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Pathology of the stomach

Terms in this set (17)

•Dyspeptic symptoms
•Endoscopy: Erythema, nodular appearance of mucosa or thickening of rugae
-Intraepithelial neutrophils, sometimes forming pit microabscess
-Lymphocytes in lamina propria with numerous plasma cells
-H. PYLORI ON THE SURFACE, demonstrated by special stains
H&E shows PMNs invading the neck of mucus gland. In the gland you can see a few H. pylori bacteria. Some eosinophil cells are also present.
2 types of gastritis by H. pylori: antral (much more dominant) and corpus predominant types.

Antral-predominant type
•H. pylori preferentially infects the antrum
•Causes hyperchlorhydria by:
-Increased production of gastrin from G-cells
-Increased production of histamine from ECL cells
-Inhibition of somatostatin release
Result: duodenal ulcer
Antral-predominant: hyperchlorhydria and duodenal ulcer
Parietal cell proliferation: pyloric gastritis (endocrine dysfunction): duodenal ulcer.

Corpus-predominant type
•Severe infection may spread to body and fundus and cause mucosal atrophy: condition referred to as Atrophic Pangastritis
•Progression to atrophic pangastritis depends on host's factors (polymorphisms of pro-inflammatory agents, e.g. IL-1) and bacterium (expression of CagA)
•Atrophic pangastritis results in hypochlorhydria and:
-Peptic ulcer
-Intestinal metaplasia
-Increased risk of adenocarcinoma
Corpus-predominant: atrophy, hypochlorhydria, gastric ulcer, intestinal metaplasia and adenocarcinoma
Body gastritis -> atrophy of gastric glands leads to gastric ulcer, acid hyposecretion and intestinal metaplasia (increase risk of stomach cancer)
•Perforation: Acute, life-threatening. Most severe: cause acute peritonitis--an emergency with high mortality
-From small vessels: Chronic bleeding, iron-deficiency anemia. Discrete bleeding. IDA in man is GI and women in menstrual usually
-From large vessel: Hematemesis, melena, shock. Pancreaticoduodenal artery: massive bleeding
•Gastric outlet obstruction: Ulcers in distal stomach and duodenal bulb may cause reversible obstruction by edema or fixed stenosis by scarring
•Penetration into adjacent organs, liver and pancreas

•In total (duodenal + gastric ulcers) 70% of patients with PUD have H. pylori
-Less than 20% of people with H. pylori develop PUD
Other etiologic factors:
•NSAIDS and corticosteroids: Inhibition of prostaglandin synthesis
•Smoking: Reduced mucosal blood flow
•Psychological stress: Possibly increased acid production
•Genetic predisposition
•Cirrhosis, COPD, chronic renal failure, hyperparathyroidism: Risk factors for duodenal ulcers

Clinical manifestations
•Epigastric gnawing, burning pain related to mealtimes
•Onset of pain in relation to meals depends on location, duodenal versus gastric:
-DU: 30 min to 3 hour after meal, relieved by antacids
-GU: immediately before or during meal, precipitated by food
•Dyspeptic symptoms: Bloating, nausea, vomiting
•Loss of appetite, weight loss. Weight: loss in gastric ulcers. Gain in duodenal ulcers
•Hematemesis, melena (cause anemia)
•Symptoms due to complications: Bleeding, perforation, penetration, gastric outlet obstruction
•Mortality: Low, but 5,000 die each year of PUD in the US