Pathology of the Esophagus

Anki Deck

List the common congenital anomalies of esophagus and describe their gross findings and relevant clinical features.

Esophageal Atresia

A, Blind upper and lower esophagus with thin cord of

connective tissue linking the two segments. B, Blind upper
segment with fistula between lower segment and
trachea(most common). C, Fistula (without atresia) between
patent esophagus and trachea.

The upper esophagus ends blindly, not connecting to the lower esophagus.

Most commonly associated with a tracheoesophageal fistula (Gross type C), where the distal esophagus is connected to the
trachea.

Clinical Features:

Prenatal: Polyhydramnios (fetus unable to swallow amniotic fluid).

Postnatal:

Excessive salivation/foaming at the mouth.

Choking, coughing, drooling, and cyanotic attacks after attempts to feed.

Inability to pass a feeding tube into the stomach.

Aspiration pneumonia.

Diagnosis: X-ray shows an air-filled pouch at the esophagus.

Tracheoesophageal Fistula
Gross Findings:

Abnormal connection between the trachea and esophagus, often with associated esophageal atresia.

Types vary based on connection to proximal or distal esophageal segments.

Clinical Features:

Proximal connection: Aspiration pneumonia, coughing, cyanotic spells, and rales.

Distal connection: Gastric distention, reflex laryngospasms causing cyanotic attacks.

Diagnosis is usually made immediately after birth based on symptoms.

Esophageal agensis

Gross Findings:

Complete absence of the esophagus.

This rare condition is incompatible with life without surgical correction.

Clinical Features:

Prenatal: Severe polyhydramnios due to inability to swallow.

Pathology of the Esophagus 1

 Postnatal: Immediate respiratory distress and inability to feed.

Explain non-neoplastic causes of esophageal obstruction and describe their pathogenesis (when relevant), clinical features, and
gross pathology (when relevant).
Stenosis

Pathogenesis:

Stenosis can occur due to chronic inflammation, fibrosis, or scarring of the esophagus. It is commonly caused by
gastroesophageal reflux disease (GERD), radiation, or ingestion of caustic substances.

usually due to fibrosis secondary to acid reflux (GERD)

Clinical Features:

Dysphagia, especially for solid foods.

Patients may have a history of chronic reflux or prior esophageal injury.

Gross Pathology:

Concentric narrowing of the esophagus, often seen at the gastroesophageal junction.

Mucosal webs

Thin, membranous structures of the mucosa, often

associated with Plummer-Vinson syndrome (iron deficiency
anemia). They arise in the upper esophagus and can
partially obstruct the lumen.

Gross Pathology:

Small mucosal outgrowths forming a web-like structure,

usually in the proximal esophagus.

Clinical Features:

Intermittent dysphagia to solids.

Prolonged history of dysphagia without significant weight loss.

Atrophic glossitis (tongue inflammation), Angular cheilosis

Esophageal rings/schatzki rings

Pathogenesis

Similar to webs but circumferential and thicker

Mostly distal , concentric

A rings (muscular rings) Above GEJ

Covered in squamous mucosa

B rings (mucosal rings) At GEJ

Covered in GEJ mucosa

Esophageal Motility disorder

Abnormal LES function

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 Gross Pathology:

Narrowing of the distal esophagus, forming a ring-like constriction.

Clinical Features:

Asymptomatic/ Intermittent dysphagia to solids especially meat or bread.

Achalasia

Pathogenesis:

Achalasia results from degeneration of inhibitory neurons

in the Auerbach (myenteric) plexus, which disrupts normal
esophageal motility. This leads to a failure of the lower
esophageal sphincter (LES) to relax during swallowing,
combined with ineffective peristalsis in the esophagus.

The result is functional obstruction at the LES and

progressive dilation of the esophagus proximal to the
sphincter.

Gross Pathology:

Dilation of the esophagus proximal to the LES, with a narrowed “bird-beak” appearance at the sphincter on barium swallow.

Clinical Features:

Dysphagia to both solids and liquids.

Regurgitation of undigested food.

Retrosternal pain, weight loss, and sometimes respiratory symptoms due to aspiration.

Diagnosis is confirmed via esophageal manometry, which shows incomplete LES relaxation and absence of peristalsis.

Functional Esophageal Obstructions

can lead to physical or functional obstructions because of disrupted coordination of peristalsis after swallowing

3 patterns of obstruction

Nutcracker esophagus

intense contractions of inner circualr and outer longitudinal smooth muscle

Diffuse esophageal spasm (corkscrew esophagus)

repetitive simultaneous contractions of distal esophageal smooth muscle

Barium Swallow

Lower esophageal sphincter dysfunction

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 high resting pressure or incomplete relaxation

Chagas disease

(caused by Trypanosoma Cruzi)

can cause abnormal LES fucntion

can affect heart, colon, esophagus causing dilation and enlargement

Esophagus

destruction of ganglion in myenteric plexus

Failure of peristalsis

esophageal dilation (mega esophagus) and mega colon

Inlet Patch

ectopic gastric mucosa commonly seen in upper 1/3 of esophagus

mostly asymptomatic, can cause esophagitis, ulcer stricture etc. due to acid secretion

Esophageal Varices

Pathogenesis

Abnormally dilated, tortuous vessels lying within the

submucosa of lower part of esophagus

Project directly into the lumen and prone to bleed

Most result from portal hypertension due to liver failure

Gross:

dilated, tortuous vessels

Causes:

Alcoholic cirrhosis (almost half of cirrhosis cases)

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 Clinical features:

Hematemesis with bright red blood or coffee-ground appearance.

Dark, tarry stools

Hemorrhoids and caput medusae (umbilical venous dilation)

Symptoms of liver failure

Compare and contrast the pathogenesis, clinical feature of Mallory- Weiss tears and Boerhaave Syndrome.

-Lacerations
Mallory-Weiss Tears

Pathogenesis:

Sudden and severe increase in intra-abdominal pressure

causes longitudinal mucosal tears at the gastroesophageal
junction. These tears are often precipitated by forceful
vomiting, coughing, or retching.

Common predisposing factors include alcohol use disorder,

bulimia, hiatal hernia, and gastroesophageal reflux
disease (GERD).

Clinical Features:

Presents with hematemesis (vomiting blood), which may range from small streaks of blood to massive hemorrhage.

Epigastric or back pain may occur, but the bleeding is typically not accompanied by systemic signs of infection.

In more severe cases, hemorrhage may cause shock if blood loss is significant.

Boerhaave Syndrome

Pathogenesis:

Characterized by transmural perforation (rupture of all

layers) of the esophagus due to a sudden increase in
intrathoracic pressure, commonly from severe vomiting or
retching. This results in air and gastric contents leaking into
the mediastinum or pleural cavity.

The rupture typically occurs in the distal third of the

esophagus, most often on the left dorsolateral wall.

Risk factors include heavy alcohol use, overeating, and

repeated vomiting.

Clinical Features:

Classic Mackler triad: vomiting, severe retrosternal pain (often radiating to the back), and subcutaneous emphysema (crepitus
in the neck and chest due to air leakage).

Additional signs may include tachypnea, dyspnea, and symptoms of sepsis (due to mediastinitis), especially if diagnosis is
delayed.

Auscultation may reveal Hamman’s sign (a crunching sound due to air in the mediastinum).

Mallory-Weiss Tears Boerhaave Syndrome

Typically occurs after forceful

Etiology Prolonged vomiting
vomiting

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 Mallory-Weiss Tears Boerhaave Syndrome

Transmural perforation of the

Gross features Longitudinal linear lacerations
esophagus

Lower 3rd esophagus

Location Usually cross GEJ
Most common

High mortality
Treatment No surgical intervention
Surgical repair in most cases

Compare and contrast the pathogenesis, clinical features, gross (if any) and microscopic pathology of chemical, infectious, reflux
and eosinophilic esophagitis.

4. Eosinophilic Esophagitis

Pathogenesis:

Immune-mediated disorder characterized by chronic

eosinophilic infiltration of the esophageal mucosa.
Triggered by food allergens or environmental allergens.

>200 neutrophils

Clinical Features:

Dysphagia, food impaction, and heartburn that is refractory to proton pump inhibitors (PPIs). Common in children and young
adults.

Food sticking in esophagus

Gross Pathology:

Concentric rings (trachealization), white exudates, and strictures on endoscopy.

Microscopic Pathology:

Prominent eosinophilic infiltration (>15 eosinophils per high-power field).

Basal cell hyperplasia and fibrosis of the lamina propria in chronic cases.

Feature Chemical Esophagitis Infectious Esophagitis Reflux Esophagitis (GERD) Eosinophilic Esophagitis

Fungal (Candida), Viral (HSV, Immune-mediated, triggered by

Pathogenesis Direct chemical injury Acid reflux from the stomach
CMV) allergens

Chest pain, odynophagia, Odynophagia, dysphagia, Heartburn, regurgitation, Dysphagia, food impaction,
Clinical Features
dysphagia fever dysphagia refractory heartburn

Mucosal erosions, White plaques (Candida), Hyperemia, erosions, Trachealization, white exudates,
Gross Pathology
ulceration, necrosis ulcers (HSV, CMV) ulceration rings

Microscopic Necrosis, inflammatory Pseudohyphae (Candida), viral Basal cell hyperplasia, Eosinophil infiltration, basal cell
Pathology infiltrates inclusions inflammatory cells hyperplasia

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 Describe the pathogenesis, clinical features, and gross and microscopic pathology of Barrett Esophagus.

Pathogenesis:

Barrett esophagus develops due to chronic

gastroesophageal reflux disease (GERD). Prolonged
exposure of the esophageal mucosa to stomach acid leads
to chronic inflammation and damage to the esophageal
lining.

As a compensatory mechanism, the normal stratified

squamous epithelium of the distal esophagus undergoes
intestinal metaplasia, where it is replaced by nonciliated
columnar epithelium with goblet cells. This condition is
considered precancerous, as it increases the risk of
developing esophageal adenocarcinoma.

Clinical Features:

Barrett esophagus itself is often asymptomatic, but patients usually present with symptoms of GERD:

Heartburn

Regurgitation

Dysphagia (difficulty swallowing)

Symptoms worsen when lying down or after eating.

Patients with Barrett esophagus have an increased risk of esophageal adenocarcinoma.

Gross Pathology:

On endoscopy, Barrett esophagus presents as a displacement of the Z-line (the squamocolumnar junction) more proximally,
with the appearance of salmon-colored mucosa (columnar epithelium) extending into the esophagus.

Microscopic Pathology:

The hallmark of Barrett esophagus is intestinal metaplasia:

The normal squamous epithelium is replaced by columnar epithelium with goblet cells.

Goblet cells appear as mucin-filled cells with a characteristic “goblet” shape.

This metaplasia is a protective response to the chronic acid exposure but increases the risk of malignant transformation to
adenocarcinoma.

List different types of esophageal tumors and describe the pathogenesis, clinical features, and gross and microscopic pathology of
esophageal tumors, particularly squamous cell carcinoma and adenocarcinoma.

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 When you see keratin or pouches think squam. cell carcinoma

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