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.

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

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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

6. All produce dysphagia (difficulty in swallowing), which is attributed either to deranged esophageal motor function or to narrowing or obstruction of the lumen.

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

9. Selected Anatomic Disorders Of The Esophagus

13. Comparison of the two forms of esophageal hiatal hernias

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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.

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.

23. Secondary achalasia may arise from pathologic processes that impair esophageal function.

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)

30. Therapy may involve:

31. Injection with botulinum toxin (Botox). This may help relax the sphincter muscles, but any benefit wears off within a matter of weeks or months.

32. Medications, such as long-acting nitrates or calcium channel blockers, which can be used to relax the lower esophagus sphincter.

33. Surgery(called an esophagomyotomy), which may be needed to decrease the pressure in the lower sphincter.

34. Wideling (dilation or balloon) of the esophagus at the location of the narrowing (done during esophagogastroduodenoscopy).8/5/2011 22

36. The presumed pathogenesis is inadequate relaxation of the musculature of the lower esophageal sphincter during vomiting,

38. Tears may involve only the mucosa or may penetrate the wall.

39. Infection of the defect may lead to an inflammatory ulcer or to mediastinitis[is inflammation of the tissues in the mid-chest].

40. Esophageal lacerations account for 5% to 10% of upper gastrointestinal bleeding episodes.

41. Most often bleeding is not profuse and ceases without surgical intervention, but life-threatening hematemesis may occur.

43. The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.

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.

49. The subsequent inflammation of the submucosa causes erosion of the thin wall of the varices with subsequent rupture.

52. Once begun, variceal hemorrhage subsides spontaneously in only 50% of cases; endoscopic injection of thrombotic agents (sclerotherapy) or balloon tamponade is often required.

53. When varices bleed, 20% to 30% of patients die during the first episode.

55. There are many presumed contributory factors:

56. Decreased efficacy of esophageal antireflux mechanisms

57. Inadequate or slowed esophageal clearance of refluxed material

58. The presence of a sliding hiatal hernia

59. Increased gastric volume, contributing to the volume of refluxed material

60. Impaired reparative capacity of the esophageal mucosa by prolonged exposure to gastric juices

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.

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65. Difficult swallowing (dysphagia), Painful swallowing (odynophagia)

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.

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.

72. Healing occurs by in growth of stem cells and re-epithelialization.

74. Microscopically, the esophageal squamous epithelium is replaced by metaplastic columnar epithelium (gastric mucosa ).

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.

80. Worldwide, Squamous cell carcinomas constitute 90% of esophageal cancers.

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.

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,

88. Long-standing esophagitis

89. Achalasia

90. Plummer-Vinson syndrome (esophageal webs, microcytichypochromic anemia, atrophic glossitis)

91. Alcohol consumption

92. Tobacco abuse

93. Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)

94. Deficiency of trace metals (zinc, molybdenum)

95. Fungal contamination of foodstuffs

96. High content of nitrites/nitrosamines

97. Genetic Predisposition

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:

100. (1) polypoidexophytic masses that protrude into the lumen;

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

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105. There is nuclear stratification, nuclear enlargement, hyperchromasia, pleomorphism, and mitoses.

106. The photomicrograph above shows pseudoinvasion but the same architectural and cytological features.

108. 8/5/2011 copyright (your organization) 2003 48 Microscopic Image of Esophageal Squamous Cell Carcinoma Microscopic image of Squamous Papilloma of the Esophagus

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.

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.

118. Definitions

120. Once food is in the stomach, a ring of muscle fibers prevents food from moving backward into the esophagus.

121. These muscle fibers are called the lower esophageal sphincter, or LES8/5/2011 53

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123. Eosinophilic esophagitis Normal esophagus GER

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.

130. Chest pain

131. Difficulty swallowing (dysphagia)

132. Hoarseness or sore throat

133. Regurgitation of food or sour liquid (acid reflux)

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135. Respiratory Symptoms of GER Apnea/ALTE Stridor and hoarseness Cough Wheezing Recurrent pneumonia

137. To note mucosal changes

138. Esophageal biopsies

139. To note changes at the cellular level

140. Motilitiy studies

141. Low LES pressures are associated with reflux

142. pH monitoring

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

145. Medical Treatment

147. Stage 0 and Stage 1 disease should never be an indication for surgery

148. Stage 2 disease should always undergo a well supervised period of medical management for at least six months to a year

149. Stage 3 disease should also undergo medical therapy first

151. Total or partial

152. Their aim is to:

153. Restore normal anatomy (intra-abdominal segment of esophagus)

154. Re-creating an appropriate high-pressure sound at the esophagogastric junction

156. QUIZ

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