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Pathology of Esophagus Pathology of Esophagus Dr.CSBR.Prasad,M.D., May-2015-CSBRP

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Pathology of EsophagusPathology of Esophagus

Dr.CSBR.Prasad,M.D.,

May-2015-CSBRP

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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

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UES & LES

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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

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@ Cricoid cartilage

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@ the aortic arch

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@ the level of the left atrium

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@ the diaphragmatic

opening

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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

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EsophagitisEsophagitis

• Candida• HSV• CMV• Chemotherapy• GVHD• Radiation• Mallory-Weis syndrome• Bullous lesion• Crohn’s disease

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• HSV• CMV

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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

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Esophageal varicesEsophageal varices

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Causes

• PHT• Superior venacaval obstruction

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Endoscopic views – bag of worms

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Gross

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Microscopy

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Complications

• Bleeding

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Bleeding varices

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Causes for massive Upper GI bleeding

• Esophageal varices• Bleeding gastric ulcer• Bleeding duodenal ulcer• Gastric leiomyoma

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Varices due to SVS & PHT

Involvement of esophagus by varices:• SVS: Entire length of esophagus• PHT: Lower 1/3rd

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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.

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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

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Benign lesionsBenign lesions

• SQUAMOUS CELL PAPILLOMA • Developmental Cysts and Duplications• Diverticulosis

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SQUAMOUS CELL PAPILLOMASQUAMOUS CELL PAPILLOMAMay-2015-CSBRP

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Case - 45yo female with weakness and difficulty in swallowingWhat are your findings? Diagnosis?

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Findings

• Angular chelitis• Esophageal web (Endoscopy, Barium swallow)• Koilonychia• Microcytic hypochromic anemia

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What is your diagnosis?

Synonyms: • Plummer-Vinson Syndrome• Patterson-Kelly Syndrome• Sideropenic dysphagia

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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?

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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

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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

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What is your diagnosis?

• Carcinoma of esophagus

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Carcinoma of EsophagusCarcinoma of Esophagus

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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

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Palmoplantar keratoderma / Tylosis

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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

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Types

• Superficial SqCC• Invasive SqCC

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SUPERFICIAL CARCINOMA

In this plaque-like gross appearance the carcinoma forms an irregular, slightly elevated lesion, covering most of the field.

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Invasive SqCC - Types

• Fungating• Ulcerative and • Infiltrating

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EXOPHYTIC OR

FUNGATING CARCINOMA

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ULCERATING CARCINOMA

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INFILTRATIVE PATTERN

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Squamous cell carcinoma - Esophagus

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MetastasisThe 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

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BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS

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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

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BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS

The importance of this disorder:• It’s associated with an increased risk of

adenocarcinoma of the esophagus

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BARRETT'S ESOPHAGUSBARRETT'S ESOPHAGUS

The most common predisposing factor:

Chronic gastroesophageal reflux – GERDAnd it’s identified by this history

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This section shows a small island of squamous epithelium replacing the surface columnar cells.

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MUCIN STAINS OF BARRETT'S MUCOSA Alcian blue stain shows the blue- staining goblet cells

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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

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Dysplasia in Barrett esophagus

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High grade dysplasia

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Treatment options

• Low grade dysplasia: Follow up• High grade dysplasia: Treated as intramucosal

carcinoma

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Adenocarcinoma of the EsophagusAdenocarcinoma of the Esophagus

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AdenocarcinomaAdenocarcinoma

• Relatively uncommon tumor• M:F = 3:1 to 7:1 • Mean age: 60yrs• GERD• Progressive dysphagia

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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

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Gross

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ADENOCARCINOMA ASSOCIATED WITH

BARRETT'S ESOPHAGUS

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Spread and prognosis

5-year survival rates:• 75% in individuals with superficial esophageal

carcinoma • With metastases to LNs: a dismal 9%

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NEOPLASMS METASTATIC TO THE ESOPHAGUS

• Same three that metastasize to the stomach: – Carcinomas of the lung– Breast, and – Melanoma

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END

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