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MS2 GI > 10/6- Esophageal Pathology > Flashcards

10/6- Esophageal Pathology Flashcards

1
Q

Describe the anatomy of the esophagus

  • Length
  • Muscle
  • Sphincters
  • Lyers
A
  • 25 cm long hollow tube (40 cm distance form incisors to GE junction)
  • Upper 1/3 = striated muscle; middle third is mixed and lower 1/3 is only smooth muscle
  • Upper and lower esophageal sphincters are functional
  • Has no serosa; rapid mediastinal spread of invasive lesions
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2
Q

What are 3 narrow points in the esophagus?

  • What can occur here?
A
  • Upper sphincter
  • Behind heart
  • Lower sphincter

Can give sensation of an object tin the esophagus

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3
Q

Label the layers

A
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4
Q

What is seen here?

A
  • Brush cell layer
  • Lamina propria
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5
Q

T/F: The esophagus is surrounded by a rich submucosal venous plexus?

A

True

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6
Q

What is a hiatal hernia?

  • Epidemiology: kids/adults
A

Separation of the diaphragmatic crura and protrusion of stomach into thorax through the gap

  • Congenital hiatal hernias usually in infants and children
  • Symptomatic in fewer than 10% of adults; generally associated with other causes of LES incompetence
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7
Q

What are symptoms of a hiatal hernia?

A
  • Heartburn and regurgitation of gastric juices

Similar to gastroesophageal reflux disease (GERD)

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8
Q

What is infectious esophagitis?

A
  • Important cause of esophagitis, especially in immunocompromised
  • Most common acute forms are from viruses and fungi
  • Bacterial esophagitis may occur in pts with systemic and upper respiratory infection (rarely biopsied)
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9
Q

Describe fungal esophagitis?

  • Etiology
  • Demographic
  • Symptoms
A
  • Most commonly from Candida albicans and Candida tropicalis
  • Primarily in pts with underlying disease (may be found in healthy pts)

Symptoms: dysphagia and odynophagia

  • Some are asymptomatic; incidental finding at esophagoscopy performed for other reasons (esp in elderly)
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10
Q

What is seen here?

A

Infectious esophagitis

  • White plaques of fibrinopurulent exudate
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11
Q

Which is worse, Candida albicans or tropicalis?

A
  • C tropicalis is more virulent than C. albicans
  • Increased potential for tissue invasion
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12
Q

What is required for diagnosis of Candida esophagitis?

A

Yeast and psuedohyphae should be detected within tissue

  • In immunosuppressed patients: only minimal inflammation
  • Special stains (silver stain, periodic acid–Schiff [PAS]) should be used to detect small numbers of invasive fungal forms
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13
Q

T/F: Candida is part of the normal flora of the GIT

A

True

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14
Q

What is a good drug to treat Candida esophagitis?

A

Fluconazole (Diflucan)

  • Safe and well tolerated

(Itraconazole and ketoconazole)

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15
Q

What is seen here?

A

Candida yeasts within cell layers (not just contamination from oral cavity)

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16
Q

What is seen here?

A
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17
Q

What can cause viral esophagitis?

A
  • Herpes simplex
  • Varicella-zoster
  • CMV
  • HIV

Most commonly in immunosuppressed patients

  • AIDS
  • Prior chemotherapy
  • Organ transplantation
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18
Q

What are symptoms of viral esophagitis?

A
  • Odynophagia
  • Dysphagia
  • Epigastric pain
  • Fever
  • Upper GI bleeding

Some are asymptomatic

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19
Q

Coexistent ____ is found in 1/4 of patients with viral esophagitis

A

Coexistent herpes labilais and oropharyngeal ulcers are found in 1/4 of patients with viral esophagitis

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20
Q

What is seen with herpetic ulcers in the esophagus?

A
  • It acts as a portal of entry for other pathogens… frequently associated with herpetic pneumonitis
  • Endoscopically: shallow and sharply punched out ulcer surrounded by relatively normal-appearing mucosa
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21
Q

What is the pathology of herpetic ulcers?

A
  • Characteristic herpetic inclusion bodies are limited to the squamous epithelial cells, margin of ulcer
  • Cowdry A intranuclear viral inclusion bodies, ground-glass nuclei, nuclear molding, multinucleated giant cells and ballooning degeneration of infected cells
  • Herpes simplex type I is the most common cause of herpetic esophagitis
  • Immunohistochemical staining and in situ hybridization
22
Q

What is seen here?

A

Multiple fragments of necro-inflammatory material (ulcer)

23
Q

What is seen here?

A
  • Chromatin pattern of a normal lymphocyte
  • Ground glass chromatin in cells that are infected by virus
24
Q

What is seen here?

A
  • Margination of chromatin to the periphery
  • Molding of nuclei
  • Multinucleation
  • Necroinflammatory debris (ulcer)
  • Ground glass appearance of nuclei
25
Q

What is seen here?

A

HSV immunohistochemical stain

26
Q

What is reflux esophagitis?

  • Prevalence
  • Causes
A
  • Common chronic condition, esp in Western countries
  • Estimated prevalence: 20-40%
  • Prolonged and repeated contact of esophageal epithelium with gastric and duodenal contents
  • Pepsin, bile, gastric acid and duodenal content: injury to esophageal mucosa.. inflammation and proliferative response
27
Q

What are predisposing factors to reflux esophagitis?

A

Decrease lower esophageal sphincter tone

  • Alcohol and tobacco use

Increase abdominal pressure

  • Obesity
  • Hiatal hernia
  • Delayed gastric emptying
  • Increased gastric volume

Most of the time no definitive cause

28
Q

What is the morphology of reflux esophagitis?

  • Endoscopy
  • Mild GERD
  • More significant disease
A

Endoscopy

  • Erosion, ulcer or stricture
  • Hyperemia (redness) or normal mucosa in up to 60% of symptomatic patient

Mild GERD: unremarkable mucosal histology

More significant disease

  • Intraepithelial eosinophils and lymphocytes
  • Basal zone and papillary hyperplasia

Congestion of small vessels with associated microhemorrhage

29
Q

What is seen here?

A

Reflux esophagitis

  • Hyperemia (redness) in the lower esophagus
30
Q

What is seen here?

A

Reflux esophagitis

  • Congestion and microhemorrhage
  • Basal cell hyperplasia (darker cells)
31
Q

What is seen here?

A
32
Q

What is the clinical presentation of reflux esophagitis?

  • Demographic
  • Symptoms
A
  • More prevalent in adults > 40 yo

Most common clinical symptoms:

  • Dysphagia
  • Heartburn
  • Regurgitation of gastric contents
33
Q

More on reflux esophagitis:

  • Treatment
  • Complications
A

Treatment:

  • Proton pump inhibitors
  • H2 histamine receptor antagonists
  • Symptomatic relief

Complications:

  • Esophageal ulceration
  • Hematemesis
  • Melena
  • Stricture
  • Barrett’s esophagus
  • Erosive esophagitis is a risk factor for Barrett’s (1-13% annually)
34
Q

What is Barrett Intestinal Metaplasia?

A

Premalignant metaplasia caused by gastroesophageal reflux disease (GERD)

  • Squamous epithelium -> metaplastic columnar epithelium (still normal morphology, just in the wrong place)
  • Common in general population: 1 – 10%
  • 12 – 15% of patients with GERD
  • Risk of cancer 30 – 125 times greater than age-matched population
  • Risk of adenocarcinoma in Barrett: 0.1-0.5% per year
  • Periodic endoscopic surveillance

(So reflux esophagitis may -> Barrett’s intestinal metaplasia, may -> adenocarcinoma)

35
Q

What is seen here?

A

Goblet cells

36
Q

What is seen here?

A

Goblet cells

37
Q

What is seen here?

A

Endoscopic lesion in Barrett’s esophagus

38
Q

Case)

  • 63 yo woman
  • Progressive dysphagia
  • Biopsy of distal esophagus
A

Adenocarcinoma

39
Q

What is seen here?

A

Esophageal squamous epithelium

40
Q

What is seen here?

A
  • Basal cell hyperplasia
  • Intraepithelial lymphocytes
41
Q

What is seen here?

A

Adenocarcinoma

  • Cells with dark nuclei with different shapes/sizes
  • Gland formation
42
Q

What are diagnostic procedures for:

  • Adenocarcinoma
  • Reflux esophagitis
A

Distal esophagus biopsies

43
Q

Describe esophageal adenocarcinoma

  • Incidence
  • Etiology
  • Predictive factors
  • Treatment
A
  • Incidence increased 350% since 1970 (US/Europe)
  • Etiology uncertain
  • Most cases detected at advanced stage with poor survival
  • Preceded by Barrett’s intestinal metaplasia
  • Esophagectomy only for either extensive high-grade dysplasia or invasive carcinoma
44
Q

What is seen here?

A

Low grade dysplasia in adenocarcinoma

45
Q

What is seen here?

A

High grade dysplasia in adenocarcinoma

46
Q

Describe squamous cell carcinoma

  • Incidence
  • Demographics
  • Symptoms
  • Location
A
  • Used to be the #1 type of esophageal cancer (90-95%) in US before 1970
  • Mostly African-American men with long hx of smoking and alcohol
  • Worldwide: the most common type of esophageal cancer
  • Adults >40 yo
  • More in men (4x)
  • Presentation: dysphagia and weight loss
  • Mostly lethal disease
  • Half of the cases: middle third of the esophagus
47
Q

What is seen here?

A

Mass in esophagus

  • This is squamous, but couldn’t tell grossly
48
Q

What is seen here?

A

Normal squamous cell epithelium

49
Q

What is seen here?

A

Desmoplasia: fibroblast trying to keep tumor from invading??

50
Q

What is treatment and prognosis for squamous cell carcinoma?

A

Prognosis: poor

Treatment:

  • Esophagectomy
  • Photodynamic therapy
51
Q

What is photodynamic therapy?

A
  • Photosensitizing chromophores, selectively retained by dysplastic malignant tissue
  • Light is delivered in the area where the photons are absorbed by the photosensitizer
  • Photosensitizer becomes photoexcited and transfers its energy to a chemical substrate that causes biologic damage to the abnormal tissue

MS2 GI (26 decks)

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