Esophagus Secretes mucous, transports food – no enzymes produced,

no absorption Mucosa – protection against wear and tear lamina propria Submucosa Muscularis divided in thirds

Superior 1/3 skeletal muscle Middle 1/3 skeletal and smooth muscle Inferior 1/3 smooth muscle 2 sphincters – upper esophageal sphincter (UES) regulates

movement into esophagus, lower esophageal sphincter (LES) regulates movement into stomach

Adventitia – no serosa – attaches to surroundings < 3 cm below diaphragm

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Esophagus Lesions of the esophagus run from bland esophagitis to highly lethal cancers.

All produce dysphagia (difficulty in swallowing), which is attributed either to deranged esophageal motor function or to narrowing or obstruction of the lumen.

Heartburn or Gastroesophageal reflux disease (GERD) (retrosternal burning pain) usually reflects regurgitation of gastric contents into the lower esophagus.

Less commonly, hematemesis (vomiting of blood) and melena (blood in the stools) are evidence of severe inflammation, ulceration, or laceration of the esophageal mucosa.

• Massive hematemesis may reflect life-threatening rupture of esophageal varices.

esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus

Patho----- Of-------Eso

Structural abnormalities of the esophagus can be either congenital or acquired.

The two most common congenital esophageal abnormalities are

Esophageal Atresia (EA) and

Tracheoesophageal Fistula (TEF).

Anatomic disorders encountered infrequently (Table).

Selected Anatomic Disorders Of The Esophagus

Disorder Clinical Presentation and Anatomy

Stenosis Adult with progressive dysphagia to solids and eventually to all foods; a lower esophageal narrowing, which is usually the result of chronic inflammatory disease, including gastroesophageal reflux

Atresia, fistula

Newborn with aspiration, paroxysmal suffocation, pneumonia; esophageal atresia (absence of a lumen) and tracheoesophageal fistula may occur together

Webs, rings Episodic dysphagia to solid foods; a (presumably) acquired mucosal web or mucosal and submucosal concentric ring partially occluding the esophagus

Diverticula Episodic food regurgitation especially nocturnal, sometimes pain is present; an acquired outpouching of the esophageal wall

ANATOMIC AND MOTOR DISORDERS

• Both esophageal anatomy and function may be affected secondarily by many esophageal disorders.

• In hiatal hernia, separation of the diaphragmatic crura and widening of the space between the muscular crura and the esophageal wall permits a dilated segment of the stomach to protrude above the diaphragm.

Two anatomic patterns are recognized: the axial, or sliding hernia and the nonaxial, or paraesophageal hernia.

The sliding hernia constitutes 95% of cases; protrusion of the stomach above the diaphragm creates a bell-shaped dilation, bounded below by the diaphragmatic narrowing.

In paraesophageal hernias, a separate portion of the stomach, usually along the greater curvature, enters the thorax through the widened foramen.

Comparison of the two forms of esophageal hiatal hernias

Only about 9% of these adults, however, suffer from heartburn or regurgitation of gastric juices into the mouth.

Other complications affecting both types of hiatal hernias include mucosal ulceration, bleeding, and even perforation.

Achalasia The term achalasia means "failure to relax" and in the present context denotes incomplete relaxation of the lower esophageal sphincter in response to swallowing.

• Three major abnormalities in

achalasia:

Achalasia

(1) Aperistalsis (absence of peristalsis )(2) partial or incomplete relaxation of the lower esophageal

sphincter with swallowing(3) increased resting tone of the lower esophageal sphincter.

Causes

Primary: achalasia there is loss of intrinsic inhibitory innervation of the lower esophageal sphincter and smooth muscle.

Secondary: achalasia may arise from pathologic processes; example is Chagas disease, caused by Trypanosoma cruzi, which causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter.

Morphology

In primary achalasia there is progressive dilation of the esophagus above the level of the lower esophageal sphincter.

The wall of the esophagus may be normal thickness, thicker than normal because of hypertrophy of the muscularis, or markedly thinned by dilation.

Symptoms• Backflow (regurgitation) of food• Nocturnal regurgitation and aspiration of undigested

food• dysphagia• Chest pain, which may increase after eating or may be felt

in the back, neck, and arms• Cough• Difficulty swallowing liquids and solids• Heartburn • Unintentional weight loss Examination • Esophageal manometry: is a test used to measure the function of the

lower esophageal sphincte by specific tube through esogh to stomach• Esophagogastroduodenoscopy • Upper GI x-ray

Treatment

• Incurable• Palliative measures

– Nonsurgical– Surgical– Both are directed toward relieving the

obstruction caused by the no relaxing LES( lower esogh)

– Injection with botulinum toxin (Botox). This may help relax the sphincter muscles, but any benefit wears off within a matter of weeks or months.

Lacerations (Mallory-Weiss Syndrome)

Longitudinal tears in the esophagus at the esophagogastric junction.

The presumed pathogenesis is inadequate relaxation of the musculature of the lower esophageal sphincter during vomiting.

with stretching and tearing of the esophagogastric junction at the moment of propulsive expulsion of gastric contents.

This thinking is supported by the fact that a hiatal hernia is found in more than 75% of patients with Mallory-Weiss tears.

Tears may involve only the mucosa or may penetrate the wall.

Infection of the defect may lead to an inflammatory ulcer or to mediastinitis [is inflammation of the tissues in the mid-chest].

Esophageal lacerations account for 5% to 10% of upper gastrointestinal bleeding episodes.

Most often bleeding is not profuse and ceases without surgical intervention, but life-threatening hematemesis may occur.

ESOPHAGITIS Injury to the esophageal mucosa with subsequent

inflammation is a common condition worldwide. There are many presumed contributory factors:

Decreased efficacy of esophageal antireflux mechanisms Inadequate or slowed esophageal clearance of refluxed

material The presence of a sliding hiatal hernia Increased gastric volume, contributing to the volume of

refluxed material Impaired reparative capacity of the esophageal mucosa by

prolonged exposure to gastric juices Any one of these influences may assume primacy in an

individual case, but more than one is likely to be involved in most instances.

MORPHOLOGY

• The anatomic changes depend on the causative agent and on the duration and severity of the exposure.

• Mild esophagitis may appear macroscopically as simple hyperemia, with virtually no histologic abnormality.

• Three histologic features are characteristic of uncomplicated reflux esophagitis, although only one or two may be present:

• (1) Eosinophils, with or without neutrophils, in the epithelial layer;

• (2) Basal Zone Hyperplasia;

• (3) Elongation of lamina propria papillae. Intraepithelial neutrophils are markers of more severe injury.

Reflux esophagitis showing the superficial portion of the mucosa. Numerous eosinophils (arrows) are present within the mucosa, and the stratified squamous epithelium has not undergone complete maturation owing to ongoing inflammatory damage.

Clinical Features The dominant manifestation of reflux disease is heartburn,

sour brash. Difficult swallowing (dysphagia), Painful swallowing

(odynophagia) Chest pain, particularly behind the breastbone, that occurs

with eating Swallowed food becoming stuck in the esophagus (food impaction).

Rarely, chronic symptoms are punctuated by attacks of severe chest pain mimicking a heart attack.

The potential consequences of severe reflux esophagitis are bleeding, development of stricture, and Barrett esophagus, with its predisposition to malignancy.

BARRETT ESOPHAGUS Barrett esophagus is a complication of long-standing

gastroesophageal reflux, occurring in up to 10% of patients with persistent symptomatic reflux disease, as well as in some patients with asymptomatic reflux.

Barrett esophagus is defined as the replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells.

Prolonged and recurrent gastroesophageal reflux is thought to produce inflammation and eventually ulceration of the squamous epithelial lining.

Healing occurs by in growth of stem cells and re-epithelialization. In the microenvironment of an abnormally low pH in the distal

esophagus caused by acid reflux, the cells differentiate into columnar epithelium.

MORPHOLOGY Barrett esophagus is apparent as a

salmon-pink, velvety mucosa between the smooth, pale pink esophageal squamous mucosa and the more lush light brown gastric mucosa.

the esophageal squamous epithelium is replaced by metaplastic columnar epithelium (gastric mucosa ).

Critical to the pathologic evaluation of patients with Barrett mucosa is the recognition of dysplastic changes in the mucosa that may be precursors of cancer.

Barrett esophagus. A, Endoscopic view showing red velvety gastrointestinal-type mucosa extending from the gastroesophageal orifice. Note paler squamous esophageal mucosa. B, Microscopic view showing mixed gastric- and intestine-type columnar epithelial cells in glandular mucosa.

Ulcer and stricture may develop as a complication of Barrett esophagus.

Patients with Barrett esophagus have a 30- to 40-fold greater risk of developing esophageal adenocarcinoma compared with normal populations.

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Gastroesophageal reflux disease (GERD)

Gastroesophageal reflux (GER) is defined as passage of gastric contents into the esophagus.

GER is a normal physiologic process that occurs throughout the day in healthy infants, children, and adults.

Gastroesophageal reflux disease (GERD) occurs when gastric contents reflux into the esophagus or oropharynx and produce symptoms.

DefinitionsGER Passage of gastric contents into

esophagus

GERD Symptoms or complications that may occur when gastric contents reflux into esophagus or oropharynx

Regurgitation Passage of refluxed gastric contents into oral pharynx

Vomiting Expulsion of refluxed gastric contents from mouth

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Causes Its mostly happen becz the weakness of the lower

esophageal sphincter, or LES Alcohol (possibly) Hiatal hernia Obesity Pregnancy Scleroderma (autoimmune disorder, ) Smoking Some types of food :drinks with caffeine, fatty and

fried foods, garlic and onions, spicy foods

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GERD Eosinophilic esophagitisNormal esophagus

The esophageal biopsy specimen shows a small number of intraepithelial eosinophils.

Basal cell thickening of the esophageal mucosal epithelium and lengthening of stromal papillae.

this patient had dysphagia and food allergies that responded to an elimination diet.

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Symptoms A burning sensation in your chest (heartburn),

sometimes spreading to the throat, along with a sour taste in your mouth

Chest pain Difficulty swallowing (dysphagia) Hoarseness or sore throat Regurgitation of food or sour liquid (acid reflux) Sensation of a lump in the throat

Respiratory Symptoms of GER

• Apnea/ALTE

• Stridor and hoarseness

• Cough

• Wheezing

• Recurrent pneumonia

DiagnosisEsophagoscopy

To note mucosal changesEsophageal biopsies

To note changes at the cellular levelMotilitiy studies

Low LES pressures are associated with reflux

pH monitoringThe most precise measure for the

presence of acid in the esophageal lumen (24 hour monitoring)

Medical Treatment

Surgical TreatmentIndications for surgical treatment are somewhat

controversialStage 0 and Stage 1 disease should never be an

indication for surgeryStage 2 disease should always undergo a well

supervised period of medical management for at least six months to a year

Stage 3 disease should also undergo medical therapy first

In stage2 and in Stage 3 disease surgical options should be entertained after failed medical management

Surgical Treatment

Nissen fundoplicationTotal or partial

Their aim is to:Restore normal anatomy (intra-abdominal

segment of esophagus)Re-creating an appropriate high-pressure

sound at the esophagogastric junctionMaintaining this repair in the normal

anatomic position

BENIGN TUMORS

Leiomyomas Fibrovascular polyps Condylomas (hpv) Lipomas “Granulation” tissue

(pseudotumor)

ESOPHAGEAL CARCINOMA There are two types: squamous cell carcinomas and

adenocarcinomas . Worldwide, Squamous cell carcinomas constitute 90% of

esophageal cancers. Adenocarcinoma arising in Barrett esophagus is more

common in whites than in blacks. There are striking and puzzling differences in the geographic

incidence of esophageal carcinoma. In the United States, there are about 6 new cases per

100,000 population per year. In regions of Asia extending from the northern provinces of

China to Iran, the prevalence is well over 100 per 100,000.

RISK FACTORS FOR SQUAMOUS CELL CARCINOMA OF THE ESOPHAGUS

Esophageal Disorders

Long-standing esophagitis

Achalasia

Plummer-Vinson syndrome (esophageal webs, microcytic hypochromic anemia, atrophic glossitis)

Alcohol consumption

Tobacco abuse

Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)

Deficiency of trace metals (zinc, molybdenum)

Fungal contamination of foodstuffs

High content of nitrites/nitrosamines

Genetic Predisposition

Tylosis (hyperkeratosis of palms and soles)

MORPHOLOGY Squamous cell carcinomas are usually

early overt lesions appear as small, gray-white, plaque like thickenings or elevations of the mucosa and taking one of three forms:

(1) polypoid exophytic masses that protrude into the lumen;

(2) Necrotizing cancerous ulcerations that extend deeply and sometimes erode into the respiratory tree, aorta, or elsewhere

(3) diffuse infiltrative neoplasms that impart thickening and rigidity to the wall and narrowing of the lumen.

Large ulcerated squamous cell carcinoma of the esophagus

Exophytic growing outward

The epithelial lining above is clearly abnormal compared to the normal single-layer ciliated epithelium below.  

There is nuclear stratification, nuclear enlargement, hyperchromasia, pleomorphism, and mitoses.

 The photomicrograph above shows pseudoinvasion but the same architectural and cytological features.

Micrograph of an esophageal adenocarcinoma (dark blue - upper-left of image) and normal squamous epithelium (upper-right of image). H&E stain.

(a) Histology of squamous cell carcinoma Keratinization is seen.

(b) The tumor cells shows characteristic morphologies of small cell carcinoma.

(c) Tubular formations are seen.

(d) Transitional zone between squamous cell carcinoma element and small cell carcinoma element of the esophageal carcinoma.

Microscopic Image of Esophageal Squamous Cell Carcinoma Microscopic image of Squamous

Papilloma of the Esophagus

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Adenocarcinomas appear to arise from dysplastic mucosa in the setting of Barrett esophagus.

Unlike squamous cell carcinomas, they are usually in the distal one third of the esophagus and may invade the subjacent gastric cardia.

Microscopically, most tumors are mucin-producing glandular tumors exhibiting intestinal-type features, in keeping with the morphology of the preexisting metaplastic mucosa.

The occasional development of tumors of other alimentary cell types supports the concept that Barrett epithelium arises from multipotential cells.

ADENOCARCINOMA

Clinical Features

Esophageal carcinoma is insidious in onset and produces dysphagia and obstruction gradually and late.

Weight loss, anorexia, fatigue, and weakness appear, followed by pain, usually related to swallowing.

Because these cancers extensively invade the rich esophageal lymphatic network and adjacent structures, surgical excision rarely is curative.

Diagnosis is usually made by imaging techniques and endoscopic biopsy.

Esophagogastroduod enoscopy

Diagnosis

QUIZ