Peptic ulcer disease

Peptic ulcer disease (PUD) refers to the presence of peptic ulcers in the stomach and/or duodenum. Duodenal ulcers are approx 3 times more common than gastric ulcers. In virtually all cases, patients with PUD either have H. pylori infection and/or use NSAIDs long-term. Few people develop PUD without either of these risk factors.

In addition to H. pylori and NSAIDs, there are multiple other “supportive” risk factors. These include smoking, alcohol, steroid use, and stress. Severe stress like trauma, burns and surgery may predispose to PUD. These ulcers sometimes have special names: Curling-ulcus after severe burn injury, and Cushing-ulcus after CNS injury.

Pathology

The ulcers may occur in any part of the GI-tract that is exposed to acidic gastric juices but is most commonly found in the minor curvature of the stomach, gastric antrum and first portion of duodenum.

We distinguish between acute and chronic ulcers. Let’s take a look at their differences:

Acute ulcer	Chronic ulcer
Mostly smaller than 1 cm	2 – 4 cm
Often multiple	Often just one
Round or oval	Radiating mucosal folds around it
At the level of the mucosa	-
Ulcer base: covered by fibrin or hematin	Ulcer base: clear
Ulcer edge: grayish, yellow and flat	Ulcer edge: Hyperemic and straight walls
Complications: bleeding, perforation, peritonitis	Complications: Bleeding, perforation, penetration, scarring formation

Clinical features

70% of peptic ulcers are asymptomatic, but they may still develop complications like bleeding or perforation.

Symptomatic peptic ulcers present with epigastric pain or discomfort, as well as other non-specific symptoms like bloating, abdominal fullness, and nausea. The symptoms of duodenal ulcers frequently improve with eating and worsen a few hours after meals and at night. The symptoms of gastric ulcers worsen with eating.

Bleeding ulcer presents with features of upper GI bleeding, like haematemesis, melena, or anaemia. Perforated ulcers are the most common cause of GI perforation and cause peritonitis. Duodenal ulcers may penetrate through the wall into adjacent organs, forming fistulas.

Diagnosis and evaluation

The diagnosis is suspected in patients with typical risk factors (chronic NSAIDs use, previous H. pylori infection) and typical symptoms, but definite diagnosis is based on upper endoscopy. All patients with suspected PUD should undergo this examination. Upper endoscopy allows not only direct visualisation but biopsy of ulcers which malignant features. Biopsy should also be taken from the gastric antrum to look for H. pylori.

Testing for H. pylori may be necessary as well if biopsy is negative or the patient does not undergo endoscopy.

Patients with features of complicated PUD require more thorough workup.

Complications

Peptic ulcers may bleed, obstruct the gastric outlet, or perforate. Perforation may lead to peritonitis.

Treatment

Treatment involves treating the underlying cause, removing risk factors, and giving PPIs.

Surgical treatment is necessary for the treatment of complications like perforation, bleeding (if endoscopic haemostasis fails), pyloric stenosis, cases which don’t respond to conservative therapy, or if malignancy is discovered.

Perforations and bleeding ulcers may be simply sutured or closed with a patch, or they may be treated with partial gastric resection and reconstruction surgeries like Billroth I, Billroth II, or Roux-en-Y. Many years ago, vagotomy was performed to reduce the production of stomach acid.

Many complications may occur after gastric resection:

• Post-gastrectomy gastritis
• Stoma stenosis
• Dumping syndrome
• Maldigestion
• B12 deficiency

Zollinger-Ellison syndrome

Zollinger-Ellison syndrome is a rare cause of PUD. It is characterized by multiple peptic ulcerations in the stomach, duodenum and even jejunum. It is caused by neuroendocrine tumors that produce gastrin, called gastrinomas, and they are often located in the pancreas, duodenum or the lymph nodes of the abdomen. Increased gastrin means increased stomach acid.