SFP: stomach Flashcards
(51 cards)
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.