Esophagous Stomach Small Intestine Pathology

Pathology of Esophagus
lect-3&4
Year Three 2022-2023
Inf. Thyroid
Arts.
R. Bronch.
Art.
Thoracic.
Aor.
Variatio
ns:
Inf,
Left Gastric Phrenic
Art. Celiac
Congenital anomalies
• 1-Atresia and fistula
Ø Uncommon, may be incompatible with life.
ØSegment of esophagus replaced by thin cord.
ØMay be connected to trachea.
ØMay be associated with heart anomalies.
ØAspiration and suffocation, pneumonia, fluid and
electrolyte imbalance.
2-Stenosis, webs and rings:
Ø Webs in females < 40 years, ID anemia, dysphagia→
(Plummer Vinson syndrome): premalignant, risk of SCC.
Esophageal web
• Thin mucosal protrusion, mostly in the upper
third.
• Dysphagia to poorly chewed food.
• Increased risk of SCC.
Plummer Vinson syndrome
• Severe IDA.
• Esophageal web.
• beefy-red tongue due to atropgic glossitis.
ESOPHAGEAL STENOSIS
Types of tracheoesophageal anomalies and their relative
frequencies.
Most common
Common type TEF
• Proximal atretic esophagus.
• Distal esophagus connected to trachea.
Four C/F
• Vomiting after feeding.
• Increased amount of amniotic
fluid(polyhydramnios).
• Abdominal distention.
• Aspiration of gastric content into the trachea.
Esophgeal atrasia+TE fistula
• Disruption of the normal physiological events of oropharyngeal
or esophageal swallowing results in one of the cardinal
symptoms of disease = DYSPHAGIA.
• Dysphagia can be categorized as oropharyngeal or esophageal
depending on which phase is involved.
• Odynophagia: painful swallowing.
• Dysphagia can be caused by two types of disease processes:
1. Structural/mechanical abnormalities.
2. Neuromuscular (motor) abnormalities.
Causes of Esophageal Dysphagia
• Mechanical disorders 85-90%
– Peptic stricture: Slowly progressive Chronic heartburn
– Esophageal cancer: Rapidly progressive
• Motor disorders 10-15%

– Achalasia
– Scleroderma
Achalasia • Mechanism:
– Absent esophageal body peristalsis.
(cardiospasm, – Incomplete LES relaxation.
esophageal – LES hypertension.
aperistalsis) • Causes:
– Idiopathic or primary
95%+
– Chagas disease (trypansoma

cruzii)
• Pathology
Primary – Loss of ganglion cells in myenteric
plexus of esophagus.
Achalasia – Failure of esophageal inhibitory
neurons.
• Etiology - unknown, ?
infectious
• Clinical features:
– Gradually progressive dysphagia to
solids & liquids.
– Chest pain in some patients.
– Nocturnal aspiration & weight loss.
Diagnosis
– Barium swallow.
– Endoscopy (to exclude underlying neoplasm)
Bird-peak sign
Hiatal Hernia
Diaphragmatic muscular defect.

Widening of the space through which the lower
esophagus passes, in all the cases the stomach is
above the diaphragm:
Two types:
• 1- Sliding(axial): most common (95%), due to
protrusion of the stomach above the diaphragm.
• 2- Para-esophageal (non-axial): the stomach herneate
up next to the esophagus.
C/F
• heartburn(mimics cardc chest pain).
• cough.
• damage to the enamel of teeth.
• ulceration, stricture and Barrett esophagus are
late complications.
The hernia prevents the food from moving normally along
the digestive tract.
Food moves back into the esophagus, creating a burning
sensation (heartburn), and sometimes food will be
regurgitated into the mouth.
Can be complicated by strangulation, obstruction,
ulceration, bleeding and perforation.
Definition Longitudinal tears in the
esopheal mucosa at the
GE junction
Lacerations
(Mallory-Weiss Cause Severe vomiting.
tear)
Clinical Upper GI bleeding
Morphology Tear in mucosa,
perforation or
esophageal rupture
Mallory-Weiss Syndrome.
• Caused by alcoholism or bulimia.
• presents with painful hematamesis.
• risk of Boerhaave syndrome.
Diverticula
• Proximal: in the upper portion of the esophagus
(Zenker diverticulum), results from outpouching of
esophageal mucosa at point of weakness in the wall of
the esophagus at the junction with the pharynx. It is
termed as pharyngoesophageal and are classified as
pulsion diverticulum.
• Distal: In the lower third of esophagus, at the level of
the hilum of the lung, inflammatory lymph nodes
(usually tuberculous) firmly attached to the esophagus
and produce traction diverticulum.
Zinker
Diverticulum
Zenker Diverticulum
• Outpouching of pharangeal mucosa through
aquired defect in the muscular wall.
• Arise above upper esophageal sphinctor at
junction of esophagus & pharynx.
• presents with dyusphagia, obstruction, and
halitosis.
Esophageal Varices
• Dilated submucosal veins in the lower esophagus.
• Arise secendory to potral HTN.
• backup of blood into the left gastric vein, dilation of
veins.
• Asymptomatic, but can rupture(painless
hematamesis).
• Gross: tortuous dilated veins in submucosa of
distal esophagus and proximal stomach.
• Massive, sudden hemorrhage is the most feared
consequence.
EV
• THREE common areas of portal/caval
anastomoses:
–Esophageal
– Umbilical
– Hemorrhoidal
• 100% related to portal hypertension.
• Found in 90% of cirrhotic patients.
Varices:
ESOPHAGITIS:
l Causes:
l RE.
l Prolonged intubation.
l Irritants.
l Cytotoxics, radiation.
l Viral and fungal infection.
Gross and microscopy
l Hyperemia, inflammation, ulceration and granulation
tissue.
l Micro.:
l Eosinophilic infiltration & neutrophils.
l Basal cell hyperplasia.
l Elongation of the
lamina properia papillae.
Gastroesophageal Reflux Disease(GERD)
• Failure of lower esophageal sphincter→ poor

closure→ gastric content enter the esophagus.
Pathogenesis of GERD:
ØDecreased efficacy of esophageal anti-reflux
mechanism.
ØInadequate or slowed esophageal clearance of
refluxed material.
ØPresence of sliding hiatal hernia.
ØIncreased gastric volume.
ØReduction in the reparative capacity of the
esophageal mucosa by chronic exposure to
gastric juice.
Risk factors of GERD:
ØObesity.
ØPregnancy.
ØSmoking.
ØHiatal hernia.
ØMedications; antihistamines, Ca-channel blockers,
antidepressants, hypnotics, steroids.
ØZollinger-Ellison Syndrome(↑ gastrin production,
from pancreatic or SI tumor; gastrinoma).
Ø scleroderma/systemic sclerosis(esophageal
dysmotility)
Severe, long-term effects:
l GIT bleeding.
l Esophageal Stricture.
l Barrett’s esophagus( intestinal metaplasia;
premalignant condition)
l Esophageal adenocarcinoma.
Barrett’s Esophagus
Ø11 % of symptomatic reflux disease.
Pathogenesis:
Øprolonged recurrent GER leads to inflammation.
ØUlceration, heal by re-epithelialization and ingrowth
of pluripotent stem cells, those differentiate in acidic
environment into gastric or intestinal cells which are
more resistant to acid.
BE
Esophagus
Squamous
epithelium Z-line
Stomach
Columnar (adeno) Columnar metaplasia
Gastric Intestinal
epithelium
Barrett Esophagous
Squamocolumnar j. in BE:
BE→ adenocarcinoma
Esophageal Biopsy:
• Pleomorphic cells
with bizarre
nuclei.
• Gland formation
• Note signet ring
form of tumor
cells
Esophageal carcinoma
• Adenocarcinoma and squamous cell carcinoma
• Adenocarcinoma is the most common
carcinoma in the west and arises from
longstanding Barrett esophagus.
• malignant proliferation of glands.
• in the lower third.

• SCC
• Malignant proliferation of squamous cells.
• most common esophageal cancer worldwide.
• usually arises in the middle & upper thirds of

esophagus.
Squamous cell Carcinoma:
• Risk factors:
Ø Smoking and alcohol.

Ø Very hot drinks.
Ø Malnutrition, vitamins A & C deficiency.
Ø Esophagitis & ingested chemicals.
Ø High nitrites in diet.
Ø HPV might play an etiologic role in esophageal
carcinogenesis either by producing carcinogens or by
acting directly on the host cells.
Ø Plummer-Vinson syndrome(esophageal web)
Ø Achalasia.
Morphology:
• Gross:
• Most commonly in the middle 1/3 of esophagus.
• Circumferential, ulcerating, or fungating.
• Muscular wall invasion.
• Extension to surrounding soft tissue and trachea.
• Intraluminal growth→ total obstruction.
• Distal tumor can invade the stomach.
Esophageal
SCC
SCC
Lower 1/3
dysplastic
changes
Invasive
SCC

Esophagous Stomach Small Intestine Pathology

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Pathology of Esophagus

• Motor disorders 10-15%

– Chagas disease (trypansoma

Diaphragmatic muscular defect.

• Failure of lower esophageal sphincter→ poor

• malignant proliferation of glands.

• in the lower third.

• most common esophageal cancer worldwide.

• usually arises in the middle & upper thirds of

Ø Smoking and alcohol.

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