135b/137b - Pathology and Clinical Features of Esophageal Disorders Flashcards

1
Q

List the histological changes seen in chronic GERD (4)

A
  • Basal cell hyperplasia
  • Extension of vascular papillae to the top 1/2
    • Due to vascular congestion
  • Inflammaotry infiltrate
    • Eosinophils, lymphocytes, few neutrophils
  • Ballooning of squamous cells
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2
Q

What defines Barrett’s Esophagus

A

Columnar metaplasia of the esophageal mucosa that contains intestinal metaplasia

  • The esophagus is only supposed to have stratified squamous epithelium
  • In Barrett’s it will contain columnar cells (columnar metaplasia) and goblet cells (intestinal metaplasia)
    • Intestinal metaplasia is specifially goblet cells
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3
Q

What abnormality is pictured here, at the gastroesophageal junction?

What cell types would histology show?

A

Barrett’s esophagus

  • Esophagus should be white-ish all the way until the GEJ
    • White = non-keratinous stratified squamous cells
  • The pinkish stomach cells should not be present here
    • These are nonciliated simple columnar cells
      (gastric metaplasia)
    • May also contain goblet cells (intestinal metaplasia)
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4
Q

Which infectious esophagitis will appear with punched out ulcers?

What is the treatment?

A

HSV1 or HSV2

Self limited; acyclovir, valacyclovir if needed

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5
Q

List 3 potential complications of GERD

A
  • Erosion/ulceration
  • Strictures
    • Secondary to fibrosis from ulceration
  • Barrett’s esophagus
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6
Q

How is GERD treated?

A
  • Lifestyle modification = mainstay
    • Smaller meals, don’t eat before bed
    • Weight reduction
  • Pharmoacotherapy
    • Decrease acid secretion w/ H2 blocker or PP1
  • Surgery is a last resort
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7
Q

Which parts of the esophagus are affected by GERD?

Which parts are affected by eosinophilic esophagitis?

A

GERD - distal

EoE - Proximal and distal

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8
Q

Describe the pathogenesis of Barrett’s esophagus

A
  • Chronic GERD
  • -> Inflammation, ulceration of esophageal squamous mucosa
  • -> Columnar/mucinous metaplasia; mucus is protective
    • This can lead to intestinal metaplasia (goblet cells)
  • May develop into adenocarcinoma
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9
Q

What is the difference between metaplasia and dysplasia?

A
  • Metaplasia = transformation of one cell type into another
    • Ex: Stratified squamous -> columnar in Barrett’s esophagus
    • However, the new columnar cells look pretty normal
  • Dysplasia = cells are ~weird~
    • Non-uniform shape, crowded, nuclear changes
    • May be accumulating mutations that could be pre-cancerous
    • High-grade dysplasia = carcinoma in situ
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10
Q

Which esophageal pathology is most strongly linked to food-antigens?

A

Eosinophilic esophagitis

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11
Q

What is the histologic hallmark of squamous cell carcinoma?

A

Keratin formation

Will also see:

  • Nucelar hyperchromasia
  • Pleomorphism (cells are not uniform)
  • Increased nucleus:cytoplasm ratio
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12
Q

What esophageal abnormaility is pictured?

What complications may result?

A

Sliding hiatal hernia

(Herniation of stomach into the mediastinum through the esophageal hiatus of the diaphragm)

Predisposes to acid reflux

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13
Q

List 4 endoscopic findings of eosinophilic esophagitis

A
  • Linear furrows
  • Rings
  • Strictures
  • White patches/plaques
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14
Q

What kind of epithelium is this?

Where might it be found?

A

Non-keratinized stratified squamous epithelium

Found in places exposed to the external environment
(Esophagus, external anal canal)

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15
Q

List 3 histologic findings of eosinophilic esophagitis

A
  • Eosinophils: 15+ in 2+ high power fields, or 25+ in any one field
    • Remeber, eosinophils are pink on H&E
  • Basal cell hyperplasia
  • Fibrosis in the lamina propria

Eosinophils and fibrosis differentiate EoE from GERD

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16
Q

What is the difference between high-grade dysplasia and adenocarcinoma?

A

Becomes adenocarcinoma when the dysplastic cells breach the muscularis mucosa

No difference in what the cells look like

17
Q

Barrett’s esophagus is a risk factor for which type of cancer?

A

Esophageal adenocarcinoma

(Squamous cell carcinoma arises from squamous cells; in Barrett’s esophagous, the cells are no longer squamous)

18
Q

Where does Zenker’s diverticulum usually occur?

What are the symptoms? (5)

A

Between transverse fibers of the cricoharyngeus and oblique fibers of the lower inferior constrictor

  • Aspiration
  • Halitosis
  • Regurgitation
  • Gurgling in throat
  • Neck fullness
19
Q

Which infectious esophagitis will appear with white plaques that are easily scraped off?

What is the treatment?

A

Candidal esophagitis (candida albicans)

Treat with fluconazole

20
Q

What is the most common cause of GERD?

A

Transient relaxation of the lower esophageal sphincter

This causes 90% of reflux

21
Q

Which infectious esophagitis will appear with linear/serpiginous ulcers?

What is the treatment?

A

CMV esophagitis

Treat with ganciclovir

(Usually in immunocompromised patients)

22
Q

Which medications are most commonly implicated in pill esophagitis?

How is it treated?

A
  • Bisphosphonates
  • Alprenolol
  • Doxycycline/Tetracycline
  • Quinidine
  • Potassium
  • Iron
  • Pinaverium
  • Emepronium

BAD Q PIPE

Stop offending medication, give PPI and Carafate

23
Q

What esophageal pathology is shown here?

What cells are we likely to see on histology?

A

Eosinophilic esophagitis

  • Rings and linear furrows are specific for EoE
  • Histology
    • Eosinophils (>15 in 2 hpfs or >25 in 1 hpf = diagnostic)
      • May also be in microabscesses
    • Hyperplasia
    • Fibrosis
24
Q

What esophageal abnormality is shown?

A

Paraesophageal hernia

25
Q

How is eosinophilic esophagitis treated?

A
  • Medicine
    • PPI
    • Swallowed topical steroids
    • Biologics (immune modulators)
  • Diet
    • Directed by allergy testing or elimination diet
  • Endoscopic therapy
    • Dilation helps open up rings/scar tissue
26
Q

What is the most important prognostic factor for esophageal cancer?

A

Stage; based on depth of invasion