- The majority of people who develop either duodenal or gastric ulcers are infected with HP.
- Just because someone is infected with HP does not mean he/she will develop a peptic ulcer. Only 15% of those infected with HP will develop a peptic ulcer
- Ammonia, cytotoxins, and mucolytic enzymes damage cells and breaks down the mucous barrier which results in mucosal injury and a decrease in mucosal defense mechanisms
- These mechanisms cause mucosal injury and decrease mucosal defense mechanisms
- Development of a peptic ulcer is considered an NSAID-related complication
- Possible mechanisms of why cigarette smoking increases PUD risks include delayed gastric emptyng, inhibition of pancreatic bicarbonate secretion, promotion of duodenogastric reflux, reduction in mucosal prostaglandin production, and production of a favorable environment for H.pylori infection
- For nocturnal epigastric pain, the pain often wakes the patient between midnight and 3:00am
- If a peptic ulcer is strongly suspected or it is visualized on endoscopy, testing to determine is the patient is infected with HP is done. Whether or not a patient has an active HP infection or not directs treatment of the peptic ulcer.
- When using either of these tests to confirm H.pylori eradication, the appropriate amount of time needs to elapse after therapy has been discontinued to perform either test to minimize the risk of false negative results
- There is a correlation between the percentage of time that the gastric pH remains above 4 and healing of erosive esophagitis.
- Antacids can interact and decrease the effectiveness of other medications through a various mechanisms including increasing gastric pH with resulting decreased absorption of some medications, increasing urinary pH, adsorbing other medications, acting as a physical barrier to the absorption of other medications, forming insoluble complexes with some medications.
- Most of the studies on sequential therapy were performed in Italy