Motor disorders, varices, esophagitis & baretts

Dr. Rubina Gulzar

Learning objectives
At the end of the lecture student should be able to understand:
Motor disorders of oesophagus.
Causes and clinical presentation of varices.
Types of esophagitis.
What is barettes oesophagus.

Motor disorders
Achalasia
Hiatal Hernia (sliding [95%], paraesophageal)
ZENKER diverticulum
Esophagophrenic diverticulum
Mallory-Weiss tear
 Types of Achalasia
Primary /idiopathic achalasia .
Primary achalasia is caused by failure of distal
esophageal inhibitory neurons.

Secondary achalasia
Its occur due to any caused like.
Chagas disease, caused by Trypanosoma cruzi infection.

Treatment
laparoscopic myotomy and pneumatic balloon dilatation.
Botulinum neurotoxin (Botox) injection, to inhibit LES cholinergic neurons,
can also be effective.

Types of esophagitis
CHEMICAL ESOPHAGITIS.
Alcohol.
Corrosive acids or alkalis.
Excessively hot fluids.
Heavy smoking.
Pill-induced esophagitis.
Cytotoxic chemotherapy.
Radiation therapy.
Graft-versus-host disease.
Types of esophagitis
2. INFECTIOUS ESOPHAGITIS.
Herpes simplex viruses.
Cytomegalo virus(CMV).
Fungal organisms.

Morphology of chemical and infectious esophagitis

Morphology of chemical and infectious esophagitis varies with etiology.

chemicals (lye, acids, or detergent).

Lack of neutrophilic infiltration which may result in outright necrosis of the
esophageal wall.
 Morphology of infectious esophagitis
Endoscopic Finding
Herpes viruses typically cause punched-out ulcers.
Histological Finding
Herpes viruses demonstrate nuclear viral inclusions within a rim of
degenerating epithelial cells at the margin of the ulcer .
CMV causes characteristic nuclear and cytoplasmic inclusions within
capillary endothelium and stromal cells .

Reflux esophagitis
DEFINATION.
Esophageal mucosal damage that results from reflux of gastric acid into the
esophagus.

CAUSES OF GERD
Decrease lower esophageal sphincter tone or increase abdominal
pressure contribute to GERD.
Alcohol and tobacco use.
Obesity
Central nervous system depressants.
Pregnancy.
Hiatal hernia (discussed below).
Delayed gastric emptying,.
Increased gastric volume.

Reflux esophagitis: morphology

Inflammatory Cells
Eosinophils
Neutrophils
Lymphocytes

Basal zone hyperplasia

Lamina Propria papillae elongated and congested, due to regeneration

Reflux esophagitis: morphology

 Reflux esophagitis
Clinical Features
Dysphagia.
Heartburn.
Noticeable regurgitation of sour-tasting gastric contents.
Treatment with
Proton pump inhibitors or
H2 histamine receptor antagonists.

Reflux esophagitis
Complications
Esophageal ulceration.
Hematemesis.
Melena.
Stricture development.
Barrett esophagus.

Histology of Barrets
INTESTINALIZED (GASTRICIZED) mucosa is AT RISK for glandular dysplasia.
Searching for dysplasia when BARRETTs is present is of utmost importance.
Dysplasia again divided in to low grade and high grade.
MOST/ALL adenocarcinomas arising in the esophagus arise from previously
existing BARRETTs

Barrett Esophagus
Barrett esophagus is a complication of chronic GERD that is characterized by
intestinal metaplasia within the esophageal squamous mucosa.
SINGLE most common RISK FACTOR for esophageal adenocarcinoma
10% of GERD patients get it BREACHED G-E junction

Morphology
Barrett esophagus can be recognized as one or several tongues or patches of
red, velvety mucosa extending upward from the gastro esophageal junction.
Endoscopically barrets classified in:
long segment, in which 3 cm or more of esophagus is involved.
short segment, in which less than 3 cm is involved..
 Morphology of Barrets

Dysplasia in Barrets
Dysplasia is define as
Increased epithelial proliferation.
Often with atypical mitoses.
Nuclear hyperchromasia and stratification.
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
 Low AND high grade dysplasia

Clinical Features
Barrett esophagus can only be identified
thorough endoscopy and biopsy.
BARRETTS ESOPHAGUS TREATMENT
Periodic endoscopy with biopsy, for detection of dysplasia, has an important
role.
Low grade dysplasia potential to regress, either spontaneously or in response
to therapy
In case of multifocal high grade dysplasia and intamucosal carcinoma
treatment options include surgical resection, or esophagectomy.
Esophageal varices
Esophageal varices are extremely dilated sub-mucosal veins in
the esophagus. They are most often a consequence of portal hypertension,
patients with esophageal varices have a strong tendency to develop bleeding.
Morphology
Varices appear as tortuous dilated veins lying primarily within the submucosa
of the distal esophagus and proximal stomach.
when varices are not ruptured, the overlying mucosa is intact .
Variceal rupture results in hemorrhage into the lumen or esophageal wall, in
which case the overlying mucosa appears ulcerated and necrotic.
If rupture has occurred in the past, venous thrombosis, inflammation, and
evidence of prior therapy may also be present.
 Endoscopic finding of varices

Histological finding of varices

Clinical Features
varices are often asymptomatic, they may rupture, causing massive
hematemesis.
Treatment.
Sclerotherapy.
Endoscopic balloon tamponade.
Endoscopic rubber band ligation.
 You must known
Achalasia is characterized by the triad of incomplete LES relaxation, increased
LES tone, and aperistalsis of the esophagus.
Herpes viruses typically cause punched-out ulcers biopsy specimens
demonstrate nuclear viral inclusions.
Gerd results from reflux of gastric acid into the esophagus.
Barettes is most common risk factor for esophageal adenocarcinoma.
Esophageal varices are most often a consequence of portal hypertension.

Reference
Pathologic Basis Of Disease. Eight Edition . Chapter 17. Gastrointestinal tract.
Page Number 767-771.
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