Download Symptoms of the esophageal disorders

PATHOLOGY OF THE
ESOPHAGUS
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).
Disorders
Hiatal hernia
Achalasia
Lacerations (Mallory-Weiss Syndrome)
Varices
Stenosis, webs and rings
Esophagitis
Esophageal carcinoma
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.
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.
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.
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).
Achalasia
Lacerations (Mallory-Weiss Syndrome)
Longitudinal tears in the esophagus at the
esophagogastric junction
common in alcoholics
5 to 10% of upper gastrointestinal bleeding
episodes.
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
Stenosis, Webs, and Rings
Non-neoplastic constrictions (stenoses):
Primary: developmental defects
Secondary (severe esophageal injury):
– gastroesophageal reflux,
– radiation,
– scleroderma,
– caustic injury.
Progressive dysphagia
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.
Plummer-Vinson syndrome
(Paterson-Kelly syndrome):
– 1. microcytic hypochromic anemia,
– 2. esophageal webs (progressive dysphagia),
– 3. atrophic glossitis.
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.
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).
– Fungal infection in debilitated or
immunosuppressed patients or during broadspectrum 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.
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
2. basal zone hyperplasia
3. elongation of lamina propria papillae .
1.
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.
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.
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.
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.
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)
Only about 5-10% of patients with Barrett's
esophagus will progress to cancer.
Endoscopy with biopsy is therefore
recommended in patients who have longstanding or frequent gastroesophageal
reflux disease (GERD) symptoms to
determine whether or not Barrett's
esophagus has developed.
Barret’s
Barrett's esophagus
No malignancy
Adenocarcinoma
TUMORS of the ESOPHAGUS
Benign tumors
– Rare
Malignant tumors
– Squamous cell
carcinoma (90%)
– Adenocarcinoma
(associated with
Barret’s esophagus)
SQUAMOUS CELL CARCINOMA
Risk factors
Esophageal disorders
– Long standing esophagitis
– Achalasia
– Plummer-Vinson syndrome
Life style
– Alcohol
– Tobacco
Virus
– Human papillomavirus
Dietary
– 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)
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).
Adenocarcinomas of the
esophagus
– Barret’s esophagus
– Lower third
– Invasion of cardia
– Forms:
Nodular
Diffuse
Infiltrative.
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