Atlas of pathophysiology, 2 Edition

Part II - Disorders

Gastrointestinal Disorders

Ulcers

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 don't extend below the epithelium. Ulcers may be acute or chronic in nature. Acute ulcers are usually multiple and superficial. Chronic ulcers are identified by scar tissue at their base.

Age Alert

Gastric ulcers are most common in middle-age and elderly men, especially in chronic users of nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, or tobacco.

Causes

· Helicobacter pylori infection

· NSAIDs

· Inadequate protection of mucous membrane

· Pathologic hypersecretory disorders

Predisposing factors

· Blood type (gastric ulcers and type A; duodenal ulcers and type O)

· Other genetic factors

· Exposure to irritants, such as alcohol, coffee, tobacco

· Emotional stress

· Physical trauma and normal aging

Pathophysiology

Ulceration stems from inhibition of prostaglandin synthesis, increased gastric acid and pepsin secretion, reduced gastric mucosal blood flow, or decreased cytoprotective mucus production.

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 production in the duodenum.

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

Signs and symptoms

Gastric ulcer

· Recent weight loss or loss of appetite

· Pain that worsens with eating

· Nausea and anorexia

· Pallor

· Epigastric tenderness

· Hyperactive bowel sounds

Duodenal ulcer

· Epigastric pain that's gnawing and dull; similar to hunger

· Pain relieved by food or antacids, but usually recurring 2 to 4 hours after ingestion

· Weight gain

· Pallor

· Epigastric tenderness

· Hyperactive bowel sounds

Clinical Tip

Complications may occur and include hemorrhage, shock, gastric perforation, and gastric outlet obstruction.

Diagnostic test results

· Barium swallow or upper GI and small bowel series reveal the presence of the ulcer.

· Esophagogastroduodenoscopy 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 detects occult blood.

· White blood cell count is elevated.

· Gastric secretory studies show hyperchlorhydria.

· Urea breath test results reflect activity of H. pylori.

Treatment

· Physical and emotional rest

· For H. pylori infection: tetracycline, metronidazole, or clarithromycin; ranitidine, bismuth citrate, bismuth salicylate, or a proton pump inhibitor

· Misoprostol (a prostaglandin analog)

· Antacids

· Avoidance of caffeine, tobacco, and alcohol

· Anticholinergic drugs

· Histamine-2 antagonists

· Sucralfate

· Prostaglandin analogs

· Dietary therapy: small frequent meals and avoidance of eating before bedtime

P.211

COMMON ULCER TYPES AND SITES

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