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Gastro-Intestinal Pathology

Esophagus

Husni Maqboul, M.D.


Normal esophagus

Squamous
esophagus

Glandular
stomach
Normal esophageal squamous mucosa
Normal GE
junction;
squamous mucosa
on the right, and
gastric cardiac
glandular mucosa
on the left
Symptoms of Esophageal Disorders

■ Dysphagia: difficulty swallowing


■ Odynophagia: pain upon swallowing
■ Heartburn: retrosternal burning pain
■ Hematemesis: vomiting of blood
■ Melena: blood in stools
– May be of upper GI origin
Esophagus, Congenital Anomalies

■ Atresia and Fistulae


– At or near Tracheal bifurcation
– Fistula connects lower or upper
pouch with a bronchus or trachea
– Other associated anomalies include
congenital heart disease and GI
malformations
Esophagus, Atresia and Fistulae
Esophagus, Anatomic Disorders

■ Stenosis : Narrowing of lumen due to


fibrous thickening of the wall
– Progressive dysphagia
– G/E reflux
– Radiation
– Scleroderma
– Caustic injury
Esophageal
Stenosis

Markedly narrowed lumen


Esophagus, Anatomic Disorders

■ Webs and Rings : Narrowing of lumen


due to mucosal protrusions
– Upper webs, lower Schatzki rings
– Episodic dysphagia
– Mostly women over 40 years
– Plummer-Vinson Syndrome : Upper
esophageal webs, iron deficiency,
glossitis, cheilosis
Motor Dysfunctions, Achalasia
■ Failure of the lower esophageal sphincter to
relax following swallowing
– Functional obstruction
– Dilation of upper esophagus
– Primary vs. secondary
■ Dysphagia, nocturnal regurgitation,
aspiration
■ Increased risk of SCC, HH, Candidiasis
■ Disorder of innervation, not muscle
– May have absent myenteric plexi
Motor Dysfunctions, Achalasia
■ Manometric studies
» Aperistalsis
» Incomplete relaxation of LES with swallowing
» Increased resting tone of LES
■ Primary
» Loss of intrinsic inhibitory innervation of
LES (autoimmune, previous viral infections?)
■ Secondary
» Chagas, polio, autonomic diabetic neuropathy
Achalasia
Motor Dysfunctions,
Hiatal Hernias
■ Caused by widening of space between
esophagus and diaphragm
– Portion of stomach protrudes above
diaphragm
– 1-20% of adults
– Significant because they may contribute to
reflux
■ Sliding : 95 % of cases
■ Rolling or Paraesophageal
Hiatal Hernia
Hiatal Hernia-Radiograph
Ectopia
● Mostly gastric type mucosa in the
upper third (Inlet patch)
● Usually asymptomatic, but may lead to
dysphagia, esophagitis and Barrett's
esophagus
Lacerations ( Mallory-Weiss )
■ Longitudinal tears at the G-E junction
■ Inadequate relaxation of muscles of
LES following retching
– Usually in chronic alcoholics
■ May be superficial or transmural
– Infection
– Upper GI bleeding or massive
hemorrhage
Diverticulae

■ Out pouching of alimentary tract


containing all viscera layers
■ Zenkers, traction, and epiphrenic
■ Food regurgitation without dysphagia
■ Aspiration
Diverticulae
Vascular Disorders: Varices
■ Collateral bypass channels where the
portal and systemic circulation
communicate
■ Dilated tortuous veins in the submucosa
– In 2/3 of all cirrhotic patients
– Asymptomatic until rupture, when
massive bleeding occurs
– 40% mortality, most survivors rebleed
within one year
Varices
Varices
Esophagitis
■ Reflux
■ Uremia
■ Corrosives/irritants
■ Radiation/Chemotherapy
■ Infection
– Viral HSV, CMV
– Fungal candida , mucor, aspergillus
– Bacterial
Herpetic
Esophagiti
note marked
ulceration
and
hemorrhage
Herpetic
Esophagitis

Herpetic
Inclusions
Eosinophilic Esophagitis
- Immune mediated disorder
- Dysphagia in adults
- Feeding intolerance and GERD like symptoms in
children
- Rings in upper and mid esophagus
- Rich eosinophilic infiltrate (away from GE junction)
- No response to PPIs
- Avoid allergens such as cow milk and soya
- Often associated with atopy. allergic dermatitis and
asthma
Reflux Esophagitis

■ 10-20% percent of adults in Western


countries
– Children and adults
■ Heartburn, regurgitation, chest pain
■ Sequelae
– Bleeding, stricture, Barrett’s esophagus
■ Pathogenesis (usually multifactorial)
– Incompetent LES, hiatal hernia, increased
gastric volume, SS, alcoholism, hypothyroidism
Reflux esophagitis

■ Gross
– Mucosal redness
– Erosions and/or ulceration
■ Microscopic
– Elongation of papillae
– Basal layer hyperplasia
– Eosinophils +/- other inflammatory
cells
Linear erosions
Typical of reflux
esophagitis
Reflux esophagitis. Note rete peg elongation and basal
layer hyperplasia.
Eosinophils in reflux
esophagitis
Barrett’s Esophagus
■ Probable complication of longstanding
reflux (up to 11% reflux patients)
■ Replacement of normal distal stratified
squamous mucosal by intestinal-type
glandular mucosa
■ Possible pathogenesis
– Reflux induces inflammation and mucosal
injury
– Healing occurs by ingrowth of stem cells and
re-epithelialization and metaplasia
Barrett’s esophagus-pathology
■ Irregular band of dark pink, velvety
mucosa extending upward as tongues
of mucosa
■ May be very patchy or focal
■ Histology
– Metaplastic columnar epithelium with
goblet cells
❖ Genetically, cells resemble
adenocarcinoma
Barrett’s esophagus

Normal white
Squamous
mucosa

Pink abnormal
Glandular
mucosa
Barrett’s esophagus
Note goblet cell metaplasia
Barrett’s esophagus-sequelae

■ Ulceration
■ Bleeding
■ Stricture
■ Adenocarcinoma
Dysplasia/Carcinoma Sequence

Barrett’s

Dysplasia

Carcinoma
Barrett’s esophagus with dysplasia. Note lack of mucin,
nuclear hyperchromasia,, and variation in size and shape.
High power
view of dysplasia in
Barrett’s esophagus..
Note
nuclear variation,
prominent nucleoli, and
increased mitoses.
Squamous mucosa

Carcinoma arising in
Barrett’s
esophagus
Benign Tumors

■ Mostly of mesenchymal origin


– Leiomyomas, lipomas, hemangiomas
■ Other Types
– Mucosal polyps
– Squamous papillomas
Malignant Tumors

■ Squamous Cell Carcinoma


– Usually > 50 years with M : F ratio of 4 : 1
– Dietary and environmental factors
– Middle third (50%), lower third (30%), and upper third
(20%)
– Gradual and late dysphagia
■ Adenocarcinoma
– Most adenocarcinomas of lower third are actually
esophageal cancers
– Barrett’s esophagus
Squamous Cell Carcinoma

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