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GI > Esophageal and Gastric Pathology > Flashcards

Esophageal and Gastric Pathology Flashcards

1
Q

What lines the fetal esophagus?

A

Ciliated epithelium.

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2
Q

What is an esophageal duplication cyst, and why do they matter?

A

There’s a second, blind out-pouching of esophagus. Food sits there and rots -> bad breath and increased risk of squamous cell carcinoma.

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3
Q

What is an inlet pouch? Importance?

A

It’s a remnant of cliated epithelium in the esophagus. It’s completely benign.

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4
Q

What does it mean to have inflammation of the esophagus? (i.e. what cells?)

A

Neutrophils and eosinophils.

Lymphocytes are normal.

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5
Q

What should you think if you see ulcers / other lesions on the esophagus that don’t start at the GE junction?

A

The etiology is something other than reflux.

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6
Q

2 viruses that can cause esophagitis in immunocompromised patients?

A

Herpes

CMV

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7
Q

What does candida esophagitis look like grossly? On histology?

A

“Cheesy” white plaques grossly.

Histologically: keratin debris with yeasts and pseudo-hyphal forms.

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8
Q

What is a Schatzki ring?

A

Muscular ring covered by squamous epithelium - common cause of dysphagia.
(treatment = dilation

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9
Q

Is achalasia classified as hypo or hypermotility?

A

Hypermotility, actually, because early in disease there’s lots of contraction as esophagus tries to get stuff past the LES.
Later on, the esophagus gives up.

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10
Q

What muscle cell layer atrophies in scleraderma?

A

The inner circular muscle layer atrophies.

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11
Q

What is a Mallory Weiss tear?

A

Longitudinal tear caused by repeated wrenching vomiting.

causes lots of bleeding, esp. in a background of alcoholic liver disease - less clotting factor production

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12
Q

How do esophageal and gastric cancers compare in incidence to colo-rectal cancer? In lethality?

A

Esophageal and gastric cancers are less common, but more lethal when they happen.

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13
Q

What’s the most common esophageal malignancy in the world? In the US?

A

World: Squamous cell carcinoma.
US: Adenocarcinoma.

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14
Q

What type of cell do you see in Barrett’s esophagus that you really shouldn’t see there?

A

Goblet cells (should only be in the intestine)

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15
Q

Take home points about the length of the lesion in Barrett’s esophagus?

A

Length is fixed at the time of injury (it doesn’t grow or regress).
Longer metaplastic region is associated with greater risk of cancer.

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16
Q

How does glandular mucosa look different from squamous mucosa, grossly, in an esophagus?

A

Squamous is white.

Glandular is salmon-colored.

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17
Q

Is HPV a risk factor for squamous cell carcinoma of the esophagus?

A

Nope.

18
Q

Risk factors for squamous cell carcinoma of the esophagus? (6 are listed)

A

EtOH, smoking, moldy foods, achalasia, lye ingestion, diverticulum.

19
Q

What’s a benign tumor of squamous epithelium?

A

Papilloma.

this is related to HPV infection - carcinoma in the esophagus is not

20
Q

What’s glycogenic acanthosis?

A

A benign growth of glycogenated squamous mucosa.

21
Q

What’s a name for the area of the stomach that makes acid, pepsin, intrinsic factor aside from “corpus/fundus”?

A

The oxyntic region.

22
Q

Acute gastritis is mainly a product of…?

A

Barrier breakdown -> acid and pepsin gets to epithelium -> bleeding and inflammation.

23
Q

Etiologies of acute gastritis? (6 are listed)

A 
Alcohol
Severe stress (including head trauma, burns)
Shock
Radiation
Caustic agents
NSAIDs
24
Q

What pills are particularly caustic when they get stuck in one’s throat?

A

Iron pills

25
Q

What kind of inflammation is in the cells in chronic gastritiis? When do you say that there is “activity”?

A

Lymphocytes are in chronic gastritis.

There is said to be “activity” when PMNs are seen.

26
Q

What’s one cause of chronic gastritis +/- PMNs?

A

H. pylori

27
Q

What is atrophic gastric gastritis?

Predominant etiology?

A

Loss of parietal and chief cells.

Predominantly caused by autoimmune disease.

28
Q

What’s the specificity of (at least some) anti-parietal cell antibodies?

A

The H+ pump.

29
Q

What do you say has happened to the oxyntic epithelium when parietal and chief cells have been lost?

A

It has been “antralized”

30
Q

How can atrophic gastritis increase risk of carcinoid tumors?

A

Less acid -> more gastrin -> ECL proliferation -> “Carcinoid tumors”

31
Q

2 problems with atrophic gastritis?

A

Less acid -> bacterial overgrowth -> cancer.

Loss of intrinsic factor -> B12 deficiency -> pernicious anemia

32
Q

What’s a fundic gland polyp?

A

Benign dilation of glands of parietal and chief cells. (of oxyntic mucosa)

33
Q

What’s a hyperplastic gastric polyp?

A

It’s also benign, but associated with inflammation, so you should look for the cause.

34
Q

Causes of large rugae?

A

Hyperplasia of parietal and chief cells (can be due to ZES)
OR
Hyperplasia of foveolar compartment (the other epithelium there?)

35
Q

What is extra-nodal marginal zone B cell lymphoma of the stomach related to? Progression? Can progression can be stopped?

A

It’s related to H. pylori infection.
It starts as small cell but can progress to large cell (which… is worse… MDTI).
Progression can often be stopped if H. pylori is treated with ABx early enough.

36
Q

2 types of gastric cancer? Which is more common?

A

Intestinal (more common)

Signet Ring

37
Q

What is intestinal type gastric cancer associated with? Precursor lesion?

A

Repeated injury, esp. H. pylori.

Has intestinal metaplasia and dysplasia precursor lesions.

38
Q

What is signet ring type gastric cancer associated with?

A

Germline mutations in E-cadherin.

39
Q

Protective factors for gastric cancer?

Aggressive factors?

A

Protective: Vit C and veggies.
Aggressive: processed meats (N-nitroso compounds)

40
Q

If you see a gastric ulcer, could it be cancer?

How about a duodenal ulcer?

A

Gastric, yes, it could be.

Duodenal, no.

GI (45 decks)

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