NON-NEOPLASTIC

DISORDERS OF
ESOPHAGUS

Dr. Naw May Emerald

Faculty of Medicine & Health Sciences
UCSI University
Learning outcomes ( Diseases of
oropharynx, non-neoplastic disorders and
neoplastic disorders of oesophagus)

The student will be able to

List the common diseases of oral cavity and tonsils .
List the causes of tonsillar enlargement and
oesophagitis.
Explain mechanisms of GERD and achalasia, and list their
important clinical features.
List aetilogical factors, histological types and describe the
morphology and clinical features of oesophageal tumours
List the causes of dysphagia
 Diseases of Esophagus
I. NON-NEOPLASTIC DISORDERS

II. NEOPLASTIC
DISORDERS
A. Obstructive &
vascular diseases
Esophageal tumours
 Mechanical obstruction
 Functional obstruction
 Ectopia B . Esophagitis
 Oesophageal varices
• Laceration
• Chemical & infectious Esophagitis
• Reflux Esophagitis (GERD)
• Eosinophilic Esophagitis
• Barrett Esophagus
A . Obstructive & vascular diseases
 Mechanical obstruction – Congenital / acquired
Congenital - agenesis ,atresia, stenosis and fistula,
Acquired - stenosis due to inflammation &
scarring,
 Functional obstruction – Esophageal dysmotility
characterized by discoordinated contraction or
spasm of muscularis , Increased LES tone e.g.
Acalasia cadia
 Ectopia – ectopic gastric mucosa in upper third of
esophagus, usu: asymptomatic but acid secretion
can result in dysphagia, esophagitis, Barrett
esophagus & rarely adenocarcinoma
 Oesophageal varices – abnormal, tortuous and
dilated oesophgeal veins due to the effects of
portal hypertension, can be ruptured and an
important cause of esophageal bleeding
 Mechanical obstruction
Esophageal atresia and tracheoesophageal fistula

A, Blind upper and lower esophagus with thin cord of connective tissue linkin
two segments.
B, Blind upper segment with fistula between lower segment
and trachea.
C, Fistula (without atresia) between patent esophagus and
trachea.
 Functional obstruction – Achalasia cardia
 Functional disorder of esophagus
 Characterized by the triad of incomplete LES
relaxation, increased LES tone and esophageal
aperistalsis , that leads to esophageal dilatation
 impaired smooth muscle relaxation,

 Increased tone of the lower

esophageal sphincter (LES)

 esophageal obstruction.

 REVISE the normal mechanism of swallowing

( Physiology)
(2) types
Primary achalasia – idiopathic, is the result of distal
esophageal inhibitory neuronal (ganglion cell)
degeneration.
 leads to increased tone, an inability to relax of the
lower esophageal sphincter, and esophageal
aperistalsis.
- degenerative changes in the neural innervation
either intrinsic to the esophagus or within the
extraesophageal vagus nerve or dorsal nucleus may
occur
 rare familial cases (+)
Secondary achalasia – occurs in Chagas disease
in which Trypanozoma cruzi infection causes
destruction of myenteric plexus & failure of LES
relaxation
Achalasia-like disease
may be caused by diabetic autonomic neuropathy;
 infiltrative disorders such as malignancy,
amyloidosis, or sarcoidosis;
lesions of dorsal motor nuclei, particularly polio or
surgical ablation;
 in association with Down syndrome

Symptoms - dysphagia for solids and liquids,

difficulty in belching, chest pain, and
regurgitation.
Esophagitis
Causes
1. Laceration
2. Chemical & infectious
Esophagitis
3. Reflux Esophagitis (GERD)
4. Eosinophilic Esophagitis
5. Barrett Esophagus
1. Lacerations
Mallory-Weiss tears
 Longitudinal mucosal tears near the
gastroesophageal junction
 most often associated with severe retching or
vomiting secondary to acute alcohol
intoxication.
 Normally, a reflex relaxation of the
gastroesophageal musculature precedes the
antiperistaltic contractile wave associated
with vomiting.
 Failure of relaxation during prolonged
vomiting with the result that refluxing gastric
contents overwhelm the gastric inlet and
cause the esophageal wall to stretch and tear
 The roughly linear lacerations are
longitudinally oriented and range in length
from millimeters to several centimeters.
 These tears usually cross the
gastroesophageal junction and may also be
located in the proximal gastric mucosa.
 superficial esophageal lacerations presents
as upper GI bleeding, (hematemesis)
(2) syndromes caused by Mallory-
Weiss tears
1. Mallory Weiss syndrome is characterized by
upper gastrointestinal bleeding secondary to
longitudinal mucosal lacerations at the
gastroesophageal junction or gastric cardia.
 do not generally require surgical intervention, and
healing tends to be rapid and complete.

2. Boerhaave syndrome is a much less common

but more serious disorder characterized by
transmural tearing and rupture of the distal
esophagus.
This catastrophic event produces severe mediastinitis
and generally requires surgical intervention.
patients can present with severe chest pain,
tachypnea, and shock, the initial differential diagnosis
can include myocardial infarction.
2. Chemical & infectious Esophagitis
Chemical – alcohol, corrosive acids or alkali,
excessively hot fluid, heavy smoking,
Medicinal pills → pill-induced esophagitis
May be caused by cytotoxic chemotherapy, radiatio
therapy or graftversus host disease
Clinical features : Odynophagia, in severe case
hemorrhage, stricture, perforation
Infectious esophagitis- common in debilitated and
immunosuppressed
Causal organisms – herpes simplex, CMV or fungal
organisms ( candida is the most common)
 3. REFLUX ESOPHAGITIS /GERD
 Inflammation of the esophagus due to the
reflux of gastric contents into the lower
esophagus
 The most frequent cause of esophagitis
 The associated clinical condition is termed
GERD ( Gastroesophageal
reflux disease)

Protective Mechanism
 Stratified squamous epithelium of the
esophagus is resistant to abrasion from foods
but sensitive to acid
 Submucosal glands of the proximal and distal
esophagus secrete mucin and bicarbonate to
Pathogenesis
Impairment of LES tone or increased
abdominal pressure lead to reflux of
gastric contents into the lower
esophagus
Reflux of gastric content is central to
the development of mucosal injury –
reflux esophagitis
Contribute to GERD
In severe cases , reflux of bile from the
duodenum may exacerbate the damage.
The most common cause of gastroesophageal
reflux is transient lower esophageal
sphincter relaxation.
thought to be mediated via vagal pathways, and
can be triggered by gastric distention by gas or
food, mild pharyngeal stimulation that does not
trigger swallowing, and stress.
Gastroesophageal reflux can also occur following
swallow-induced lower esophageal sphincter
relaxations or due to forceful opening of a relatively
hypotensive lower esophageal sphincter by an
abrupt increase in intra-abdominal pressure, such
as that due to coughing, straining, or bending.

Other conditions that decrease lower
esophageal sphincter tone or increase
abdominal pressure and contribute to GERD
include
1. alcohol & tobacco use
2. obesity
3.CNS depressants
4. Pregnancy
5. Hiatal hernia
6. Delayed gastric emptying
7. Increased gastric volume
8. No definite cause in many cases
 Endoscopic view

Morphology

Gross – Mucosal Hyperemia –

redness are seen at the
lower esophagus
Histology – mild case –
unremarkable
Significant disease –
Mucosa – eosinophils
recruitment followed by
neutrophils
Basal zone hyperplasia
leading to epithelial
thickness and elongation of
lamina propria papillae
Ref: J C E Underwood: General & Systematic Pathology : 5th Edition
Clinical Features
GERD is most common in individuals
older than age 40 but also occurs in
infants and children.
The most frequent clinical symptoms
are heartburn, dysphagia, and
regurgitation of sour-tasting gastric
contents.
Rarely, chronic GERD is punctuated by
attacks of severe chest pain that may
be mistaken for heart disease.
Complications of reflux
esophagitis
ulceration,
hematemesis, melena,
stricture development, and
Barrett esophagus.
 Hiatal hernia ( Hiatus
hernia)
It is characterized by separation of the
diaphragmatic crura and protrusion of the stomach
into the thorax through the resulting gap.
can give rise to symptoms, such as heartburn

and regurgitation of gastric juices, that are similar

to
those of GERD.
Congenital hiatal hernias are recognized in infants
and children, but many are acquired in later life.
Hiatal hernia is symptomatic in fewer than 10% of
adults, but can be a cause of lower esophageal
sphincter incompetence.
4. BARRETT ESOPHAGUS
Barrett esophagus is a complication of
chronic GERD
is characterized by intestinal
metaplasia within the esophageal
squamous mucosa.
occurs in as many as 10% of
individuals with symptomatic GERD.
most common in white males and
typically presents between 40 and 60
years of age
Importance - an increased risk of
esophageal adenocarcinoma.
Genomic sequencing of biopsies from Barrett
esophagus has revealed the presence of
mutations that are shared with esophageal
adenocarcinoma,
Potentially oncogenic mutations are more
numerous when biopsies demonstrate
dysplasia,
The presence of dysplasia, a preinvasive
change, is associated with prolonged
symptoms, longer segment length, increased
patient age, and Caucasian race.
Although the vast majority of esophageal
adenocarcinomas are associated with Barrett
esophagus, but most individuals do not
develop esophageal tumors.
MORPHOLGY
GROSS
 one or several tongues

or patches of red, velvety

mucosa extending upward
from the gastroesophageal
junction.
Normal Barrett esophagus

This metaplastic mucosa alternates with residual

smooth, pale
squamous (esophageal) mucosa and interfaces with
light-brown columnar (gastric) mucosa distally
HISTOLOGY - metaplastic columnar mucosa above
the gastroesophageal junction.
Microscopically, gastric or intestinal-type metaplasia
is seen as replacement of the squamous esophageal
epithelium with goblet cells (intestinal metaplasia)
 Low grade dysplasia High grade dysplasia

etaplastic glandular epithelium

Dysplasia if present, classified as low grade or high grade.
 Atypical mitoses, nuclear hyperchromasia, irregularly clumped
chromatin, increased nuclear-to-cytoplasmic ratio, and a
failure of epithelial cells to mature as they migrate to the
esophageal surface are present in both grades of dysplasia
 Gland architecture is frequently abnormal and is
characterized by budding, irregular shapes, and cellular
crowding.
 High-grade dysplasia exhibits more severe cytologic and
architectural changes. With progression, epithelial cells may
Clinical Features
 Presents with GERD symptoms.
 Only be identified through endoscopy
and biopsy
 Periodic endoscopy with biopsy should be
performed for dysplasia surveillance.
 However, randomized trials have failed to
demonstrate that surveillance improves
patient survival.
 Furthermore, uncertainties regarding the
potential of dysplasia, particularly low grade,
to regress spontaneously and limited
information on the risk of progression
complicates clinical decisions.