Lec 4 Flashcards

(56 cards)

1
Q

How does mucosa of gastric body differ from that of gastric antrum?

A

both = lines by tall mucous cell pits

have different gland morphology

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2
Q

What part of stomach has more prominent rugae?

A

more prominent in corpus than antrum

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3
Q

What is purpose of gastric rugae?

A

allow for gastric expansion and become flat when stomach filled with food

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4
Q

What is gland morphology of corpus of stomach? What types of cells

A

long straight tubules with parietal and chief cells, mucous neck cells, enterochromaffin-like [ECL] cells, and D cells

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5
Q

What is gland morphology of antrum?

A

short coiled mucous glands

some parietal cells, few G cells

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6
Q

What is gland morphology of cardia?

A

similar to antrum [short coiled glans] but no G cells

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7
Q

What do you see in acute erosive gastritis?

A
  • surface of stomach punctuated by areas of necrosis/erosions
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8
Q

What are some potential complications of acute erosive gastritis?

A

potential source of GI bleeding

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9
Q

How does erosive gastritis lesion differ from ulcer?

A

ulcer is a deeper defect –> goes through mucosa into submucosa

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10
Q

What are some etiologies of acute erosive gastritis?

A
  • NSAIDs

- severy physiological stress (stress ulcers) from sepsis, hypoxia, trauma, etc

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11
Q

What causes a curling ulcer?

A

burn

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12
Q

What causes a cushing ulcer?

A

trauma or surgery; brain injury

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13
Q

What is acute hemorrhagic gastritis?

A

acute erosive gastritis w/ necrosis of entire gastric mucosa

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14
Q

What causes chemical gastropathy?

A

NSAIDS, bile reflux

irritate gastric mucosa and get erosions

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15
Q

What do you see endoscopically/microscopically to distinguish chemical gastropathy?

A

endoscopically: erythema/redness
microscopically: no inflammation = distinguishes it from gastritis

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16
Q

What are 3 features of chemical gastropathy microscopically?

A
  • loss of epithelial mucin
  • dilated capillaries
  • corkscrew-shaped gastric pits
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17
Q

What do you see in chronic gastritis?

A
  • mucosa heavily infiltrated by chronic inflammatory cells
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18
Q

What do you see in atrophic gastritis

A
  • atrophy –> thin mucosa, reduced number of glands

- intestinal antral or metaplasia: body glands start to look like antrum or have goblet cells like in intestine

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19
Q

What are the 3 different types of chronic gastritis and their distributions?

A

type A: autoimmune; body

type B: antral-predominant gastritis

type C: Multifocal atrophic gastritis: pangastritis

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20
Q

What is pathogenesis of type A gastritis?

A

autoantibodies against parietal cells and/or intrinsic factor

causing loss of parietal cells and B12 deficiency

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21
Q

What findings in type A gastritis?

A
  • B12 deficiency
  • achlohydria or hypochlorhydria
  • antral G cell hyperplasia
  • hypergastrinemia
  • ECL cell hyperplasia
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22
Q

High or low acid in autoimmune gastritis?

A

low acid [hypochlorhydria]

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23
Q

What do you see microscopically in autoimmune gastritis?

A
  • atrophy
  • metaplasia of fundic glands with antral and instestinal epithelium
  • ECL cell hyperplasia
  • G cell hyperplasia
24
Q

Where in the stomach do you get autoimmune gastritis?

A

fundus/body of stomach

25
What are some complications associated with chronic autoimmune gastritis?
- carcinoid tumors
26
Why do you get carcinoid tumors in type A chronic gastritis?
have ECL cell hyperplasia as a result of hypergastrinemia can end up with neuroendocrine tumors
27
What do you see grossly in chronic autoimmune gastritis?
loss of rugae
28
What lab features in chronic autoimmune gastritis?
- anti-parietal and anti-IF antibodies - elevated gastric pH - elevated serum gastrin - low B12 - megaloblastic anemia
29
What stain for neuroendocrine cells?
chromogranin
30
Are carcinoids in setting of type A gastritis slow or fast growing?
slow growing compaired to sporadic gastric and intestinal carcinoids
31
Gastric ulcer in setting of hypochlorhydria should make you think what?
think cancer chronic autoimmune gastritis
32
Where do you usually see Type B chronic gastritis?
antrum
33
What is pathogenesis of type B chronic gastritis?
H pylori infection
34
What stain is best way to look for H pylori?
silver impregnation
35
Where does H pylori usually reside?
gastric mucosa
36
How does H pylori protect itself?
- urease --> bicarb and ammonia to neutralize gastric acid | - virulence factors: cytotoxins, breakdown of acid-protective barriers
37
How do you diagnose H pylori infection?
- histology - urease-based tissue or breath tests - serology [anti-H pylori antibodies]
38
What are some complications associated with chronic H pylori gastritis?
- increase risk MALT lymphoma | - 2-5x increase risk gastric carcinoma
39
What type of ulcers most highly associated with H pylori?
duodenal ulcers
40
What is MALT lymphoma?
B cell lymphoma associated with H pylori regresses in response to H pylori eradication
41
What is pathogenesis of Type C chronic gastritis?
- effects entire stomach | - environmental / H pylori associated
42
Which type of chronic gastritis has highest risk of adenocarcinoma?
multifocal atrophic gastritis = 10x increase risk
43
What do you see in multifocal atrophic gastritis?
- atrophy leading to reduced acid output - entire stomach has flattened mucosa - widespread chronic inflammation - ulcerations
44
Where do gastric ulcers usually occur?
distal stomach at junction between corpus and antrum
45
Which location of ulcers in H pylori gastritis? In multifocal atrophic gastritis?
H pylori gastritis = mostly duodenal ulcers, some antral ulcers multifocal atrophic gastritis = only gastric ulcers
46
What are some complications of peptic ulcer disease?
- bleeding - perforation - penetration into adjacent organs - pyloric scarring and stenosis --> gastric outlet obstruction + vomitting
47
How long does it take ordinary ulcers to heal when treated properly?
~ 6 weeks
48
What should you think if delayed healing of peptic ulcers?
may indicate gastric cancer
49
What should you think if 3 or more ulcers in duodenal bulb?
zollinger-ellison = gastrinoma
50
What are some risk factors for gastric adenocarcinoma?
- dietary: nitrosamines [smoked foods] - older age - genetics - chronic atrophic gastritis - H pylori - smoking
51
Intestinal gastric cancer - age/gener - risk factors - characteristics
age/gender: older, mostly males risks: environmental, dietary [nitrosamines], H pylori, smoking characteristics: in background of chronic gastritis, intestinal metaplasia, usually discrete mass with malignant glands and tubules
52
Diffuse gastric cancer - age/gender - risk factors - characteristics
age/gender: lower age [48 vs 55], more in women risks: not associated with H pylori, probably genetic characteristics: ill-defined, stomach wall thick and leathery [linitis plastica], signet ring cells
53
Where does diffuse gastric cancer usually metastasize to?
met to lymph nodes, peritoneal cavity, ovaries
54
Where does intestinal gastric cancer usually met to?
met to lymph nodes and liver via portal circulation
55
What are krukenberg tumors?
bilateral enlarged ovaries with metastatic diffuse gastric cancer
56
How have rates of each type of gastric cancer changed in the US? overall gastric cancer?
- declining overall gastric cancer due to a decline in intestinal-type; diffuse remain constant