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.
How can you differentiate MALT lymphoma from regular old MALT?
Only in lymphoma will you have lymphoepithelial lesions, which are collections of lymphocytes that appear to be eating glands.
MALT lymphoma cells also have a characteristic morphology.
MALT lymphoma
MALT lymphoma is a marginal zone-type lymphoma with monocytoid appearance (fried-egg-like cells, small round nuclei with a halo of clear cytoplasm).
Lymphoepithelial lesions are present (inset). Here the glands look like little more than islands of pink cytoplasm.
You can confirm with immunostains: CD20+ CD43+. T cells will also stain CD43+, so you should subtract them out with a CD3 stain. Usually most cells will be either CD20+CD43+ or CD3+CD43+, as most lymphocytes in chronic gastritis are T cells.
MALT lymphoma immunophenotype
CD20+CD43+
CD3-
Chronic gastritis immunophenotype
CD3+CD43+
CD20-
Gastric amyloidosis
Note the abundance of pink, amorphous material in the lamina propria. Give it the good-old Congo red stain to confirm.
A potential cause of gastroparesis in a patient with the right risk factors.
Fundic gland polyp
Most common type of polyp found on upper endoscopy.
These polyps look like oxyntic mucosa, but with occasional cystically dilated glands (circled). They are common in older individuals.
They are associated with chronic PPI use. Also, multiple fundic polyps may occur in a young individual with FAP. There is thought to be a connection to superphysiologic levels of gastrin, which can act as a hyperplastic and hypertrophic factor for parietal cells in oxyntic glands.
Hyperplastic gastric polyp
Characterized by elongated or cystic foveolar pits with mild inflammation. Usually associated with background gastritis and may have intestinal metaplasia.
Glands reminiscent of chemical gastritis with an elongated corkscrew appearance may be seen.
Foveolar-type gastric adenoma
By definition, gastric adenomas have at least low-grade dysplasia (like an intestinal tubular adenoma).
Note the foveolar-like epithelium
Intestina-type gastric adenoma
By definition, gastric adenomas have at least low-grade dysplasia (like an intestinal tubular adenoma).
Note the presence of goblet cells.
Intestinal-type gastric adenocarcinoma
Note its morphological similarity to colon cancer, hence the name. Often found in association with gastric atrophy and intestinal metaplasia.
Diffuse-type gastric adenocarcinoma
May creep through the entire stomach and cause linitus plastica (rigid, non-distendable stomach).
Often has a signet-ring cell morphology. These cells can look like foamy macrophages and hide on low-power. For this reason every stomach biopsy should get a once-over on high power. When they are there, the more you look the more you will see.
Gastrointestinal stromal tumor (GIST)
There is just way too much stroma here. On high power you might see multiple mitotic figures or cytoplasmic/paranuclear vacuoles.
This tumor arises from the interstitial cells of Cajal. They are driven by c-Kit (CD117) and also stain for DOG1. Their malignant potential is assessed by size, location, and mitotic rate.
DDx includes schwannoma (S100+), leiomyoma (smooth muscle markers), and heterotopic pancreas (pancreas tissue that just got lost).
Normal duodenal histology
Brunner glands
Normal mucous glands of the muscularis mucosa in the duodenum
Stain bright in PAS/AB
Only appear in the duodenum. They disappear in the transition to the jejunum.
Rules of a healthy duodenum
- The villi should be 3x as tall as the crypts are deep
- There should not be any collections of lymphocytes within villi
- There should be no neutrophils in the epithelium
Chronic peptic duodenitis
Note the foveolar metaplastic change at the tips of the villi (arrow). There is increased chronic inflammation in the lamina propria and Brunner gland hyperplasia (arrowhead). Sometimes neutrophils may also be seen in the epithelium.
Be wary of gastric heterotopia – misplaced nodule of totally normal gastric tissue within the duodenal wall.
Rule of thumb for Celiac’s disease
The earliest change in Celiac’s disease is prominent intraepithelial lymphocytes (IELs), long before there is villous blunting:
Over 40 IELs / 100 enterocytes (roughly 1 villus-worth) is considered diagnostic of a malabsorptive pattern.
However, whether this malabsorption is due to Celiac’s disease will require supportive serology and/or clinical picture.
Duodenal giardiasis
You can see them if you squint! Those aren’t shed epithelial cells. Zoom in to high power to confirm.
Strongyloides
There are tiny worm bodies visible within the duodenal crypts.
Duodenal tubular adenoma
As in the colon, characterized by low-grade dysplasia with crowded and elongate nuclei and loss of mucinous differentiation.
Duodenal carcinoid tumor (aka well-differentiated neuroendocrine tumor)
G cells
Appear as haloed neuroendocrine cells within pyloric glands
Small intestinal bacterial overgrowth on histology
Has a comparable pattern to Celiac’s disease with villous blunting and intraepithelial lymphocytes.
