Molavi Chapter 7 - Stomach and Duodenum Flashcards
Two types of gastric mucosa
Antral (mucinous or protective, shown in B). Thinner muucosa with mucinous glands and overlying foveolar epithelium.
Oxyntic (secretory). Thick mucosa with secretory cells including the parietal and chief cells and an overlying foveolar epithelium.
Transitional mucosa is where the two overlap and features are mixed.
Foveolar epithelium
Lining of the stomach
Stains bright pink with PAS/AB
Cells within an oxyntic gland
Cells within a pyloric gland
Intestinal metaplasia
When the epithelium is lined with occasional goblet cells.
Marker of chronic irritation in the stomach.
Note that the goblet cells should be interspersed. You will probably never see just back-to-back goblet cells on the stomach epithelium.
Active vs Inactive gatsritis
Neutrophils in the stomach epithelium indicate “active” inflammation (by convention “active” instead of “acute” in the stomach)
If you have only mononuclear cells, you have “inactive” chronic gastritis
If you have both, you have “active chronic” gastritis
Active chronic gastritis and lymphoid follicles in the gastric mucosa typically indicate ___
Active chronic gastritis and lymphoid follicles in the gastric mucosa typically indicate H. pylori infection
Active or inactive chronic gastritis with a granuloma
Crohn’s disease is most likely
Chemical gastritis in the antrum
Note the foveolar hyperplasia with a corkscrew-papillary appearance, low-power blue appearance, and prominent thin strands of smooth muscle between glands.
May be caused by bile reflux or pill-induced chemical irritation.
Autoimmune gastritis with gastric atrophy
Atrophy is indicated by intestinal metaplasia and inflammation.
There is replacement of secretory glands by mucinous, antral-type glands (2).
Some residual oxyntic cells are visible (3).
Gastric atrophy and what causes it
Gastric atrophy is loss of glands in the stomach, in any region.
True atrophy will have intestinal metaplasia and inflammation.
Two principal causes are H. pylori and autoimmune metaplastric atrophic gastritis (which may progress to pernicious anemia).
Disease course of autoimmune metaplastic atrophic gastritis
- Autoimmune response against parietal cells in the gastric body
- Progression to gastric atrophy
- Loss of intrinsic factor due to parietal cell destruction (pernicious anemia)
- Compensastory antral gastrin-cell response with hypergastrinemia
- ECL cell hyperplasia which may progress to microcarcinoids or tumorlets
- “Antralized” atrophic oxyntic mucosa due to replacement of oxyntic glands.
Presence of lymphoid follicles in the gastric mucosa in the setting of gastric atrophy suggests. . .
. . . H. pylori, NOT autoimmune metaplastric atrophic gastritis
In the setting of chronic autoimmune gastritis with “antralized” atrophic oxyntic mucosa and true antral mucosa, how can you tell if you biopsied the right site?
Only the true antrum will have G-cells.
So, a gastrin stain can differentiate “antralized” from “antral” mucosa.
DLBCL of the stomach
Truly “sheets” of large B cells.