The document discusses the anatomy and pathologies of the esophagus. It describes the layers of the esophagus and contains sphincters. Lesions can cause dysphagia due to narrowing or obstruction. Gastroesophageal reflux disease is a common cause of heartburn. Varices are dilated veins caused by portal hypertension. Achalasia is a motility disorder causing difficulty swallowing. Barrett's esophagus is a complication of long-term reflux and increases cancer risk. Squamous cell carcinoma and adenocarcinoma are the two main types of esophageal cancer.
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Esophagus Anatomy and Disorders
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2. 2 Esophagus Upper 1/3 is skeletal muscle Lower 1/3 is smooth muscle middle is combo of both Contains two sphincters Lined by squamous epithelium < 3 cm below diaphragm
4. The act of swallowing is comprised of a series of events requiring intact central, autonomic, and enteric nervoussystems as well as a set of functional striated and smooth muscles Interference with these precise mechanisms will result in dysphagia
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6. All produce dysphagia (difficulty in swallowing), which is attributed either to deranged esophageal motor function or to narrowing or obstruction of the lumen.
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8. 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). 8/5/2011 7
16. These symptoms more likely result from incompetence of the lower esophageal sphincter than from the hiatal hernia and are accentuated by positions favoring reflux (bending forward, lying supine) and obesity.
17. Although most patients with sliding hiatal hernias do not have reflux esophagitis, those with severe reflux esophagitis are likely to have a sliding hiatal hernia.
18. Other complications affecting both types of hiatal hernias include mucosal ulceration, bleeding, and even perforation.
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20. This produces functional obstruction of the esophagus, with consequent dilation of the more proximal esophagus.
21. Three major abnormalities in achalasia: Aperistalsis(absence of peristalsis ) partial or incomplete relaxation of the lower esophageal sphincter with swallowing increased resting tone of the lower esophageal sphincter.
28. Treatment Incurable Palliative measures Nonsurgical Surgical Both are directed toward relieving the obstruction caused by the no relaxing LES( lower esogh I don’t know)
41. Most often bleeding is not profuse and ceases without surgical intervention, but life-threatening hematemesis may occur.
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43. The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.
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46. The net effect is irregular protrusion of the overlying mucosa into the lumen, although varices are collapsed in surgical or postmortem specimens .
47. When the varixis unruptured, the mucosa may be normal, but often it is eroded and inflamed because of its exposed position, further weakening the tissue support of the dilated veins.
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49. The subsequent inflammation of the submucosa causes erosion of the thin wall of the varices with subsequent rupture.
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52. Once begun, variceal hemorrhage subsides spontaneously in only 50% of cases; endoscopic injection of thrombotic agents (sclerotherapy) or balloon tamponade is often required.
62. 33 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 damage.
66. Chest pain, particularly behind the breastbone, that occurs with eating Swallowed food becoming stuck in the esophagus (food impaction).
67. Rarely, chronic symptoms are punctuated by attacks of severe chest pain mimicking a heart attack.
68. Although largely limited to adults older than age 40, reflux esophagitis is occasionally seen in infants and children.
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70. Barrett esophagus is defined as the replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells.
71. Prolonged and recurrent gastroesophageal reflux is thought to produce inflammation and eventually ulceration of the squamous epithelial lining.
77. Ulcer and stricture may develop as a complication of Barrett esophagus. However, the chief clinical significance of Barrett esophagus relates to the development of adenocarcinoma.
81. Adenocarcinoma arising in Barrett esophagus is more common in whites than in blacks. By contrast, squamous cell carcinomas are more common in blacks worldwide.
82. 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.
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84. An important contributing factor is retarded passage of food through the esophagus, prolonging mucosal exposure to potential carcinogens such as those contained in tobacco and alcoholic beverages.
85. There is a well-defined predisposing role for chronic esophagitis, itself associated with alcohol and tobacco.
86. The role of genetic predisposition is extremely ill defined, but the rare genetic syndrome of tylosis,
99. Early overt lesions appear as small, gray-white, plaque like thickenings or elevations of the mucosa. In months to years, these lesions become tumorous, taking one of three forms:
101. (2) Necrotizing cancerous ulcerations that extend deeply and sometimes erode into the respiratory tree, aorta, or elsewhere; and
102. (3) diffuse infiltrative neoplasms that impart thickening and rigidity to the wall and narrowing of the lumen. Whichever the pattern, about 20% arise in the cervical and upper thoracic esophagus, 50% in the middle third, and 30% in the lower third. Large ulcerated squamous cell carcinoma of the esophagus Exophytic growing outward
108. 8/5/2011 copyright (your organization) 2003 48 Microscopic Image of Esophageal Squamous Cell Carcinoma Microscopic image of Squamous Papilloma of the Esophagus
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110. Unlike squamous cell carcinomas, they are usually in the distal one third of the esophagus and may invade the subjacent gastric cardia.
111. Initially appearing as flat or raised patches on an otherwise intact mucosa, they may develop into large nodular masses or exhibit deeply ulcerative or diffusely infiltrative features.
112. Microscopically, most tumors are mucin-producing glandular tumors exhibiting intestinal-type features, in keeping with the morphology of the preexisting metaplastic mucosa.
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114. Weight loss, anorexia, fatigue, and weakness appear, followed by pain, usually related to swallowing. Diagnosis is usually made by imaging techniques and endoscopic biopsy.
115. Because these cancers extensively invade the rich esophageal lymphatic network and adjacent structures, surgical excision rarely is curative.
116. Thus, there is emphasis on routine screening procedures, particularly for those with manifestations of chronic esophagitis or known Barrett esophagus.
125. Basal cell thickening of the esophageal mucosal epithelium and lengthening of stromal papillae, also depicted, are additional markers of GER.
126. If biopsy reveals extensive eosinophilia, for example, >20 intraepithelial eosinophils per high-power microscopic field (HPF), an allergic condition or idiopathic esophagitis, rather than GER, should be considered.
127. The histologic picture at right is of primary eosinophilic esophagitis, showing clusters of eosinophils and papillary and basal increases; this patient had dysphagia and food allergies that responded to an elimination diet.
144. The presence of inflammation in the esophagus suggests significant peptic injury, whereas inflammation in the stomach or duodenum may support other conditions, such as food allergy.8/5/2011 copyright (your organization) 2003 61 Diagnosis
Hematoxylin and eosin staining of tongue (a and b) and esophagus (c and d). (a and c) Wild-type mouse at 12 months of age. (b and d) L2D1+/p53+/– mouse at 12 months of age. b and d show evidence of nuclear atypia, enlargement, and hyperchromasia of cells as well as loss of polarity with migration of atypical cells into intermediate and superficial layers as cellular and histologic features of dysplasia. In particular, there is invasion of malignant cells into the submucosa and muscle of the tongue and into the submucosa of the esophagus. Cancer lesions are marked by arrows. (e) Hematoxylin and eosin staining and (f) pancytokeratin immunohistochemistry from one representative paraesophageal lymph node metastasis. There are keratin-positive epithelial cells within the lymphatic tissue. Magnification, ×400.