Dysphagia pathophysiology

Dysphagia Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Dysphagia from other Conditions
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X Ray
Barium Swallow
Endoscopy
CT
MRI
Echocardiography and Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Dysphagia pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Dysphagia pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Dysphagia pathophysiology
CDC on Dysphagia pathophysiology
Dysphagia pathophysiology in the news
Blogs on Dysphagia pathophysiology
Directions to Hospitals Treating Dysphagia
Risk calculators and risk factors for Dysphagia pathophysiology

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

Overview

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]

Pathophysiology

Physiology of normal swallowing

Anatomically, swallowing can be divided into three phases:

• Oral preparatory phase
• Oral voluntary phase
• Pharyngeal phase
• Esophageal phase

(a)Oral preparatory phase:

• This phase involves mastication and formation of a bolus in the oral cavity.

(b)Oral voluntary phase:

• It is characterized by propelling the bolus into the pharyngeal phase.
• It is controlled by the corticobulbar tracts and cranial nerves V(trigemenal),VII(facial)and XII(hypoglossal).

(c)Pharyngeal phase:

• This phase is a reflex
• It is controlled by the cranial nerves V(trigemenal),X(vagus)XI(accessory) and, XII(hypoglossal).

(d)Esophageal phase:

• 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(ZD): It is 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	Pseudo diverticulum Only mucosa and submucosa present Chronic submucosal inflammation Epithelial atypia or dysplasia
				•Webs
•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 •Esophageal Cancer	Yes	No	Progressive	Strictures:	The following genes can be involved: ACD CTC1 DKC1 NHP2 NOP10 PARN RTEL1 TERC TERT TINF2 WRAP53
				•Esophageal Cancer:	Mutations in the following genes can cause esophageal cancer: Chromosomal losses (4q, 5q, 9p, and 18q) Chromosomal gains (8q, 17q, and 20q) Gene amplifications (7, 8, and 17q) PT53 genes and P16 genes  Variants in ADH and/or ALDH2 genes
•Rings •Webs	Yes	No	Intermittent	Rings: Webs: Multiple theories have been found: Webs may form due to the chronic damage to the esophageal mucosa Or due to failure of the esophagus to recanalize.
•Achalasia •Diffuse esophageal spasm(DES)	Yes	Yes	Intermittent	•Achalasia:	HLA class II moleculesVasoactive intestinal peptide KIT Interleukin 23 receptor|	There is defect in the nerves that control the motility of the esophagus (the myenteric plexus).  The esophagus is dilated and hypertrophied.
				•Diffuse esophageal spasm(DES): Impairment of inhibitory myenteric plexus neurons Dysregulation of endogenous NO synthesis or/and degradation	There is a genetic association between DES and achalasia	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