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

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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

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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

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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

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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

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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

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Pyloric Metaplasia

Pyloric Metaplasia

- pyloric glands get replacement of fundic specialized glands by mucous glands

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Intestinal Metaplasia

Intestinal Metaplasia

- intestinal metaplasia occurs when the gastric glands and cells become replaced by Paneth cells, brush border cells and importantly goblet cells

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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

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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

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