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Peptic ulcer disease (PUD) of the stomach and duodenum

Definition

Peptic ulcers are raw patches that are usually 1-2cm in diameter. The surface mucosa (protective skin) has been removed. An ulcer in the stomach is called a gastric or stomach ulcer. In the duodenum it's called a duodenal ulcer.

Causes

There are several factors that increase a person's risk of getting a peptic ulcer:

• infection with bacteria called Helicobacter pylori (H. pylori) - this is almost always present in people with ulcers, although it's also found in the stomachs of many people without ulcers or indigestion symptoms
• regularly taking certain medicines, particularly aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen and diclofenac
• smoking
• blood group O
• drinking alcohol in excess

Clinical picture

Gastric ulcer typically causes a sharp pain in the stomach soon after eating, whereas the pain of a duodenal ulcer is typically relieved by eating, or by drinking milk. Other symptoms may include:

• Belching
• General discomfort in the stomach
• Loss of appetite or, rarely, increased appetite
• Nausea
• Vomiting
• Loss of weight

Complications

1. Bleeding peptic ulcer

2. Perforation

3. Obstruction

4. Intractable pain

Diagnosis

Diagnosis is established either by endoscopy or indirectly by UGI series. In this case if gastric ulcer is seen a biopsy is mandatory. 

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Treatment

Patients under 50 years that do not exhibit anemia, gastrointestinal bleeding, anorexia, early satiety or weight loss with the 1st episode of dyspepsia can be given emperic antiulcer therapy 4-6 weeks. Failure to respond by 2 weeks or recurrence warrants further investigation.

Document H.pylori infection and document other aetiological factors that would lead to recurrence.

1. Active ulcer not attributable to H.pylori:

Options include:

1.     H2 receptor antagonists: PO bid for 8 wks
cimetidine 400mg
ranitidine 150mg
famotidine 20 mg
nizatidine 150 mg
* parenteral therapy is reserved for those
* all H2 antagonists at the above doses are equal in efficacy

2.     Proton pump inhibitors: PO bid 4wks in duodenal and 8 wks in gastric
Omeprazole 20mg
Lanzoprazole 30 mg

3.     Sucralfate:1 g qid for acute therapy
Should not be administered with H2 antagonist or antacid as it requires an acid pH to become activated.

4.     Antacids: because of their frequent dosing and side effects they are best used as supplemental therapy for pain relief. However, due to their low cost they are sometimes prescribed for patients with low funds.

2. Patients with active peptic ulcer associated with H.pylori:

Antisecretory therapy as above + erradication therapy for 1^st 2 weeks. Irradication requires triple antibiotic therapy.

Prevention of relapse

• Recurrence rate is as high as 75% in the 1^st year.

• Maintenance therapy by ½ dose H2 antagonists before bedtime for 6 months.

• Alternatively if patient was on sucralfate he is maintained with 1g bid.

• Erradicating H. pylori decreases the recurrence rate to as low as 10%.

Evaluation of response and follow up

Duodenal Ulcer:

80% DU heal on the above regimen. if not successful then note patient compliance, the use of risk factors. One must document unhealed ulcer by endoscopy. If these patients were on H2 antagonists then switch to proton pump blockers. Consider the possibility of Zollinger – Ellison syndrome.

Gastric Ulcer:

Therapy takes longer and should be continued for 8 weeks then evaluation with endoscopy is done and biopsy is taken. If these are negative then treatment is continued for longer. If this fails then either the dose is increased or switched to proton pump blockers. Otherwise consider surgery.

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