SFP: stomach Flashcards
What is the GE junction?
Area between the esophagus and start of the stomach where there is a transition from stratified squamous epithelium to gastric epithelium.
Compare gastric pits/glands in the pyloric and cardiac mucosa to those in the antrum.
The pits are shorter in the antrum and the glands are more mucinous.
What are oxyntic glands?
Glands in the fundus of the stomach that are lined by cells like parietal cells and chief cells. They also contain D cells and ECFL cells.
Describe antral glands.
Glands in the antrum of the stomach that notably contain G cells. They also contain D cells and ECFL cells.
What is acute gastritis?
Short term inflammation of the stomach. Can be related to stress, infections, irritation, etc.
Describe gross pathology of acute gastritis.
Hemorrhagic mucosa, gastric erosions.
Describe the histology of acute gastritis.
Lots of neutrophils present.
What are clinical features of acute gastritis?
Pain, nausea, vomiting, blood loss, potentially asymptomatic.
Compare erosion and ulceration.
Erosion is a break in surface epithelium that does not go past the MM, and ulceration enters the submucosa.
What is reactive gastropathy and its histologic features?
A type of gastritis with minimal inflammation.
What are histologic features of reactive gastropathy?
No neutrophilic infiltrate, basophilic stain due to a loss of mucin, corkscrew glandular structure.
What is the major cause of chronic gastritis?
H pylori.
What are the 4 virulence features of H pylori?
Adhesins, urease, flagella, toxins.
What are histologic features of H pylori chronic gastritis?
Lymphocytes, plasma cells, neutrophils, lymphoid aggregates with germinal centers.
How do we treat H pylori chronic gastritis?
Antibiotics and PPIs.
What is an outcome of chronic gastritis?
Intestinal metaplasia; glandular structures will transform to an intestine-like mucosa. This can later lead to gastric adenocarcinoma.
What is chronic atrophic gastritis?
An autoimmune gastritis where antibodies attack parietal cells in the stomach. This leads to lost acidity, lowered IF/B12 absorption, and pernicious anemia.
What will fundic mucosa resemble in atrophic gastritis?
Antral mucosa due to loss of parietal cells.
What causes peptic ulcers?
Damage to the epithelium via things like NSAIDs, H pylori gastritis, areas exposed to acid secretion.
What are clinical manifestations of peptic ulcers?
Epigastric burning, aching pain, bleeding, anemia.
When does pain begin in a patient with a gastric ulcer?
Right after eating.
When does pain begin in a patient with a duodenal ulcer?
2-3 hours after eating; it may also be relieved right after eating.
What is seen histologically with peptic ulcers?
Granulation tissue, fibrin, neutrophils, large vessel at the base of the ulcer, necroinflammatory debris.
What are clinical consequences of peptic ulcers?
Bleeding, perforation, obstruction, intestinal metaplasia that can lead to dysplasia/carcinoma.
Compare surrounding epithelium in benign vs malignant ulcers.
In benign ulcers surrounding epithelium will have radiating folds (kind of looks like sun rays), whereas it will be nodular and irregular in malignant ulcers.
What is Zollinger-ellison syndrome?
Neuroendocrine tumors producing gastrin; they can lead to multiple peptic ulcers in unusual locations.
What are histologic features of Zollinger-Ellison syndrome?
Hypertrophy of parietal cells and increased acid production, elongated and dilated glands, hyperplasia of gastric pits.
What are gastric polyps?
Protruding mass that may be benign or precursors/dysplastic.
What are hyperplastic (benign) polyps associated with?
Chronic gastritis.
What are clinical features of hyperplastic polyps?
Pain, bleeding/anemia, may be asymptomatic.
What is seen histologically with hyperplastic polyps?
Hyperplasia of gastric pits and mild chronic inflammation.
What causes fundic gland polyps?
PPI use.
What is the pathogenesis of fundic gland polyps?
Increased gastrin production.
What is seen histologically in fundic gland polyps?
Dilated and irregular glands lined by flattened chief/parietal cells.
What are adenomas of the stomach?
Lesions with risk for adenocarcinoma transformation that are caused by chronic gastritis and intestinal metaplasia.
What is a common mutation seen in diffuse gastric cancer?
CDH1 mutation.
What are the different variations of early gastric cancer morphology?
- Protruded 2. Superficial 3. Excavated.
What are the different varieties of advanced gastric cancer morphology?
- Polypoid 2. Excavating 3. Ulcerating 4. Infiltrating.
What is linitis plastica?
An infiltrating type of gastric cancer that involves a thickening of the mucosa wall of the stomach due to signaling cells infiltrating the wall.
What is intestinal type gastric cancer?
Formation of malignant glands infiltrating the stroma.
What is signet ring type gastric cancer?
A poorly differentiated cancer with diffuse thickening of the stomach wall containing cells filled with mucin.
What is MALT lymphoma?
The lymphoma of the stomach often seen in the US that may be associated with H pylori; treating the H pylori will reduce the tumor.
Describe histology of MALT lymphoma.
Diffuse infiltrate with lymphoepithelial lesions attacking the glandular structure.
What is carcinoid syndrome?
Syndrome associated with neuroendocrine tumors that may cause serotonin secretion. This can lead to diarrhea, skin rashes/flushing, cyanosis, bronchospasm, etc.
What is the histology of carcinoid tumors?
Salt and pepper chromatin within the nuclei.
Describe GIST (gastrointestinal stroma) tumors.
They are the most commonly in the stomach, but may be anywhere in the submucosa/wall of the GI tract.
GIST tumors originate from…
Cells of cajal.
What mutation is associated with GIST tumors?
c-KIT gene or PDGFRA.
What are diagnostic markers of GIST?
CD117 or DOG1.
How do we treat GIST tumors?
Tyrosine kinase inhibitors.
Describe histology of GIST tumors.
Spindle cell/epithelioid lesions.
