GI: Stomach and Duodenum Flashcards
How is a peptic ulcer diagnosed?
Peptic ulcers are diagnosed not by symptoms but instead by the presence of a mucosal break 5 mm or larger in the stomach or duodenum.
Upper endoscopy is the gold standard for diagnosis of peptic ulcer disease.
What type of peptic ulcers DO NOT require endoscopic follow-up?
Duodenal ulcers and low-risk gastric ulcers (for example, a young patient on NSAIDs) do not typically require endoscopic follow-up.
How do you manage dyspepsia for people UNDER the age of 50-55 and with NO RED FLAG SYMPTOMS?
For patients younger than age 50 to 55 years who present with dyspepsia without alarm features, testing and treating for Helicobacter pylori infection or a trial of proton pump inhibitor therapy should be pursued before any further testing is done.
How do you manage dyspepsia in someone older than 50-55 and/or with red flag symptoms and/or persistent symptoms despite eradication of H. pylori?
Further structural testing should be performed in patients older than 50 to 55 years, those with alarm features at any age, or those with persistent dyspeptic symptoms despite eradication of H. pylori and/or a trial of PPI therapy. Upper endoscopy is considered the gold standard for the exclusion of upper gastrointestinal structural causes of dyspepsia.
What are the indications for H. pylori testing?
Clearly established indications for Helicobacter pylori testing are:
- active peptic ulcer disease (gastric and/or duodenal ulcer)
- confirmed history of peptic ulcer disease
- gastric mucosa–associated lymphoid tissue lymphoma
- uninvestigated dyspepsia in patients younger than age 60 years without alarm symptoms
- following endoscopic resection of early gastric cancer.
Is GERD in itself an indication for H. pylori testing?
Gastroesophageal reflux disease is not a clinical indication for Helicobacter pylori testing.
How do you test and treat for H. pylori? What medications should be avoided when testing?
**Noninvasive tests that identify ACTIVE infection include the urea breath test and fecal antigen test.
- To improve the diagnostic accuracy of the urea breath test and fecal antigen test, antimicrobial agents and bismuth should be avoided for 28 days prior to testing. PPIs should be avoided for 7 to 14 days prior to testing, and H2 blockers should be avoided for 1 to 2 days prior to testing.
- Serum testing for IgG antibodies to H. pylori does not identify active infection in populations with low prevalence of disease; however, it remains popular given its ease of administration, rapidity of results, and low cost. Given its marginal sensitivity (85%) and specificity (79%), antibody testing should not be used when there is a low background prevalence of H. pylori (prevalence <20%).
- Invasive (endoscopic) tests for H. pylori include the rapid urease test, histology, and culture; all invasive testing modalities identify active infection.
**Owing to the increased risk of false-negative endoscopic and fecal antigen test results in patients with bleeding PUD, serologic antibody testing should also be performed as a second test in this clinical setting, and treatment should be pursued if either test modality is positive.
Treatment of H. pylori
Patients should be asked about previous treatment with a macrolide antibiotic. Use of a clarithromycin-containing regimen as first-line therapy should be limited to patients with no prior macrolide exposure who do not reside in areas with high clarithromycin resistance. In these situations, bismuth quadruple therapy should be considered for first-line therapy.
How do you confirm eradication of H. pylori?
Noninvasive testing to confirm eradication of Helicobacter pylori (with the urea breath test or fecal antigen test) should be performed given the high rate of treatment failure (roughly 25% in the United States); antibody testing is not appropriate for confirming eradication because antibodies can remain in the serum long after H. pylori has been eradicated.
What are the two causes of atrophic gastritis?
The two forms of atrophic gastritis are H. pylori–associated and autoimmune.
How is atrophic gastritis treated?
H. pylori–associated atrophic gastritis typically resolves with H. pylori eradication. Autoimmune atrophic gastritis, however, has no cure.
What are the clinical manifestations of atrophic gastritis?
Important clinical manifestations include pernicious anemia, iron deficiency anemia, and hypergastrinemia, which result from the long-term effects of the associated parietal cell loss and subsequent development of achlorhydria.
What is lymphocytic gastritis? How is it treated?
Lymphocytic gastritis is a rare, benign chronic inflammatory condition of the gastric mucosa. Clinical manifestations may include dyspepsia, iron deficiency anemia, and diarrhea.
Treatment is directed at the underlying condition, which in most cases is celiac disease or H. pylori infection.Endoscopic surveillance is not required; however, small-bowel and colon biopsies should be obtained to determine the extent of the inflammation and to identify underlying conditions.
Do the following conditions require endoscopic surveillance?
- Lymphocytic gastritis
- Atrophic gastritis
- intestinal metaplasia
- Atrophic gastritis
- Lymphocytic gastritis: No
- Atrophic gastritis: No
- intestinal metaplasia:Not unless they have a family history of gastric cancer or are from an area with high gastric cancer
- Atrophic gastritis: No
What is the preferred agent for treatment and prophylaxis of NSAID and aspirin related GI injury?
PPIs are the preferred agent for treatment and prophylaxis of NSAID- and aspirin-related gastrointestinal injury.