A defensive mechanism anatomically with epithelium, subepithelial and pre-epithelial components is present on the duodenal and gastric surfaces. Damage to the mucosal membrane that spreads over the superficial layer leads to ulceration.
Although dyspepsia is the key symptom of most duodenal ulcers, other severe symptoms exist, such as restriction of the gastric outlet, gastrointestinal bleeding, perforation, or the development of a fistula.
Epidemiology
The prevalence of duodenal ulcers is between 5-15% in Western populations. Since H. pylori were not appropriately diagnosed and treated in the past, the prevalence and recurrence rates were relatively high.
In light of increasing patient and physician knowledge about the use of NSAIDs, the potential side effects of misuse, the gradually declining cigarette smoking prevalence among younger people, and duodenal ulcer diagnosis rates have decreased overall.
Anatomy
Pathophysiology
Due to the corrosive effect of gastric secretions on the previously damaged small intestine surface epithelium, duodenal ulcers develop. It is believed that H. pylori colonization and ongoing inflammation cause the mucosal surface layer to deteriorate, making it susceptible to exposure to stomach acid.
The protective mucosa of the gastrointestinal system, particularly the stomach and small intestine mucosa, is developed due to prostaglandins. COX (Cyclooxygenase), which comprises two variants, COX-1 and COX-2, catalyzes their production.
NSAIDs inhibit their pathways to provide therapeutic effects. Prostaglandin levels significantly decrease with repeated use of NSAIDs, increasing the risk of mucosal damage.
Etiology
A history of frequent or chronic NSAID use and H. pylori infection are the two leading causes of duodenal ulcers.
Although H. pylori are the secondary diagnosis in most patients, other unusual etiologies are increasingly common as infection prevalence has decreased.
Other etiologies that affect the duodenum lining, similar to NSAIDs and H. pylori, are also causes of duodenal ulcers. These include cancer, Zollinger-Ellison syndrome, chemotherapy, and vascular insufficiency.
Genetics
Prognostic Factors
Depending on the severity of the first presentation, the prognosis for duodenal ulcers varies. It is possible to treat duodenal ulcers, mainly brought on by using NSAIDs, by discontinuing the medication and receiving treatment for symptoms with a high remission rate.
Patients with ulcers because of H. pylori must be treated for the infection, and recovery times depend on eradicating the infection. Patients with significant perforation or ulceration at their initial visit have a greater mortality rate and are more vulnerable to postoperative complications.
A defensive mechanism anatomically with epithelium, subepithelial and pre-epithelial components is present on the duodenal and gastric surfaces. Damage to the mucosal membrane that spreads over the superficial layer leads to ulceration.
Although dyspepsia is the key symptom of most duodenal ulcers, other severe symptoms exist, such as restriction of the gastric outlet, gastrointestinal bleeding, perforation, or the development of a fistula.
The prevalence of duodenal ulcers is between 5-15% in Western populations. Since H. pylori were not appropriately diagnosed and treated in the past, the prevalence and recurrence rates were relatively high.
In light of increasing patient and physician knowledge about the use of NSAIDs, the potential side effects of misuse, the gradually declining cigarette smoking prevalence among younger people, and duodenal ulcer diagnosis rates have decreased overall.
Due to the corrosive effect of gastric secretions on the previously damaged small intestine surface epithelium, duodenal ulcers develop. It is believed that H. pylori colonization and ongoing inflammation cause the mucosal surface layer to deteriorate, making it susceptible to exposure to stomach acid.
The protective mucosa of the gastrointestinal system, particularly the stomach and small intestine mucosa, is developed due to prostaglandins. COX (Cyclooxygenase), which comprises two variants, COX-1 and COX-2, catalyzes their production.
NSAIDs inhibit their pathways to provide therapeutic effects. Prostaglandin levels significantly decrease with repeated use of NSAIDs, increasing the risk of mucosal damage.
A history of frequent or chronic NSAID use and H. pylori infection are the two leading causes of duodenal ulcers.
Although H. pylori are the secondary diagnosis in most patients, other unusual etiologies are increasingly common as infection prevalence has decreased.
Other etiologies that affect the duodenum lining, similar to NSAIDs and H. pylori, are also causes of duodenal ulcers. These include cancer, Zollinger-Ellison syndrome, chemotherapy, and vascular insufficiency.
Depending on the severity of the first presentation, the prognosis for duodenal ulcers varies. It is possible to treat duodenal ulcers, mainly brought on by using NSAIDs, by discontinuing the medication and receiving treatment for symptoms with a high remission rate.
Patients with ulcers because of H. pylori must be treated for the infection, and recovery times depend on eradicating the infection. Patients with significant perforation or ulceration at their initial visit have a greater mortality rate and are more vulnerable to postoperative complications.
daily in 3 to 4 divided doses for 4 to 8 weeks
(Do not exceed 300mg/dose)
Maintenance dose: 5 to 6 mg/kg orally once a day at bedtime
https://www.ncbi.nlm.nih.gov/books/NBK557390/
medtigo
Duodenal Ulcer
Updated :
September 17, 2022
A defensive mechanism anatomically with epithelium, subepithelial and pre-epithelial components is present on the duodenal and gastric surfaces. Damage to the mucosal membrane that spreads over the superficial layer leads to ulceration.
Although dyspepsia is the key symptom of most duodenal ulcers, other severe symptoms exist, such as restriction of the gastric outlet, gastrointestinal bleeding, perforation, or the development of a fistula.
The prevalence of duodenal ulcers is between 5-15% in Western populations. Since H. pylori were not appropriately diagnosed and treated in the past, the prevalence and recurrence rates were relatively high.
In light of increasing patient and physician knowledge about the use of NSAIDs, the potential side effects of misuse, the gradually declining cigarette smoking prevalence among younger people, and duodenal ulcer diagnosis rates have decreased overall.
Due to the corrosive effect of gastric secretions on the previously damaged small intestine surface epithelium, duodenal ulcers develop. It is believed that H. pylori colonization and ongoing inflammation cause the mucosal surface layer to deteriorate, making it susceptible to exposure to stomach acid.
The protective mucosa of the gastrointestinal system, particularly the stomach and small intestine mucosa, is developed due to prostaglandins. COX (Cyclooxygenase), which comprises two variants, COX-1 and COX-2, catalyzes their production.
NSAIDs inhibit their pathways to provide therapeutic effects. Prostaglandin levels significantly decrease with repeated use of NSAIDs, increasing the risk of mucosal damage.
A history of frequent or chronic NSAID use and H. pylori infection are the two leading causes of duodenal ulcers.
Although H. pylori are the secondary diagnosis in most patients, other unusual etiologies are increasingly common as infection prevalence has decreased.
Other etiologies that affect the duodenum lining, similar to NSAIDs and H. pylori, are also causes of duodenal ulcers. These include cancer, Zollinger-Ellison syndrome, chemotherapy, and vascular insufficiency.
Depending on the severity of the first presentation, the prognosis for duodenal ulcers varies. It is possible to treat duodenal ulcers, mainly brought on by using NSAIDs, by discontinuing the medication and receiving treatment for symptoms with a high remission rate.
Patients with ulcers because of H. pylori must be treated for the infection, and recovery times depend on eradicating the infection. Patients with significant perforation or ulceration at their initial visit have a greater mortality rate and are more vulnerable to postoperative complications.
https://www.ncbi.nlm.nih.gov/books/NBK557390/
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