PATHOLOGY

DISEASES OF THE ESOPHAGUS

Dr. Janet L. Dy

November 17, 2011

DISEASES OF THE ESOPHAGUS

Diseases of the esophagus tend to produce similar symptoms
which include:
1. Dysphagia
- Difficulty in swallowing
- Due to obstruction or motor dysfunction like in
Achalasia or hernia
- Usually due to narrowing of lumen (obstruction)
2. Odynophagia
- Pain in swallowing
- Due to infection or gastric reflux
3. Heartburn
- Pain in the retrosternum
- Reflux esophagitis
4. Hematemesis
5. Melena
Note:
The last two are less common manifestation

CONGENITAL ABNORMALITIES
Atresia
Defined as the incomplete development of the esophagus
Thin, non-canalized cord replaces a segment of esophagus,
causing a mechanical obstruction
Occurs most commonly at or near the tracheal bifurcation
Usually associated with a fistula
Also associated with congenital heart defects, genitourinary
malformations, neurologic diseases
Stenosis
o Incomplete form of atresia
o Lumen is markedly reduced in calibre as a result of fibrous
thickening Partial or complete obstruction

Fistulae
Abnormal communication between two hollow organs
Can lead to aspiration, suffocation, pneumonia, severe fluid
and electrolyte imbalance
Type C
o Most common form
o Fistula which frequently combined with esophageal atresia
(90%)
Type E
o Least common
o Fistula between an intact esophagus & trachea

DISORDERS OF MOTOR DYSFUNCTION

Hallmark Dysphagia
Consists of:
1. Achalasia
2. Hiatal Hernia
3. Laceration
4. Diverticula

Achalasia
Also known as esophageal achalasia, esophagosapasm,
achalasia cardiae, cardiospasm, and esophageal
aperistalsis, esophageal motility disorder
Involves the smooth layer of the esophagus and the LES
Due to impaired smooth muscle relaxation
Release of NO and VIP from inhibitory neurons along with
interruption of normal cholinergic signalling Allows LES to
relax
Produces functional obstruction of the esophagus
Characterized by the triad of:
1. Incomplete lower esophageal sphincter (LES)
relaxation
2. Increased LES tone
3. Aperistalsis of esophagus Impaired swallowing
Note:
In the absence of other explanations like cancer or fibrosis
Epidemiology:
- Incidence rate: 1 every 100,000 population/year
- Sex: F:M = 1:1
- Age: 25-60
Types:
1. Primary Achalasia
Idiopathic
Degenerative changes in neural innervations (either
intrinsic, within extraesophageal vagus nerve or dorsal
motor nucleus of vagus)
Loss of intrinsic inhibitory innervations (NO, VIP) and
myenteric ganglion cells
2. Secondary Achalasia
May arise in Chagas disease in which Trypanosoma
cruzi causes destruction of the myenteric plexus, failure
of peristalsis and esophageal dilatation
May also developed from polio as a result of destruction
of dorsal motor nuclei from the diabetic autonomic
neuropathy
Achalasia-like Diseases
- May be caused by diabetic neuropathy, malignancy,
amyloidosis, sarcoidosis, polio, surgical ablation

Note:
In infants the immediate response/manifestation is
regurgitation of milk and aspiration So when this two
are present in newborn infants then considered Esophageal
atresia/fistulae
Atresia and fistula are the most important congenital
malformations

SECTION B

Fig. 2. This figure is an example of Megaloesophagus: There is progressive

dilatation (that is why MEGALO) at oral end because food stays in this are due to
constricted LES or Aperistalsis of esophagus thus obstructions. Take note that as it
approaches the LES, it is progressively narrowed

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Pathophysiology:
- Disrupted innervations results in loss of neuromuscular
coordination and muscle tone at the lower end of the
esophagus Decreased peristalsis and relaxation of LE
Morphology:
A. Gross:
- Progressive dilatation of esophagus above the level of
LES
- Distal end is narrowed while the proximal end is dilated
(Birds beak appearance diagnostic in achalasia)
- Wall: may present with normal, thin, or thick
- May present with + or mucosal changes
B. Histology:
- Absence of ganglion cells
- Inflammation on myenteric plexus area

Sliding Hernia (Axial)

95 % of cases
This is the more common type of hernia
GEJ moves above the diaphragm together with some of the
stomach (cardia and fundus)
Stomach herniates through the diaphragmatic opening
through which the LE normally passes
Creates a bell shaped dilatation of protruding stomach
Developed from muscle weakness
Common symptoms in sliding reflux are esophagitis
(aggravated by bending forward, supine position, and obesity)
and reflux of gastric contents
Reflux esophagitis are sometimes present.
Sliding hiatal hernias develop from muscle weakening in the
esophageal hiatus.

Rolling/Paraesophageal Hernia (Non-axial)

Clinical Features:
- Progressive dysphagia (classic symptom)
- Nocturnal regurgitation
Aspiration

When a part of the stomach (usually the greater curvature)

herniates through the esophageal hiatus and lies beside the
esophagus, without movement of the GEJ
Developed from an anatomic defect when stomach is not
properly anchored
Paraesophageal hernia is less common, but is more cause for
concern
Esophagus and stomach stay in their normal locations, but
part of the stomach squeezes through the hiatus, landing it
next to the esophagus.
Symptom is usually a vague epigastric pain
Although you can have this type of hernia without any
symptoms, the danger is that the stomach can become
"strangled," or have its blood supply shut off.
There is no reflux esophagitis unlike in sliding hernia

Fig. 3. Birds beak appearance of LES in radiographic image. By the look of the xray, it is obvious that LES is constricted, thus no food passages Dysphagia is
manifested (classic symptom) It is confirmatory diagnosis using Barium Enema (BE)
and Manometry.

Complications:
- 5% of cases progress to squamous carcinoma
- Candida esophagitis
- Lower esophageal diverticula
- Aspiration pneumonia
- Airway obstruction
Notes:
Regurgitation occurs at night time because by the end of
the day not all food is conveyed to the stomach thus
leading to accumulation of food. Note that the undigested
form of food is regurgitated.
Bird;s beak: Diagnostic for achalasia

Hiatal Hernia (Diaphragmatic Hernia)

A congenital defect due to incomplete formation of the
diaphragm which allows the abdominal viscera to herniate
into the thoracic cavity
Very common
Females > Males
Incidence increases with age
Separation of diaphragmatic crura and widening of muscular
crura and esophageal wall
Associated with reflux esophagitis
Etiology: Unknown ;
The stomach moves into thorax
2 Types:
1. Sliding Hernia (Axial)
2. Rolling/Paraesophageal Hernia (Non-Axial)

Fig. 4. Examples of Hiatal Hernia

Diverticula
True diverticulum Blind outpouching of the alimentary
tract, lined by mucosa, communicates with the lumen, and
includes all 3 layers of the bowel wall (mucosa, submucosa,
muscularis)
Outpouching of esophagus in areas of muscular weakness
brought about by increase intraluminal pressure
o Meckel diverticulum
Most common type and is found in the ileum
Formed by the failure of involution of vitelline duct
(connects lumen of developing gut to yolk sac)
Rule of 2s (REMEMBER this)
1. Occur in 2% of population
2. 2 feet from ileocecal valve
3. 2 inches long
4. Symptomatic by age 2
Pseudodiverticulum lack true muscularis and is formed
due to weakness of the esophageal wall and/or increase in
esophageal wall stress

Fig. 5. True diverticulum versus Pseudodiverticulum

SECTION B

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PATHOLOGY
Types of Esophageal Diverticula:
1. Zenker / Paraesophageal diverticulum
Insert lecturer
here
- More common,
esophago-pharyngeal
junction, often
large
- Associated with esophago-pharyngeal motor
dysfunction
- May accumulate significant amounts of food, producing
a mass and symptoms that include regurgitation in
episodic
- Causes dysphagia
2. Traction diverticulum
- Midpoint of the esophagus
- Less common
- Rarely collect food
- Tuberculous lymphadenitis
3. Epiphrenic diverticulum
- Just above the LES
- No dysphagia (different from Zenker)
- May manifest nocturnal regurgitation of massive amount
of fluid.
Note:
Regurgitation in Zenker diverticulum are episodic. As food
particles pass some may fall in the pocket. Slowly the pocket fills
up with food Symptom: Regurgitation

Clinical Features:
- Mallory Weiss syndrome (superficial lacerations)
Healing tends to be rapid and complete
Surgical intervention no generally required
Represents up to 5-10% of upper gastrosintestinal
bleeding (UGIB) which often presents as hematemesis
- Boerhaave syndrome
Complication of Mallory Weiss syndrome
Characterized by distal esophageal rupture, perforation
and mediastinitis
Occurs rarely and a catastrophic event
Requires surgical intervention

Fig. 8. Boerhave syndrome.Probe = Area of perforation. There are also sign of

ulceration

Notes:
Most of the time tear is superficial; one tear involves entire
mucosa Perforation, rupture, secondary to acute
inflammation
Normal: Reflex relaxation of the GE musculature precedes
the antiperistaltic contractile wave associated with vomiting

ESOPHAGEAL OBSTRUCTION
Esophageal Stenosis

Fig. 6. Types of esophageal diverticula

Lacerations (Mallory-Weiss tears)

Longitudinal tears at the gastro-esophageal junction
Associated with severe retching or vomiting secondary
to acute alcohol intoxication

Fibrous thickening of esophageal submucosa with atrophy

of muscularis layer
Most often due to inflammation and scarring
Progressive dysphagia
Causes:
1. Chronic gastroesophageal reflux
2. Irradiation
3. Caustic injury
4. Scleroderma
Note: Mostly acquired

Esophageal Webs

Fig. 7. Take note of the black arrows. These are the MW tears. Remember it is
longitudinal tears along esophagus. If not treated immediately, a lot of blood will be
out to our system via hematenesis or blood in our stool. May lead to Boerhave
syndrome. Treatment can be medication like vasoconstrictor drugs or balloon is
inserted. S: stomach, E: Esophagus

Pathogenesis:
- Failure of reflex LES relaxation and the refluxing gastric
contents suddenly overwhelm the contraction of the
musculature of gastric inlet Cause the esophageal wall to
stretch and tear
Morphology:
- Linear, irregular lacerations
Longitudinally oriented
Range in length from mm to several cm
- Usually cross the E-G junction
- May also be in proximal gastric mucosa

SECTION B

Ledge-like , circumferential mucosal protrusions into the

lumen in the upper esophagus
Episodic dysphagia (partial occlusion)
Semicircumferential, eccentric lesions protruding less than 5
mm with a thickness of 2-4 mm
Composed of fibrovascular connective tissue and overlying
epithelium
Unknown pathogenesis
Frequently encountered in women over age 40
Main symptom is dysphagia associated with incompletely
chewed food
Paterson-Brown-Kelly / Plummer-Vinson syndrome
1. Upper esophageal webs
2. Iron-deficiency anemia
3. Atrophic glossitis
4. Cheilosis
5. Post-cricoid Esophageal Ca

Esophageal Rings/Schatzki Rings

Circumferential mucosal protrusions in the distal esophagus.
Similar to webs but are thicker and circumferential
Types according to location:
1. A rings
- Above the gastroesophageal (squamocolumnar
junction)
- Covered by squamous mucosa

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PATHOLOGY
2. B rings
- At the squamocolumnar junction of the lower esophagus
Insert
- Have
gastriclecturer
cardia-typehere
mucosa on their undersurface
- Symptom: Episodic dysphagia

ESOPHAGEAL VARICES
Tortuous dilated veins at the distal esophagus and proximal
stomach
Portal hypertension Most common cause
Found in 90% of cirrhotic patients
Formation of collaterals in the lower esophagus when the
portal blood flow is shunted into the plexus of esophageal
subepithelial and submucosal veins

Pathogenesis/Etiology:
- Reflux of gastric acid is central to the development of injury
- Decrease anti-reflux mechanism ( secondary to
hypothyroidism, CNS depressants, alcohol, tobacco,
pregnancy)
Pregnancy Increase intrabdominal pressure Reflux
of gastric contents
- Sliding hiatal hernia
- Delayed gastric emptying, increase gastric volume
- Acid peptic juice action in esophageal mucosa
- Bile reflux

Pathogenesis:
- Portal HTN Development of collateral channels (where
portal and caval systems communicate) Lead to
development of a congested subepithelial and submucosal
venous plexus within distal esophagus
Note:
THREE common areas of portal/caval anastomoses
- Hepatic schistosomiasis is the second most common cause
- Net effect:
Irregular protrusion of the overlying mucosa in the
lumen
Thus high risk for bleeding when food pass the lumen
Morphology:
- Appear as tortuous dilated veins lying primarily within the
submucosa of distal esophagus and proximal stomach
- Collapse in absence of blood flow
- Rupture results in hemorrhage into the lumen or esophageal
wall
Clinical Features:
- Often asymptomatic until they rupture causing massive
hematemesis and hemorrhage which is a medical
emergency
- Contributing factors that lead to rupture:
a. Inflammatory erosion of thinned overlying mucosa
b. Increased tension in progressively dilated veins
c. Increased vascular hydrostatic pressure associated
with vomiting
- 40-50% fatality rate in the first bleeding episode
- Fatal hemorrhage is the most feared consequence

Fig. 9. Nonspecific findings: Hyperemia and edema.

Long standing: may develop ulcers Bleeding

Morphology:
- Morphologic changes depend on the cause, duration, &
severity of exposure to injury
A. Gross:
- Esophagus appears red and hemorrhagic with linear
ulcers obliterating the z-line (simple hyperemia May
be the only alteration)
B. Histology:
- 3 important features:
Presence of inflammatory cells: Eosinophils
(early finding ), neutrophils (severe injury ) or
lymphocytes in the epithelial mucosa
Basal zone hyperplasia exceeding 20 % of
epithelial thickness
Part where reserve cells are found
Thickening of the epithelium with increase in the
height of the vascular papillae of the lamina
propria, to greater than 50% of the thickness of the
epithelium

ESOPHAGITIS
Heartburn is the common symptom among the different
types
Causes:
1. Chemical (alcohol, acids, alkalis, smoking, pill,
chemotherapy)
2. Physical (hot fluids, radiation, prolonged intubation)
3. Biological
- Infectious agents (especially in debilitated or
immunosuppressed individuals)
4. GERD
- Most frequent cause of esophagitis

Reflux Esophagitis (aka GERD)

Gastro-esophageal reflux disease
Most common cause of esophagitis
Normal protective mechanisms against acid-peptic juice
action:
1. Submucosal glands secrete mucin and bicarbonate
2. Constant LES tone prevents reflux of acid gastric
contents

SECTION B

Fig. 10. L: Early Reflux Esophagitis, eosinophils is appreciated (black arrow)

R: Severe Reflux Esophagitis, being infiltrated by neutrophils

Note:
These 3 features may not all be present, only 1 or 2 may be
observed. Regarding the inflammatory cells the eosiniphils are
the 1st. Presence of neutrophils indicates severity
Clinical Features:
- Dysphagia and heartburn are the most common symptoms
- Less frequent regurgitation of sour-tasting gastric contents
- Severity of symptoms not closely related to degree of
histologic damage Increase with disease duration
Complications:
- Bleeding
- Ulceration
- Hematemesis
- Melena
- Strictures
- Barretts Esophagus Most important complication,
especially from long standing reflux esophagitis
Treatment:
- Proton pump inhibitors or H2 histamine receptor antagonists

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PATHOLOGY
Infectious Esophagitis

Chemical/radiation Esophagitis

Occur most frequently in those who are immunosuppressed

Insert
lecturer
hereof full blown: AIDS
especially (+)
HIV Pxs
often indicative
Bacterial esophagitis occurs 10-15%

Damage in stratified squamous mucosa by a variety of

irritants
Implicated agents: Alcohol, corrosive acids or alkali, (suicidal
attempt ) , detergents , excessive hot fluid , heavy smoking
Cytotoxic anticancer treatment
Radiation
Generally only causes self limited pain, particulary dysphagia

1. Candida esophagitis
- Found in 20 % among adults
- Associated with disturbance in the normal GI flora
- Associated with conditions of reduced host resistance,
Morphologic:
immunodeficiency and malignancies
- Dense infiltrates of neutrophils are present in most cases;
- Surface proliferation in the absence of epithelial invasion
may be absent following injury induced by chemicals
is not considered infection (colonization )
(outright necrosis)
- Epithelial invasion by fungi accompanied by an
- Esophageal irradiation: intimal proliferation and luminal
inflammatory tissue reaction
narrowing of submucosal and mural blood vessels.
- Many are asymptomatic
- Final common pathway for all
- Characterized by adherent, gray-white pseudomembranes
Severe acute inflammation
- Composed of densely matted fungal hyphae and
Superficial mucosal necrosis and ulceration
inflammatory cells
Formation of granulation tissues
Late stage: Fibrosis

Fig. 11. Image shows Candida esophagitis. You can see the fungal masses along
the esophagus (blue arrow) creamy white-yellow patches of fungal masses.

Clinical features:
- Uncomplicated ingestion: Acute oral burns, pain, and
dysphagia
- Complications:
1030% with scar and stricture formation
Acute dysphagia
Acute respiratory compromise
Laryngeal edema, tracheitis and pneumonitis
Esophageal perforation
Septicemia, mediastinitis, peritonitis, empyema
Hemorrhage

BARRETTS ESOPHAGUS
Fig. 12. Histologic image of Candida esophagitis: to be sure that esophagitis is due
to fungal infection then hyphae or fungal elements must be appreciated in the slide
that came from fungal masses from previous picture.

Epidemiology:
- Seen in 50 % of AIDS patient
- Seen in other immunodeficient states (leukemia,
lymphoma, chemotherapy, steroid therapy, hereditary
immunodeficient states , diabetes mellitus, severe
debilitation, elderly )
2. Herpes simplex virus
- Causes punched out-ulcers
- Nuclear viral inclusions within a rim of degenerating
epithelial cells at the margin of the ulcer

Fig. 13. Shows viral esophagitis, in the left picture, you can see the tan-brown base
lesion as the arrow pointed. This can cause punched out ulcers once it is remove
from the mucosa; the right picture just show histologic characteristic of a viral
infected cell. It is large multinucleated with inclusion bodies

Note:
Infected squamous cells becomes larger and
multinucleated.
Nuclei show molding? Margination at periphery,
glassy/empty appearance.
3Ms: Multinucleation, molding and margination of nuclear
chromatin.
3. Cytomegalovirus
- Causes shallower, linear ulcers
- Characteristic: Nuclear and cytoplasmic inclusions
within capillary endothelium and stromal cells

SECTION B

Etiology:
- Complication of long standing G-E reflux with replacement
of distal squamous by metaplastic columnar epithelium
containing goblet cells
- Presence of GOBLET CELLS in the esophageal mucosa
is DIAGNOSTIC
- Characterized by intestinal metaplasia within the esophageal
squamous mucosa
- Occurs in 5-15%
- Greatest concern: Increased risk of esophageal
carcinoma (precursor to malignancy), however, most do not
develop esophageal tumors)
Notes:
This condition was initially thought to represent a
congenitally short esophagus. Results from alteration in the
different program of stem cells
This patient have long history of heartburn and other reflux
symptoms like sinisikmura
Pathogenesis:
- Increased exposure to gastric acid Reflux esophagitis
Erosion and ulceration Stimulation of pluripotential stem
cells in the basal layer Intestinal metaplasia
Morphology:
- Located in the G-E junction
- Velvety red (sometimes pink salmon) appearance
- Often multifocal, irregular patches or tongues of tissue
- Alternates with residual smooth, pale squamous mucosa
- Interfaces with light brown columnar mucosa distally
- 2 criteria for the diagnosis of Barrett esophagus:
1. Endoscopic evidence of abnormal mucosa (columnar
epithelium) above the gastroesophageal junction
Note:
Helps to prevent misdiagnosis if metaplastic goblet cells
within the cardiac are included in the biopsy

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PATHOLOGY
2. Histologically documented intestinal metaplasia
- Goblet cells (have distinct mucous vacuoles)
Insert
here
Definelecturer
intestinal metaplasia
Necessary for diagnosis of Barrett esophagus
Note:
Simple yet important: when the gross images are pale red like
in esophagus or maybe oral mucosa -> strat. Squamous epith;
but if it is velvety red or pink salmon like most of our visceral GI
organs then it is simple columnar epith. That is why when you
see pink salmon patches in esophagus, then it may be Barretts
Esophagus due to metaplasia. (kasi nga dapat strat. Squamous
ang esophagus, e naging columnar kaya metaplasia)

Fig. 14. L: Normal. R: BE; So as previously discussed, in the left there is smooth
delineated boundary between the two organs Normal. Unlike the right picture;
there are already infiltrates of patchy velvety red lesion in the esophagus thus
intestinal metaplasia thus BE

Fig. 15. B: note presence of goblet cells (red arrow; top right shows basal zone
hyperplasia A: Normal GEJ

Classification:
1. Long segment: >3cm of esophagus is involved
2. Short segment: <3 cm of esophagus is involved
Dysplasia in Barretts Esophagus
- Low grade dysplasia
- High grade dysplasia

ESOPHAGEAL TUMORS
1. Benign tumors - Uncommon/mesenchymal origin
1. Squamous papilloma
2. Leiomyoma , fibroma, hemangioma
3. Fibrovascular polyps
4. Inflammatory pseudo-tumors
2. Malignant tumors Epithelial in nature
1. Squamous cell carcinoma
2. Adenocarcinoma
3. Melanocarcinoma
4. Leiomyosarcoma
Esophageal carcinoma statistics:
o 6 % of GIT cancers
o 90 % of esophageal Ca are Squamous cell carcinoma
(worldwide stats)
o In US , Adeno CA incidence > SCCA
Notes:
The very best way to classify ALL tumors of a major organ
is to remember BASIC HISTOLOGY. You do NOT need to
memorize a stupid list from a pathology lecture, just
remember an organs native cells! (Dr. Dys notes in the
PPT)
Dr. Dys notes above is correct! Example, skin, normally
lined by strat. Squamous cell, of course when it begins to
produce neoplastic cells Become Squamous Cell CA,
not Skin AdenoCA. Same goes with Esophagus, highly it
will be SCCA UNLESS! It undergoes intestinal metaplasia
like Barretts esophagus thus prone to become Esophageal
AdenoCA. Gets?
Another classic info: worldwide Esophageal SCCA
incidence > AdenoCA except in US, why? They always use
Aspirin which can cause ulcer Reflux problem
Barretts Esophagus AdenoCA. Kaya impossible
magkaka Esophageal AdenoCA ka w/o having intestinal
metaplasia 1st.

Esophageal Squamous Cell Carcinoma

Note:
Present in both grades: inc. epithelial proliferation w/ atypical
mitoses and nuclear hyperchromasia, irreg. clumped chromatin,
inc. N:C ratio and failure of epith.cells to mature
High grade More severe changes
If high grade dysplasia is present in biopsy specimen, there is
70% chance of AdenoCA present
Precursor to malignancy
Clinical Features:
- Only identified through endoscopy and biopsy, prompted by
GERD symptoms
- Symptoms are related to reflux esophagitis Single risk
factor to development of adenoCA
Complications:
- Ulceration
- Hemorrhage
- Stricture
- Dysplasia
- Development of adenocarcinoma Dysplasia is the single
determinant

SECTION B

Note:
Periodic surveillance (endoscopy with biopsy) for detection of
dysplasia should be undertaken, as the incidence of
adenocarcinoma in Barrett's is 30x that of the general population
Searching for dysplasia when Barretts is present is of utmost
importance. MOST/ALL adenocarcinomas arising in the
esophagos arise from previously existing Barretts.

Affects males more (2:1 to 20:1)

Affects African-Americans (blacks) than Caucasians (whites)
More common in rural and underdeveloped areas
Regions with highest incidences: Iran, central China, Hong
Kong, Brazil, South Africa
Etiopathogenesis:
- Molecular pathogenesis of esophageal SCC remains
incompletely defined
1. Dietary
- Def of Vit (A, C, Riboflavin, B12 )
- Def of trace metals (zinc , molybdenum )
- Fungal contamination of food (mutagenic compounds)
- High nitrites/nitrosamines content
2. Lifestyle
- Alcohol
- Tobacco
- Urban environment
3. Esophageal disorders
- Chronic esophagitis , HPV infection
- Achalasia
- Plummer-Vinson syndrome
Triad of esophageal web, Fe deficiencies and
glossitis

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PATHOLOGY
4. Genetic predisposition
- Long standing celiac disease
Insert
lecturer here
- Ectodemal
dysplasia
- Tylosis palmaris et plantaris
- Racial predisposition
- Chromosomal abnormalities: mutations in p53,
- p16/INK4 tumor suppressor gene
Note:
Etiopathogenesis is multifactorial ranging from nutritional
deficiencies as well as carcinogenic compounds like nitosamines
and others like from fungal. Alcohol and tobacco synergize to
increase risk. Environment and diet contribute synergistically,
modified by genetic factors.
Morphology:
- Begins as an in situ lesion termed squamous dysplasia
- early lesions appear as small, gray-white, plaque-like
thickenings
- SCCs may invade the respiratory tree, aorta, mediastinum,
or pericardium
- Half occur in the middle third of the esophagus
- Morphologic patterns :
Exophytic 60 %
Flat/ diffusely infiltrative - 15 %
Excavated / ulcerated 25 %
- Location :
Upper third 20 % (linked to PV synd.elderly women)
Middle third 50 %
Lower third 30 %
Most SCC moderately to well-differentiated
Epithelial dysplasia Regional lymph node spread is early
and common
Rich submucosal lymphatic network promotes circumferential
and longitudinal spread
Spread-transmural invasion
Sites of lymph node metastases vary with tumor location
o Cancers in upper third of esophagus favor cervical
lymph nodes
o Cancers in middle third favor mediastinal, paratracheal,
tracheobronchial nodes
o Cancers in lower third favor gastric and celiac nodes

Esophageal Adenocarcinoma
Usually involves the lower third of the esophagus
Commonly arises from metaplastic columnar epithelium
(i.e. Barretts esophagus)
May also arise from heterotropic gastric mucosa or from
submucosal glands
It is one of the most significant complications of barretts
esophagus
Risk is reduced by diets rich in fruits and vegetables
Epidemiology:
- Most frequent among Caucasians
- 7-fold more common in men
- Usually seen between the ages of 40 and 60
- Incidence of adenocarcinoma in Barrett's esophagus is
probably less than 5-10% but is really unknown because the
true incidence of Barrett's is not known

Fig. 17. The transition of a normally squamous esophageal mucosa to a glandular

or intestinal type of a mucosa is called BARRETTS

Pathogenesis:
- Progression of Barrett esophagus to adenocarcinoma occurs
over an extended period through the stepwise acquisition of
genetic and epigenetic changes
- The evolution of esophageal adenocarcinoma:
Reflux esophagitis Metaplastic Barrett's esophageal
mucosa Glandular epithelial dysplasia AdenoCA
Morphology:
- Occur almost exclusively in the distal third of the esophagus
- May invade the adjacent gastric cardia
- May infiltrate diffusely or ulcerate and invade deeply
- First appears as a thickened plaque-like white mucosa
- Larger lesions form white, exophytic, polypoid masses
- Tumors may infiltrate diffusely or ulcerate and invade deeply
- May be multifocal

Fig. 18. Esophageal AdenoCA

Fig. 16 L: well-differentiated, keratin pearls? Formation, solid nest infiltrating

stroma,intracellular bridges indicates it originated from squamous?
R: moderately differentiated

Clinical Features:
- Dysphagia, odynophagia (pain on swallowing), obstruction,
extreme weight loss, debilitations
- Hemorrhage and sepsis may accompany tumor ulceration
- Prognosis is poor
- Overall 5 year survival = 9%
Note:
Overall is 9%, this may be d/t very early spread of the
neoplasm because of rich lymphatic network, another
reason would be the absence of serosa thus less barrier.

SECTION B

Microscopic Features:
- Microscopically indistinguishable from gastric adeno Ca
- Majority are moderate to well differentiated intestinal type
- Most commonly produce mucin and form glands
- Minority with signet ring type
- Prognosis for both types is poor

Clinical Features:
- Commonly present with pain or difficulty in swallowing,
progressive weight loss,
- Hematemesis, chest pain, vomiting
- When symptoms appear, tumor has usually spread to
submucosal lymphatic vessels.
- In advanced stages, overall 5-yr survival is less than 25%

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