Esophagitis + Esophageal Cancer Flashcards

1
Q

What are 3 causes of esophagitis?

A

Erosive esophagitis

Eosinophillic esophagitis

Infectious esophagitis

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2
Q

What are the different types of erosive esophagitis? How can they be characterized? How can they be caused? What are some symptoms?

A

Chemical and pill esophagitis
Reflux esophagitis
(erosive)

Endogenous:
acid in reflux

Exogenous:
lye, acids, or
detergent
pill

Strong or mild
Acute or chronic

Necrosis? ulcer?erosion?inflammation
Barrett?s (premalignant)

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3
Q

What are some symptoms of iron pill esophagitis? Pill esophagitis in general? What else can cause pill esophagitis? Where does it usually occur? How is it treated?

A

Iron pill (ferrous-sulfate)

Ulcertation
Acute inflammation
Pigmented material, blue on Perls? stain

Chest pain, pain with swallowing, acute
heartburn

NSAID

antibiotics

Usually mid 
esophagus/aor
tic arch
Transition 
zone between 
skeletal/smoot
h muscle

Avoid offending agent

Symptom control

Acid reflux prevention (no clear data)

Behavioral changes - drink 8 oz water with
pill, stay upright for 30 minutes, look for
alternative drugs

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4
Q

What are the cells like that are characteristic of herpes esophagitis? Where are they seen? How are they differentiated from CMV cells? What are the ulcers like? When does HSV infectious esophagitis occur? What are the symptoms? What is the path. like? Where should a biopsy be taken? What will be seen? What is the treatment? What are the ulcers like in CMV infectious esoph.? What are the cells like? How should it be treated?

A

Cells are:
Margination
Molding
Multinucleation

They are seen at the edge of the ulcers not in the ulcer

They ulcers are punched out.

Immunocompromised (solid organ transplant or
BMT) or immunocompetent

Odynophagia, dysphagia, chest pain, fever

Vesicles, small ulcers, ?volcano like?

Biopsy from edge of ulcer

Multi-nucleated giant cells, ground glass nuclei,
eosinophilic inclusions (Cowdry type A
inclusion bodies)

Treatment: Acyclovir, famcyclovir, valcyclovir

CMV cells have:

Cytoplasmic and nuclear inclusions

Ulcers linear and deeper, larger

Intranuclear inclusion bodies

Rx: ganciclovir (IV), foscarnet (IV)

Switch to valganciclovir

3-6 weeks

Eye exam to evaluate for retinopathy

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5
Q

In which patients does infectious esophagitis occur? What is the most common bug? What are the symptoms? How is this most common cause diagnosed? What is often coexistent with? How is it treated? What is seen grossly? Microscopically?

A

Immunosuppression

Use of inhaled corticosteroids

Candida most common in immunocompetent and
immunocompromised

Odynophagia or dysphagia

Brushings KOH/PAS stain

Oral thrush coexistent in 2/3

Trial of empiric fluconazole

Requires systemic therapy

Grossly: white plaques

Tissue invasive pseudohyphae and budding yeast
forms

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6
Q

What is the pathology of eosinophilic esophagitis compared to reflux esophagitis? How else does it differ from reflux esophagitis? What is it associated with? What is the treatment? What can be seen on endoscopy? What is this due to? What patients might have eosinophilic esophagitis? What will they have a history of? Symptoms? What will be found on lab tests, endoscopy, and barium swallow? What must be excluded? How? How is it treated?

A

Larger numbers of intraepithelial eosinophils and
more superficially located than reflux esophagitis

Absence of acid reflux and failure of PPI

Atopic: atopic dermatitis, allergic rhinitis, asthma or
peripheral eosinophilia

Treatment: dietary restriction, corticosteroids

Furrows—>Dysphasia Rings—>Food impaction

Initially disease of children but more
common now in adults

Young men

History of atopy (allergies, asthma,
hayfever)

Symptoms: dysphagia, food impaction,
heartburn

Lab tests: elevated IgE, peripheral
eosinophilia

Barium swallow-small caliber, focal or long
tapered strictures, concentric rings

EGD-ringed esophagus, linear furrows,
eosinophilic abscesses, strictures (1/3
normal esophagus)-Biopsies: >15 eos/HPF

Must exclude GERD (Trial of PPI)

Trial of PPI
Topical or systemic corticosteroids
Dietary changes (wheat, soy, egg, dairy, 
shellfish, peanuts)
Allergy referral
Cautious dilation
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7
Q

What is the most common cause of esophagitis? What are some risk factors? What % of population? Define it? Symptoms? Complications? What is the path.? What are the symptoms? What is the treatment? Describe reflux esophagitis grossly. Microscopically?

A

Definition: Inflammation of the lower esophagus, resulting from damage caused by acid reflux from the stomach

Most common cause of esophagitis, 10% of
population

B. Risk factors include alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia

Heartburn and regurgitation

Complications: severe ulcerations,
strictures, Barrett?s esophagus, and
adenocarcinoma

Reflux of gastric contents into the
esophagus

Hyperemia, eosinophils/neutrophils on
pathology

Clinical symptoms: dysphagia, heartburn,
epigastric pain, reflux, asymptomatic

Treatment: Acid suppression, behavioral
modifications

GROSSLY:
Reddish, hyperhemic areas at
the squamocolumnar junction

Erosions, or ulcers followed
by strictures

Barrett?s esophagus (salmon-
colored mucosal tongues) in
long-standing cases

MICROSCOPICALLY:
Basal cell hyperplasia
>20% (nl

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8
Q

Define Barrett’s esophagus Why is it important? What causes barretts esoph. ? Why is it serious? What are some treatments? What is the main difference between low grade dysplasia and high grade dysplasia? Why is that important?

A

Definition

intestinal
metaplasia
within the 
esophageal
squamous
mucosa. 

Is a
consequence
of GERD

Why important?
Precursor for
cancer

Replacement of normal squamous epithelium with
specialized columnar epithelium (?intestinal-like?)
resulting from epithelial injury (esophagitis) and
healing/repair in an acid environment

Found in 2%-20% of GERD Patients

Increased risk for esophageal adenocarcinoma

Chemoprevention
NSAIDs/Aspirin/Statins

Antisecretory therapy
Acid suppression

Ablative therapies
Thermal (Radiofrequency ablation)
Mechanical (Endoscopic mucosal resection,
Endoscopic submucosal dissection,surgical)
Photodynamic therapy, Cryotherapy

LGD: Architecture still maintained
HGD: Architecture lost somewhat

Important for prognosis.

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9
Q

What are some malignant neoplasms that occur in the esophagus? Benign? To which LNs do malignant neoplasms metastasize ?

A

Squamous Cell CA
Adenocarcinoma

Leiomyoma
fibrovascular polyp of esophagus
Squamous papilloma

o Upper 1/3 – cervical lymph nodes

o Middle 1/3 – mediastinal, paratracheal, and tracheobronchial nodes

o Lower 1/3 – gastric and celiac nodes.

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10
Q

Why is the TNM staging different in the colon compared to elsewhere in the GI system? What is the T staging like for neoplasms in the GI system? In the colon?

A

Colon is unique in that it lacks rich lymphatics in the mucosa as compared to other portions of the gut

** Mucosal adenocarcinoma in colon virtually has no risk
for lymphatic invasion and metastasis. It is therefore
regarded as carcinoma in situ when staging.

Tumor Invasion of lamina propria:
Colon: Tis
Elsewhere: T1a

Invasion of submucosa
Colon:T1
Elsewhere:T1b

Invasion of muscularis propria: T2
Serosa: T3
Through Serosa: T4

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11
Q

What are some risk factors for esophageal cancer? What are the symptoms?

A

IRRITATION:

Alcohol

Barrett?s esophagus

Cigarettes

Dietary (Very Hot Tea)

Esophageal Diseases (Plummer Vinson 
syndrome, achalasia, esophagitis) 

Familial

11, Esophageal carcinoma presents late (poor prognosis).
1 . Symptoms include progressive dysphagia (solids to liquids), weight loss, pain, and hematemesis.
2. Squamous cell carcinoma may additionally present with hoarse voice (recurrent laryngeal nerve involvement) and cough (tracheal involvement)

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12
Q

What is squamous cell CA like grossly? Where in the esophagus is it located? Microscopically?

A

Gross-Middle 1/3 in 50% of cases

Polypoid or exophytic mass with
gray-white cut surface

Can be ulcerated or 
diffusely infiltrative 
that spread within 
the esophageal wall 
causing thickening,
rigidity, and luminal 
narrowing.
Local extension into
respiratory tree, 
aorta, medistinum, 
and pericardium can
occur

Microscopic:

Nests of malignant cells that partially
recapitulate the organization of squamous
epithelium

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13
Q

What is Adenocarcinoma like grossly? Where is it located in the esoph? Microscopically? What is it like if its developed due to barretts?

A

Gross:

Flat or raised

Ulcerated or
infiltrative

Lower 1/3

MICROSCOPIC:

Malignant tumors
forming glandular
structures

Mucin producing

BARRETS ADENOCARCINOMA:

large exophytic
tumor fills distal
esophagus

Barrett?s epithelium
is tan mucosa above
and to one side of
tumor

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14
Q

Describe leiomyoma.

A

leiomyoma are the most common
benign tumors of esophagus

5 cm lobulated
leiomyoma has bulging,
white, whorled cut
surface

Submucosal leiomyoma

circumscribed

composed of intersecting
fascicles of bland spindle cells
with abundant cytoplasm

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15
Q

What is a fibrovascular polyp of esophagus? Where is it located? What is it like grossly and microscopically? What are the complications?

A
A 7.0-cm polyp lies 
posterior to the larynx 
and extends from the 
cervical esophagus
causing asphyxiation

squamous epithelial lining

core of mature fibromyxoid
tissue with scattered thin-walled
blood vessels and variable
adipose tissue

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16
Q

What is a squamous papilloma like grossly and microscopically?

A

Gross: small (5 mm or less),
white-pink sessile mass

Micro:mature thickened
squamous epithelium
covering delicate
fibrovascular stalks

17
Q

How is an HIV infectious esoph. diagnosed? What is the ulcer like? How should it be treated?

A

HIV

Idiopathic ulcer

Diagnosis of exclusion

CD4 count<100

Responds well to steroids (IV, oral,
intralesional)

HAART therapy

Thalidomide for refractory cases