Chapter 15: Stomach

Question 1

The stomach is divided into four major anatomic regions: the cardia, fundus, body and antrum. In these regions there are foveolar cells, G cells, parietal cells and chief cells. What do these cells produce?

Answer 1

Foveolar cells secrete mucus

G cells secrete gastrin

Parietal cells secrete acid (upon gastrin stimulation).

Chief cells produce and secrete digestive enzymes such as pepsin.

Question 2

The stomach is divided into four major anatomic regions: the cardia, fundus, body and antrum. In these regions there are foveolar cells, G cells, parietal cells and chief cells. What cells reside in the different regions of the stomach?

Answer 2

Foveolar cells -> in cardia and antral glands.

G cells -> in antral glands

Parietal cells -> in the fundus and body

Chief cells -> glands of the body and fundus

Question 3

When do we refer gastritis to acute gastritis and when do we refer gastritis to gastropathy?

Answer 3

When neutrophils are present, the lesions is reffered to as acute gastritis. When cell injury and regeneration are present but inflammatory cells are absent, the term gastropathy is applied.

Question 4

What are agents that cause gastropathy?

Answer 4

Nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, bile, stress-induced injury and H. pylori.

Question 5

What is the most common cause of chronic gastritis and what is a less common cause?

Answer 5

Infection with tha bacillus Helicobacter pylori. A less common cause would be auto-immune gastritis.

Question 6

How does H. pylori infection usually present?

Answer 6

As an antral gastritis with increased acid production which may give rise to peptic ulcers in the duodenum or stomach.

Question 7

Which four features are linked to H. pylori virulence?

Answer 7

• Flagella (bacteria are motile in viscous mucus)
• Urease, generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach.
• Adhesions, which enhance bacterial adherence to surface foveolar cells
• Toxins, that may be involved in ulcer or cancer development.

Question 8

What can be seen in histologic pictures of a H. pylori infection in the stomach?

Answer 8

Neutrophils are prominent in intraepithelial and lamina propria. Lymphoid aggregates are present and there’s also intestinal metaplsia.

Question 9

What are characteristics of autoimmune gastritis?

Answer 9

• Antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions.
• Reduced serum pepsinogen I levels
• Antral endocrine cell hyperplasia
• Vitamin B12 deficiency leading to pernicious anemia and neurologic changes.
• Impaired gastric acid secretion

Question 10

Describe autoimmune gastritis in short.

Answer 10

This type of gastritis is associated with immune-mediated loss of parietal cells and subsequent reductions in acid and intrinsic factor secretion.

Question 11

What are morphological characterisations of autoimune gastritis?

Answer 11

Diffuse damage of the oxyntic (acid-producing) mucosa. Here, the oxyntic mucosa of the body and fundus are thinned and rugal folds are lost.

Question 12

What are morphological characterisations of H. pylori gastritis?

Answer 12

Inflammatory reaction is deep and centered on the gastric glands. Parietal and chief cell loss can be extensive, and intestinal metaplasia may develop.

Question 13

What are three complications of chronic gastritis?

Answer 13

Peptic ulcer disease, mucosal atrophy and intestinal metaplasia and dyplasia.

Question 14

With what is peptic ulcer disease most often associated?

Answer 14

H. pylori infection or NSAID use.

Question 15

Just read

Answer 15

Gastric acid is fundamental to the pathogenesis of Peptid Ulcer Disease (PUD). Hyperacidity may be caused by H. pylori infection, parietal cell hyperplasia, and excessive secretory responses. Insufficient inhibition of stimulatory mechanisms such as gastrin release may also contribute.

Question 16

The classic peptic ulcer is a…

Answer 16

round to oval, sharply punched-out defect

Question 17

What is a complication of a peptic ulcer?

Answer 17

Perforation

Question 18

Long-standing chronic gastritis may be associated with…

Answer 18

intestinal metaplasia, recognized by the presence of goblet cells.

Question 19

With what increased risk is intestinal metaplasia associated with?

Answer 19

Gastric adenocarcinoma

Question 20

How does dysplasia occur in chronic gastritis?

Answer 20

Gastritis exposes epithelium to inflammation-related free radical damage and proliferative stimuli. This can lead to accumulation of genetic alterations, which eventually leads to carcinoma. Before this, preinvasive in situ lesions can be recognized histologically as dysplasia.

Question 21

What are polyps?

Answer 21

Nodules/masses that project above the level of the surrounding mucosa.

Question 22

Polyps occur as a result of…

Answer 22

epithelial or stromal cell hyperplasia, inflammation, ectopia or neoplasia.

Question 23

There are different types of polyps, just know that in the book only the following types of polyps are discussed.

Answer 23

• Inflammatory and Hyperplastic polyps
• Fundic gland polyps (sporadic)
• Gastric adenoma

Question 24

What are early symptoms of gastric adenocarcinoma?

Answer 24

Dyspepsia, dysphagia and nausea. Therefore the cancer is usually diagnosed at advanced stages when clinical manifestations such as weight loss, anorexia, altered bowel habits, anemia, and hemorrhage trigger diagnostic evaluation.

Question 25

The majority of gastric cancers are not hereditary, but mutations in familial gastric cancer identified important insights. Which gene is usually mutated?

Answer 25

CDH1, which encodes E-cadherin. It doesn’t need to be mutated, it can also be gene-silencing through methylation of CDH1 promotor. Thus a change (and loss) the E-cadherin function.

Question 26

What is the Lauren classification?

Answer 26

Gastric cancers are seperated into intestinal and diffuse types that correlate with distinct patterns of molecular alterations.

Question 27

What are characterisations of the intestinal type of a gastric adenocarcinoma?

Answer 27

Intestinal type cancers tend to be bulky and have a precize location in the stomach and are composed of glandular structures that invade the deeper layers.

Question 28

Why is the intestinal type of gastric adenocarcinoma called intestinal type?

Answer 28

Because the intestinal metaplasia is a precursor lesion of this type of adenocarcinoma.

Question 29

What are characterisations of the diffuse type of a gastric adenocarcinoma?

Answer 29

There’s no localized tumor, macroscopically your can hardly recognize it. Only the bowel wall has visibly thickened. The lesions have spread everywhere and these cancercells don’t grow into tubular structures but cells grow seperately. The cells have large mucin vacuoles that expand the cytoplasm and push the nucleus to the periphery, creatin a signet ring cell (displayed in picture).

Question 30

What are the best prognostic indicators for gastric cancer?

Answer 30

The depth of invasion and the extent of nodal and distant metastasis at the time of diagnosis

Question 31

Where do extranodal lymphomas commonly arise?

Answer 31

In gastrointestinal tract, particularly the stomach.

Question 32

From what do neuroendocrine tumors (or carcinoid tumors) arise from?

Answer 32

From neuroendocrine organs and neuroendocrine-differentiated gastrointestnial epithelia.

Question 33

What kind of tumor is the gastrointestinal stromal tumor (GIST)?

Answer 33

A mesenchymal tumor of the abdomen, half of these occur in the stomach.

Question 34

What is the most common genetic change underlying the pathogenesis of gastrointestinal stromal tumors (GISTs)?

Answer 34

A gain-of-function mutation of the gene encoding the tyrosine kinase KIT, the receptor for stem cell factor.

Question 35

What are morphological characterisations of gastrointestinal stromal tumors (GISTs)?

Answer 35

Primary tumors form a solitary, well-circumscribed, fleshy, submucosal mass. Metastases may form multiple small serosal nodules or fewer large nodules in the liver.

Question 36

From normal mucosa to chronic gastritis to intestinal metaplasia to dysplasia and finally to gastric adenocarcinoma. What two things increase as a gastric adenocarcinoma develops?

Answer 36

Morphological and genomic changes.