GIT.Lec.

2
Dr.BASIM
The esophagus:
It is muscular tube of 25cm.
Functions:
 Conduct food & fluid from the pharynx to the stomach.
 Prevent reflux of gastric contents by the presence of two physiological
sphincters.
 Upper esophageal sphincter at the cricopharyngeal muscle.
 Lower esophageal sphincter proximal to the esophageo-gastric
junction.
Mic:
 Mucosa: non keratinizing Squamous epithelium.
 Lamina properia: connective tissue.
 Submucosa: containing glands.
 Muscularis properia: all consist of smooth muscle, except first 6-8cm
contains skeletal muscle.
 No serosal coat.
Congenital anomalies:
1. Esophageal atresia:
 Is congenital absence of normal esophageal canal (blind end of the
canal).
 Usually associated with tracheoesophageal fistula.

2. Tracheoesophageal fistula:
 It will lead to passage of food from the esophagus to the
trachea…….. Leading to aspiration pneumonia which leads to
suffocation.

Aquired lesions:
Stenosis:
 Is a fibrous thickening of the esophageal wall forming constrictions.
e.g. lower esophageal narrowing due to gastroesophageal reflux disease.

Webs:
 Protrusion of the esophageal mucosa into the esophageal lumen.
 Common in female > 40 years.
Etiology is unknown.
1. Upper esophageal Web: (web + iron deficiency anemia +
glossitis + chelosis), this is called plummer Vinson
syndrome……. Predispose to adenocarcinoma.
2. Lower esophageal Web (rings): called schtzki's ring
(pathological annular narrowing at the lower
esophagogastric junction; could be congenital or
inflammatory (reflux disease).

Lesions of motor dysfunctions:

Achalasia (FAILURE TO RELAX):
Incomplete relaxation of lower esophageal sphincter in response to
swallowing; result in functional obstruction of esophagus with
consequent dilation of more proximal esophagus.
By manometric studies, there are three abnormalities in achalasia:
1. Aperistalsis.
2. Partial or incomplete relaxation of lower esophageal sphincter
with swallowing.
3. Increased resting tone of lower esophageal sphincter.

Etiology:
Primary achalasia: mostly unknown causes (autoimmune, viral
infection??)
 There is loss of intrinsic inhibitory innervations of lower
esophageal sphincter & smooth muscles of body.
Secondary achalasia:
 Due to Chagas disease (due to Trypanosoma Cruzi…….. destruction
of myentric plexus of esophagus).
Gross: in primary disease
 Progressive dilation of the esophagus above the level of the lower
esophageal sphincter.
 Wall of esophagus either normal in thickness OR thicker than normal
because of hypertrophy of the muscular coat OR thinned & dilation.
MIC:
 Myentric plexus are usually absent from the body of esophagus.
 Myentric plexus are either normal or reduced in number in the
region of lower esophagus sphincter.
 Inflammation in the region of Myentric plexus (pathognomonic).

Complications:
 Squamous cell carcinoma in 5% of achalasia.
 Aspiration pneumonia.
 Candida esophagitis.
 Lower esophageal diverticuli.
Diverticuli:
 Is an outpouching of the alimentary tract containing all the
visceral layers.
Types:
1. Congenital Zenker 's diverticulum:
 Site: immediate above the upper esophageal sphincter.
 Cause: congenital weakness in the inferior constrictor muscle of
pharynx.
2. Traction diverticulum:
 Site: near the mid point of esophagus (lower third).
 Cause: T.B madiastinal lymphadenitis ……..pulling esophageal
wall….. sac like formation.
3. Pulsion diverticuli:
 Site: any part of esophagus.
 Cause: abnormal peristalsis of esophagus.
 Mic: lined by stratified Squamous epithelium.
Complications:
 Food regurgitation & aspiration.
 Mass in the neck.
Hiatus hernia:
 Separation & widening of diaphragmatic crura………. Protrusion
of dilated segment of stomach above the diaphragm.
Types:
1.Sliding hernia:
 Constitute 95% of cases.
 Associated with displacement of gastroesophageal junction above
the diaphragm…………. Protrusion of stomach above the
diaphragm as bell- like dilation.
 Usually associated with reflux esophagitis.
2. Rolling (Paraesophageal hernia):
 Here separated portion of stomach (mainly fundus) enter the thorax
through a wide diaphragmatic foramen, without displacement of
gastroesophaageal junction.
 Not associated with reflux esophagitis.
Complications:
1. Mucosal ulceration.
2. Bleeding.
3. Perforation.
3. Mixed type.

Lacerations of esophagus (Mallory – Weiss Syndrome):

 Longitudinal tearing in the esophagus at the gastroesophageal
junction.
 Seen in alcoholic individuals after severe retching, & vomiting.
 Tear can extend through mucosa, submucosa……. Upper
gastrointestinal bleeding.
 It forms 10% of Upper gastrointestinal bleeding.
Esophagitis:
 Inflammation of esophagus with injury to mucosa.
 Types:
 Infective 2. Non infective.
Non infective causes:
 Acute esophagitis:
 Ingestion of mucosal irritants (alcohol, corrosive acids & alkali, hot
tea).
 Uremia.
 Drugs
 Irradiation.
 Reflux esophagitis:
Is reflux of gastric contents into the lower esophagus in which the acid-
peptic action of the gastric juice is the main cause of injury leading to
inflammation of the lower esophagus.
Predisposing factors:
1. Decrease of efficacy of esophageal anti reflux mechanisms (of LES).
2. Inadequate or slowed esophageal clearance of refluxed material.
3. Presence of sliding hernia.
4. Increased gastric volume.
5. Impaired reparative capacity of the esophageal mucosa by prolonged
exposure to gastric juices.
Mic:
Three characteristics features:
1. Eosinophils with or without neutrophils in epithelial layer.
2. Basal cells hyperplasia.
3. Intraepithelial neutrophils are marker of severe injury.
 Elongation of lamina propria papillae.
Symptoms:
 Age more than 40years, dysphagia, heartburn, regurgitation.
Complications:
 1. Bleeding 2. Stricture. 3. Barrett esophagus
4. Predisposing to malignancy.

Barrett esophagus:
Is a replacement of the normal distal stratified Squamous mucosa by
metaplastic columnar epithelium containing goblet cells.
 Is a complication of long standing gastroesophageal reflux disease.

Pathogenesis:
 Prolonged & recurrent reflux………. Inflammation & ulceration of
Squamous esophageal mucosa ……. Then healing by ingrowth of stem
cells & re-epithelialization……. Formation of metaplastic columnar
cells (resistant to gastric acid).
 Sex: male>female, white > than other races.
Complications:
1. Esophageal ulcer.
2. Stricture formation.
3. Develpement of adenocarcinoma (risk of 30 – 40 times than normal
population).
Tumors of Esophagus:
1. Benign tumors:
 Leiomyoma (commonest tumor).
 Squamous cell papilloma.
2. Malignant tumors:
 Squamous cell carcinoma 90% of cases.
 Adenocarcinoma, carcinoid, undifferentiated 10%

Squamous cell carcinoma:

 Age: >50years.
 Sex: male >female, black > white.
 Geographic differences: most common in iran, china, central asia.
Etiology:
1. Dietary causes:
 Deficiency of vitamins & trace minerals e.g. vita A,C,Zn.
 Fungal contamination of foodstaffs.
 High contents of nitrites/ nitrosamines.
3. Life style:
 Alcohol consumption.
 Tabacco abuse.
4. Esophageal disorders:
 Long standing esophagitis.
 Achalasia.
 Plummer Vinson syndrome.
5. Genetic predisposition.

Sites:
 50% occur in the middle third.
 30% occur in the lower third.
 20% occur in the upper third.
Gross:
 Polypoid mass protrude into the lumen (60%).
 Ulcerative (25%).
 Diffuse thickening of wall …… narrowing thelumen.
Mic:
 Early lesions are dysplasia…….. carcinoma in situ……… invasive
carcinoma (Squamous cell carcinoma).

Spread:
1. Local spread to the mediastinum, resp. tract, aorta.
2. Lymphatics……… regionallymph nodes.
3. Hematogenous ……… liver, lung.

Adenocarcinoma:
 Mainly at distal third.
 Commonest predisposing cause is Barrett esophagus.
 Mic: mucin producing malignant glands.
THANK YOU