Sandbox: mahda20

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]. 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 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.
• [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.

Peptic strictures are the endstage result of chronic reflux esophagitis. They account for 90% of benign esophageal strictures and, by definition, imply a stricture arising as a result of exposure to the acid-peptic content of the stomach. The esophagus normally is exposed to frequent episodes of reflux of small amounts of gastric fluid which are limited by a competent lower esophageal sphincter and rapidly cleared by normal esophageal peristalsis. A defect in these and other esophageal protective mechanisms leads to inflammation due to prolonged esophageal exposure to acid, pepsin, and possibly bile and pancreatic enzymes. Stricture formation occurs in 7–23% of patients with reflux esophagitis. The process is progressive, beginning with mucosal edema and inflammatory cell infiltrates of the lamina propria. Chronic esophagitis progresses transmurally, even into periesophageal tissues, with subsequent fibrosis and scarring leading to luminal compromise and esophageal foreshortening (Kuo and Kalloo 1998,Mamazza et al 1998).

A stricture is an esophageal narrowing, usually 13 mm or less in diameter, that causes dysphagia. The normal esophagus measures up to 30 mm in diameter. Peptic strictures occur usually at the squamocolumnar junction and measure 1–4 cm in length. The typical patient with a peptic stricture is elderly with a long history of gastroesophageal reflux (GER). Significant predictors of stricture formation in patients with GER are lower esophageal sphincter (LES) tone of less than 8 mmHg, impaired esophageal motility, and duodenogastric reflux (Marks and Richter 1993,Stein et al 1992). Hiatus hernia is twice as prevalent in GER patients with stricture (85%) as compared to those with no esophagitis (42%) (Kuo and Kalloo 1998).

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:
  • gastroesophageal reflux disease

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].

Mahshid

Normal physiology:

Gastric acid frequently get back as reflux to esophagus. Lower esophageal sphincter normally prevent large amount of gastric acid reflux. The esophagus normally has the ability to clear gastric acid effect by normal esophageal peristalsis.