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G.I & Nutrition > Esophageal and Gastric Pathology > Flashcards

Esophageal and Gastric Pathology Flashcards

1
Q

What kind of cells line the esophagus?

A

non keratinized stratified squamous epithelium

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2
Q

What are the bridges one sees on microscopy of the esophagus?

A

tight junctions between esophageal epithelium

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3
Q

What kind of cell lines the fetal esophagus?

A

respiratory type ciliated columnar epithelium –> common embryologic derivation of the trachea and esophagus

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4
Q

Is the GEJ an anatomical or functional sphincter?

A

functional –> no clear muscle group but still functions as a sphincter

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5
Q

Where are minor salivary glands located?

A

in the pharynx, esophagus and no where distally

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6
Q

What is the function of minor salivary glands?

A

lubrication and enzymes like amylase

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7
Q

Is the LES an anatomical or functional sphincter?

A

functional –> no clear muscle group but still functions as a sphincter due to controlled contraction of smooth muscle via neural input

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8
Q

What is an esophageal duplication cysts?

A

a congenital abnormality involving a “branched” esophagus that has all layers (can be squamous or respiratory type cells as it has to do with embryologic divergence of the two structures)

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9
Q

Where are inlet patches found?

A

cervical esophagus –> multiple glandular types of mucosa

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10
Q

What is the significance of inlet patches?

A

none –> just a developmental abnormality

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11
Q

What is esophagitis?

A

injury to the mucosal lining of the esophagus

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12
Q

Do all people have chest/mid epigastric pain with esophagitis?

A

no

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13
Q

How do we detect esophagitis?

A

endoscopy and biopsy –> may appear reddish when mild to ulcerated when severe

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14
Q

What kinds of cells are involved in esophagitis?

A

neutrophils and eosinophils // lymphocytes are normal b/c of MALT (but can be an inflammatory mediator too)

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15
Q

What is the endoscopic finding in reflux esophagitis?

A

linear erythema with variable linear ulcers w/neutrophils and reactive epithelium

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16
Q

Dysphagia

A

difficulty on swallowing

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17
Q

What are the endoscopic/histologic findings of Herpes esophagitis?

A

ulcers “punched out”, multinucleated squamous cells, intranuclear inclusions

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18
Q

What are the endoscopic/histologic findings of CMV esophagitis?

A

ulcers, intranuclear AND intracytoplasmic inclusions (vs herpes which only has intranuclear)

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19
Q

What are the endoscopic/histologic findings of candida esophagitis?

A

white “cheesy” plaques, keratin debris, admixed yeast and psuedohyphae

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20
Q

What are the endoscopic/histologic findings of eosinophilic esophagitis?

A

white papules of intraepithelial eosinophils (12-15/hpf), ring esophagus/felinization/trachealization, stricture

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21
Q

T/F the incidence of eosinophilic esophagitis is falling in children and adults.

A

F –> rising

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22
Q

Pathogenesis of eosinophilic esophagitis

A

atopic allergic response to antigen in food or air

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23
Q

Tx of eosinophilic esophagitis

A

oral swish and low dose steroids

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24
Q

Dyspepsia

A

pain in the upper abdomen associated with feeding

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25
Q

Name 3 skin disorders that can present as esophagitis.

A

pemphigus, pemphigoid, lichenoid reactions

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26
Q

Schatzki Ring

A

muscular ring covered by squamous epithelium that can cause dysphagia –> 10% of people

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27
Q

Odynophagia

A

pain on swallowing

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28
Q

Pathogenesis Achalasia

A

LES has high tone impeding progress of bolus into stomach and dilates over time due to increased pressure and food –> food stasis with enzymes can increase risk of carcinoma/dysplasia progression

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29
Q

Pathogenesis Scleroderma/Crest

A

selective ATROPHY (not fibrosis) of inner circular muscle layer –> lower esophagus only

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30
Q

Pathogenesis Mallory Weiss Tear

A

with repeated wrenching vomiting, a rip may occur in distal esophagus causing massive bleeding

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31
Q

Where are most common cancers of GI tract?

A

colorectal

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32
Q

4 categories of benign esophageal tumors

A

papilloma, granular cell, mixed, leiomyoma

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33
Q

4 categories of malignant esophageal tumors

A

squamous and adenocarcinoma, malignant nerve sheath, adenoid cystic, leiomyosarcoma

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34
Q

Worldwide, what is the most common esophageal tumor?

A

squamous cell carcinoma

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35
Q

In the occident, what is the most common esophageal tumor?

A

adenocarcinoma

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36
Q

Risk factors for adenocarcinoma

A

reflux, diet, obesity, male, microbiome

“DORMM”

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37
Q

Are the esophagus and stomach sterile?

A

the esophagus isn’t, the stomach is

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38
Q

T/F >50% of those with Barrett’s have no symptoms

A

T

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39
Q

T/F >99% of BE develops before initial endoscopy

A

T (BE = barrett’s)

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40
Q

Pathogenesis of Barrett’s risk factors

A

obesity promotes GERD mechanically and by secreting inflammatory factors, high fat diet has delayed gastric emptying + MHC variants + long segment BE

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41
Q

T/F screening for BE based on reflux symptoms is effective

A

F –> will miss >50% w/only reflux screening

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42
Q

How do we identify BE histologically?

A

goblet cells/intestinal metaplasia

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43
Q

When is the length of intestinal metaplasia in BE established?

A

at the initiation of the injury

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44
Q

Do short segments convert to long segments in BE?

A

NO

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45
Q

Which has a higher risk of cancer in BE? long/short segment

A

long segment

46
Q

When may surgical resection become necessary w/regards to esophagus dysplasia/cancer?

A

once invasion has developed

47
Q

Staging of esophageal adenocarcinoma?

A

TNM

48
Q

What term is used for peri-esophageal fat?

A

adventitia

49
Q

Does the esophagus have a serosal surface?

A

no –> adventitia

50
Q

What are the endoscopic findings of esophageal BE/dysplasia/cancer?

A

salmon colored tongue of glandular mucosa

51
Q

What some etiologic factors in squamous cell carcinoma of the esophagus?

A

ETOH, smoking, moldy foods, achalasia, lye, diverticulum

52
Q

Is HPV a prominent etiologic factor in squamous cell carcinoma of the esophagus?

A

No

53
Q

How common is squamous cell carcinoma of the esophagus in the US?

A

quite rare actually

54
Q

What set of genes increases risk of squamous cell carcinoma of the esophagus?

A

alcohol dehydrogenases

55
Q

What would a geographic high risk area for squamous cell carcinoma of the esophagus look like?

A

low altitude, drought, low vegetable intake

56
Q

What is the staging system used in squamous cell carcinoma of the esophagus?

A

TNM

57
Q

Another name for an isolated patch of glycogenated squamous mucosa in the esophagus.

A

glycogenic acanthosis –>benign

58
Q

What part of the stomach mucosa makes acid and pepsinogen?

A

oxyntic –> basically fundus and body and cardia

59
Q

What part of the stomach mucosa makes gastrin?

A

antrum

60
Q

Does the antrum have rugae?

A

no –> smooth

61
Q

Does the antrum have MALT?

A

no

62
Q

Pathogenesis of acute gastritis

A

epithelial injury resulting in breakdown of mucosal barrier allowing gastric luminal contents to back diffusely into the lamina causing ulcerations and bleeding

63
Q

Etiologic factors in acute gastritis

A

alcohol, severe stress (“cushing type” ulcers in burn patients and head trauma patients), shock, radiation, caustic agents, NSAIDs

64
Q

Histologic features of acute gastritis

A

fibrin, erosion, ulcer beds, no chronic inflammation, may have neutrophils, blood

65
Q

What distinguishes an erosion from an ulcer?

A

ulcer goes all the way through mucosa vs. erosion is just surface epithelium

66
Q

What is implied if there are lymphocytes in the gastric lamina propria?

A

chronic gastritis

67
Q

What is chronic gastritis without activity vs with activity?

A 
without = lymphocytes
with = lymphocytes + neutrophils
68
Q

4 tests for H.pylori

A

biospy with thiazine stain, CLOtest (pH/urease), blood test for Ab, breath test

69
Q

How do we get duodenal ulcers with H.pylori?

A

antral H.pylori can kill off D cells reducing inhibition of acid production

70
Q

What is atrophic chronic gastritis?

A

loss of parietal and chief cells –> autoimmune or migration of antral H.pylori – // can increase risk of carcinoma and lymphoma

71
Q

Autoimmune gastritis pathogenesis

A

auto antibodies against H+ pump –> antibody and cell mediated killing follows

72
Q

What is another word for gastric atrophy?

A

antralization

73
Q

What are the negative effects of autoimmune gastritis?

A
  1. rise in gastric pH due to loss of inhibition of G cells –> proliferation of ECL cells –> carcinoid tumors
  2. reduced B12 absorption b/c no intrinsic factor production –> pernicious anemia
  3. long term low acid production
74
Q

Histologic features of ECL clusters

A

round nuclei, chromogranin
–> microscopic ball = microcarcinoid
endoscopic mass = macrocarcinoid

75
Q

H.pylori or autoimmune gastritis? begins in antrum

A

H.pylori

76
Q

H.pylori or autoimmune gastritis? involves body and fundus

A

autoimmune –> antrum NOT effected

77
Q

H.pylori or autoimmune gastritis? acute and chronic

A

both

78
Q

H.pylori or autoimmune gastritis? + CLO

A

H.pylori

79
Q

H.pylori or autoimmune gastritis? -CLO

A

autoimmune

80
Q

H.pylori or autoimmune gastritis? antiparietal antibodies

A

usually autoimmune (rarely H.pylori)

81
Q

H.pylori or autoimmune gastritis? microcarcinoid

A

autoimmune

82
Q

2 categories of malignancies in stomach

A

lymphoma and carcinoma

83
Q

2 categories of benign growths of stomach

A

polyps, enlarged folds

84
Q

What is the most common stomach malignancy?

A

carcinoma

85
Q

T/F gastric cancer prevalence is increasing in the USA

A

F –> unlike esophagus, on the decline

86
Q

Fundic gland polyps

A

usually incidental, most common polyp, single/multiple, benign, always in those with FAP gene (familial adenomatous polyposis), sporadic ones occur via beta catenin mutations

87
Q

What mutation can lead to sporadic fundic gland polyps?

A

beta catenin mutation

88
Q

Histologic features of fundic gland polyps

A

oxyntic mucosa, dilation of glands, no proliferation

89
Q

Hyperplastic gastric polyp

A

usually antral, single/multiple, usually arise on underlying gastritis, low risk of neoplastic transformation, inflamed and proliferating mucosa

90
Q

Etiologies of enlarged gastric folds

A

lymphoma, gastric cancer, metastatic breast lobular cancer, diffuse gastritis, benign increase called hypertrophic gastropathy

91
Q

What is the normal ratio of parietal/chief cells to surface foveolar cell compartment?

A

3:1

92
Q

What cell layer is expanded in hypertrophic gastropathies?

A

epithelium

93
Q

In what condition is parietal cell compartment expanded?

A

ZES/MEN

94
Q

*probably not testable b/c only in notes: pathogenesis of Metrier’s disease

A

foveolar/epithelial expansion in stomach leads to lots of mucin production –> abnormal protein signaling –> loss of protein –> secretion of serum albumin –> loss of pressure, body edema

95
Q

Most common primary lymphoma in stomach

A

extra nodal marginal zone b cell lymphoma

96
Q

Pathogenesis of extra nodal marginal zone b cell lymphoma

A

H.pylori –> stomach MALT –> proliferation and mutations –> indolent or large cell lymphoma

97
Q

Can we treat extra nodal marginal zone b cell lymphoma with antibiotics?

A

yes, if it is indolent/small then it will respond to antibiotics

98
Q

2 types of gastric cancer

A

intestinal type, signet ring type

99
Q

What are the features of intestinal type gastric cancer

A

repeated injury/chronic gastritis –> metaplasia/dysplasia –> glands

100
Q

Does signet ring type gastric cancer undergo dysplasia/metaplasia sequence?

A

NO, no injury or gastritis so no metaplasia/dysplasia –> instead, 2 e cadherin mutations

101
Q

M:F Intestinal gastric cancer

A

M>F

102
Q

M:F Signet Ring gastric cancer

A

M = F

103
Q

Avg Age: Intestinal gastric cancer

A

58

104
Q

Avg Age: Signet Ring gastric cancer

A

48

105
Q

Diet and geographic effects: Intestinal gastric cancer

A

both have an association

106
Q

Diet and geographic effects: Signet Ring gastric cancer

A

no association

107
Q

Does ETOH increase risk of intestinal gastric cancer?

A

No

108
Q

Does Vitamin C increase risk of intestinal gastric cancer?

A

No –> protective

109
Q

Does processed meat increase risk of intestinal gastric cancer?

A

yes –> 50g/day = 2.5x increase

110
Q

Do vegetables increase risk of intestinal gastric cancer?

A

No –> 100g/day = 1/3 risk

111
Q

Presentation of gastric cancers

A

enlarged folds, ulcers, glands

112
Q

Presentation of pure genetic signet ring gastric cancer

A

leather bottle stomach/linitus plastica

G.I & Nutrition (43 decks)

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