Dysphagia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

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

Normal physiology of the food motility through the esophagus

• The esophagus is a part of the gastrointestinal tract which is responsible of moving the food from the mouth to the rectum.
• The esophagus has anti-reflux barrier which prevents the return of the acidic contentof the stomach back to the esophagus. The anti-reflux barrier consists of the lower esophageal sphincter (LES) and the related part of the diaphragm.
• The lower esophageal sphincter is contracting smooth muscle at the end of the esophagus responsible for the food passage to the stomach. LES has high pressure tone which helps keeping it a strong barrier between the esophagus and the stomach.

Pathogenesis of Dysphagia

The pathogenesis of dysphagia can be explained on the basis of etiology. There are a number of causes of different types of dysphagia of which the most common being esophageal food impaction. The following table elaborates the mechanism of each cause.

Cause of dysphagia	Type of food		Type of progression	Mechanism of development	Genes involved	Gross pathology findings	Microscopic findings
Oropharyngeal dysphagia	Soilds	Liquids	Intermittent/Progressive
•Zenker's diverticulum •Webs	Yes	No	Progressive	•Zenker's diverticulum: Zenker's diverticulum (ZD) is thought to be due to the result of motor abnormalities of the esophagus ZD is a defect over the Killian's triangle, a point of weakness in the muscular wall of the hypopharynx Killian's triangle is surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle.  ZD should be considered a pseudodiverticulum as it includes only mucosa and submucosa.		Diverticulum or a sac is seen in the esophagus	Psuedo diverticulum Only mucosa and submucosa present Chronic submucosal inflammation Epithelial atypia or dysplasia
				•
•Neoplasm	Yes	Yes	Progressive	•Neoplasm
Myogenic causes •Myasthenia gravis •Connective tissue disorder •Myotonic dystrophy Neurogenic causes •ALS •Parkinsonism •Stroke	Yes	Yes	Progressive
Esophageal dysphagia
•Pill esophagitis •Caustic injury •Chemotherapy	Yes	No
•Strictures •Cancer	Yes	No	Progressive
•Rings •Webs	Yes	No	Intermittent	Rings: Webs: Multiple theories have been found: Esophageal webs are thought to be due to the chronic damage to the esophageal mucosa Esophageal webs are thought to be due to failure of the esophagus to recanalize.
•Achalasia •Diffuse esophageal spasm(DES)	Yes	Yes	Intermittent	•Achalasia:
				•Diffuse esophageal spasm(DES): Impairment of inhibitory myenteric plexus neurons Dysregulation of endogenous NO synthesis or/and degradation	There is a genetic association	Gross thickening of muscularis propria layer and lower esophageal sphincter (LES) due to hyperplasia are characteristic findings of DES	There is degeneration of vagal fibres, inflammatory infiltration of myenteric plexus, and hyperplasia of smooth muscles are characteristic findings of DES
•Scleroderma	Yes	Yes	Progressive