Lect 3 Diseasesofesophagus 121203074045 Phpapp01

7/27/2019 Lect 3 Diseasesofesophagus 121203074045 Phpapp01

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Esophagus Secretes mucous, transports food no enzymes produced,

no absorptionMucosa protection against wear and tear

lam ina propr ia

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

Adventitia no serosa attaches to surroundings

< 3 cm below diaphragm


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EsophagusLesions of the esophagus run from bland

esophagitis to highly lethal cancers.

All produce dysphagia(difficulty in swallowing),

which is attributed either to deranged esophagealmotor 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.


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Less commonly,

hematemesis(vomiting of

blood) andmelena(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


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

Structural abnormalities of the esophagus can be

eithercongenital or acquired.

The two most common congenital esophageal

abnormalities areEsophageal Atresia (EA) and

Tracheoesophageal Fistula (TEF).

Anatomic disorders encountered infrequently (Table).

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Selected Anatomic Disorders Of The Esophagus

Disorder Clinical Presentation and Anatomy

Stenosis Adult with progressive dysphagia to solids and eventually to allfoods; 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 tracheoesophagealfistula 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


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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 stomachto protrude above the

diaphragm.


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Two anatomic patterns arerecognized: the axial, or slidinghernia and the nonaxial, orparaesophageal hernia.

The sliding hernia constitutes95% of cases; protrusion of thestomach above the diaphragm

creates a bell-shaped dilation,bounded below by thediaphragmatic narrowing.

In paraesophageal hernias, aseparate portion of the stomach,usually along the greatercurvature, enters the thoraxthrough the widened foramen.


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Comparison of the two forms of esophageal

hiatal hernias


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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.


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Achalasia The term achalasia means

"failure to relax" and in the present

context denotes incomplete relaxation ofthe 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.


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Causes

Primary: achalasia there is loss of

intrinsic inhibitory innervation of thelower esophageal sphincter and

smooth muscle.

Secondary: achalasia may arise

from pathologic processes; exampleis Chagas disease, caused by

Trypanosoma cruzi, which causes

destruction of the myenteric plexus of

the esophagus, duodenum, colon,

and ureter.


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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.


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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-ray17


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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.


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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 ofgastric contents.


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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.


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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

materialThe presence of a sliding hiatal hernia

Increased gastric volume, contributing to the volume of

refluxed material

Impaired reparative capacity of the esophageal mucosa byprolonged 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.


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MORPHOLOGY

The anatomic changes depend on the causative agent and on

the duration and severity of the exposure.

Mild esophagitis may appear macroscopically as simplehyperemia, 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 ofmore severe injury.


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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.


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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 Barrettesophagus, with its predisposition to malignancy.


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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 somepatients 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


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MORPHOLOGY

Barrett esophagus is apparent as a

salmon-pink, velvety mucosa

between the smooth, pale pinkesophageal squamous mucosa and

the more lush light brown gastric

mucosa.

the esophageal squamous

epithelium is replaced by

metaplastic columnarepithelium

(gastric mucosa ).

Critical to the pathologic evaluation

of patients with Barrett mucosa is the

recognition ofdysplasticchanges in

the mucosa that may be precursors

ofcancer.


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Barrett esophagus.

A, Endoscopic view showing red

velvety gastrointestinal-type mucosa

extending from the

gastroesophageal orifice. Note palersquamous esophageal mucosa.

B, Microscopic view showing mixed

gastric- and intestine-type columnar

epithelial cells in glandular mucosa.


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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 adenocarcinomacompared with normal populations.


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Gastroesophageal reflux disease

(GERD)

Gastroesophageal reflux (GER) is defined as passage ofgastric 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.

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Definitions

GER Passage of gastric contents intoesophagus

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 epitheliumand 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

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Respiratory Symptoms of

GER

Apnea/ALTE

Stridor and hoarseness Cough

Wheezing

Recurrent pneumonia


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DiagnosisEsophagoscopyTo note mucosal changes

Esophageal biopsiesTo note changes at the cellular level

Motilitiy studiesLow LES pressures are associated with

reflux

pH monitoring

The most precise measure for thepresence of acid in the esophageallumen (24 hour monitoring)


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Medical Treatment


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Surgical TreatmentIndications for surgical treatment are somewhat

controversialStage 0 and Stage 1 disease should never be an

indication for surgery

Stage 2 disease should always undergo a wellsupervised period of medical management for atleast six months to a year

Stage 3 disease should also undergo medical

therapy firstIn stage2 and in Stage 3 disease surgical options

should be entertained after failed medicalmanagement


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Surgical Treatment

Nissen fundoplicationTotal or partial

Their aim is to:

Restore normal anatomy (intra-abdominalsegment of esophagus)

Re-creating an appropriate high-pressuresound at the esophagogastric junction

Maintaining this repair in the normalanatomic position


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BENIGN TUMORS

Leiomyomas

Fibrovascular polyps

Condylomas (hpv)

Lipomas

Granulation tissue

(pseudotumor)

ESOPHAGEAL CARCINOMA


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ESOPHAGEAL CARCINOMA

There are two types: squamous cell carcinomas and

adenocarcinomas.

Worldwide, Squamous cell carcinomas constitute 90% ofesophageal cancers.

Adenocarcinoma arising in Barrett esophagus is more

common in whites than in blacks.

There are striking and puzzling differences in the geographicincidence 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 ofChina to Iran, the prevalence is well over 100 per 100,000.

RISK FACTORS FOR SQUAMOUS CELL CARCINOMA OF THE


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RISK FACTORS FOR SQUAMOUS CELL CARCINOMA OF THE

ESOPHAGUS

Esophageal Disorders

Long-standing esophagitisAchalasia

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

Alcohol consumption

Tobacco abuseDeficiency of vitamins (A, C, riboflavin, thiamine,pyridoxine)

Deficiency of trace metals (zinc, molybdenum)

Fungal contamination of foodstuffsHigh content of nitrites/nitrosamines

Genetic Predisposition

Tylosis (hyperkeratosis of palms and soles)

MORPHOLOGY


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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 ofthe esophagus

Exophytic

growing outward


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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


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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 cellcarcinoma element of the esophageal

carcinoma.


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Microscopic Image of Esophageal

Squamous Cell Carcinoma Microscopic image of SquamousPapilloma of the Esophagus


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Adenocarcinomas appear to arise from dysplastic mucosa


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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 thedistal one third of the esophagus and may invade the

subjacent gastric cardia.

Microscopically, most tumors are mucin-producingglandular 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


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ADENOCARCINOMA

Cli i l F t


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Clinical Features

Esophageal carcinoma is insidious in onset and

produces dysphagia and obstruction gradually and

late.

Weight loss, anorexia, fatigue, and weaknessappear, 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.


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Diagnosis is usually made by imaging techniques

and endoscopic biopsy.

Esophagogastroduod enoscopy


Diagnosis


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QUIZ


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Documents

Lect 3 Diseasesofesophagus 121203074045 Phpapp01