anions. | ||
==== Secretory diarrhea ==== | ==== Secretory diarrhea ==== | ||
* | * | ||
* | * | ||
* | * | ||
==Genetics== | ==Genetics== | ||
Revision as of 15:19, 9 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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
Pathogenesis
The exact pathogenesis of acute diarrhea is different for infectious and non-infectious causes. Diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiology of acute diarrhea include osmotic, secretory, inflammatory, altered motility, and iatrogenic mechanisms.[1]
Osmotic diarrhea
Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gap >125 mOsm/kg. In case of osmotic diarrhea, fasting leads to cessation of diarrhea.
- Acute diarrhea due to an osmotic cause includes osmotic laxatives such as lactose intolerance antacids, fructose, lactulose, laxatives magnesium, phosphate, and sorbitol, which induce a secretory state.[2][3]
- Maldigestion syndromes such as disaccharidase deficiency may also result in osmotic chronic diarrhea.
Secretory diarrhea
Secretory diarrhea results from disordered electrolyte transport and is the result of alteration of the absorptive role of the gut to a secretory one. In secretory diarrheas, stool osmotic gap is <50 mOsm/kg and fasting does not lead to diarrhea cessation.
- Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions.
- Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling.
- Cytokines activate release of inflammatory mediators such as platelet activating factor and prostaglandins which stimulate secretion.
Inflammatory diarrhea
Disruption of the normal colonic epithelial barrier by microorganisms is mainly responsible for inflammatory chronic diarrhea. This disruption can lead to exudative, secretory, or malabsorptive components of inflammatory chronic diarrhea.
- Inflammatory causes of chronic diarrhea might present with features that suggest malabsorption or rectal bleeding.
- The nature of the malabsorption depends on the regions affected (e.g., proximal vs. distal small bowel), and rectal bleeding is usually a manifestation of colonic or rectal ulcerations.
- Anti-inflammatory agents, including bismuth subsalicylate or other, more potent anti-inflammatory medications, appear to benefit patients with microscopic or collagenous colitis.[4]
Motility disorders causing chronic diarrhea
Both rapid transit time and slow transit time are associated with motility disorders causing chronic diarrhea.
- Rapid transit time delivers fluid secreted during digestion to the distal small bowel or colon. This prevents reabsorption of normally secreted fluid in the small bowel, overwhelming the reabsorptive capacity of the colon.
- Slow transit time results in bacterial overgrowth with bile acid deconjugation, poor micelle formation, and steatorrhea.
- The clinical manifestations of chronic diarrhea caused by motility disorders include steatorrhea, usually up to 14 g per day.
- Osmotic laxatives result in acceleration of transit through the bowel, which is associated with up to 14 g of fat in the stool.
- Presence of more than 14 g per day of fat in the stool suggests the presence of bacterial overgrowth or associated disease such as celiac disease.[5]
Iatrogenic causes of chronic diarrhea
After abdominal surgeries such as cholecystectomy, about 5%–10% of patients develop chronic diarrhea.
- Most of these cases resolve completely or significantly improve within a couple of months.
- Iatrogenic diarrhea is related to excessive bile acids being delivered into the intestine.[6][7]
- After a cholecystectomy, bile is delivered directly into the small bowel, overcoming the terminal ileum's ability to reabsorb adequately, leading to cholerheic diarrhea.
- Some other iatrogenic causes of chronic diarrhea might result from vagal injury and ileal resection.
Osmotic diarrhea
- Diarrhea induced by enterotoxins generate a secretory state by increasing secretion of anions.
Secretory diarrhea
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Sweetser S (2012). "Evaluating the patient with diarrhea: a case-based approach". Mayo Clin Proc. 87 (6): 596–602. doi:10.1016/j.mayocp.2012.02.015. PMC 3538472. PMID 22677080.
- ↑ Suarez FL, Savaiano DA, Levitt MD (1995). "A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance". N Engl J Med. 333 (1): 1–4. doi:10.1056/NEJM199507063330101. PMID 7776987.
- ↑ Morris AI, Turnberg LA (1979). "Surreptitious laxative abuse". Gastroenterology. 77 (4 Pt 1): 780–6. PMID 467934.
- ↑ Pardi DS, Smyrk TC, Tremaine WJ, Sandborn WJ (2002). "Microscopic colitis: a review". Am J Gastroenterol. 97 (4): 794–802. doi:10.1111/j.1572-0241.2002.05595.x. PMID 12003412.
- ↑ Hammer HF, Santa Ana CA, Schiller LR, Fordtran JS (1989). "Studies of osmotic diarrhea induced in normal subjects by ingestion of polyethylene glycol and lactulose". J Clin Invest. 84 (4): 1056–62. doi:10.1172/JCI114267. PMC 329760. PMID 2794043.
- ↑ Breuer NF, Jaekel S, Dommes P, Goebell H (1986). "Fecal bile acid excretion pattern in cholecystectomized patients". Dig Dis Sci. 31 (9): 953–60. PMID 3731987.
- ↑ Arlow FL, Dekovich AA, Priest RJ, Beher WT (1987). "Bile acid-mediated postcholecystectomy diarrhea". Arch Intern Med. 147 (7): 1327–9. PMID 3606289.