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The document summarizes the pathology of the esophagus. It describes that the esophagus is lined by stratified squamous epithelium and has two muscle coats. It notes four narrow regions where food can become lodged. Various pathologies are described, including esophagitis, varices, benign lesions like papillomas, and cancers like squamous cell carcinoma and adenocarcinoma associated with Barrett's esophagus. Risk factors for cancers include alcohol, tobacco, and chronic reflux. Spread of cancer is described along with survival rates.
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Git 3-csbrp
- 1. Pathology of EsophagusPathology of Esophagus Dr.CSBR.Prasad,M.D., May-2015-CSBRP
- 2. Salient featuresSalient features • Lined by stratified squamous epithelium • Muscle coat: – Inner circular (Thinner) – Outer longitudinal (Thicker) • Upper portion – voluntary • Lower portion – involuntary • No serosa • Spincters: – UES (at the level of the sixth cervical vertebra) – LES (1 to 2 cm above the hiatus) • 4 narrow regions May-2015-CSBRP
- 4. Narrow regionsNarrow regions Occur at the following sites: – at the level of the cricoid cartilage – at the aortic arch – at the level of the left atrium – at the diaphragmatic opening • Importance: These are potential sites at which food and pills may become lodged May-2015-CSBRP
- 7. @ the level of the left atrium May-2015-CSBRP
- 10. Lymphatic drainageLymphatic drainage • The lymphatics within the muscle coats are predominantly oriented in a longitudinal direction • They freely interconnect Because of the extensive interconnections metastatic disease from the esophagus is frequently unpredictable May-2015-CSBRP
- 11. May-2015-CSBRP
- 12. May-2015-CSBRP
- 13. EsophagitisEsophagitis • Candida • HSV • CMV • Chemotherapy • GVHD • Radiation • Mallory-Weis syndrome • Bullous lesion • Crohn’s disease May-2015-CSBRP
- 15. Reflux esophagitis • Reflux of gastric juices • Conditions: – Decrease LES tone – Increase abdominal pressure – Alcohol and tobacco use – Obesity – Central nervous system depressants – Pregnancy – Hiatal hernia – Delayed gastric emptying and increased gastric volume May-2015-CSBRP
- 17. Causes • PHT • Superior venacaval obstruction May-2015-CSBRP
- 18. Endoscopic views – bag of worms May-2015-CSBRP
- 23. Causes for massive Upper GI bleeding • Esophageal varices • Bleeding gastric ulcer • Bleeding duodenal ulcer • Gastric leiomyoma May-2015-CSBRP
- 24. Varices due to SVS & PHT Involvement of esophagus by varices: • SVS: Entire length of esophagus • PHT: Lower 1/3rd May-2015-CSBRP
- 25. Redirection of flow through the left gastric vein secondary to portal hypertension or portal venous occlusion. Uphill varices develop in the distal one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava. May-2015-CSBRP
- 26. Direction of flow with superior vena cava (SVC) obstruction involving or distal to the azygous vein. Flow is redirected through the azygous vein, the esophageal veins, and into the portal circulation. Flow enters the systemic circulation through the inferior vena cava (IVC). Downhill varices develop the entire length of the esophagus. IMC = inferior mesenteric vein May-2015-CSBRP
- 27. Benign lesionsBenign lesions • SQUAMOUS CELL PAPILLOMA • Developmental Cysts and Duplications • Diverticulosis May-2015-CSBRP
- 28. SQUAMOUS CELL PAPILLOMASQUAMOUS CELL PAPILLOMAMay-2015-CSBRP
- 29. Case - 45yo female with weakness and difficulty in swallowing What are your findings? Diagnosis? May-2015-CSBRP
- 30. Findings • Angular chelitis • Esophageal web (Endoscopy, Barium swallow) • Koilonychia • Microcytic hypochromic anemia May-2015-CSBRP
- 31. What is your diagnosis? Synonyms: • Plummer-Vinson Syndrome • Patterson-Kelly Syndrome • Sideropenic dysphagia May-2015-CSBRP
- 32. Case – Old woman presented with this swelling of 3months duration. No h/o fever. Tenderness +. Give your DDs In the history what are all the questions you will ask? May-2015-CSBRP
- 33. This is what we should ask…. • Any evening rise of temperature • Any thyroid swelling / surgery • Change in voice • Difficulty in swallowing – solids / liquids • Non-healing oral ulcers • Cough , lung complaints May-2015-CSBRP
- 34. She gave a h/o …. • Difficulty in swallowing • At first it was for solids, some times associated with vomiting • She was comfortable with liquids • Lost weight • Recently she developed difficulty in swallowing for liquids May-2015-CSBRP
- 35. What is your diagnosis? • Carcinoma of esophagus May-2015-CSBRP
- 36. Carcinoma of EsophagusCarcinoma of Esophagus May-2015-CSBRP
- 37. The risk factors include: • Alcohol consumption • Tobacco • Vitamin and mineral deficiencies • Staple diet: rich in cereals, poor in fresh fruits & vegetables • Plummer-Vinson Syndrome (10%) • Thermal injury (eating hot food) • Lye strictures • Viruses (HPV 16, 18) • Nitrosamines and other nitrogenous compounds • Genetic factors: Palmoplantar keratoderma / Tylosis May-2015-CSBRP
- 38. Palmoplantar keratoderma / Tylosis May-2015-CSBRP
- 39. Clinical Features • M:F = 3-5:1 • 6-7th decade • The most common presenting symptom is dysphagia, beginning with solid foods and then progressing to liquid May-2015-CSBRP
- 40. Types • Superficial SqCC • Invasive SqCC May-2015-CSBRP
- 41. SUPERFICIAL CARCINOMA In this plaque-like gross appearance the carcinoma forms an irregular, slightly elevated lesion, covering most of the field. May-2015-CSBRP
- 42. May-2015-CSBRP
- 43. Invasive SqCC - Types • Fungating • Ulcerative and • Infiltrating May-2015-CSBRP
- 47. Squamous cell carcinoma - Esophagus May-2015-CSBRP
- 48. May-2015-CSBRP
- 49. Metastasis The node groups affected differ, depending upon the site of the tumor: • Cervical esophagus: – Cervical and – Superior mediastinal nodes • Upper and middle thoracic esophagus: – Mediastinal nodes – Superior gastric nodes • Lower thoracic part: – Lower mediastinal – Superior gastric – Celiac artery, and – Splenic artery nodes • The most common extranodal metastatic sites: – Liver – Lung May-2015-CSBRP
- 51. BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS • In Barrett's esophagus the normal stratified squamous epithelium lining the esophagus is replaced by columnar epithelium for variable lengths from the lower esophageal sphincter region cephalad May-2015-CSBRP
- 52. May-2015-CSBRP
- 53. BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS The importance of this disorder: • It’s associated with an increased risk of adenocarcinoma of the esophagus May-2015-CSBRP
- 54. BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS The most common predisposing factor: Chronic gastroesophageal reflux – GERD And it’s identified by this history May-2015-CSBRP
- 55. This section shows a small island of squamous epithelium replacing the surface columnar cells. May-2015-CSBRP
- 56. MUCIN STAINS OF BARRETT'S MUCOSA Alcian blue stain shows the blue- staining goblet cells May-2015-CSBRP
- 57. BARRETT'S DYSPLASIABARRETT'S DYSPLASIA • Dysplasia is defined as neoplastic change of the epithelium of the glands without any evidence of invasion • Grades: – Low grade – High grade May-2015-CSBRP
- 58. Dysplasia in Barrett esophagus May-2015-CSBRP
- 60. Treatment options • Low grade dysplasia: Follow up • High grade dysplasia: Treated as intramucosal carcinoma May-2015-CSBRP
- 61. Adenocarcinoma of the EsophagusAdenocarcinoma of the Esophagus May-2015-CSBRP
- 62. AdenocarcinomaAdenocarcinoma • Relatively uncommon tumor • M:F = 3:1 to 7:1 • Mean age: 60yrs • GERD • Progressive dysphagia May-2015-CSBRP
- 63. Gross and Endoscopic Findings • Site: 80% of esophageal adenocarcinomas are located in the lower third of the esophagus • Gross: slight mucosal irregularities or plaques, large exophytic, fungating, or deeply ulcerated masses May-2015-CSBRP
- 66. Spread and prognosis 5-year survival rates: • 75% in individuals with superficial esophageal carcinoma • With metastases to LNs: a dismal 9% May-2015-CSBRP
- 67. NEOPLASMS METASTATIC TO THE ESOPHAGUS • Same three that metastasize to the stomach: – Carcinomas of the lung – Breast, and – Melanoma May-2015-CSBRP
Editor's Notes
- The upper fourth of the esophagus consists entirely of striated muscle, the next quarter contains a mixture of striated and smooth muscle, and the lower half consists entirely of nonstriated muscle. The inner circular muscle coat is usually thinner than the outer longitudinal muscle coat, a histologic feature that is the opposite of the rest of the gastrointestinal tract.
- These indentations occur at the following sites: at the level of the cricoid cartilage, caused by the cricopharyngeus muscle; at the aortic arch; at the level of the left atrium, where the left main bronchus crosses the esophagus; and at the diaphragmatic opening.
- This consists primarily of a rich network of lymphatics within the mucosa and submucosa that connect with lymphatics within the muscle and adventitial coats. The lymphatics within the muscle coats are predominantly oriented in a longitudinal direction. They freely connect with one another and these interconnections explain the frequency of intramucosal and submucosal spread of a primary tumor. In the cervical esophagus the adventitial lymphatics tend to drain into the paratracheal and internal jugular lymph nodes; the latter flow into the left thoracic duct. Lymphatics of the thoracic esophagus drain into the superior, middle, and lower mediastinal nodes; they then, in most instances, flow upwards into the thoracic duct on the left side and into the right lymph duct on the right side and into the right subclavian vein. The lymphatics of the abdominal esophagus drain into the superior gastric, celiac, common hepatic, and splenic artery lymph nodes. Because of the extensive interconnections of all the lymphatic channels, metastatic disease from the esophagus is frequently unpredictable: tumors of the lower esophagus which tend to metastasize to the upper abdominal lymph node chains mentioned above, also metastasize to the cervical lymph nodes in some cases.
- FIGURE 17-4 Viral esophagitis. A, Postmortem specimen with multiple herpetic ulcers in the distal esophagus. B, Multinucleate squamous cells containing Herpesvirus nuclear inclusions. C, Cytomegalovirus-infected endothelial cells with nuclear and cytoplasmic inclusions.
- UL-Normal esophagus UR-Varices LR-Varices LL-Erosion /ulceration
- Figure 2: Endoscopic image of the brisk hemorrhage that resulted after inadvertent dislodgement of the platelet-fibrin plug. Blood spurting or oozing from a varix confirms the diagnosis of variceal hemorrhage.Most of the attention has focused on red color signs, such as red wale markings, described by Beppu et al. [Gastrointest Endosc 1981;27:213-218] and well known to endoscopists.Here we describe our experience with a less recognized stigma of variceal hemorrhage known as the 'white nipple sign', which resulted in active hemorrhage when manipulated.
- SVS = superior venacaval syndrome PHT = Portal hypertension
- Normal venous flow through the portal and systemic circulation. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.
- This is an exaggerated version of the common form. It has an elaborate branching core of lamina propria that is covered by mature squamous epithelium.
- Plummer-Vincent (Patterson-Kelly) Syndrome: 10% develop esophageal cancer. Lye strictures: Alkali injury resulting in strictures. The carcinomas occur after a long latent period, usually 30 years or more.
- Symmetric thickened scaly hyperpigmented plaques on the soles. And in other case involving the palms.
- Superficial SqCC: Any carcinoma of the esophagus that extends no deeper than the submucosa is referred to as a superficial esophageal carcinoma
- In this plaque-like gross appearance the carcinoma forms an irregular, slightly elevated lesion, covering most of the field.This is classified as plaque type, coarse type, or the slightly elevatedflat type, depending upon the classification scheme used.
- The deepest invasion is in the middle of the submucosa. There is a thin layer of submucosa between the carcinomaand the muscularis propria.
- The infiltrative pattern is characterized by an elevatedplaque that obliterates the folds and thickens the wall.
- The node groups affected differ, depending upon the site of the tumor. Carcinomas of the cervical esophagus metastasize mostly to the cervical and superior mediastinal nodes; those in the upper and middle thoracic esophagus spread to the mediastinal nodes at all levels and to the superior gastric nodes; and those in the lower thoracic part most frequently involve the lower mediastinal, superior gastric, celiac artery, and splenic artery nodes . The most common extranodal metastatic sites in all reported series are the liver and lung.
- FIGURE 17-6 Barrett esophagus. A, Normal gastroesophageal junction. B, Barrett esophagus. Note the small islands of paler squamous mucosa within the Barrett mucosa. C, Histologic appearance of the gastroesophageal junction in Barrett esophagus. Note the transition between esophageal squamous mucosa (left) and Barrett metaplasia, with abundant metaplastic goblet cells (right).
- The sequence of events leading to Barrett's esophagus has not been clearly defined. It is probable that ulceration of the squamous epithelium occurs in response to gastroesophageal reflux of acid, bile, and duodenal contents and that reepithelialization occurs via multipotential stem cells which in turn differentiate into the variety of epithelial cells found in Barrett's esophagus. There may, however, be other mechanisms. It is possible, although unproven, that metaplasia occurs simply by the upward migration and overgrowth of columnar epithelium from the gastric cardia, in response to gastroesophageal reflux. Alternatively, as was postulated in the past, Barrett's esophagus may arise from congenital rests of gastric columnar epithelium, which usually occur in the cervical esophagus but have also been documented in the distal esophagus. Although these rests may account for rare cases of childhood Barrett's esophagus, there is no evidence of this mechanism in adults.
- MUCIN STAINS OF BARRETT'S MUCOSA: Alcian blue stain of Barrett's mucosa shows the blue- staining goblet cells, a few specialized columnar cells, and the clear- staining gastric- type surface columnar cells.
- FIGURE 17-7 Dysplasia in Barrett esophagus. A, Abrupt transition from Barrett metaplasia to low-grade dysplasia. Note the nuclear stratification and hyperchromasia. B, Architectural irregularities, including gland-within-gland, or cribriform, profiles in high-grade dysplasia.
- This case shows a markedly atypical villiform epithelium on top of ducts and glands and adjacent to squamous epithelium. There are scattered goblet cells, which are consistent with Barrett mucosa of the distinctive type. The atypical epithelium is diagnostic of high-grade dysplasia because it shows (1) prominent architectural distortion, (2) loss of cellular polarity, even at the very surface of the epithelium, (3) marked cytologic atypia, including nuclear hyperchromasia and irregularity, and (4) a lack of significant inflammation. No invasive carcinoma is seen within this specimen.
- B: A tiny adenocarcinoma consisting of a small pinkish plaque just above the esophagogastric junction H: Large, exophytic, fungating adenocarcinoma of the esophagus occupying the full circumference of the lumen