Category Archives: Stomach
Gastric Juvenile Polyp
Juvenile Polyp
Clinical presentation:
- increased risk of colorectal and gastric carcinoma
Gross appearance:
- smooth-surfaced, 1-2 cm, short narrow stalk
Histology:
- irregular cysts in lamina propria with normal foveolar epithelium
Fundic Gland Polyp
Fundic Gland Polyp
Gross appearance and location:
- multiple sessile polyps
- fundus or body of stomach
Histology:
- mixture of mucous and specialized glands
- associated with familial adenomatous polyposis syndrome (FAP) if numerous
Genetics:
sporadic: β-catenin mutations
FAP: APC mutations
Stomach Hyperplastic Polyp
Stomach Hyperplastic Polyp
Histology:
- dilated, tortuous foveolar lined glands
- inflammatory cells and increased regenerative atypia in epithelium
- surface maturation is usually present
Zollinger Ellison Syndrome
Zollinger Ellison Syndrome
Gastrinoma
Pathophysiology:
- gastrin-secreting endocrine tumor in pancreas (gastrinoma) or in ectopic gastric tissue (duodenum or Meckel’s diverticulum)
- causes hypergastrinemia and an increase in serum gastrin
- 20% associated with MEN-1, 80% sporadic
Gross Appearance and Location:
- fundus and body (where parietal cells are)
- massive rugal folds
Histology:
- increase in parietal cells and hypertrophy of the fundus and body of the stomach
- enterochromaffin-like cell linear hyperplasia in body of stomach
Immunohistochemistry:
- gastrinoma is chromogranin, synaptophysin and gastrin positive
Autoimmune Gastritis
Autoimmune Gastritis
Clinical:
- older, white women, Helicobacter pylori negative, associated with pernicious anemia
Pathophysiology:
- autoimmune disease with an antibody directed at parietal cells, intrinsic factor
- results in decreased acid production
- causes G cell hyperplasia in the antrum of the stomach
- leads to ECL cell linear hyperplasia in the fundus of the stomach
Gross appearance and location:
- fundus and body of the stomach
- thinning and loss of rugal folds
Histology:
- decreased parietal, chief cells in fundus, body of stomach
- linear and nodular hyperplasia of G endocrine cells (antrum)
- ECL cell linear hyperplasia (body)
Laboratory findings:
- increased serum gastrin, intrinsic factor antibody, decrease in parietal cells, decrease in vitamin B12 n
Autoimmune gastritis is a risk factor for:
- increased risk of stomach adenocarinoma, carcinoid tumours, peptic ulcer disease
Hemorrhagic Gastritis
Hemorrhagic Gastritis
Also known as Acute Erosive Gastritis
Causes:
Aspirin, non steroidal anti-inflammatory drugs (NSAIDs), ASA, steroids, iron pills, crack cocaine, radiation, chemotherapy, hypoperfusion, Cushing ulcer (from head injury, severe burns)
Gross appearance:
- pinpoint hemorrhages
Histology:
- sloughing epithelium, necrotic debris, hemorrhage, reactive epithelium
Stomach Histology
Stomach
Histology and Physiology
Fundus, body
- specialized glands containing chief and parietal cells
- pit:gland ratio = 3:1
Antrum, cardia
- mucous glands
- pit:gand = 1:1
Stomach Cells
- parietal cells appear pale eosinophilic, located more proximal in the neck
- chief cells located more in the base of the pits
- mucus neck cells
- endocrine cells
- foveolar cells
- APUD cells
- endocrine {G cells secrete gastrin, EnterChromaffin cells secrete serotonin, D cells secrete somatostatin} antrum and EnterChromaffin-like cells (fundus secrete histamine),
Immunohistochemistry:
- stomach: MUC1, MUC5AC, MUC6, PAS
- intestine: MUC2, Alcian blue pH=2.5
Helicobacter Pylori Gastritis
Helicobacter Pylori Gastritis
- gram negative curvilinear organism
Factors that increase virulence:
Invasive factors:
- vacA – vacuolating cytotoxin and cagA genes
- lipopolysaccharide (endotoxin)
- adhesion
- urease → converts urea into NH3 (buffers the gastric acid)
Protective factors:
- mucous production
- HCO3- bicarbonate secretion into mucous
- mucosal blood flow
- prostaglandin production
- regenerative capacity of epithelium
Gross appearance and location of Helicobacter Pylori
- stomach antrum and body
- Helicobacter pylori infection causes the stomach to appear red (erythema), granular, erosions OR normal!
Helicobacter Pylori Infection Histology
Chronic active gastritis with:
- lymphocytes, plasma cells and neutrophils in pits, abscesses
- lymphoid aggregates
- organisms present in lumen, often in mucous
Chronic atrophic gastritis with:
- gland atrophy
- intestinal metaplasia
- lymphoplasmacytic infiltrate
Ulcer:
- fibrinous exudate
- neutrophils
- granulation tissue
- fibrosis
Gross appearance:
- flat edge (not rolled, not friable = malignant), punched out appearance
- usually lesser curvature at antral-body region
- occur anywhere bathed in gastric acid
duodenal more common than gastric regions
Special stains
- Giemsa
Immunohistochemistry
- antibody for Helicobacter pylori
Helicobacter pylori infection increases the risk for:
- adenocarcinoma, MALToma, peptic ulcer disease



