Stomach Flashcards
Pancreatic acinar metaplasia in the stomach suggests. . .
A history of autoimmune gastritis.
This type of metaplasia is present in 50% of autoimmune gastritis, but is rare in other forms of gastritis.
Phlegmonous gastritis
Basically necrotizing fasciitis of the stomach. Seen in immunocompromised/diabetic patients.
What’s worse than H. pylori?
Sarcina ventriculi
This organism has been associated with phlegmonous and emphysematous gastritis. It usually colonizes in the setting of delayed gastric emptying, which may be neuropathic or obstructive in etiology.
Pseudopyloric metaplasia
This is when the oxyntic mucosa resembles the antral mucosa, with a paucity of parietal and chief cells.
However, there will be no true G cells, and staining for gastrin will be stone cold negative.
Instead, you may see hypertrophy of other neuroendocrine cells due to hypergastrinemia from the true antrum (appreciated better with chromogranin stain). This may be associated with the development of indolent neuroendocrine tumors in the stomach.
Changes in the histology of the body/fundus and antrum in autoimmune gastritis
Body/Fundus:
* Loss of parietal cells
* Intestinal metaplasia
* Pseudopyloric metaplasia
* Pancreatic acinar cell metaplasia
Antrum:
* Essentially normal histologic appearance
* G cells present on gastrin stain
* Normal number of cells on chromogranin stain
How do you distinguish IPEX-type autoimmune gastritis from typical autoimmune gastritis?
- Involvement of the antrum
- Absence of ECL cell hyperplasia
- Concurrent autoimmune enteritis
- Multiple serum autoantibodies (anti-parietal cell, anti-intrinsic factor)
Dieulafoy lesion on histology
This is a cause of UGI bleed! Don’t forget to include this in your ddx when assessing endoscopy specimens from a UGIB case.
Check the endoscopy report, because in some cases a protruding vessel will even be seen grossly.
Also, check the histology for amyloid! Amyloid deposition may thicken the wall of a tortuous gastric artery and cause it to burst through into the gastric lumen, ultimately precipitating a Dieulafoy lesion.
Hyperplastic gastric polyp
Characterized by elongated and architecturally distorted, irregular foveolar epithelium with cystic dilatations, often with smooth muscle strands extending from muscularis mucosa towards surface.
85% occur in the presence of chronic gastritis (H. pylori and non-H. pylori).
If multiple are seen, you must consider Peutz-Jegher syndrome.
Gastritis cystica polyposa
Uncommon - typically occurs in gastroenterostomy stomas.
Essentially, it is a form of mucosal prolapse. 1-3 cm polyps form a circular ring or fullness surrounding the stoma. Enlarged pits with serration, hyperplasia, and cystic dilation of pyloric glands which have herniation into the submucosa. Disorganized strands of muscularis mucosae may be seen in irregular bundles.
Lymphocytic gastritis
Lymphocytosis of the foveolar and surface epithelium. Usually greater in the antrum than in the body.
May be found in association with celiac, H. pylori, and varioliform gastritis.
Collagenous gastritis
Pattern of injury with prominent subepithelial collagen, intraepithelial lymphocytosis, and surface epithelial damage with flattening and detachment.
Associated with Celiac’s disease and collagenous sprue, lymphocytic and collagenous colitis, lymphocytic gastritis, and other adult autoimmune disease.
Two clues to Crohn’s gastritis
- Granulomas (obviously)
- “Focally enhanced gastritis” – this refers to small foci of intense inflammation separated by normal mucosa (rather than a diffuse process).
DDx for granulomatous gastritis
- Obviously, Crohn’s disease. Roughly ~50% of cases.
- Sarcoidosis
- Vasculitis
- Infection
Generally, all of these will require clinical correlation – you can’t diagnose any of them on gastric biopsy alone.
