Acute diarrhea pathophysiology: Difference between revisions

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{{Acute diarrhea}}
{{Acute diarrhea}}


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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
[[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]].


OR
==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>


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].
===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]], [[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 chronic [[osmotic]] [[diarrhea]].  


OR
===Secretory diarrhea===
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 [[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.
*[[Cytokine|Cytokines]] activate the release of [[inflammatory]] mediators such as [[Platelet-activating factor|platelet activating factor]] and [[Prostaglandin|prostaglandins]] which stimulate secretion.


[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
===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]].
*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> 


OR
===Motility disorders causing diarrhea===
 
Both rapid and slow transit time are associated with motility [[disorders]] causing [[diarrhea]].  
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 physiological mechanisms of [[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>
 
===Osmotic chronic diarrhea===
[[Osmotic]] chronic [[diarrhea]] involves an unabsorbed substance that draws water from the [[plasma]] into the [[intestinal]] lumen along [[osmotic]] gradients. If excessive amounts of unabsorbed substance are retained in the [[intestinal]] lumen, water will not be absorbed and [[diarrhea]] will result.
*Chronic [[diarrhea]] due to an [[osmotic]] cause includes [[osmotic]] [[laxatives]] such as [[lactose intolerance]] [[Antacid|antacids]], [[fructose]], [[lactulose]], [[laxatives]] [[magnesium]], [[phosphate]], and [[sorbitol]].<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> 
*[[Maldigestion]] [[syndromes]] such as [[disaccharidase]] deficiency and [[Pancreatic insufficiency|pancreatic exocrine insufficiency]] can also result in [[osmotic]] chronic [[diarrhea]].
*[[Osmotic]] diarrheas might result in [[steatorrhea]] and [[azotorrhea]] (passage of [[fat]] and nitrogenous substances into the [[stool]]), but they typically do not cause any [[rectal bleeding]].<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>
 
===Secretory chronic diarrhea===
Secretory chronic [[diarrhea]] results from disordered [[electrolyte]] transport and, despite the term, is more commonly caused by decreased [[absorption]] rather than net [[secretion]].
*Secretory [[Diarrhea|diarrheas]] include [[congenital]] abnormalities such as [[congenital]] chloridorrhea, in which an abnormality in the [[genetic]] control of [[Chloride-bicarbonate exchanger|chloride-bicarbonate exchange]] in the [[ileum]] results in the loss of [[chloride]] into the [[stool]].
*Another example is the loss of α2-adrenergic function in [[enterocytes]] of patients with [[autonomic neuropathy]] caused by [[diabetes mellitus]].
*The typical features of secretory [[diarrhea]] include the persistence of the [[diarrhea]] with fasting and the absence of [[steatorrhea]], [[azotorrhea]], or [[Rectal bleeding|blood per rectum]].
*Secretory diarrheas caused by [[neuroendocrine tumors]] have been identified by measurement of [[plasma]] levels of the [[hormone]] or its [[metabolite]] in the [[urine]].
*Investigations include measurements of [[VIP]], [[gastrin]], or [[calcitonin]] in [[plasma]] or 24-hour collections of urine for [[5-Hydroxyindoleacetic acid|5-hydroxyindoleacetic acid]].<ref name="pmid8371728">{{cite journal| author=von der Ohe MR, Camilleri M, Kvols LK, Thomforde GM| title=Motor dysfunction of the small bowel and colon in patients with the carcinoid syndrome and diarrhea. | journal=N Engl J Med | year= 1993 | volume= 329 | issue= 15 | pages= 1073-8 | pmid=8371728 | doi=10.1056/NEJM199310073291503 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8371728  }} </ref>
 
===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]].
*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|anti-inflammatory medications]], appear to benefit patients with [[microscopic]] or [[collagenous colitis]].<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 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]].  
*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]].  
*The clinical manifestations of chronic [[diarrhea]] caused by motility disorders include [[steatorrhea]], usually up to 14 g per day.
*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>  
*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]].<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>
 
===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 acid|bile acids]] being delivered into the [[intestine]].<ref name="pmid3731987">{{cite journal| author=Breuer NF, Jaekel S, Dommes P, Goebell H| title=Fecal bile acid excretion pattern in cholecystectomized patients. | journal=Dig Dis Sci | year= 1986 | volume= 31 | issue= 9 | pages= 953-60 | pmid=3731987 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3731987  }} </ref><ref name="pmid3606289">{{cite journal| author=Arlow FL, Dekovich AA, Priest RJ, Beher WT| title=Bile acid-mediated postcholecystectomy diarrhea. | journal=Arch Intern Med | year= 1987 | volume= 147 | issue= 7 | pages= 1327-9 | pmid=3606289 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3606289  }} </ref>
*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 [[Ileum|ileal]] resection.


 
==Genetics, Associated conditions, Gross pathology and Microscopic pathology==
==== Osmotic diarrhea ====
For the details of the [[genetics]], associated conditions, [[Gross examination|gross]] and [[microscopic]] [[pathology]] of the following causes of acute [[diarrhea]], click the links below.
* Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gap >125 mOsm/kg and fasting leads to cessation of diarrhea. 
*[[Rotavirus]]
* This may occur due to increased osmolarity due to nonabsorbable carbohydrates within the intestinal lumen, such as lactulose which induces a secretory state.
*[[Traveler's diarrhea]]
* Diarrhea induced by enterotoxins generate a secretory state by increasing secretion of anions.
*[[Ulcerative colitis pathophysiology#Pathphysiology|Ulcerative colitis]]
 
*[[Crohn's disease pathophysiology#Pathophysiology|Crohn's disease]]
==== Secretory diarrhea ====
*[[Lactose intolerance pathophysiology#Pathophysiology|Lactose intolerance]]
*It is understood that diarrhea is the result of alteration of the absorptive role of the gut to a secretory one.
*[[Cholera pathophysiology#Pathophysiology|Cholera]]
*In secretory diarrheas, stool osmotic gap is <50 mOsm/kg and fasting does not lead to diarrhea cessation.
*[[Microsporidiosis pathophysiology#Pathophysiology|Microsporidiosis]]
*Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions.  
*[[Giardiasis pathophysiology#Pathophysiology|Giardiasis]]
*Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling.
*[[Cryptosporidiosis pathophysiology#Pathophysiology|Cryptosporidiosis]]
*Cytokines activate release of inflammatory mediators such as platelet activating factor and prostaglandins which stimulate secretion.
*[[Hyperthyroidism pathophysiology#Pathophysiology|Hyperthyroidism]]
 
==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==
==References==
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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.

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.

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.

Motility disorders causing diarrhea

Both rapid and slow transit time are associated with motility disorders causing diarrhea.

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.

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ Morris AI, Turnberg LA (1979). "Surreptitious laxative abuse". Gastroenterology. 77 (4 Pt 1): 780–6. PMID 467934.
  4. ↑ 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.
  5. ↑ 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.

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