diseases of esophagus

2. 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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5. 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.

6. 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

7. 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).
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8. 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, Newborn with aspiration, paroxysmal suffocation, pneumonia;
fistula 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

9. 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.

10. 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.

11. Comparison of the two forms of esophageal
hiatal hernias

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13.  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.

14. Achalasia
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:
(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.

15.  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.

16. 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.

17. 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
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• Upper GI x-ray

18. 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.

19. 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.

20.  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.

21. 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.

22. 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.

23. 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
23
damage.

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25. 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.

26. 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.

27. 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.

28. 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.
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29.  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.

30. 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.
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31. Definitions
GER 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

32. 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
32

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34. Normal esophagus GERD Eosinophilic esophagitis
 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.

35. 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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36. Respiratory Symptoms of
GER
• Apnea/ALTE
• Stridor and hoarseness
• Cough
• Wheezing
• Recurrent pneumonia

37. Diagnosis
Esophagoscopy
To note mucosal changes
Esophageal biopsies
To note changes at the cellular level
Motilitiy studies
Low LES pressures are associated with
reflux
pH monitoring
The most precise measure for the
presence of acid in the esophageal
lumen (24 hour monitoring)

38. Medical Treatment

39. Surgical Treatment
Indications for surgical treatment are somewhat
controversial
Stage 0 and Stage 1 disease should never be an
indication for surgery
Stage 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

40. Surgical Treatment
Nissen fundoplication
Total or partial
Their aim is to:
Restore normal anatomy (intra-abdominal
segment of esophagus)
Re-creating an appropriate high-pressure
sound at the esophagogastric junction
Maintaining this repair in the normal
anatomic position

42. BENIGN TUMORS
 Leiomyomas
 Fibrovascular polyps
 Condylomas (hpv)
 Lipomas
 “Granulation” tissue
(pseudotumor)

43. 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.

44. 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)

45. 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
Large
extend deeply and sometimes erode into the
ulcerated
respiratory tree, aorta, or elsewhere
squamous cell
 (3) diffuse infiltrative neoplasms that impart carcinoma of
thickening and rigidity to the wall and the esophagus
narrowing of the lumen. Exophytic
growing outward

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47.  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.
47

48. 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.
48

49. Microscopic Image of Esophageal
Squamous Cell Carcinoma Microscopic image of Squamous
Papilloma of the Esophagus
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51.  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.
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52. ADENOCARCINOMA

53. 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.

54. Diagnosis
Diagnosis is usually made by imaging techniques
and endoscopic biopsy.
Esophagogastroduod enoscopy
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55. QUIZ

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