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Long-term use of PPIs is associated with the development of benign polyps from fundic glands (which is distinct from fundic gland polyposis); these polyps do not cause cancer and resolve when PPIs are discontinued. [33] There is concern that use of PPIs may mask gastric cancers or other serious gastric problems. [33]
Complications of an ulcer can cause severe signs and symptoms such as black or tarry stool indicative of bleeding into the stomach or duodenum; blood - either red or coffee-ground colored in vomit; persistent sharp or severe abdominal pain; dizziness, and a fast heartbeat. [67] [68] Bleeding is the most common complication.
Often blood transfusions are not recommended unless the hemoglobin is less than 70 or 80 g/L. [7] [12] Treatment with proton pump inhibitors, octreotide, and antibiotics may be considered in certain cases. [5] [6] [13] If other measures are not effective, an esophageal balloon may be attempted in those with presumed esophageal varices. [2]
Proton pump inhibitors are prodrugs and their actual inhibitory form is somewhat controversial. In acidic solution, the sulfenic acid is isolated before reaction with one or more cysteines accessible from the luminar surface of the enzyme, a tetracyclic sulfenamide. This is a planar molecule thus any enantiomer of a PPI loses stereospecifity ...
Fundic gland polyposis is a medical syndrome where the fundus and the body of the stomach develop many fundic gland polyps.The condition has been described both in patients with familial adenomatous polyposis (FAP) and attenuated variants (AFAP), and in patients in whom it occurs sporadically.
PPI is the most popular agent in peptic ulcer prevention. [15] However, there is no evidence that H2 antagonists can prevent stomach bleeding for those taking NSAIDs. [15] Although misoprostol is effective in preventing peptic ulcer, its properties of promoting abortion and causing gastrointestinal distress limit its use. [15]
The gastric hydrogen potassium ATPase or H + /K + ATPase is the proton pump of the stomach.It exchanges potassium from the intestinal lumen with cytoplasmic hydronium [2] and is the enzyme primarily responsible for the acidification of the stomach contents and the activation of the digestive enzyme pepsin [3] (see gastric acid).
Mucosal disruption in acid peptic disease patients can be caused by infection, barrier disruption, or gastric acid hypersecretion.Acid peptic diseases can arise due to various risk factors such as Helicobacter pylori infection, alcoholism, tobacco use, cocaine and amphetamine use, nonsteroidal anti-inflammatory drug use (NSAIDs), fasting, Zollinger-Ellison syndrome, angiogenesis inhibitor ...