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Esophagus
L2
Dr. Hadeel Karbel
Esophagus
OBSTRUCTIVE AND VASCULAR DISEASES
Mechanical Obstruction
Passage of food can be impeded by esophageal stenosis. The
narrowing generally is caused by fibrous thickening of the submucosa,
atrophy of the muscularis propria, and secondary epithelial damage.
Stenosis most often is due to inflammation and scarring, which may be
caused by chronic gastroesophageal reflux, irradiation, or caustic injury.
Stenosis associated dysphagia usually is progressive; difficulty eating
solids typically occurs long before problems with liquids
Functional Obstruction
Increased lower esophageal sphincter (LES) tone can result from
impaired smooth muscle relaxation with consequent functional
esophageal obstruction. Achalasia is characterized by the triad of
incomplete LES relaxation, increased LES tone, and esophageal a
peristalsis.
Primary achalasia is caused by failure of distal esophageal inhibitory
neurons and is, by definition, idiopathic. Degenerative changes in neural
innervations also may occur.
Secondary achalasia may arise in Chagas disease, in which
Trypanosoma cruzi infection causes destruction of the myenteric plexus,
failure of LES relaxation, and esophageal dilatation.
ESOPHAGITIS
Reflux Esophagitis
The stratified squamous epithelium of the esophagus is
resistant to abrasion from foods but is sensitive to acid. The
submucosal glands of the proximal and distal esophagus
contribute to mucosal protection by secreting mucin and
bicarbonate. More important, constant LES tone prevents
reflux of acidic gastric contents, which are under positive
pressure. Reflux of gastric contents into the lower esophagus
is the most frequent cause of esophagitis.
Esophagus
L2
Dr. Hadeel Karbel
PATHOGENESIS Reflux of gastric juices is central to the development
of mucosal injury in GERD. In severe cases, duodenal bile reflux may
exacerbate the damage. Conditions that decrease LES tone or increase
abdominal pressure contribute to GERD and include alcohol and
tobacco use, obesity, central nervous system depressants, pregnancy,
hiatal hernia , delayed gastric emptying, and increased gastric volume.
In many cases, no definitive cause is identified.
Barrett Esophagus
Barrett esophagus is a complication of chronic GERD that is
characterized by intestinal metaplasia within the esophageal squamous
mucosa.
The incidence of Barrett esophagus is rising; it is estimated to occur in
as many as 10% of persons with symptomatic GERD. White males are
affected most often and typically present between 40 and 60 years of
age.
The greatest concern in Barrett esophagus is that it confers an
increased risk of esophageal adenocarcinoma.
Although the vast majority of esophageal adenocarcinomas are
associated with Barrett esophagus, it should be noted that most persons
with Barrett esophagus do not develop esophageal cancer.
MORPHOLOGY
Barrett esophagus is recognized endoscopically as tongues or patches
of red, velvety mucosa extending upward from the gastroesophageal
junction. This metaplastic mucosa alternates with residual smooth, pale
squamous (esophageal) mucosa proximally and interfaces with lightbrown columnar (gastric) mucosa distally.
goblet cells, which have distinct mucous vacuoles that stain pale blue
by H&E and , define intestinal metaplasia and are a feature of Barrett
esophagus.
ESOPHAGEAL TUMORS
Adenocarcinoma
Esophageal adenocarcinoma typically arises in a background of Barrett
esophagus and long-standing GERD.
Risk of adenocarcinoma is greater in patients with documented
dysplasia and is further increased by tobacco use, obesity, and previous
radiation therapy. Conversely, reduced adenocarcinoma risk is
associated with diets rich in fresh fruits and vegetables
Esophagus
L2
Dr. Hadeel Karbel
Esophageal adenocarcinoma occurs most frequently in whites and
shows a strong gender bias, being seven times more common in men
than in women.
MORPHOLOGY
Esophageal adenocarcinoma usually occurs in the distal third of the
esophagus and may invade the adjacent gastric cardia. While early
lesions may appear as flat or raised patches in otherwise intact mucosa,
tumors may form large exophytic masses, infiltrate diffusely, or ulcerate
and invade deeply.
On microscopic examination, Barrett esophagus frequently is present
adjacent to the tumor. Tumors typically produce mucin and form glands
Squamous Cell Carcinoma
Esophageal squamous cell carcinoma typically occurs in adults older
than 45 years of age and affects males four times more frequently than
females.
Risk factors : alcohol and tobacco use, poverty, caustic esophageal
injury, achalasia, Plummer-Vinson syndrome, frequent consumption of
very hot beverages, and previous radiation therapy to the mediastinum.
PATHOGENESIS
A majority of esophageal squamous cell carcinomas in Europe and the
United States are at least partially attributable to the use of alcohol and
tobacco, However, esophageal squamous cell carcinoma also is
common in some regions where alcohol and tobacco use is uncommon.
Thus, nutritional deficiencies, as well as polycyclic hydrocarbons,
nitrosamines, and other mutagenic compounds, such as those found in
fungus-contaminated foods, have been considered as possible risk
factors. HPV infection also has been implicated in esophageal
Squamous cell carcinoma.
MORPHOLOGY
In contrast to the distal location of most adenocarcinomas, half of
squamous cell carcinomas occur in the middle third of the esophagus.
Squamous cell carcinoma begins as an in situ lesion in the form of
squamous dysplasia. Early lesions appear as small, gray-white plaque
like thickenings. Over months to years they grow into tumor masses that
may be polypoid and protrude into and obstruct the lumen. Other tumors
are either ulcerated or diffusely infiltrative lesions that spread within the
esophageal wall, where they cause thickening, rigidity, and luminal
narrowing.
Esophagus
L2
Dr. Hadeel Karbel
Most squamous cell carcinomas are moderately to well differentiated.
Less common histologic variants include verrucous squamous cell
carcinoma, spindle cell carcinoma, and basaloid squamous cell
carcinoma.
Regardless of histologic type, symptomatic tumors are generally very
large at diagnosis and have already invaded the esophageal wall. The
rich submucosal lymphatic network promotes circumferential and
longitudinal spread, and intramural tumor nodules may be present
several centimeters away from the principal mass.