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Pathology of the Stomach Flashcards

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1
Q

What are the cells that accumulate in an acute gastritis? Chronic?

A 
Acute = PMNs
Chronic = lymphocytes or plasma cells
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2
Q

Erosions of the stomach do not go past what layer of the GI tract? What happens it does?

A

Muscularis mucosa

Becomes an ulcer

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3
Q

What are the causes of acute gastritis?

A
  • Disruption of the mucus layer
  • Decrease bicarb secretion
  • Decreased mucosal blood flow
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4
Q

What are the two major chemicals that are absorbed through the stomach?

A

NSAIDs and EtOH

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5
Q

How can renal disease lead to gastritis?

A

Uremia

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6
Q

What is the morphology of acute gastritis?

A

Hyperemia and edema with PMNs above the BM

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7
Q

What is the morphology of more severe gastritis?

A

Entire mucosal thickness eroded and/or hemorrhage.

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8
Q

What is acute erosive hemorrhagic gastritis?

A

When the mucus layer of the stomach has eroded away, and is bleeding

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9
Q

What are the ssx of acute gastritis?

A

Hematemesis

Melena

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10
Q

What is chronic gastritis?

A

Chronic mucosal inflammatory changes eventually leading to mucosal atrophy and intestinal metaplasia

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11
Q

What CA can result from chronic gastritis?

A

Carcinoma

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12
Q

What is the autoimmune cause of gastric gastritis?

A

Pernicious anemia

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13
Q

What is the cause of granulomatous gastritis?

A

Crohn’s disease

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14
Q

What are the gram staining and morphological characteristics of chronic gastritis?

A

S shaped gram negative rod

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15
Q

Is H.Pylori invasive?

A

no

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16
Q

True or false: most H.pylori infections are asymptomatic

A

True

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17
Q

What are the risk factors of having an H.Pylori infection?

A

Increase peptic ulcer
carcinoma
Lymphoma

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18
Q

Where does H.pylori reside in the stomach?

A

In the mucus layer

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19
Q

What are the virulence factors that some strains of H.pylori produce? MOA?

A

CagA
VacA (forms vacuoles)

Both are inflammatory cytokines

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20
Q

True or false: H.pylori are flagellated

A

True

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21
Q

What are the protein that allow H.pylori to bind to the epithelial cells of the stomach?

A

Adhesins

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22
Q

What is a major cause of gastric epithelial degradation?

A

Pepsin is allowed in, degrading proteins

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23
Q

What is the major difference between acute an chronic gastritis secondary to H.pylori infection?

A

PMNs cause damage in chronic infections

Atrophy / dysplasia

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24
Q

What happens when H.pylori infections become symptomatic? (2 scenarios) where does this usually occur?

A

Increase acid and gastrin secretion. OR just increased gastrin.

usually occurs in the antrum.
Less commonly in the body

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25
Autoimmune gastritis can have antibodies to what?
Parietal cells and IF
26
What are the microcytic anemias? (5)
``` Fe deficiency Chronic disease Pb exposure Sideroblastic Thalassemias ```
27
What is the MOA of CagA that H.pylori produces?
Activates IL-8, attracting PMNs
28
What are the histological characteristics of H.pylori dysplasia?
PMN infiltration | Dysplasia
29
What is the late morphology of Chronic gastritis?
Atrophy, dysplasia | carcinoma in situ
30
What is the early morphological characteristics of chronic gastritis?
Coarse, red mucosa; inflammatory infiltrate
31
What are the more severe morphological changes associated with chronic gastritis?
Variable atrophy Thin, flattened mucosa Regenerative changes
32
What happens to the rugal folds in chronic gastritis?
Flattening
33
What are the symptoms of autoimmune chronic gastritis (besides pernicious anemia?
Achlorhydria and hypergastrinemia
34
What is an ulcer?
Erosion below the muscularis mucosa
35
Where do peptic ulcers form?
Antrum of the stomach Pylorus body of the stomach Duodenum
36
Who is affected with PUD more often: men or women
Men
37
What is the relationship between hyperparathyroidism and PUD?
Hypercalcemia increases gastrin production
38
What are the ssx of PUD?
Gnawing epigastric pain occurring 1-3 hours, worse at night
39
How do you diagnose PUD?
Endoscopy and imaging
40
Does eating improve or worsen the ssx of PUD?
Improve
41
Which ulcers are usually cancerous: duodenal or stomach
Duodenal
42
What is the main pathological cause of PUD?
Imbalance between mucosal defense and damaging forces
43
H. Pylori is present in almost all (___) ulcers and most of the time in (___) ulcers?
Duodenal Gastric
44
What are some of the defensive forces against developing an ulcer?
Mucosal blood flow Mucus Bicarb secretion Prostaglandins
45
What are the pro-inflammatory cytokines that are secreted by H.pylori?
IL-1 IL-6 TNF IL-8
46
What is the role of IL-8 in H.pylori infection
Recruits PMNs
47
What is the effect H.Pylori has on gastric acid secretion? Bicarb?
Increased gastric acid Decreased bicarb
48
What are the three enzymes that H.pylori secretes?
Urease Protease Phospholipase
49
What is Zollinger-ellison syndrome?
Gastrinoma producing extra HCl
50
What are the problems with the lower pyloric sphincter that can contribute to ulcer formation?
Delayed gastric emptying | Duodenal-gastric reflux
51
What are the severe symptoms of gastric ulcers?
Hematemesis | Melena
52
Where are the vast majority of ulcer located?
1st portion of the duodenum
53
What is the best way to diagnose an ulcer?
Look at it (EGD)
54
What are the characteristics of a benign gastric ulcer?
Small, punched out appearance without other signs of inflammation or dysplasia
55
What do gastric carcinomas look like?
Raised edges around an ulcer
56
What are the four demonstrable zones histologically of a peptic ulcer?
1. Necrosis of ulcer base and margins 2. Inflammatory infiltrate 3. Granulation tissue 4. Scarring (fibrosis)
57
What are the 4 major complications with PUD?
Bleeding Perforation Obstruction Intractable pain
58
What causes the obstructive problems with PUD?
Edema or scarring
59
What is the characteristic of stress ulcers? Where do these usually occur?
Multiple, small ulcers that Do not breach the muscularis mucosa Stomach and the duodenum, esophagus
60
True or false: stress ulcers are a precursor to chronic PUD
False
61
What are Curling ulcers?
an acute peptic ulcer of the duodenum resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa.
62
What are Cushing ulcers?
Increased intracranial pressure may lead to overstimulation of the vagus nerve, causing increased gastric acid secretion, and ulcer formation
63
What are polyps?
Mass lesions arising from and projecting above the mucosa
64
What are hyperplastic or inflammatory polyps?
Usually nonneoplastic but hyperplastic epithelium overlying dilated glandular tissue
65
What are adenomatous polyps?
True neoplasms--
66
What type of polyps in the stomach are precancerous?
Adenomatous polyps
67
What are the histological characteristics of hyperplastic gastric polyps?
Tons o' glands in the epithelium
68
What is the most common type of malignancy of the stomach?
Gastric carcinoma
69
What are the two types of gastric carcinomas?
Intestinal types | Diffuse type
70
Where, geographically, are most gastric carcinomas found?
Asia
71
What is the most important factor for the development of the intestinal type of gastric carcinoma?
H.Pylori infection
72
What are the major environmental influences on the intestinal type of gastric carcinoma?
nitrosamines | Benzopyrenes
73
Where in the stomach does gastric carcinoma usually occur?
Lesser curvature of the stomach
74
What is the most important prognostic factor for gastric carcinoma?
Depth of invasion
75
What is the shape, generally, of a malignant ulcer?
Ragged edges with elevated edges
76
What is the shape, generally, of a benign ulcer?
Smooth, round edges
77
What is linitis plastic?
Diffuse gastric carcinoma that spreads out, causing diffuse thickening of the walls of the stomach
78
Signet rings in gastric cells is indicative of what?
"Diffuse" typu adenocarcinoma
79
What is the gene that is mutated that causes gastric carcinoma?
APC

Gastrointestinal (42 decks)

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