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Factors associated with pathogenesis of acute gastritis. (p.17)
- Erosive gastritis
- Involves focal necrosis of mucosa
- Leads to erosion into deeper tissues
- Then acute ulcer, inflammation, and hemorrhage
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Mechanism of injury of acute gastritis. (p.17)
- Chemical irritants - ASA, NSAIDs, ETOH
- Severe illness - trauma, sepsis, surgery, burns, hypothermia, bile reflux, drugs given during course of illness
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Cushing's Ulcer (p.18)
- Response to traumatic/surgical injury to CNS or rapidly progressing ICH
- Brain injury --> increased vagal tone & increased acid secretion in stomach
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Curling's Ulcer (p.18)
- Occurs in severely burned patients, in shock, sepsis, and other forms of trauma
- Probably due to autonomic response to shock
- Shunts blood from GI tract to more critical areas --> ischemia --> inhibits PG synthesis --> impairs mucus-bicarb layer
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Autoimmune gastritis
(chronic gastritis)
- Antibodies attack parietal cells --> destruction of gastric glands
- Causes parietal cell malfunction and eventual absence of HCl secretion (achlorydia) and intrinsic factor secretion (needed for B12 absorption)
- Lack of B12 causes impaired folic acid metabolism, needed for DNA synthesis of new cells.
- Ultimately leads to atrophy of gastric epithelium.
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Infectious gastritis
(chronic gastritis)
- Primarily Helicobacter pylori (H. pylori), gram-negative bacteria
- Causes chronic gastritis of antrum and body of stomach
- H. pylori burrows through mucus layers, attaches to epithelial cells, and colonizes
- H. pylori damages cells by producing urease, which increases ammonia levels in stomach, increasing pH
- H. pylori disrupts bicarb layer with mucolytic enzymes
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What is the gold standard for diagnosing peptic ulcers and H. pylori? (p.21)
Biopsy and rapid urease test (CLO test - campylobacter-like organism)
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What is the least invasive test to document H. pylori and document bacterial eradication
after treatment?
Urea breath test
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Describe Zollinger-Ellison syndrome. How is it related to peptic ulcer disease? (p.20)
- Endocrine syndrome affecting islet cells of pancreas (pancreatic tumor)
- Produces gastrin, which increases secretion of acid by the stomach
- Leads to chronic inflammation and eventual ulceration of mucosal lining
- Further ulceration can occur as submucosa exposed to acid and gastrin
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