CTL Week 7 - Stomach: ulcerations, gastritis, cancer
CTL Week 7 - Peptic ulcer dz: H. Pylori
Mallory-Weiss lacerations
Chronic gastritis
Esophageal candidiasis
Peptic ulcer disease
Ruptured esophageal varices
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Autoimmune mechanisms
High doses of aspirin
Clostridium difficile
Diet of smoked fish and red meat
Ménétrier disease
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Acute gastric ulcers
Acute gastritis
Chronic gastritis
Linitis plastica
Peptic ulcer
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More rapid healing of the ulcer
Prevention of ulcer recurrence
Prevention of gastro-esophageal reflux disease
More rapid resolution of symptoms
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It is acquired at earlier ages in developing countries than in USA
Children are more likely than adults to show antibodies against Helicobacter pylori
It is acquired earlier in life in white persons than in African Americans and Hispanic persons in USA
Nausea and vomiting usually develop after acquisition
A normal immune system will clear the organism from the stomach within a month of acquisition.
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Chronic gastritis
Linitis plastic
Acute gastric ulceration
Peptic ulcer
Zollinger-Ellison syndrome
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The bacterium can invade the tissues through the stomach wall by increasing local acidity which then causes the actual ulcer
The bacterium invades the tissue and causes an alkaline environment, which causes the stomach to produce more acid leading to tissue damage and an ulcer
The bacterium doesn’t invade the tissue, but it does decrease the protective mucous layer by increasing acidity, causing local stomach damage
The bacterium doesn’t actually invade the tissues but it does damage them, allowing stomach acid to damage the underlying tissues and cause the actual ulcer
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Perforation
Bleeding
Obstruction
Chronic renal failure
Cirrhosis
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Patients with ulcers caused by H. pylori acquire their infections through food or water in the few weeks preceding their symptoms
H. pylori causes ulcers by the actions of urease and cytotoxin
Ulcers caused by H. pylori heal faster when antibiotics are administered
H. pylori infection predisposes persons to both peptic ulcers and esophageal reflux disease
Most persons with H. pylori infection will develop duodenal ulcers or gastric carcinoma
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After he ingested pathogenic bacteria, the bacteria invaded his duodenal mucosa where a cytotoxin caused an ulcer
Pathogenic bacteria secreted urease and a cytotoxin into his gastric epithelial cells to result in an ulcer
Pathogenic bacteria attached to his antral epithelium and secreted urease; ammonia produced from urea acted to damage his epithelium
Pathogenic bacteria produced urease and damaged the epithelium by secreting acid to result in ulcer formation
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Multiple episodes of gastritis causing nausea and vomiting
Development of a duodenal ulcer with epigastric pain and occult blood in his stools
Development of adenocarcinoma of the gastric antrum
Asymptomatic but will show diagnostic serum antibodies if tested
Immune-mediated clearance of the bacteria within a year
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Achalasia
Barrett esophagus
Adenocarcinoma
Sliding hiatal hernia
Zenker diverticulum
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Infection was recently acquired and was causing symptomatic gastritis
Infection was acquired several years ago and is now causing symptoms
Infection was never acquired because the patient practiced meticulous hand hygiene and dietary habits
Infection was acquired several years ago and was treated a year ago with antibiotics
His esophagitis was unrelated to H. pylori, likely caused by Candida albicans or cytomegalovirus
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