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Duodenal Ulcer

Updated : September 17, 2022





Background

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.

Clinical History

Physical Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

 

bismuth subcitrate metronidazole and tetracycline

3

Capsules

4 times a day

after dinner at bedtime with omeprazole 20 mg twice a day for 10 to 14 days



sucralfate

Initial:

1

g

tablet/suspension four times a day for 4 to 8 weeks.



rabeprazole

15

mg

Orally 

once a day

4

weeks


Maintenance: 15 mg once daily



vonoprazan fumarate 

20 mg to be taken orally one time daily for a duration of 6 weeks



dexrabeprazole 

Take 10 mg one time a day for the duration of four to eight weeks, which depends upon the condition and body response
The recommended maintenance dose is 5 to 10 mg one time a day



almasilate 

Neutralizing excess acid in the stomach needs an antacid. almasilate is an antacid used to treat heart burns and stomach and duodenal ulcers caused by excess acid inside the stomach. almasilate is used for the symptomatic treatment
Two teaspoons of almasilate, which is equivalent to 10 mL, is recommended daily four times



Dose Adjustments

Limited data is available

vonoprazan fumarate 

The dosage is 20 mg to be taken orally one time daily for a duration of 6 weeks



metronidazole/tetracycline/bismuth subsalicylate 

Bismuth subsalicylate- 525mg(two chewable tablets of 262.4mg), metronidazole- 250mg, tetracycline- 500mg orally every 6 hours along with meals for two weeks
Note: histamine(H2) antagonist should be taken along with the therapy
Indication: used in the treatment of infection due to Helicobacter pylori in patients with a history of duodenal ulcers in combination with a histamine(H2) antagonist



Dose Adjustments

Renal dose adjustments
Contraindicated in patients with kidney failure
Hepatic dose adjustments
To be used with caution in patients with liver failure

lansoprazole 

Administer 15 mg orally every day for a month as active dose Administer 15 mg orally every day as maintenance dose



 

cimetidine

Children 5 to 16 years:

20 - 40

mg/kg

Orally 

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



 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK557390/

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.

bismuth subcitrate metronidazole and tetracycline

3

Capsules

4 times a day

after dinner at bedtime with omeprazole 20 mg twice a day for 10 to 14 days



sucralfate

Initial:

1

g

tablet/suspension four times a day for 4 to 8 weeks.



rabeprazole

15

mg

Orally 

once a day

4

weeks


Maintenance: 15 mg once daily



vonoprazan fumarate 

20 mg to be taken orally one time daily for a duration of 6 weeks



dexrabeprazole 

Take 10 mg one time a day for the duration of four to eight weeks, which depends upon the condition and body response
The recommended maintenance dose is 5 to 10 mg one time a day



almasilate 

Neutralizing excess acid in the stomach needs an antacid. almasilate is an antacid used to treat heart burns and stomach and duodenal ulcers caused by excess acid inside the stomach. almasilate is used for the symptomatic treatment
Two teaspoons of almasilate, which is equivalent to 10 mL, is recommended daily four times



Dose Adjustments

Limited data is available

vonoprazan fumarate 

The dosage is 20 mg to be taken orally one time daily for a duration of 6 weeks



metronidazole/tetracycline/bismuth subsalicylate 

Bismuth subsalicylate- 525mg(two chewable tablets of 262.4mg), metronidazole- 250mg, tetracycline- 500mg orally every 6 hours along with meals for two weeks
Note: histamine(H2) antagonist should be taken along with the therapy
Indication: used in the treatment of infection due to Helicobacter pylori in patients with a history of duodenal ulcers in combination with a histamine(H2) antagonist



Dose Adjustments

Renal dose adjustments
Contraindicated in patients with kidney failure
Hepatic dose adjustments
To be used with caution in patients with liver failure

lansoprazole 

Administer 15 mg orally every day for a month as active dose Administer 15 mg orally every day as maintenance dose



cimetidine

Children 5 to 16 years:

20 - 40

mg/kg

Orally 

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/

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