Toxic megacolon pathophysiology: Difference between revisions
Farima Kahe (talk | contribs) |
Farima Kahe (talk | contribs) |
||
Line 35: | Line 35: | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
*It is believed that oxic megacolon is the result of defective smooth muscle contraction, lowered basal pressure in the colonic lumen, and an inhibited gastro-colic reflex is caused by changes in colonic response to vasoactive intestinal polypeptide, substance P, neurotensin, leukotrienes, and nitric oxide.<ref name="BassottiAntonelli2014">{{citejournal|last1=Bassotti|first1=Gabrio|last2=Antonelli|first2=Elisabetta|last3=Villanacci|first3=Vincenzo|last4=Baldoni|first4=Monia|last5=Dore|first5=Maria Pina|title=Colonic motility in ulcerative colitis|journal=United European Gastroenterology Journal|volume=2|issue=6|year=2014|pages=457–462|issn=2050-6406|doi=10.1177/2050640614548096}}</ref><ref name="GanBeck2003">{{cite journal|last1=Gan|first1=S. Ian|last2=Beck|first2=P. L.|title=A new look at toxic megacolon: an update and review of incidence, etiology, pathogenesis, and management|journal=The American Journal of Gastroenterology|volume=98|issue=11|year=2003|pages=2363–2371|issn=0002-9270|doi=10.1111/j.1572-0241.2003.07696.x}}</ref> | *It is believed that oxic megacolon is the result of defective smooth muscle contraction, lowered basal pressure in the colonic lumen, and an inhibited gastro-colic reflex is caused by changes in colonic response to vasoactive intestinal polypeptide, substance P, neurotensin, leukotrienes, and nitric oxide.<ref name="BassottiAntonelli2014">{{citejournal|last1=Bassotti|first1=Gabrio|last2=Antonelli|first2=Elisabetta|last3=Villanacci|first3=Vincenzo|last4=Baldoni|first4=Monia|last5=Dore|first5=Maria Pina|title=Colonic motility in ulcerative colitis|journal=United European Gastroenterology Journal|volume=2|issue=6|year=2014|pages=457–462|issn=2050-6406|doi=10.1177/2050640614548096}}</ref><ref name="GanBeck2003">{{cite journal|last1=Gan|first1=S. Ian|last2=Beck|first2=P. L.|title=A new look at toxic megacolon: an update and review of incidence, etiology, pathogenesis, and management|journal=The American Journal of Gastroenterology|volume=98|issue=11|year=2003|pages=2363–2371|issn=0002-9270|doi=10.1111/j.1572-0241.2003.07696.x}}</ref> | ||
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. | *[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. | ||
*The progression to [disease name] usually involves the [molecular pathway]. | *The progression to [disease name] usually involves the [molecular pathway]. |
Revision as of 18:31, 31 October 2017
Toxic Megacolon Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Toxic megacolon pathophysiology On the Web |
American Roentgen Ray Society Images of Toxic megacolon pathophysiology |
Risk calculators and risk factors for Toxic megacolon pathophysiology |
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
- It is believed that oxic megacolon is the result of defective smooth muscle contraction, lowered basal pressure in the colonic lumen, and an inhibited gastro-colic reflex is caused by changes in colonic response to vasoactive intestinal polypeptide, substance P, neurotensin, leukotrienes, and nitric oxide.[1][2]
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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
- ↑ Template:Citejournal
- ↑ Gan, S. Ian; Beck, P. L. (2003). "A new look at toxic megacolon: an update and review of incidence, etiology, pathogenesis, and management". The American Journal of Gastroenterology. 98 (11): 2363–2371. doi:10.1111/j.1572-0241.2003.07696.x. ISSN 0002-9270.