Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI/Liver > Lec 4 > Flashcards

Lec 4 Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What part of stomach has more prominent rugae?

A

more prominent in corpus than antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is purpose of gastric rugae?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is gland morphology of antrum?

A

short coiled mucous glands

some parietal cells, few G cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is gland morphology of cardia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do you see in acute erosive gastritis?

A
  • surface of stomach punctuated by areas of necrosis/erosions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some potential complications of acute erosive gastritis?

A

potential source of GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does erosive gastritis lesion differ from ulcer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some etiologies of acute erosive gastritis?

A
  • NSAIDs

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes a curling ulcer?

A

burn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes a cushing ulcer?

A

trauma or surgery; brain injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is acute hemorrhagic gastritis?

A

acute erosive gastritis w/ necrosis of entire gastric mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes chemical gastropathy?

A

NSAIDS, bile reflux

irritate gastric mucosa and get erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 3 features of chemical gastropathy microscopically?

A
  • loss of epithelial mucin
  • dilated capillaries
  • corkscrew-shaped gastric pits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do you see in chronic gastritis?

A
  • mucosa heavily infiltrated by chronic inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What findings in type A gastritis?

A
  • B12 deficiency
  • achlohydria or hypochlorhydria
  • antral G cell hyperplasia
  • hypergastrinemia
  • ECL cell hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

High or low acid in autoimmune gastritis?

A

low acid [hypochlorhydria]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are some complications associated with chronic autoimmune gastritis?

A
  • carcinoid tumors
26
Q

Why do you get carcinoid tumors in type A chronic gastritis?

A

have ECL cell hyperplasia as a result of hypergastrinemia

can end up with neuroendocrine tumors

27
Q

What do you see grossly in chronic autoimmune gastritis?

A

loss of rugae

28
Q

What lab features in chronic autoimmune gastritis?

A
  • anti-parietal and anti-IF antibodies
  • elevated gastric pH
  • elevated serum gastrin
  • low B12
  • megaloblastic anemia
29
Q

What stain for neuroendocrine cells?

A

chromogranin

30
Q

Are carcinoids in setting of type A gastritis slow or fast growing?

A

slow growing compaired to sporadic gastric and intestinal carcinoids

31
Q

Gastric ulcer in setting of hypochlorhydria should make you think what?

A

think cancer

chronic autoimmune gastritis

32
Q

Where do you usually see Type B chronic gastritis?

A

antrum

33
Q

What is pathogenesis of type B chronic gastritis?

A

H pylori infection

34
Q

What stain is best way to look for H pylori?

A

silver impregnation

35
Q

Where does H pylori usually reside?

A

gastric mucosa

36
Q

How does H pylori protect itself?

A
  • urease –> bicarb and ammonia to neutralize gastric acid

- virulence factors: cytotoxins, breakdown of acid-protective barriers

37
Q

How do you diagnose H pylori infection?

A
  • histology
  • urease-based tissue or breath tests
  • serology [anti-H pylori antibodies]
38
Q

What are some complications associated with chronic H pylori gastritis?

A
  • increase risk MALT lymphoma

- 2-5x increase risk gastric carcinoma

39
Q

What type of ulcers most highly associated with H pylori?

A

duodenal ulcers

40
Q

What is MALT lymphoma?

A

B cell lymphoma
associated with H pylori
regresses in response to H pylori eradication

41
Q

What is pathogenesis of Type C chronic gastritis?

A
  • effects entire stomach

- environmental / H pylori associated

42
Q

Which type of chronic gastritis has highest risk of adenocarcinoma?

A

multifocal atrophic gastritis = 10x increase risk

43
Q

What do you see in multifocal atrophic gastritis?

A
  • atrophy leading to reduced acid output
  • entire stomach has flattened mucosa
  • widespread chronic inflammation
  • ulcerations
44
Q

Where do gastric ulcers usually occur?

A

distal stomach at junction between corpus and antrum

45
Q

Which location of ulcers in H pylori gastritis? In multifocal atrophic gastritis?

A

H pylori gastritis = mostly duodenal ulcers, some antral ulcers

multifocal atrophic gastritis = only gastric ulcers

46
Q

What are some complications of peptic ulcer disease?

A
  • bleeding
  • perforation
  • penetration into adjacent organs
  • pyloric scarring and stenosis –> gastric outlet obstruction + vomitting
47
Q

How long does it take ordinary ulcers to heal when treated properly?

A

~ 6 weeks

48
Q

What should you think if delayed healing of peptic ulcers?

A

may indicate gastric cancer

49
Q

What should you think if 3 or more ulcers in duodenal bulb?

A

zollinger-ellison = gastrinoma

50
Q

What are some risk factors for gastric adenocarcinoma?

A
  • dietary: nitrosamines [smoked foods]
  • older age
  • genetics
  • chronic atrophic gastritis
  • H pylori
  • smoking
51
Q

Intestinal gastric cancer

  • age/gener
  • risk factors
  • characteristics
A

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
Q

Diffuse gastric cancer

  • age/gender
  • risk factors
  • characteristics
A

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
Q

Where does diffuse gastric cancer usually metastasize to?

A

met to lymph nodes, peritoneal cavity, ovaries

54
Q

Where does intestinal gastric cancer usually met to?

A

met to lymph nodes and liver via portal circulation

55
Q

What are krukenberg tumors?

A

bilateral enlarged ovaries with metastatic diffuse gastric cancer

56
Q

How have rates of each type of gastric cancer changed in the US? overall gastric cancer?

A
  • declining overall gastric cancer due to a decline in intestinal-type; diffuse remain constant

GI/Liver (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions