1. PATHOLOGY OF THE ESOPHAGUS

2. Symptoms of the esophageal disorders
Upper gastrointestinal bleeding (lacerations, varices)
Odynophagia (painful swallowing)--infections, other inflammatory insults
Dysphagia (difficulty swallowing)-disorders of motility (solids and liquids), obstructions such as tumors and benign strictures (solids first, progressing to liquids).

3. Disorders Hiatal hernia Achalasia Lacerations (Mallory-Weiss Syndrome)
Varices
Stenosis, webs and rings
Esophagitis
Esophageal carcinoma

4. ANATOMIC & MOTOR DISORDERS
Hiatal hernia
1-20% of population; 9% symptomatic
Characterized by
separation of the diaphragmatic crura and
widening of the space between the muscular crura and the esophageal wall.
Complications: Ulceration, bleeding, perforation, reflux esophagitis.

5. Types of Hiatal hernia
Type 1 (Sliding)--95%; protrusion of the stomach above the diaphragm creates a bell shaped dilation
Type 2 (Paraesophageal)--stomach rolls along side of lower esophageal sphincter (LES), may strangulate or obstruct and thus is often managed surgically.

6. ACHALASIA
Failure of relaxation with consequent dilatation of the esophagus
Clinically progressive dysphagia and regurgitation
Manifest in young adulthood but may appear in infancy or childhood
Manometric studies show three major abnormalities of the achalasia:
(1) aperistalsis,
(2) partial or incomplete relaxation of the lower esophageal sphincter (LES) with swallowing,
(3) increased resting tone of the LES.

7. Primary achalasia: primary degenerative changes in neural innervation
Secondary achalasia:
Chagas’ disease (Trypanosoma cruzi) causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter, with resultant dilatation of these structures
Diseases of the vagal dorsal motor nuclei, particularly polio or surgical ablation,
Diabetic autonomic neuropathy,
Infiltrative disorders (malignancy, amyloidosis, sarcoidosis),
Infectious diseases (pneumonia, candida albicans esophagitis).

8. Achalasia

9. Lacerations (Mallory-Weiss Syndrome)
Longitudinal tears in the esophagus at the esophagogastric junction
common in alcoholics
5 to 10% of upper gastrointestinal bleeding episodes.

10. Varices
Portal hypertension  collateral bypass channels (wherever the portal and caval systems communicate)
The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.
Two-thirds of all cirrhotic patients and are most often associated with alcoholic cirrhosis.
No symptoms until they rupture.
Massive hematemesis

12. Stenosis, Webs, and Rings
Non-neoplastic constrictions (stenoses):
Primary: developmental defects
Secondary (severe esophageal injury):
gastroesophageal reflux,
radiation,
scleroderma,
caustic injury.
Progressive dysphagia

13. Perforation of the esophagus
Boerhaave syndrome
Most commonly due to trauma (nasogastric tube)
or excessive vomiting
Gross: may be indistinct, or associated with a small amount of hemorrhage
Complications: bacterial mediastinitis, which has a high mortality, even with the use of broad-spectrum antibiotics.

14. Plummer-Vinson syndrome (Paterson-Kelly syndrome):
1. microcytic hypochromic anemia,
2. esophageal webs (progressive dysphagia),
3. atrophic glossitis.

15. INFLAMMATORY DISORDERS
ESOPHAGITIS
Types
Corrosive
Infectious--CMV/Herpes/Candida
Reflux.
Injury to the esophageal mucosa with subsequent inflammation is common worldwide.
In northern Iran, the prevalence of esophagitis is more than 80% (hot tea).
It is also extremely high in regions of China.

16. Disease and Origin Reflux esophagitis, via reflux of gastric contents.
Prolonged gastric intubation.
Ingestion of irritants, such as alcohol, corrosive acids or alkalis (in suicide attempts), excessively hot fluids (i.e., hot tea in Iran), and heavy smoking.
Cytotoxic anticancer therapy, with or without superimposed infection.
Infection following bacteremia or viremia (herpes simplex viruses and cytomegalovirus are the more common offenders in the immunosuppressed).

17. Fungal infection in debilitated or immunosuppressed patients or during broad-spectrum antimicrobial therapy. Candidiasis is the most common; mucormycosis and aspergillosis may occur.
Uremia.
Radiation.
Systemic conditions associated with decreased LES tone, including hypothyroidism, systemic sclerosis, and pregnancy.
In association with systemic desquamative dermatologic conditions, such as pemphigoid and epidermolysis bullosa.
Graft-versus-host disease.

18. In reflux esophagitis, three features are characteristic:
Morphology
The anatomic changes depend on the causative agent and on the duration and severity of the exposure:
Simple hyperemia
In reflux esophagitis, three features are characteristic:
eosinophils, with or without neutrophils, in the epithelial layer
basal zone hyperplasia
elongation of lamina propria papillae .

19. The final common pathway for all is
severe acute inflammation,
superficial necrosis (erosion),
ulceration with the formation of granulation tissue,
accumulation of adherent purulent debris,
and eventual fibrosis.
In infectious dieseases:
Candidiasis: gray-white pseudomembranes
Herpes and cytomegalovirus: punched-out ulcers, inclusions
Pathogenic bacteria: bacterial invasion with ulcerations.

20. Chemically induced injury ( acids, detergents):
Irradiation:
intimal proliferation with luminal narrowing in blood vessels,
fibrosis and mucosal atrophy.
Chemically induced injury ( acids, detergents):
severe necrosis of the esophageal wall,
hemorrhage
severe inflammation.
Graft-versus-host disease:
karyorrhexis of basal epithelial cells,
atrophy,
fibrosis of the lamina propria with minimal inflammation.

21. Candida albicans
Superficial, curdy, gray to white inflammatory membrane composed of matted organisms
fibrinosuppurative exudate with an underlying erythematous inflammatory base
Risk factors:
Diabetes mellitus,
neutropenia,
immunoincompetent,
AIDS,
Xerostomia, antibiotic therapy.

23. Barrett’s Esophagus
A premalignant condition in which the normal stratified squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium as a complication of chronic gastroesophageal reflux disease (GERD).
The metaplastic epithelium of Barrett's esophagus is variously called
Barrett's metaplasia,
specialized columnar metaplasia
intestinal metaplasia.

24. Red, velvety mucosa located between the smooth, pale pink esophageal squamous mucosa and the more lush, light brown gastric mucosa.
Microscopically:
the esophageal squamous epithelium is replaced by metaplastic columnar epithelium.
dysplasia (the presumed precursor of malignancy)

25. Only about 5-10% of patients with Barrett's esophagus will progress to cancer.
Endoscopy with biopsy is therefore recommended in patients who have long-standing or frequent gastroesophageal reflux disease (GERD) symptoms to determine whether or not Barrett's esophagus has developed.

26. Barret’s

27. Barrett's esophagus
No malignancy Adenocarcinoma

28. TUMORS of the ESOPHAGUS
Malignant tumors
Squamous cell carcinoma (90%)
Adenocarcinoma (associated with Barret’s esophagus)
Benign tumors
Rare

29. SQUAMOUS CELL CARCINOMA
Risk factors
Esophageal disorders
Long standing esophagitis
Achalasia
Plummer-Vinson syndrome
Life style
Alcohol
Tobacco
Virus
Human papillomavirus

30. Dietary Genetic disposition Hypovitaminosis (A,B,C)
Deficiency of trace elements (zinc, molybdenum)
Fungal contamination of foodstuff
High contents of nitrits / nitrosamines
Genetic disposition
Tylosis (hyperkeratosis of palms and soles)

31. Squamous cell carcinoma
Usually preceed by epithelial dysplasia and carcinoma in situ,
Early lesions: small, gray-white mucosal thickenings,
Three forms:
1. Polypoid exophytic
2. Necrotizing-ulcerative
3. Diffuse infiltrative
Localization:
Upper upper third (20%)
Middle third (50%)
Lower third (% 30).

32. Adenocarcinomas of the esophagus
Barret’s esophagus
Lower third
Invasion of cardia
Forms:
Nodular
Diffuse
Infiltrative.

35. THANK YOU