Peptic ulcer

Peptic ulcers, circumscribed lesions in the mucosal membrane extending below the epithelium, can
develop in the lower

esophagus, stomach, pylorus, duodenum, or jejunum. Although erosions are often referred to as ulcers,
erosions are

breaks in the mucosal membranes that do not extend below the epithelium. Ulcers may be acute or
chronic in nature.

Chronic ulcers are identified by scar tissue at their base. (See A closer look at peptic ulcers.) About 80%
of all peptic

ulcers are duodenal ulcers, which affect the proximal part of the small intestine and occur most
commonly in men

between ages 20 and 50. Duodenal ulcers usually follow a chronic course with remissions and
exacerbations; 5% to 10%

of patients develop complications that necessitate surgery.

Gastric ulcers are most common in middle-aged and elderly men, especially in chronic users of
nonsteroidal

anti-inflammatory drugs, alcohol, or tobacco.

Causes
Infection with Helicobacter pylori

Use of nonsteroidal anti-inflammatory drugs (NSAIDs)

Pathologic hypersecretory disorders.

Pathophysiology

Although the stomach contains acidic secretions that can digest substances, intrinsic defenses protect
the gastric

mucosal membrane from injury. A thick, tenacious layer of gastric mucus protects the stomach from
autodigestion,

mechanical trauma, and chemical trauma. Prostaglandins provide another line of defense. Gastric ulcers
may be a result

of destruction of the mucosal barrier.

The duodenum is protected from ulceration by the function of Brunner's glands. These glands produce a
viscid, mucoid,

alkaline secretion that neutralizes the acid chyme. Duodenal ulcers appear to result from excessive acid
protection.

Helicobacter pylori releases a toxin that destroys the gastric and duodenal mucosa, reducing the
epithelium's resistance
to acid digestion and causing gastritis and ulcer disease.

Salicylates and other NSAIDs inhibit the secretion of prostaglandins (substances that block ulceration).
Certain illnesses,

such as pancreatitis, hepatic disease, Crohn's disease, preexisting gastritis, and Zollinger-Ellison
syndrome, also

contribute to ulceration.

Besides peptic ulcer's main causes, several predisposing factors are acknowledged. They include blood
type (gastric

ulcers and type A; duodenal ulcers and type O) and other genetic factors. Exposure to irritants, such as
alcohol, coffee,

and tobacco, may contribute by accelerating gastric acid emptying and promoting mucosal breakdown.
Emotional stress

also contributes to ulcer formation because of the increased stimulation of acid and pepsin secretion and
decreased

mucosal defense. Physical trauma and normal aging are additional predisposing conditions.

Signs and symptoms

Symptoms vary by the type of ulcer.

A gastric ulcer produces the following signs and symptoms:

pain that worsens with eating due to stretching of the mucosa by food

nausea and anorexia secondary to mucosal stretching.

A duodenal ulcer produces the following signs and symptoms:

epigastric pain that is gnawing, dull, aching, or “hunger like” due to excessive acid production

pain relieved by food or antacids, but usually recurring 2 to 4 hours later secondary to food acting as a
buffer for

acid.

Complications

Hemorrhage

Shock

Gastric perforation

Gastric outlet obstruction.

Diagnosis

Barium swallow or upper GI and small bowel series may reveal the presence of the ulcer. This is the first
test

performed on a patient when symptoms aren't severe.

Endenoscopy confirms the presence of an ulcer and permits cytologic studies and biopsy to rule out H.
pylori or

cancer.

Upper GI tract X-rays reveal mucosal abnormalities.

Stool analysis may reveal occult blood.

Serologic testing may disclose clinical signs of infection, such as elevated white blood cell count.

Gastric secretory studies show hyperchlorhydria.

Carbon13 urea breath test results reflect activity of H. pylori.

Treatment

Antimicrobial agents (tetracycline, bismuth subsalicylate, and metronidazole) to eradicate H. pylori

infection (See

Treating peptic ulcer.)

Misoprostol (a prostaglandin analog) to inhibit gastric acid secretion and increase carbonate and mucus
production,

to protect the stomach lining

Antacids to neutralize acid gastric contents by elevating the gastric pH, thus protecting the mucosa and
relieving

pain

Avoidance of caffeine and alcohol to avoid stimulation of gastric acid secretion

Anticholinergic drugs to inhibit the effect of the vagal nerve on acid-secreting cells

H2 blockers to reduce acid secretion

Sucralfate, mucosal protectant to form an acid-impermeable membrane that adheres to the mucous
membrane and

also accelerates mucus production

Dietary therapy with small infrequent meals and avoidance of eating before bedtime to neutralize gastric
contents

Insertion of a nasogastric tube (in instances of gastrointestinal bleeding) for gastric decompression and
rest, and
also to permit iced saline lavage that may also contain norepinephrine

Gastroscopy to allow visualization of the bleeding site and coagulation by laser or cautery to control
bleeding

Surgery to repair perforation or treat unresponsiveness to conservative treatment, and suspected

malignancy.

Treating peptic ulcer

Peptic ulcers can result from factors that increase gastric acid production or from factors that impair
mucosal barrier

protection. This illustration highlights the actions of the major treatments used for peptic ulcer and
where they interfere

with the pathophysiologic chain of events.