OESOPHAGEAL PATHOLOGY
Dr Purushotham
Krishnappa
Copyright reserved 2023, IMU. All rights reserv
Objectives
• Describe the etiopathogenesis & Clinicopathological features
of
• Reflux oesophagitis
• Achalasia
• Tumours of oesophagus.
Oesophageal Disorders
Anatomic /
Reflux Infectious
Structural
Motility Neoplastic
STRUCTURAL DISORDERS OF Oesophagus
• Atresia, Fistula (tracheoesophageal)
• Diverticula
• Stenosis
• Hiatal hernia
• Esophageal webs & Rings
• Lacerations (Mallory- Weiss syndrome)
4
Tracheoesophageal fistula
Most dangerous Most common
Diverticulum
• Are uncommon small mucosal outpouchings.
• Zenker diverticulum (pharyngoesophageal
diverticulum) is located immediately above the upper
oesophageal sphincter.
• Traction diverticulum occurs near the midpoint of the
oesophagus.
• Epiphrenic diverticulum is immediately above the
lower oesophageal sphincter.
Hiatus Hernia
Sliding Rolling (para-
oesophageal)
• >90%
• <10%
• Shortened oesophagus
• Part of the stomach
• Dragging part of the
(fundus) herniates
stomach into the
alongside oesophagus
thoracic cavity
into the thorax
(stomach continuous with • .Vulnerable to serious
oesophagus)
strangulation
prone to ulceration, bleeding, dysphagia
Oesophageal webs & Rings
Webs (produce dysphagia to solids)
• Plummer-Vinson / Paterson-Kelly syndrome post cricoid web, IDA,
Glossitis, cheilosis in perimenopausal female, Risk of postcricoid
Squamous cell carcinoma.
Schatzki’s rings
• At LES
• Cause narrowing (Stenosis)
Lacerations
Mallory- Weiss syndrome
• At the gastro esophageal junction
• Caused by excessive vomiting in presence of spasm of LES
Boerhaave’ syndrome – tear penetrates all layers of oesophagus.
REFLUX OESOPHAGITIS
• Gastroesophageal reflux: Reflux of gastric contents
to the oesophagus
• Gastroesophageal reflux disease (GERD): Any
significant symptomatic clinical condition or
histopathological changes resulting from reflux.
• Reflux esophagitis: GERD patients with
histopathologically demonstrable changes in the
oesophageal mucosa.
Etiopathogenesis of reflux oesophagitis
Reflux of gastric contents;
1. Inefficiency of Antireflux mechanisms --
- CNS depressants,
- hypothyroidism,
- pregnancy,
- systemic sclerosing disorders,
- Alcohol,
- Tobacco,
- Nasogastric tube,
2. Sliding hiatal hernia,
3. Inadequate clearance of refluxed material
4. Delayed gastric emptying;
Effect: [ Injury ]
Protracted exposure to gastric juices,
Acid - peptic action
Inflammation and ulceration.
GERD
• Clinical features • Complications:
• HEARTBURN
• REGURGITATION
• Bleeding
• Dysphagia • Stricture
• Chest pain • Barrett oesophagus
• Water brash
• Nausea and vomiting
• Belching
• Hicough
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BARRETT Oesophagus :
Distal squamous mucosa
replaced by metaplastic
columnar epithelium as a
response to prolonged
injury.
Pathogenesis
• Not clearly known,
• Ulceration
Ingrowth by pluripotent stem cells
[Resistant to acid-peptic injury]
16
Clinical features
• Reflux oesophagitis features,
• With complications like
• Bleeding and stricture,
• Dysplasia
• 30 to 40 fold = Adenocarcinoma;
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Normal oesophagus and stomach
Normal oesophagus - microscopy
Barrett oesophagus with
ulcerating adenocarcinoma
Pathology
Gross Microscopy
• Tongues or patches of red, velvety • Diagnosis requires both
mucosa extending upward from the endoscopic evidence of abnormal
gastroesophageal junction. mucosa above the
• This metaplastic mucosa alternates gastroesophageal junction and
with residual smooth, pale squamous histologically documented
(esophageal) mucosa and interfaces intestinal metaplasia.
with light-brown columnar (gastric)
mucosa distally .
• Long segment, in which 3 cm or more
• short segment, in which less than 3 cm
is involved.
Barrett Oesophagus
Motility Disorders
Primary Secondary
motility motility
disorders disorders
1. Achalasia 1. Severe esophagitis
2. Diffuse esophageal spasm 2. Scleroderma
3. Nutcracker oesophagus 3. Diabetes
4. Nonspecific esophageal 4. Parkinson’s
dysmotility 5. Stroke
Achalasia
• Dual Pathology
– LES fails to relax
• resistance to flow into stomach
• not spasm of LES but an increased basal LES pressure often seen
(55-90%)
– loss of peristalsis in distal 2/3 oesophagus
• Pathogenesis
loss of ganglionic cells in the myenteric plexus (distal to
proximal)
– vagal fiber degeneration
– underlying cause: unknown
• autoimmune?
Achalasia
• Clinical presentation
– Dysphagia 90-100%
– Post-prandial regurgitation 60-90%
– Chest pain 33-50%
– Pyrosis 25-45%
– Weight loss
– Nocturnal cough and recurrent aspiration
• Diagnosis
– Plain film (air-fluid level, wide mediastinum, absent gastric
bubble, pulmonary infiltrates)
– Barium oesophagram (dilated oesophagus with taper at LES)
• good screening test (95% accurate)
– Endoscopy (rule out GE junction tumors, esp. age>60)
– Esophageal manometry (absent peristalsis, LES relaxation, &
resting LES >45 mmHg)
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Tumors
Benign: Malignant:
• Leiomyoma, • Carcinoma –
• Fibroma, Squamous
• Lipoma, Adeno
• Neurofibroma, • Sarcoma
• Hemangioma,
• Polyps
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SQUAMOUS CELL CARCINOMA
• Geographic Variability in incidence,
• Age 50 yrs.,
• M : F = 20 : 1,
• Incidence - Variable,
Northern Iran to Northern China
--- 100 / 100,000
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Etiology & pathogenesis:
•Genetic : •Lifestyle: •Preexistent Dietary:
not clear, • Alcohol Esophageal disorders: • Vitamins [ A, C ]
consumption • Longstanding • Trace metals
• Tobacco use oesophagitis [ Zn, Mo ]
• Urban • Achalasia • Fungal
environment • Plummer-Vinson contamination
syndrome of food
• Nitrites /
nitrates,
• Betel chewing;
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Morphology:
• GROSS: 20%
* Polypoid - 60%,
* Flat - - - - - 15%, 50%
* Excavating - 25%
30%
STARTS AS
IN-SITU-CARCINOMA
Clinical Features
• Insidious onset,
• Dysphagia - gradual obstruction,
• Weight loss & debility,
• Haemorrhage,
• Sepsis,
• Tracheoesophageal fistula,
Prognosis:
• 5 yr. Survival: superficial - 75%
• Advanced - 25%
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[Local & distant spread common ]
ADENOCARCINOMA
• 50% OF TUMORS,
ETIOLOGY & PATHOGENESIS:
POINT MUTATION OF p53 gene with
functional inactivation
•COMMON AT LOWER END,
•5 - YR. SURVIVAL is < 30%.
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Irregular, reddish, ulcerated mass -
mid-oesophagus:
32
References
1. The gastrointestinal tract. Kumar et al: Robbins and Cotran
Pathologic Basis of Disease 9th edition. Chapters 16 & 17.
2. "Diseases of the oesophagus." In Oxford Textbook of Medicine 5th
edition. Edited by David A. Warrell, Timothy M. Cox, John D. Firth
3. https://next.amboss.com/us/library/Qh0udf/zi0r8f/WQ0PEf/rQ0fxf
4. Goyal, Raj K. "Diseases of the oesophagus." In Harrison's Principles
of Internal Medicine, edited by Anthony S. Fauci, et al. New York:
McGraw-Hill, 1997.
Q 1:
• A 57-year-old man comes to the physician for a follow-up evaluation
of chronic, retrosternal chest pain. The pain is worse at night and
after heavy meals. He has taken oral pantoprazole for several months
without any relief of his symptoms. Esophagogastroduodenoscopy
shows ulcerations in the distal oesophagus and a proximally
dislocated Z-line. A biopsy of the distal oesophagus shows columnar
epithelium with goblet cells. Which of the following microscopic
findings underlie the same pathomechanism as the cellular changes
seen in this patient?
A. Pseudostratified columnar epithelium in the bronchi
B. Squamous epithelium in the bladder
C. Paneth cells in the duodenum
D. Branching muscularis mucosa in the jejunum
Q 2:
• A 68-year-old man comes to the
physician because of a 4-
month history of bad breath and
progressive difficulty
swallowing solid food. Physical
examination shows no
abnormalities. An upper endoscopy
is performed and
a photomicrograph of a biopsy
specimen obtained from the mid-
oesophagus is shown. Which of the
following best explains the findings
in this patient?
A. Well-differentiated neoplastic glandular proliferation
B. Atrophy and fibrosis of the oesophageal smooth muscle
C. Metaplastic transformation of oesophageal mucosa
D. Neoplastic proliferation of squamous epithelium
