Revised Gi 1 Esophagus

8/10/2019 Revised Gi 1 Esophagus

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The GI System, Part 1:

The Esophagus

Mark Galan, MD

October 2, 2014


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Esophageal Disorders

Congenital

Inflammatory (Esophagitis)

Vascular Neoplastic

But first.


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First Things FirstWhat Is Normal?

Epithelium (squamous)

Lamina propria

Muscularis mucosa

Submucosa

Muscularis propria(inner circumferential)

Muscularis propria

(outer longitudinal)

Layers of the esophagus: Mucosa, Submucosa, Muscularis Propria


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More Normal

The Squamous epithelium of the

esophagus gives way to the

glandular epithelium of the

stomach at the gastroesophageal

junction at the Z-line.

The GE junction is where a lot of

important pathology occurs


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Tracheo-Esophageal Fistula

Most common congenital anomaly

Associated with esophageal atresia in

90% of cases (usually the middle 3rd)

Presents in neonatal period

Can lead to death due to aspiration

pneumonia To help understand the concept, a little

embryology is useful.


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Development of the Foregut


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Hernias

Two major types:

Hiatal (sliding). The

entire proximal

stomach protrudes intothe mediastinum

Paraesophageal

(rolling). Only part of

the fundus protrudes

into the mediastinum


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Esophagitis

Reflux: most important cause: distal 1/3

Certain foods or drugs (NSAIDs, Fe)

Hypersensitivity reaction

N/G tubes Infections: e.g. Herpes, Candida, CMV (in

immunosuppressed individuals)

Caustic bases (NaOH) or acids

Complications: Erosions, ulcers, perforation,Barretts metaplasia (reflux), strictures (lye)


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Reflux Esophagitis

Most common cause of esophagitis

Passage of gastric/duodenal contents

back up through the lower esophageal

sphincter

Incidence in the US is ~30-40%

More common in adults >40; also commonin babies


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Classic elements of

reflux esophagitis:

Elongation of rete

Basal cell

hyperplasia

Intraepithelialeosinophils (which

are also seen in

hypersensitivity

esophagitis)


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Endoscopically, an esophagus with

eosinophilic esophagitis is described as

feline esophagusalso known astrachealization. Compare to normal (right)


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Now Lets Take a Brief Detour to Talk about

What Can Happen As A Result of Reflux

Esophagitis

Repeated injury to the esophagus will cause the

glandular-type epithelium of the stomach to

move into the esophagus.

This glandular epithelium can then become

intestinalizeda condition known as Barretts

Esophagus

Barretts Esophagus is the background fromwhich esophageal adenocarcinoma can arise

(more about that shortly.)


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Review: Normal gastroesophageal junction (Z-line)


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On the left is normal esophagus, with the Z-line right where it is

supposed to be. But in Barretts esophagus, the glandular epitheliummoves up into the esophagus


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Barretts EsophagusGross Pathology

Barrettsred,

velvety, salmon-

colored mucosa

Normal esophaguspale

pink mucosa (normal

squamous)


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In addition to the glandular, gastric-type epithelium

moving upward, Barretts esophagus is

characterized by intestinalization of the glandular

epithelium (goblet cells)

OK, now back to the discussion of esophagitis.


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Candida

Most common cause of infectious esophagitis

Usually C. albicans or C. tropicalis

Associations/risk factors:

Immunosuppression

HIV, BMT, immunosuppressive tx, bone marrow disorders Acid-suppression tx

Diabetes

Esophageal motility disorders

Rheumatic diseases

Presentation:

Dysphagia

Treatment:

Antifungals (like fluconazole)

The characteristic white


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The characteristic white

plaques of candidal

esophagitis, seen on

endoscopy

NASPGHN


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PAS stain


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Herpes Simplex Virus (HSV)

2ndmost common cause of

infectious esophagitis after

Candida

Usually affects

immunosuppressed people, but

can also be a problem withimmunocompetent children

You may also see superinfection

with bacteria and fungi

Causes esophageal ulcers, which

can turn into perforations; the

infection can also become

disseminated

Treat with antivirals (like acyclovir)


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An HSV ulcer. Note the large cells.


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HSV esophagitis. Note the Multinucleation, Margination, and Molding

Dr. D. Wiedbrauk, Warde Medical Laboratory


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Cytomegalovirus (CMV)

Infection Virtually always in

immunocompromised patients

Up to ~30% of HIV patients

not on HAART have CMV,

HSV, or Candida

esophagitis

Can cause ulcers that grossly

resemble HSV ulcers

Therapy:

Antivirals

Modulation of immunosuppression

Treat the underlying cause (as

with HAART in HIV patients)

Indian J Pathol Microbiol 2011;54:852-3


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Mallory-Weiss Syndrome

Longitudinal tears in the lower esophagus,

possibly extending into the upper stomach

hematemesis

Complication of violent vomiting

Most commonly seen in alcoholics

Tears are usually superficial and do notlead to perforation

A transmural perforation due to violent

vomiting is known as Boerhaave Syndrome


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Mallory-Weiss tear


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Esophageal Varices

Complication of portal hypertension, occurs in90% of cirrhotic patients

Results from an increase in pressure in theportal vein, which shunts blood into associatedveinswhich are not built to withstand theincreased pressure.

Alcohol is #1 cause

Can result in massive hematemesisand deathifnot treated immediately (#1 cause of death incirrhotics)

Anatomy of the portal venous


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Anatomy of the portal venous

system, which shows how

esophageal varices can form. A

major player in this process is the

left gastric vein, aka the cardiac

vein.


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Esophageal varix


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Esophageal Carcinoma

Two Main Types:

Squamous cell carcinoma

Adenocarcinoma

The interesting epidemiologic differences worldwide

between the two:

While SCC accounts for about 90% of esophageal cancers

worldwide, here in America the incidences of SCC and

adenocarcinoma are roughly comparable. Environmental and genetic factors are believed to be the

reasons


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Squamous Cell Carcinoma of the

Esophagus

Obligatory epidemiology slide

M>F (About 4:1)

In America, the main causes are EtOH and tobacco(which work synergistically)

Other factors Environmental

Food

HPV

Corrosives and thermal injury

RTX for other mediastinal tumors

Celiac disease


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High-grade dysplasia


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High grade dysplasia,

or carcinoma in-situ

(CIS)

Compare the CIS to

normal squamous

epithelium


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Another image of squamous cell carcinoma that has invaded

Gross photograph of


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p g p

squamous cell

carcinoma, showing an

ulcerated plaque


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The Road to Adenocarcinoma

Over time, repeated injury to an esophagus

that has already undergone intestinal

metaplasia (Barretts) will generate mutations

that will lead to dysplasia (carcinoma in-situ),and eventually carcinoma in-situ.


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The Road to Adenocarcinoma

High-grade glandular


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dysplasia, compared

to a simple case of

Barretts esophagus.

S13-796


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Esophageal Adenocarcinoma

Eventually, the dysplastic cells will start to

invade and become invasive adenocarcinoma

Invasive


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adenocarcinoma of

the esophagus


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Another example of invasive adenocarcinoma arising in a background of

Barretts

Documents

Revised Gi 1 Esophagus