Pathology of GIT ESOPHAGUS Sept. 30 2015 Prof. Dr Faeza Aftan Col of Med. Aliraqia University.

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Presentation transcript:

Pathology of GIT ESOPHAGUS Sept Prof. Dr Faeza Aftan Col of Med. Aliraqia University

ESOPHAGUS Congenital Anomalies; atresia & fistula Diverticula mucosal webs (Plummer-Vinson syndrome, Paterson-Brown- Kelly ) Achalasia Laceration (Mallory-Weiss tears,) Esophagitis,  Reflux (GERD) Barretts Neoplasm

Obstruction Mechanical; - atresia, Fistula, duplication. - Inflammation & scarring. - tumor Functional; - Achalasia, (primary & secondary)

Normal esophageal-gastric junction

Esophageal atresia and Tracheoesophageal fistula. A, Blind upper and lower esophageal segments. B, Blind upper segment with fistula between lower segment and trachea. C, Fistula between patent esophagus and trachea. Type B is the most common. most commonMechanical Obstruction

Functional obstruction  Achalasia incomplete LES relaxation, increased LES tone, aperistalsis of the esophagus. failure of distal inhibitory neurons. 1ry; idiopathic, most common. 2ry ; cancer, Chagas dis. or fibrosis, amyloidosis, DM

 Achalasia LES are regulated by excitatory (ACH, substance P) & inhibitory (NO, VIP) neurotransmitters. achalasia lack inhibitory subst. The result is a nonrelaxed esophageal sphincter. Autopsy specimens, on L/M, shown an inflammatory response ( lymphocytes, eosinophils and mast cells), loss of ganglion cells, and neurofibrosis. Unknown cause. an autoimmune, hereditary, neurodegenerative, genetic and infections.

DIVERTICULA ZENKER (HIGH)‏ TRACTION (MID)‏ EPIPHRENIC (LOW)‏ TRUE vs. FALSE?

Esophageal diverticulum Zenker diverticulum Traction Epiphrenic diverticulum

Dilated portion of stomach protrudes above diaphragm Common! Usually asymptomatic. Heartburn, reflux esophagitis Danger: ulceration, bleeding Hiatal Hernia

Sliding (L) & rolling (R) hiatal hernias Hiatal hernias

VARICES THREE common areas of portal/caval anastomoses – Esophageal – Umbilical – Hemorrhoidal 100% related to portal hypertension Found in 90% of cirrhotics MASSIVE, SUDDEN, FATAL hemorrhage is the most feared consequence

Esophagial Varices

Esophagitis Infective esophagitis viral, Bacterial, Fungal Non infective eophagitis Alcohol, Pills, Acid & alkali, chemotherapy & radiotherapy. Reflux esophagitis Laceration (Mallory-Weiss tears)

Candida esophagitis

ESOPHAGITIS - Herpes

Factors associated with the development of gastro-oesophageal reflux disease. Severe reflux oesophagitis Barrett’s oesophagus REFLUX/GERD

Barrett esophagus; long segment= >3 cm Vs. short segment< 3 cm is involved Barrett esophagus

Replacement of squamous epithelium by columnar epithelium with goblet cells Complication of long-standing reflux esophagitis Danger: risk of adenocarcinoma screen for high-grade dysplasia Barrett Esophagus

Barrett esophagus

Molecular studies suggest that Barrett epithelium may be more similar to adenocarcinoma than to normal esophageal epithelium, consistent with the view that Barrett esophagus is ???? a pre-malignant condition

LACERATION Tears are LONGITUDINAL Usually secondary to severe VOMITING Usually in ALCOHOLICS Usually MUCOSAL tears By convention, they are all called: MALLORY-WEISS

Mallory-Weiss tears

TUMORS BENIGN MALIGNANT – Squamous cell carcinoma – Adenocarcinoma

 SQUAMOUS CELL CARCINOMA >45 Years males 4X > females. underdeveloped areas. 50% occur in the middle 1/3 of esophagus

Tobacco, > 3/4 Alcohol polycyclic hydrocarbons, nitrosamines, fungus-contaminated foods, HPV radiation therapy Very hot beverages loss of tumor suppressor genes, including p53 and p16. Other: poverty, caustic esophageal injury, Achalasia, Plummer-Vinson syndrome, Nutritional deficiencies,

Esophageal Sq cell ca.

Squamous dysplasia

SQUAMOUS CARCINOMA DYSPLASIA  IN-SITU  INFILTRATION

Squamous Cell Carcinoma

Squamous cell carcinomas The rich submucosal lymphatic network promotes spread, even away from the principal mass. ca of up 1/3 of esophagus __ cervical LN. middle 1/3 __ mediastinal, paratracheal, & tracheobronchial LN; lower 1/3 spread to gastric and celiac LN.

ADENOCARCINOMA BARRETT’s Obesity Tobacco & alcohol H. pylori ‏ Female hormones

ADENOCARCINOMA Progression of Barrett esophagus to adenocarcinoma occurs through genetic and epigenetic changes. accumulate mutations.

ADENOCARCINOMA

Esophageal adenoca. Sq cell ca.

Adenocarcinoma Commonest type in US Risk factor: Barrett esophagus Distal 1/3 of esophagus Symptoms: late obstruction Squamous cell carcinoma Commonest type worldwide Risk factors: smoking, alcohol, genetics, esophagitis. Middle 1/3 of esophagus Symptoms: insidious onset; late obstruction Esophageal Carcinoma

Esophageal cancer. A, adenoca B, Sq cell ca.

BENIGN TUMORS LEIOMYOMAS POLYPS CONDYLOMAS (HPV)‏ LIPOMAS‏