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GI, Liver, GallBladder, Pancreas > P- Stomach > Flashcards

Flashcards in P- Stomach Deck (67):
1

What are the 4 layers of the stomach?

1. mucosa
2. submucosa
3. muscle layer
4. Serosa (this is what the esophagus lacks, making it easier to tear)

2

How does the mucosa of the fundus/body of the stomach differ from that of the antrum?

Fundus/Body
- shallow gastric pits
- tubular glands with parietal (HCl) and chief (pepsinogen) cells and mucus cells

Antrum
-longer gastric pits
- shorter, branched glands with G (gastrin) cells

3

How does mucosa in the body region of the stomach protect itself from autodigestion?

Its surface is covered in mucus secreted by the foveolar epitheleal cells that line it

4

What cells are found in the glands in the body of the stomach and what does each secrete?

Gastric glands are oxyntic and are composed of:

1. parietal cells -HCl (intermixed with foveolar cells
2. Chief cells - proteolytic enzyme pepsin (pepsinogen) at the bottom of the gland

5

What cells are found in the glands in the antrum of the stomach. What do they produce?

G cells are endocrine cells that make gastrin.

Gastrin promotes secretion of pepsin from the chief cells and acid from the parietal cells in the body of the stomach

6

What is gastritis?
What is the cause of MOST gastritis?

inflammation, irritation, and/or erosion/ulceration of the mucosa of the stomach.

H. pylori is the cause of most gastritis but other causes are irritation due to:
-alcohol use
- chronic vomit
- stress
- meds (aspirin/NSAIDs)
-bile reflux from duodenum
-pernicious anemia

7

What are the most common symptoms of gastritis?

What can occur if the irritation leads to erosions/ulcers?

1. nausea
2. abdominal bloating
3. hiccups
4. heartburn, epigastric pain

With erosions/ulcers:
1. hematemesis- vomiting blood ("coffee ground emetesis")
2. melena - black tarry stool

8

What is the main histological finding of chronic gastritis (regardless of cause)?

Chronic inflammatory cells (lymphocytes and plasma cells) in the lamina propria of the mucosa.
This inflammation can lead to the destruction of parietal cells/glandular atrophy and development of intestinal metaplasia.

9

When the etiology of gastritis is H. pylori, the tissue damage is usually associated with what?

1. Active (neutrophils, PMNs, acute)
2. Chronic (lymphocytes, plasma cells)

T and B cells respond to H. pylori and this is followed by neutrophilic infiltration of the gastric epithelium to phagocytize the bacteria.

There will be dense lymphoid follicles with germinal centers (like those seen in lymph nodes)

10

You do a biopsy of a stomach and notice neutrophilic infiltrate in the mucosa. There are also lymphoid follicles with germinal centers. What is the likely cause of the problem?

H. pylori

11

When the etiology of gastritis is autoimmune, what will the tissue damage show?
How does this differ from H. pylori?

1. destroyed parietal cells
2. glandular atropy
3. lymphocyte infiltrate in the mucosa/lamina propria
4. intestinal metaplasia

All 4 of those are also seen with H. pylori, however, there are NO neutrophils with autoimmune and there are neutrophils with H. pylori

12

Describe the structure of H. pylori.

It is a helix-shaped, G- curved rod

13

How does H. pylori colonize the gastric mucosa?

1. H. pylori uses flagella to burrow into the mucus to get close to the epithelial cell layer

mucus is constantly being produced and removed on the luminal side.

2. H. pylori avoids being carried into the lumen via chemotaxis. It senses the pH gradient and swims away from acidic content

3. It produces adhesins to attach to the membrane associated lipids on the epithelial cell surface

4. It produces urease which turns urea into ammonia. It accepts an H+ to become ammonium lower the pH around it to promote survival ***

The survival of H. pylori in the acidic stomach is dependent on urease activity

14

Why is H. pylori toxic to epithelial cells of the stomach destroying the mucosa and causing mucosal cell death?

1. Mucosal damage - mucinase in H. pylori
2. Mucosal cell death - ammonia, cytotoxin A
3. Inflammation - gastric acid, proteases, leukocyte chemotaxis

15

H. pylori-associated chronic gastritis progresses by one of two topographic patterns. What are they?

1. Diffuse antral gastritis
2. multi-focal atrophic gastritis

16

Describe diffuse antral gastritis.
What is the histology?
What disease is it associated with?

H. pylori causes chronic gastritis with activity in the antrum only.
This is associated with peptic ulcers.

17

Describe multifocal atrophic gastritis.
What is the histology?
What disease is associated with it?

H. pylori causes chronic gastritis that involves the body AND antrum.
Histologically there is:
1. glandular atropy
2. replacement of glands by intestinal-type epithelium (intestinal metaplasia)

This is associated with gastric carcinoma and ulcers.

18

What are the 2 non-invasive and 1 invasive test for H. pylori?

1. serological tests for antibodies (s/s 85%)

2. urea breath test (s/s >90%)

3. EGD for biopsy and the tissue is used for Rapid Urease Test (RUT) or histology (>90%)

19

How does RUT work?

It is called the CLOTest.
EGD is used to biopsy. Some tissue is plated on agar.
Urea is added and if it changes to red than that means urease was present (a sign of H. pylori)

20

What is the incidence of H. pylori in the US? Why does the incidence have to be determined indirectly?

It is 0.5% of the susceptible population become infected each year and has been decreasing over time.

It is determined indirectly because acute H. pylori infections invariable pass undetected

21

What is treatment for H. pylori?

Triple therapy:
1. bismuth, metronidazole, tetracyline

or

2. PPI, metronidazole, clarithromycin

Basically you need acid suppressant and antibiotic

22

How do PPIs help treat H. pylori?

They increase gastric pH which can enhance tissue concentration/efficiency of antimicrobials

23

What are the major complications of H. pylori induced chronic gastritis?

1. gastric/duodenal ulcers
2. gastric adenocarcinoma
3. gastric lymphoma (MALT)

MOST remain asymptomatic

24

What is the inheritance pattern of autoimmune chronic gastritis?
What is it characterized by?

AD disorder that is characterized by autoantibodies against:
1. parietal cell H/K ATPase
2. parietal cell intrinsic factor.

25

What are the changes seem over time with autoimmune chronic gastritis?

1. Autoimmune destruction of the parietal cells leads to decreased acid production and hypochorhydria. It also leads to gastrin overproduction.

2. Inadequate IF leads to vit B12 malabsorption and pernicious anemia (megaloblastic)

26

Why is autoimmune chronic gastritis limited to the body and fundus?

Because that is where parietal cells are and the autoantibodies are directed against parietal cells

27

Why is there an increase in gastrin in autoimmune chronic gastritis?

The decrease in HCl influences G cells to produce more gastrin to try to secrete acid into the stomach.
This results in G cell hyperplasia and hypergastrinemia.

28

What is the negative effect of hypergastrinemia on the body?

Gastrin is thought to have an effect on enterochromaffin-like cells (ECL- the cells that secrete histamine) that transforms them into carcinoid tumors.

29

What are the histological changes associated with acute gastritis?

1. superficial neutrophilic infiltrate (above BM not in lamina propria like h. pylori)

2. mucosal edema

3. reactive and regenerating changes to the surface epithelium

30

What is the difference between erosion and ulcer?

Erosion is acute inflammatory injury and necrosis of the superficial epithelium only.

Ulcer is when acute inflammation/necrosis injures deeper layers of the wall (into the submucosa)

31

The pathogenesis of acute gastritis is related to compromised mucosa defenses and increasedHCl/decreased bicarb. What scenarios is acute gastritis frequently associated with?

1. NSAIDs (increased acid)
2. excess alcohol
3. smoking
4. physical stress (trauma, burn, shock, surgery)
5. chemo/radiation
6. bile reflux (from duodenum

32

What are the 3 most common causes of gastric/peptic ulcers?

1. increased pepsin/acid secretion (Zollinger-Ellison)
2. H. pylori
3. NSAIDs

33

Where in the stomach are most gastric ulcers typically found? Where are most duodenal ulcers found?

Gastric- lower curvature of the antrum

Duodenal - first portion of the duodenum

34

What is the morphology of a peptic ulcer?

1. single, sharp "punched out" mucosal defect
2. "clean" base because of peptic digestion of necro-inflammatory debris
3. Flat rim on the periphery
4. chronic gastritis mucosa adjacent to the ulcer

35

How do the borders of peptic ulcers and ulcers associated with gastric cancers differ?

Peptic ulcers have flat rim/periphery

Gastric cancer ulcers have rolled/heaped borders

36

What are the 4 zones of a chronic active ulcer from top to base?

1. fibrinoid necrosis/debris
2. neutrophils/lymphocytes mixed
3. granulation tissue
4. fibrosis/scar

37

What two conditions are key for the development of MOST peptic ulcers?

1. h. pylori infection
2. mucosal exposure to pepsin/acid

38

What determines the type of ulcer that will develop?

The location of the chronic gastritis:

39

What is the mechanism by which duodenal ulcers form?

In people that secrete a lot of acid, H. pylori will colonize in the antrum of the stomach.
Inflammation in the antrum will induce G cells which travel through the blood to the body of the stomach to stimulate parietal cells.
Even more acid is produced.

Chronically, there will be hyperplasia of parietal cells further escalating the situation

40

What is the mechanism by which gastric ulcers form?

They are associated with normal/reduced acid production suggesting a defect in the mucosal protection.

Because there is not that much acid, H. pylori can colonize in the body of the stomach. Chronic inflammation reduces acid secretion even more leading to atropy of the stomach lining--> ulcer? cancer?

41

What is the major cause of PUD in patients who are helicobacter negative?
What are the 2 mechanisms by which is causes ulcers?

NSAIDs
1. direct chemical irritation
2. inhibition of COX1 (which normally produces a prostaglandin that protects the lining of the stomach and control bleeding)

42

What are the 3 risk factors for NSAID-related gastroduodenal toxicity?

1. old age
2. higher doses
3. prolonged use

43

What substance was noted not to cause ulcers, but rather to increase the risk of complications FROM ulcers?

corticosteroids

44

What is used to temporarily relieve pain from peptic ulcers? When does the pain recur?

Food or antacids are used to neutralize stomach acid.
Pain recurs after 1-2 hours because the stomach is still producing acid but the food is no longer there to buffer

45

"Cancers often _________, but _______ rarely cancer-ate".

cancer can cause ulcers, but ulcers very rarely if ever cause cancer.

Still, biopsy ulcers to see if they are a result of cancer

46

What are the 3 major complications of peptic ulcers?

1. GI bleeding (most common)
2. perforation/penetration
3. gastric outlet obstruction

47

Why is there a higher incidence of GI bleeds in the elderly?

Because this group is likely to have increased NSAID use

48

What are the negative sequelae of perforation/penetration associated with peptic ulcers?

Duodenal ulcers can perforate and penetrate into the pancreas causing pancreatitis.

Gastric ulcers can perforate and penetrate into the left lobe of the liver

49

Describe the gastric outlet obstruction that can occur with peptic ulcer disease. What are the signs/symptoms?

1. obstruction due to ulcer related inflammation and edema in peripyloric region {resolves when ulcer heals]
2. obstruction due to fibrosis/scar formation in the peripyloric region [needs balloon dilation/surgery to fix]

Signs: early satiety, ab pain post-prandial, weight loss, nausea

50

How does a stress ulcer differ from a peptic ulcer?

Stress ulcer:
1. develops acutely
2. are multiple
3. more shallow (do not penetrate muscularis propria)
4. heal without fibrosis/scarring

51

What are the 4 major conditions where stress ulcers form?

1. severe trauma (sepsis, shock, surgery)
2. NSAIDs and corticosteroids
3. burns (curling ulcers)
4. CNS trauma (cushing)

52

What are the 3 most common kinds of gastric polyps?
Which has the potential for malignant transformation?

1. hyperplastic gastric
2. fundic gland
3. adenoma (potential for malignant transformation)

53

What is seen histologically with a gastric hyperplastic polyp?

1. foveolar hyperplasia
2. edematous inflamed mucosa

54

What is seen histologically with fundic gland polyps?
What patient are they typically seen in?

dilated gastric glands lined by parietal, chief, and mucus cells

Seen in patients on PPIs

55

What are the 3 major types of gastric tumors? What is the major cause of each?
Which malignancy constitutes *90-95% of gastric carcinomas?

*1. Adenocarcinoma- H. pylori or autoimmune
2. MALT lymphoma - H. pylori
3. Carcinoid- autoimmune (gastrin->ECL)

56

What is the 5YSR for gastric adenocarcinoma?

less than 20%.

It is the 2nd leading cancer death world wide

57

What is the favored location for gastric carcinomas?

Lesser curvature of the antropyloric region (the same as multifocal atrophic gastritis)

58

What are the 2 major types of gastric adenocarcinoma? Describe the incidence of each.

1. intestinal type gastric adenocarcinoma- decreasing trend

2. diffuse infiltrative gastric adenocarcinoma- remains steady

59

From what cells do intestinal type gastric adenocarcinomas arise?

Who is typically affected by this type of gastric adenocarcinoma?

gastric surface mucosa that has undergone intestinal metaplasia (chronic gastritis)
-h. pylori
-autoimmune

affects men >50

60

What are the 5 risk factors for developing intestinal type gastric adenocarcinoma?

1. chronic gastritis with intestinal metaplasia
2. h. pylori
3. diet high in nitrites
4. partial gastrectomy
5. pernicious anemia (a sign of autoimmune chronic gastritis)

61

From what cells do diffuse infiltrative gastric adenocarcinomas arise?

They arise de novo from gastric mucus cells causing small glands of polyhedral cells with round tame nuclei

62

What do you see microscopically for diffuse infiltrative gastric adenocarcinoma?

1. glands of small polyhedral cells with tame nucleus
2. signet-ring phenotype which leads to
- linitis plastica (leather bottle stomach)

63

A patient presents with diffuse gastric adenocarcinoma that has metastasized to the ovaries. What is this called?

Krukenberg tumor

64

A patient presents with diffuse gastric adenocarcinoma that has metastasized to the peri-umbilical lymphatics. What is this called?

Sister Mary Joseph nodule

65

What are the risk factors for diffuse infiltrative gastric adenocarcinoma?

Largely undefined
- mutation in E cadherin

NO H PYLORI OR CHRONIC GASTRITIS

66

What are the 3 different gross appearances for gastric cancers?

1. exophytic- polyploid adenoma
2. flat- associated with diffuse gastric adenocarcinoma
2. excavated - mimics peptic ulcer but with "heaped up sides"

67

What is linitis plastica?

Extreme form of flat or excavated advanced gastric adenocarcinoma that makes the stomach non-distendible