GIT.Lec. 2 Dr.BASIM

1. GIT.Lec. 2Dr.BASIM

2. 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.

3. Congenital anomalies: • 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.

4. Etiology is unknown. • Upper esophageal Web: (web + iron deficiency anemia + glossitis + chelosis), this is called plummer Vinson syndrome……. Predispose to adenocarcinoma. • 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.

8. By manometric studies, there are three abnormalities in achalasia: • Aperistalsis. • Partial or incomplete relaxation of lower esophageal sphincter with swallowing. • 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 TrypanosomaCruzi…….. destruction of myentric plexus of esophagus).

9. 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.

11. Diverticuli: • Is an outpouching of the alimentary tract containing all the visceral layers. Types: • 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.

13. 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.

14. Complications: • Mucosal ulceration. • Bleeding. • 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.

17. 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: • Decrease of efficacy of esophageal anti reflux mechanisms (of LES). • Inadequate or slowed esophageal clearance of refluxed material. • Presence of sliding hernia. • Increased gastric volume. • Impaired reparative capacity of the esophageal mucosa by prolonged exposure to gastric juices.

18. Mic: Three characteristics features: • Eosinophils with or without neutrophils in epithelial layer. • Basal cells hyperplasia. • Intraepithelial neutrophils are marker of severe injury. • Elongation of lamina propria papillae. Symptoms: • Age more than 40years, dysphagia, heartburn, regurgitation.

19. 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: • Esophageal ulcer. 2. Stricture formation. 3. Develpement of adenocarcinoma (risk of 30 – 40 times than normal population).

22. 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.

23. 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.

24. Mic: • Early lesions are dysplasia…….. carcinoma in situ……… invasive carcinoma (Squamous cell carcinoma). Spread: • Local spread to the mediastinum, resp. tract, aorta. • Lymphatics……… regionallymph nodes. • Hematogenous ……… liver, lung. Adenocarcinoma: • Mainly at distal third. • Commonest predisposing cause is Barrett esophagus. • Mic: mucin producing malignant glands.

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