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Revision as of 13:29, 19 October 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, esophageal motor disorder, inflammation and fibrosis and scar of esophagus scarry esophagus and esophageal anastomosis strictures.
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 [disease name] is not fully understood.
OR
- It is thought that esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, , esophageal motor disorderor, [hypothesis 3].[1] inflammation and fibrosis and scar of esophagus scarry esophagus and esophageal anastomosis strictures.all possible variations of scarry esophageal strictures according their etiology, localization and the extension[2] Histologically, the mucosal epithelium and lamina propria had regenerated as in the normal area. In the EBD group, the circumferential stricture site showed marked thickening, and there were hypertrophic scars associated with epithelial defects on the luminal surface. Histologically, defects of the mucosal epithelium and full-thickness proliferation of connective tissue were observed.[3]
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [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
- The most important conditions/diseases associated with esophageal stricture include:
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
- ↑ Ahtaridis G, Snape WJ, Cohen S (1979). "Clinical and manometric findings in benign peptic strictures of the esophagus". Dig. Dis. Sci. 24 (11): 858–61. PMID 520106.
- ↑ Belevich VL, Ovchinnikov DV (2013). "[Treatment of benign esophageal stricture]". Vestn. Khir. Im. I. I. Grek. (in Russian). 172 (5): 111–4. PMID 24640761.
- ↑ Takase K, Aikawa M, Okada K, Watanabe Y, Okamoto K, Sato H, Nonaka K, Yamaguchi S, Sakuramoto S, Koyama I, Miyazawa M (2015). "Development of novel treatment with a bioabsorbable esophageal patch for benign esophageal stricture". Dis. Esophagus. 28 (8): 728–34. doi:10.1111/dote.12281. PMID 25286827.