Stomach Flashcards
Cells of the stomach
Fundus and body contain GASTRIC GLANDS which contain two cell types
PARIETAL –> secrete ACID, Intrinsic factor
CHIEF –> secrete PEPSIN and other
digestive enzymes
Antrum contains G CELLS which secrete GASTRIN and mucous cells
The stomach is lined by COLUMNAR EPITHELIUM! Remember that the esophagus is SQUAMOUS
Layers
Mucosa (inner) –> includes surface mucous cells that protect the lining of the stomach; also contains deep gastric glands that start there and dive deep past the mucosa
Submucosa
Muscularis
Serosa (outer)
These are the same layers as the esophagus
How does the stomach normally protect itself against the super acidic environment?
Surface mucous secretion Bicarb secretionMucosal blood flow Apical sufrace membrane transport Epithelial regenerative capacity Elaboration of prostaglandins
Acute Gastritis
Transient inflammatory process that disrupts the protective mechanisms
Causes –> H PYLORI, CMV, Candida, Drugs (NSAIDs, Alcohol), GASTRIC REFLUX
Gastric glands infiltrated by neutrophils to create a glandular abscess
Edema, hyperemia, increased mucous, erosions, hemorrhage
Epigastric pain, N/V
Fully corrected once infection resolves
Chronic Gastritis
Not always related to acute
LESS SEVERE, but more PERSISTENT SYMPTOMS (N/V, upper abdominal discomfort)
Can occur with acute lasting too long, but is MORE OFTEN ASSOCIATED WITH H. PYLORI –> this is the MOST COMMON CAUSE
Mucosa is infiltrated with chronic inflammatory cells, while the surface epithelium has less mucous, atrophy of glands, and eventual metaplasia to cells similar to those of the INTESTINAL mucosa
Lymphoid aggregates possible
Possible for acute AND chronic to present together –> stain with WARTHIN-STARRY SILVER stain to detect spiral shaped H. Pylori
Progression of H. Pylori
Usually presents in the ANTRUM (get biopsy here)
2 possible directions: Antral predominant gastritis that can progress to a duodenal ulcer and essentially stays in the antrum
OR
Pangastritis –> spreading to the gastric body, fundus –> multifocal gastritis with atrophy –> intestinal metaplasia –> INCREASED RISK OF GASTRIC ADENOCARCINOMA
Autoimmune Gastritis
Inflammatory condition associated with AUTOANTIBODIES TO PARIETAL CELLS OF THE FUNDUS/BODY which can result in PERNICIOUS ANEMIA (loss of intrinsic factor = loss of B12 absorption = pernicious anemia) and CARCINOID TUMORS
Normally, G cells produce GASTRIN (in antrum) which stimulates production of HISTAMINE in enterochromaffin cells which activates parietal cells to produce ACID
At high concentrations of Acid, D CELLS will activate in antrum, producing SOMATOSTATIN which INHIBITS G Cells and lowers GASTRIN/ACID
In Autoimmune Gastritis –> autoantibodies DESTROY parietal cells –> no acid build up –> no negative feedback –> results in Gastrin constantly stimulating the enterochromaffin cells –> these then PROLIFERATE and cause DYSPLASIA and potentially a CARCINOID TUMOR!
Commonly associated with intestinal metaplasia – want to diagnose early to prevent malignant transformation!
Ulcer vs. Erosion
Ulcer = destruction of the FULL THICKNESS of the mucosa
Erosion = Partial loss of mucosa that can potentially progress to an ulcer or just heal
Peptic Ulcers
Involve the focal destruction of the mucous membrane and the underlying tissues by gastric secretions
Causes –> HYPERACIDITY –> Gastrin, histamine, ACh, vagus all play roles;—> DECREASED MUCOSAL PRODUCTION; MOTILITY
Risk factors –> H PYLORI, NSAIDs, trauma, cerebral lesions, tobacco, hormones, gastrin producing tumors, genetics
Gross - sharply defined, clear cut edges, neither raised nor rolled
Histo - Chronic peptic ulcer has 4 layers: Fibrinopurulent exudate on the surface, coagulative necrosis, granulation tissue, scar tissue replacing muscle
Can heal, but repeated ulcers possible/likely
Complications include PERFORATION, HEMORRHAGE, OBSTRUCTION
Treatment –> Drugs that neutralize acid secretion, antibiotics to eliminate H Pylori
Precancerous Gastric Lesions
Adenomas - much less common than they are in the colon; present as polyps
Pernicious anemia - associated with increased dysplasia
Menetrier Disease – giant rugal hypertrophy; increased mucous glands and thickened gastric folds
Gastric peptic ulcer
H. Pylori
Atrophic gastritis and intestinal metaplasia
Epithelial Dysplasia
Gastric Adenocarcinoma
MOST COMMON malignancy of the stomach
Most common cause of cancer deaths worldwide – comprises 2.5% of cancer deaths in the US
Types:
intestinal-type adenocarcinoma – polyploid, elevated, well-demarcated ulcerative mass
Diffuse Type Adenocarcinoma – thickened gastric wall that is much harder; associated with linitis plastic –> extensive fibrosis without a localized mass (leathery)
Prognosis of Gastric Adenocarcinomas
Correlates with DEPTH OF PENETRATION into the submucosa/muscle
Presence of lymph node involvement and distant metastasis possible
Overall 5-year survival = 27%
GI Stromal Tumors
Most common MESENCHYMAL TUMORS of the abdomen –> > 50% occur in stomach
Common mutations associated –> tyrosine kinase c KIT –> receptor for stem cell factor, can be stained for when diagnosing
FLESHY, WHITE TUMOR MASS in the intact mucosa and muscular wall that projects into the lumen as a SESSILE MASS (immobile)
Usually covered by ULCERATED or INTACT mucosa
Can have ATROPHY, ULCERATION, BLEEDING
Made of fascicles of spindle-shaped tumor cells
Overall less aggressive than carcinoma
NEUROENDOCRINE Tumors
Gastric carcinoid tumors
Associated with endocrine cell hyperplasia, chronic atrophic gastritis, Zollinger-Ellison syndrome
Well-differentiated neuroendocrine carcinomas that can metastasize
Present as an elevated tumor within the normal gastric mucosa, composed of tumor cells in a tubular or nest pattern
Coarse and fine chromatin patterns, salt and pepper
LYMPHOMAS of the stomach
GI tract is the MAIN EXTRANODAL SITE of primary malignant lymphomas with marginal B cell lymphomas (MALTomas) most common, followed by DIFFUSE LARGE B CELL LYMPHOMAS
5% of all gastric malignancies are primary lymphomas
MALTomas –> present with diffuse nodules along the gastric wall, with a dense infiltrate of lymphocytes and reactive follicle formation
Infiltration of cells DISRUPTS the gastric glands and creates LYMPHOEPITHELIAL LESIONS with neoplastic lymphocytes around and within gastric glands
Associated with H PYLORI
CD20+
Can be associated with t(11;18)
