GI 1 Flashcards

1
Q
A

Barrett Esophagus

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1
Q

Where do adenocarcinomas of the esophagus occur?

What are some other risk factors?

What are adenocarcinomas?

What is it associated with?

Prognosis?

A

Majortiy arise in distal esophagus in association with Barrett esophagus

Risk Factors: smoking tobacco, obesity

Adenocarcinoma = gland-forming malignancy

Associated with dysplasia of adjacent glandular epithelium

Prognosis: Varies depending on stage, but overall 5yr survival

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2
Q
A

Normal Stomach

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3
Q

What is reflux esophagitis?

What is it characterized by?

A

Due to acid reflux; characterized by intra-epithelial inflammatory cells (esp. eosinophils), basal layer hyperplasia, spongiosis, and elongation of papillae of lamina propria

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4
Q
A

Gastric Ulcer

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5
Q
A

Adenocarcinoma of Esophagus

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6
Q
A

Esophageal Varices (ulceration that became thrombosed)

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6
Q
A

Normal Stomach (Antrum)

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6
Q

What is the change that happens in Barrett’s esophagus?

A

Intestinal metaplasia (goblet cell metaplasia) of distal esophagus in response to acid-reflux

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6
Q

What is the histology of gastritis?

A

Increased numbers of inflammatory cells within lamina propria, including lymphocytes, plasma cells, and neutrophils.

Neutrophils often infiltrate mucosal epithelium (“active” gastritis)

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7
Q
A

Gastric Ulcer

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8
Q
A

Adenocarcinoma of Esophagus

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9
Q
A

Herpes Esophagitis

Ground glass appearance

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10
Q
A

Acute Hemorrhagic Gastritis

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11
Q
A

Barrett Esophagus

Left side replaced by columnar glandular mucosa

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11
Q
A

Normal Stomach (fundus)

Chief cells - purple (Pepsinogen)

Parietal cells - pink (HCl, IF)

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11
Q
A

Gastric Adenocarcinoma

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11
Q

What is an erosion?

What is an ulcer?

A

Erosion: Partial thickness loss of mucosal tissue

Ulcer: Full-thickness loss of mucosa

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11
Q

What are the 2 main disorders of Hypertrophic Gastropathy?

A

Menetrier diseaes: hyperplasia of mucous neck cells due to elevated levels of TGF-alpha. Protein-losing enteropathy (diarrhea, edema). Associated with increased risk of gastric adenocarcinoma.

Zollinger Ellison Syndrome: Triad of gastrinoma (gastrin-secreting tumor usually in pancreas or duodenum due to hyperplasiz of oxyntic mucosa - parietal and chief cells), hypertrophic gastropathy and peptic ulcers due to hypersecretion of acid.

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12
Q
A

Candida Esophagitis

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12
Q
A

Herpes Esophagitis

(sharply demarcated lesions)

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12
Q
A

Gastric Adenocarcinoma

Signet Ring Cell Morphology

With stain for cytokeratin (ensures that it’s carcinoma, not macrophage)

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12
Q
A

Gastric Lymphoma

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14
Q
A

Gastric Ulcer

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15
Q
A

Adenocarcinoma of Esophagus

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16
Q
A

Normal Esophagus and stomach

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17
Q
A

Gastritis

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18
Q
A

Gastric Ulcer

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18
Q
A

Metastatic Gastric Carcinoma in liver

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19
Q

What is metaplasia?

A

Reversible change from one mature cell type into another. May represent adaptive (protective) change in response to injury

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19
Q

How is GIST treated?

A

Majority of GIST express CD117 (“c-kit”) which is the molecular target of tyrosine kinase inhibitor (Imatinib)

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20
Q
A

Hypertrophic gastropathy

Hyperplasia of mucus-secreting cells

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20
Q
A

Barrett’s esophagus

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20
Q

What are the different parts of the stomach?

A
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21
Q
A

Gastric Adenocarcinoma

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22
Q
A

Gastric Adenocarcinoma

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23
Q
A

Barrett Esophagus

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24
Q
A

Squamous Cell Carcinoma of Esophagus with keratin pearls

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25
Q
A

Herpes Esophagitis

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26
Q
A

Squamous Cell Carcinoma of Esophagus

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27
Q
A

Candida Esophagitis

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27
Q

What is the most common malignancy of th esophagus?

What are risk factors?

Where does it occur?

What is the prognosis?

What is the histology?

A

Squamous cell carcinoma

Risk factors: Alcohol, tobacco, consumption of hot beverages, dietary foods

Location: Upper 1/3 - 20%, Middle 1/3 - 50%, Lower 1/3 - 30%

Prognosis: usually advanced stage at time of Dx, poor prognosis, overall 5yr survival 20%

Histo: polygonal tumor cells with prominent intercellular bridges and foci and keratinization (Squamous pearls)

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27
Q

What is Adenocarcinoma of the stomach associated with?

A

H. pylori infection

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29
Q
A

Esophageal Varices

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29
Q
A

Gastrointestinal stromal tumor

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31
Q
A

Gastric Adenocarcinoma

Signet ring cell morphology

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33
Q
A

Esophagitis (acute)

-Intercellular edema (spongiosis) and inflammatory cells in lamina propria

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34
Q
A

Hypertrophic Gastropathy

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35
Q
A

Squamous Cell Carcinoma of Esophagus

50% mid-esophagus, 30% distal, 20% proximal

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36
Q
A

Gastric Adenocarcinoma

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38
Q

What are some copmlications of ulcers?

A

Bledding, performation, obstruction

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40
Q
A

Gastric Adenocarcinoma

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41
Q
A

Adenocarcinoma arising in Barrett Esophagus

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41
Q
A

Gastric Carcinoma

Signet Ring Cell Morphology

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42
Q
A

Reflux Esophagitis (increased eosinophils)

42
Q

What are the damaging and defensive forces of the stomach?

What causes each?

A

Damaging: gastric acid, peptic enzymes

Caused by: H. pylori, NSAIDS, aspirin, cigarettes, alcohol, gastric hyperacidity, duodenal gastric reflux

Defensive: surface mucus secretion, HCO3 secretion into mucus, mucosal blood flow, apical surface membrane transport, epithelial regenerative capacity, elaboration of prostaglandins

Caused by: Ischemia, shock, delayed gastric emptying, and host factors

43
Q
A

Gastrinoma Triangle

44
Q

Describe a normal Esophagus

A

Gross: Pale esophageal mucosa (as compared with tan-brown gastric mucosa) and discrete gastro-esophageal junction

Histo: Squamous-lined mucosa of esophagus with submucosal glands and muscularis propria

45
Q
A

Gastric Adenocarcinoma

46
Q

What are some features that favor GIST malignancy?

A

Tumor size (>5 cm)

Increased mitotic rate (>5 mitotic figures/50 high power fields)

Presence of tumor necrosis

Mucosal invasion

47
Q
A

Gastric Ulcer

49
Q
A

Esophageal Varices

51
Q
A

Herpes Esophagitis

53
Q
A

Gastric Adenocarcinoma

54
Q
A

Malignant Gastrointestinal stromal tumor

55
Q
A

Adenocarcinoma of Esophagus

56
Q
A

Barrett Esophagus

57
Q

Compare and contrast Menetrier Disease (adult) and Zollinger-Ellison Syndrome

A

Both are examples of Hypertrophic gastropathy

58
Q
A

Barrett Esophagus

Low grade dsyplasia

59
Q
A

Esophageal Varices

60
Q
A

Gastric Carcinoma (Polyploid/ulcerated)

62
Q

What is the prognosis of stomach adenocarcinoma?

A

Depends on stage, overall 5 year survival about 30%

63
Q

Describe a normal stomach

A

Gross: Tan brown mucosa and gastric rugae (folds)

Microscopic: gastric pits lined by mucous neck cells with glands lined by parietal (red-pink) and chief (pale) cells. Little/no inflammatory cells normally present in gastric mucosa.

65
Q
A

Gastric Polyploid Carcinoma

66
Q
A

Squamous Cell Carcinoma of Esophagus

67
Q
A

Gastric Ulcer

68
Q
A

Hypertrophic gastropathy

69
Q

What are some associated findings of gastritis?

A

Erosion/ulceration

Intestinal metaplasia

Atrophy & fibrosis

71
Q
A

Gastric Ulcer (Malignant)

72
Q
A

Gastric Ulcer

72
Q
A

Gastric Lymphoma

74
Q
A

Squamous Cell Carcinoma of Esophagus

75
Q
A

Herpes Esophagitis

77
Q
A

Hypertrophic gastropathy

78
Q
A

Barrett Esophagus

High grade dysplasia

79
Q
A

Gastrointestinal stromal tumor

Can arise anywhere in GI tract, thought to be due to Cajal cells

79
Q

What are the associated metastases of stomach adenocarcinoma?

A

Left supraclavicular lymph node (Virchow’s node) or both ovaries (Krukenberg tumor)

80
Q
A

Metastatic Gastric Carcinoma in Lung

81
Q
A

Squamous Cell Carcinoma of Esophagus

82
Q
A

Adenocarcinoma of Esophagus

83
Q

What is the difference between a malignant and benign ulcer?

A

Can’t absolutely distinguish between benign and malignant ulcers by macroscopic exam alone.

Benign: small, regular smooth edges

Malginant: large, irregular with “rolled” or “heaped up” borders

85
Q
A

Gastric Adenocarcinoma

86
Q

What are the different causes of gastritis?

A

Alcohol, drugs (NSAIDS), bile reflux, stress, radiation, chemotherapy

88
Q
A

Malignant Gastrointestinal stromal tumor

90
Q
A

Herpes Esophagitis

Loss of mucosa + exudate forming

91
Q
A

Gastric Ulcer

92
Q
A

Esophageal Varices (ulceration + hemorrhage)

93
Q

What are some differences between H. pylori and autoimmune gastritis?

Location, inflammatory infiltrate, acid production, gastrin, other lesions, serology, sequelae, and associations

A
95
Q

What is dysplasia?

A

Pre-malignant change involving abnormalities in nuclear size, shape, and (lack of) maturation

96
Q
A

Metastatic Gastric Carcinoma

Virchow’s node

97
Q

What is a GIST?

A

Gastrointestinal stromal tumor of stomach

Major of mesenchymal tumors of GI tract now classified as GISTs.

Thought to be dervied from interstitial cells of Cajal (pacemaker cells of GI tract).

Histo: Spindled (elongated) tumor cells

98
Q
A

Gastric Ulcer

99
Q
A

Candida Esophagitis

100
Q
A

Gastric Adenocarcinoma

Signet ring cell morphology

101
Q

What are esophageal varices?

A

Collateral, dilated veins which develop in response to portal hypertension. Tortuous dilated veins within submucosa that may cause massive upper GI bleeding

10-30% of upper GI hemorrhage

25-35% of cirrhotic patients

30% of initial bleeds fatal

102
Q
A

Reflux Esophagitis

104
Q
A

Gastrointestinal stromal tumor

105
Q
A

Gastric Lymphoma

106
Q
A

Hypertrophic gastropathy

108
Q
A

Gastric Ulcer

109
Q

What is the most common cause of chronic gastritis?

A

Helicobacter pylori. Spiral bacteria may be found in gastric biopsies

110
Q
A

Gastritis

112
Q

What is the clinical relevance of Barrett’s esophagus?

A

Increased risk of adenocarcinoma (dysplasia –> carcinoma)

113
Q
A

Gastric Lymphoma

114
Q
A

Normal esophagus by endoscopy

115
Q
A

Candida Esophagitis

Pseudomembranes

116
Q
A

Esophageal Varices

117
Q
A

Gastritis with erosions

118
Q

What are the gross and histologic patterns of adenocarcinoma of the stomach?

A

Gross: 1) Exophytic or polypoid, ulcerated mass

2) Diffuse thickening of stomach (linitis plastica “leather bottle” stomach)

Histologic: 1) “intestinal” type: cohesive, gland-forming tumor cells

2) “Diffuse” type: discohesive “signet” ring cells w/ intracytoplasmic mucin

119
Q
A

Gastric Adenocarcinoma

120
Q
A

Chronic Gastritis

Loss of glands + fibrosis

122
Q
A

Gastric Adenocarcinoma

123
Q

What is hypertrophic gastropathy characterized by?

A

Giant, “cerebriform” enlargement of rugal folds of gastric mucosa due to hyperplasia of epithelial cells

124
Q
A

Gastrointestinal stromal tumor

125
Q
A

Normal Stomach (Fundus)

126
Q
A

Gastric Lymphoma

127
Q

What are 2 types of infectious esophagitis?

Describe them.

A

Herpes esophagitis: Sharply “punched out” ulcers with multinucleated giant cells and intranuclear “ground glass” inclusions

Candida esophagitis: Gray-yellow exudates with yeast/pseudohyphae

128
Q
A

Gastric Lymphoma

129
Q
A

Normal Stomach

130
Q
A

Gastrointestinal stromal tumor

131
Q

How is Barrett’s esophagus diagnosed?

A

Combination of clinical & pathologic criteria

Clinical: Endoscopic presence of salmon-colored mucosa above GE junction

Pathologic: Histologic evidence of intestinal metaplasia (presence of goblet cells) within columnar epithelium biopsied

132
Q

What is autoimmune gastritis?

What are some symptoms?

A

Autoantibodies against parietal cells, H/K ATPase, or IF

Chronic inflammation leads to mucosal injury and eventual atrophy.

Achlorhydria (low acid production) and hypergastrinemia

Pernicious anemia (B12 deficiency)

Increased risk for gastric cancer

133
Q
A

Gastrointestinal stromal tumor

134
Q
A

Normal

135
Q
A

H. Pylori

136
Q

Lymphomas of the stomach

What is the most common form?

A

Most common site of extranodal lymphomas

5% of gastric malignancies, 20% of all extranodal lymphomas

Most common form: low-grade B-cell lymphoma of MALT (mucosa-associated lymphoid tissue)

Associated with H. pylori infection

Composed of dense infiltrate of small lymphoid cells, often showing plasma cell differentiation and invasion of gastric glands (lymphoepithelial lesions)