Acute diarrhea pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The pathophysiology of acute [[diarrhea]] includes [[osmotic]], secretory, [[inflammatory]] types, and diarrhea due to altered [[motility]]. Acute [[diarrhea]] due to | [[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The pathophysiology of acute [[diarrhea]] includes [[osmotic]], secretory, [[inflammatory]] types, and diarrhea due to altered [[motility]]. Acute [[diarrhea]] due to [[osmotic]] causes includes [[osmotic]] [[laxatives]] such as [[lactose intolerance]], [[Antacid|antacids]], [[fructose]], [[lactulose]], and increased concentration of [[magnesium]], [[phosphate]], and [[sorbitol]], which induce a secretory state. [[Infection|Bacterial infection]] of the [[intestine]] leads to activation of [[epithelial]] [[ion channels]] with increased secretion of [[anions]]. Invasion of the [[epithelium]] by various [[Pathogen|pathogens]] lead to [[exotoxin]] production and enhancement of [[enterocyte]] secretion by [[Cytotoxicity|cytotoxins]] or [[intracellular]] signalling. In case of motility disorders of the [[Gastrointestinal tract|gut]], 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]]. | ||
==Pathogenesis== | ==Pathogenesis== | ||
The exact pathogenesis of acute diarrhea is different for [[Infection|infectious]] and non-infectious causes. [[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The pathophysiology of acute [[diarrhea]] includes [[osmotic]], secretory, [[inflammatory]] types, and diarrhea due to altered [[motility]].<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> | The exact [[pathogenesis]] of acute diarrhea is different for [[Infection|infectious]] and non-[[infectious]] causes. [[Diarrhea]] is a condition of altered [[intestinal]] water and [[electrolyte]] transport. The pathophysiology of acute [[diarrhea]] includes [[osmotic]], secretory, [[inflammatory]] types, and diarrhea due to altered [[motility]].<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> | ||
===Osmotic diarrhea=== | ===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. | 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]] causes 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> | *Acute [[diarrhea]] due to an [[osmotic]] causes includes [[osmotic]] [[laxatives]] such as [[lactose intolerance]], [[Antacid|antacids]], [[fructose]], [[lactulose]], [[laxatives]] and high concentration of [[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]] | *[[Maldigestion]] [[syndromes]] such as [[disaccharidase]] deficiency may also result in chronic [[osmotic]] [[diarrhea]]. | ||
===Secretory diarrhea=== | ===Secretory diarrhea=== | ||
Secretory [[diarrhea]] results from disordered [[electrolyte]] transport and is the result of alteration of the [[Absorptive state|absorptive]] role of the gut | Secretory [[diarrhea]] results from disordered [[electrolyte]] transport and is the result of alteration of the [[Absorptive state|absorptive]] role of the gut and increased secretory capacity. In secretory diarrheas, stool osmotic gap is <50 mOsm/kg and fasting does not lead to diarrhea cessation. | ||
*[[Infection|Bacterial infection]] of the [[intestine]] leads to activation of epithelial ion channels with increased secretion of anions. | *[[Infection|Bacterial infection]] of the [[intestine]] leads to activation of [[Epithelium|epithelial]] [[ion channels]] with increased secretion of [[anions]]. | ||
*Invasion of the [[epithelium]] by various [[Pathogen|pathogens]] lead to [[exotoxin]] production and enhancement of [[enterocyte]] secretion by [[Cytotoxicity|cytotoxins]] or intracellular signalling. | *Invasion of the [[epithelium]] by various [[Pathogen|pathogens]] lead to [[exotoxin]] production and enhancement of [[enterocyte]] secretion by [[Cytotoxicity|cytotoxins]] or [[intracellular]] signalling. | ||
*[[Cytokine|Cytokines]] activate release of inflammatory mediators such as [[Platelet-activating factor|platelet activating factor]] and [[Prostaglandin|prostaglandins]] which stimulate secretion. | *[[Cytokine|Cytokines]] activate the release of [[inflammatory]] mediators such as [[Platelet-activating factor|platelet activating factor]] and [[Prostaglandin|prostaglandins]] which stimulate secretion. | ||
===Inflammatory diarrhea=== | ===Inflammatory diarrhea=== | ||
Disruption of the normal colonic [[epithelial]] barrier by microorganisms is mainly responsible for [[inflammatory]] [[diarrhea]]. This disruption may lead to [[Exudate|exudative]], [[Secretory component|secretory]], or [[Malabsorption|malabsorptive]] components of inflammatory [[diarrhea]]. | Disruption of the normal [[Colon|colonic]] [[epithelial]] barrier by [[microorganisms]] is mainly responsible for [[inflammatory]] [[diarrhea]]. This disruption may lead to [[Exudate|exudative]], [[Secretory component|secretory]], or [[Malabsorption|malabsorptive]] components of inflammatory [[diarrhea]]. | ||
*[[Inflammatory]] causes of [[diarrhea]] might present with features that suggest [[malabsorption]] or [[rectal bleeding]]. | *[[Inflammatory]] causes of [[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]].<ref name="pmid12003412">{{cite journal| author=Pardi DS, Smyrk TC, Tremaine WJ, Sandborn WJ| title=Microscopic colitis: a review. | journal=Am J Gastroenterol | year= 2002 | volume= 97 | issue= 4 | pages= 794-802 | pmid=12003412 | doi=10.1111/j.1572-0241.2002.05595.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12003412 }} </ref> | *The nature of the [[malabsorption]] depends on the regions affected (e.g., [[proximal]] vs. distal [[Small intestine|small bowel]]), and [[rectal bleeding]] is usually a manifestation of [[Colon|colonic]] or [[rectal]] [[ulcerations]].<ref name="pmid12003412">{{cite journal| author=Pardi DS, Smyrk TC, Tremaine WJ, Sandborn WJ| title=Microscopic colitis: a review. | journal=Am J Gastroenterol | year= 2002 | volume= 97 | issue= 4 | pages= 794-802 | pmid=12003412 | doi=10.1111/j.1572-0241.2002.05595.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12003412 }} </ref> | ||
===Motility disorders causing diarrhea=== | ===Motility disorders causing diarrhea=== | ||
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*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]]. | *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]]. | *Slow transit time results in [[bacterial overgrowth]] with [[bile acid]] deconjugation, poor [[micelle]] formation, and [[steatorrhea]]. | ||
*Delayed transit time may lead to symptoms such as [[steatorrhea]], usually up to 14 g per day.<ref name="pmid2794043">{{cite journal| author=Hammer HF, Santa Ana CA, Schiller LR, Fordtran JS| title=Studies of osmotic diarrhea induced in normal subjects by ingestion of polyethylene glycol and lactulose. | journal=J Clin Invest | year= 1989 | volume= 84 | issue= 4 | pages= 1056-62 | pmid=2794043 | doi=10.1172/JCI114267 | pmc=329760 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2794043 }} </ref> | *Delayed transit time may lead to [[symptoms]] such as [[steatorrhea]], usually up to 14 g per day.<ref name="pmid2794043">{{cite journal| author=Hammer HF, Santa Ana CA, Schiller LR, Fordtran JS| title=Studies of osmotic diarrhea induced in normal subjects by ingestion of polyethylene glycol and lactulose. | journal=J Clin Invest | year= 1989 | volume= 84 | issue= 4 | pages= 1056-62 | pmid=2794043 | doi=10.1172/JCI114267 | pmc=329760 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2794043 }} </ref> | ||
==Genetics, Associated conditions, Gross pathology and Microscopic pathology== | ==Genetics, Associated conditions, Gross pathology and Microscopic pathology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]
Overview
Diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiology of acute diarrhea includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility. Acute diarrhea due to osmotic causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, and increased concentration of magnesium, phosphate, and sorbitol, which induce a secretory state. 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. In case of motility disorders of the gut, 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.
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 includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility.[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 causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, laxatives and high concentration of magnesium, phosphate, and sorbitol, which induce a secretory state.[2][3]
- Maldigestion syndromes such as disaccharidase deficiency may also result in chronic osmotic diarrhea.
Secretory diarrhea
Secretory diarrhea results from disordered electrolyte transport and is the result of alteration of the absorptive role of the gut and increased secretory capacity. 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 the 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 diarrhea. This disruption may lead to exudative, secretory, or malabsorptive components of inflammatory diarrhea.
- Inflammatory causes of 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.[4]
Motility disorders causing diarrhea
Both rapid and slow transit time are associated with motility disorders causing 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.
- Delayed transit time may lead to symptoms such as steatorrhea, usually up to 14 g per day.[5]
Genetics, Associated conditions, Gross pathology and Microscopic pathology
For the details of the genetics, associated conditions, gross and microscopic pathology of the following causes of acute diarrhea, click the links below.
- Rotavirus
- Traveler's diarrhea
- Ulcerative colitis
- Crohn's disease
- Lactose intolerance
- Cholera
- Microsporidiosis
- Giardiasis
- Cryptosporidiosis
- Hyperthyroidism
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.