- Clinical science
Peptic ulcer disease (PUD) refers to the presence of one or more ulcerative lesions in the stomach or lining of the duodenum. Possible etiologies include infection with the bacterium Helicobacter pylori (most common), prolonged use of nonsteroidal anti-inflammatory medicines (possibly in combination with glucocorticoids), conditions associated with an overproduction of stomach acid (hypersecretory states), and stress. Epigastric pain is a typical symptom of PUD, however, some patients may remain asymptomatic. Diagnosis occurs via direct visualization of the ulcer on esophagogastroduodenoscopy (EGD) and H. pylori detection (via biopsy or non-invasive testing). The first-line treatment for most peptic ulcers involves H. pylori eradication via triple therapy (a course of two different antibiotics in combination with a proton-pump inhibitor) and the withdrawal of offending agents. Antisecretory drugs (e.g., proton-pump inhibitors, or PPIs), which reduce stomach acid production, are continued for 4–8 weeks after eradication therapy and may be considered for maintenance therapy if symptoms recur. Surgical intervention may be necessary in rare cases, especially if complications such as perforation or massive bleeding occur. Stomach cancer is an important differential diagnosis and must be ruled out if risk factors are present.
- Chronic gastritis caused by H. pylori, a curved, flagellated gram-negative rod
- Chronic gastritis of other etiology
- Long-term use of NSAIDs (e.g., patients with rheumatoid arthritis, SLE, etc.):
- Long-term use of NSAIDs plus glucocorticoids: Risk increases 10 to 15-fold!
- Chronic alcohol consumption
- Patients with blood type O have a higher risk for duodenal ulcers.
- Age > 65 years
- Stress (see “Subtypes and variants” below)
- Rare risk factors:
- Gastric ulcer: : an ulcerative lesion in the stomach lining; typically manifests along the lesser curvature and the gastric antrum
- Duodenal ulcer: : an ulcerative lesion located in the duodenum, typically in the first part (i.e., the duodenal bulb)
- Erosive gastritis: acute mucosal inflammation of the stomach that does not extend beyond the muscularis mucosae
An atypical location is suspicious for carcinoma!
- Parietal cells
- Mucosal cells
- Chief cells
- Helicobacter pylori gastritis: increased acid secretion, decreased protective factors/mucus production
- NSAIDs inhibit COX-1 and COX-2 → decrease in PGE2 (normally decreases gastric acid secretion and increases HCO3- and mucus secretion) → gastric mucosa erosions
Findings common to both
|Pain and eating|| |
|Nocturnal pain|| || |
Gastric ulcer is associated with pain after light (weight loss) Gorging. Duodenal ulcer is associated with relief after massive (weight gain) Desserts."
Taking NSAIDs can often mask PUD symptoms until complications such as hemorrhage and perforation occur!
- Description: In this rare disease, minor mucosal trauma can lead to major bleeding. It is caused by an abnormal submucosal artery.
- Location: proximal stomach
- Clinical presentation: signs of acute upper GI bleeding
- Treatment: endoscopic hemostasis (injection therapy, hemoclips, etc.), excision of the susceptible mucosa
- Causes: polytrauma, major surgery, SIRS, kidney failure, etc.
- Curling ulcer: severe burns → decreased plasma volume → decreased gastric blood flow → hypoxic tissue injury of stomach surface epithelium → weakening of the normal mucosal barrier
- Cushing ulcer: In patients with brain injury, increased vagal stimulation leads to increased production of stomach acid via acetylcholine release.
- Nonulcer dyspepsia; : Symptoms including bloating, nausea, and belching persisting ≥ 3 months without organic cause (synonym: functional dyspepsia).
Imagine a brain resting on a cushion to remember that patients with brain injury can develop Cushing ulcers.
- ≤ 60 years of age without alarm features: for H. pylori
- > 60 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori
- Negative for H. pylori infection and NSAID intake; trial therapy unsuccessful
Testing for Helicobacter pylori
- See “”
- Most accurate test
- Patients > 60 years of age or presence of ≥ 1 alarm features, which include:
- Certain symptoms: progressive dysphagia, painful swallowing (odynophagia), and/or persistent vomiting
- Signs of active GI bleeding (e.g., melena, unexplained iron-deficiency anemia)
- Signs of malignancy (e.g., unintended weight loss, lymphadenopathy, palpable mass)
- Family history of upper GI malignancy in a first-degree relative
- Biopsy samples from:
- If active bleeding, EGD can be performed for diagnosis and subsequent hemostasis treatment (electrocautery) in the same session.
General management of dyspepsia
- H. pylori positive → eradication therapy (with antibiotics and a PPI) and supportive treatment → continue PPIs for 4–8 weeks → follow-up
- H. pylori negative → medical acid suppression (with a PPI) and supportive treatment for 4–8 weeks → follow-up
- (with antibiotics)
- Acid suppression: PPIs (most effective), H2 blockers, antacids (mainly used for symptom relief)
- Mucosal protection: misoprostol , sucralfate (both substances are rarely used in PUD)
- Discontinue NSAIDs
- Restrict alcohol use/smoking/emotional stress
- Avoid eating before bedtime
- With the advent of potent acid suppression in the form of PPIs, surgical intervention is rarely needed.
- Refractory syndromes despite appropriate medical treatment
- If cancer is suspected
- Complications that cannot be treated endoscopically (see “Complications” below)
Partial gastrectomy (Billroth)
- Billroth I: distal gastrectomy with end-to-end or side-to-end gastroduodenostomy
- Billroth II: resection of the distal ⅔ of the stomach with a blind-ending duodenal stump and end-to-side gastro-jejunostomy. The Billroth I and II methods without a Brown's anastomosis often lead to bile reflux into the stomach. This may result in type C gastritis in the region of the anastomosis. The chronic inflammation causes atrophic changes and increases the risk of cancer (anastomosis carcinoma).
- Start a PPI (e.g., omeprazole ). 
- Consider alternative therapies (see ).
- H. pylori eradication therapy 
- Lifestyle changes: Recommend avoidance of spicy foods and caffeine, remaining upright after eating, smoking cessation, and limiting/ceasing alcohol intake.
- Discontinue NSAIDs, if possible.
- Identify and treat complications
Bleeding (see )
- Most common complication of PUD
- Located posterior more commonly than anterior
- Perforated gastric ulcers of the lesser curvature may cause hemorrhage of the left gastric artery.
- Duodenal ulcers of the posterior wall are more likely to cause massive bleeding because of their proximity to the gastroduodenal artery.
- Gastric/duodenal perforation (see also and )
- Subhepatic abscess
Gastric outlet obstruction (GOO)
- Definition: mechanical obstruction of the pyloric channel or duodenum
- Postprandial, nonbilious vomiting
- Succussion splash
- Early satiety
- Progressive gastric dilation
- Weight loss
- Fistula formation
- Malignant transformation
Posterior ulcers are more likely to bleed and anterior ulcers are more likely to perforate: Postal workers wear Blue collars and should not have an Antisocial Personality.
We list the most important complications. The selection is not exhaustive.
- Smoking cessation and avoidance of other offending agents such as alcohol
- Reduce coffee consumption
- Avoid medications that are associated with the development of ulcers
- Rule out: Zollinger-Ellison syndrome, hyperparathyroidism
Stress ulcer prophylaxis
- PPIs or H2 blockers
- Indicated in severe organic disease/stress → shock, acidosis, brain trauma, severe burns, major surgery
- Disadvantage of prolonged PPI intake: potentially higher risk of pneumonia and gastroenteritis!