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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.