Topic: Bleeding peptic ulcer, tuberculosis of bowel, ulcerative colitis
Question: Describe the etiology, laboratory findings and treatment options available for peptic ulcer disease.
Reference Material-This material is informational alone and is not specifically prepared as an answer for any question. Readers may do their own research before finalising diagnoses according to the characteristics unique to each question. Readers should not proceed without cross-referencing with relevant textbooks as well as standard guidelines available.
- Etiology:
- Helicobacter pylori infection is the most common cause of peptic ulcer disease (PUD). H. pylori is a gram-negative bacterium that infects nearly half the world’s population. It colonizes the gastric mucosa and causes a chronic active gastritis which impairs mucosal defense and resistance leading to ulcers. All patients with PUD should be tested for H. pylori and treated if positive.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are the second most common cause of PUD. Long term or high dose NSAID use inhibits cyclooxygenase enzymes (especially COX-1) which mediate prostaglandin synthesis important for mucosal defense and repair. This impairment in mucosal integrity results in ulcers and erosions. Patients at high risk of NSAID-induced ulcers should receive PPI prophylaxis. Risk factors include: age >65 years, high NSAID dose/multiple NSAIDs, history of PUD, H. pylori infection, corticosteroid use, diabetes, CVD, and smoking.
- Zollinger-Ellison syndrome (ZES) is caused by gastrinomas, usually in the pancreas and duodenum, which secrete excess gastrin and stimulate gastric acid secretion leading to ulcers. Diagnosis is by serum gastrin >1000 pg/mL (basal) and >2000 pg/mL (stimulated). Treatment includes high dose PPIs, H2 blockers, octreotide to reduce hormone and acid secretion. Chemotherapy or surgical resection may be required for refractory or complicated cases.
- Other causes include severe physiological stress, Crohn’s disease, sarcoidosis, lymphoma, gastric adenocarcinoma, smoking, alcohol, previous gastric surgery, hyperparathyroidism, and mastocytosis. Approximately 5-10% of PUD cases have no identifiable cause.
- Laboratory findings:
- • Serum gastrin: Elevated in ZES as described above. Mild elevations (<300 pg/mL) in 20% of duodenal ulcer patients.
- • Stool guaiac test: Checks for occult blood in stool from ulcer bleeding. Negative test is normal.
- • Urea breath test: 96-98% sensitive and 100% specific for H. pylori. False negatives can occur in bleeding ulcers or if antibiotics/PPI used in the past 4 weeks.
- • Endoscopy: Most accurate test for diagnosis of PUD. Can detect ulcers, erosions, tumors. Biopsies determine etiology – H. pylori, malignancy (gastric adenocarcinoma, lymphoma), Crohn’s disease, etc.
- • CBC: May show iron deficiency anemia in chronic blood loss. Significant drops in Hb/Hct suggest active bleeding.
- Barium swallow: Can detect ulcers via x-ray after barium contrast agent is swallowed. Not as sensitive as endoscopy.
- Medical management:
- • H. pylori infection: Triple therapy – PPI (omeprazole 20 mg BD), amoxicillin 1 g BD or metronidazole 400 mg BD if penicillin allergic), clarithromycin 250-500 mg BD for 14 days. Alternative treatment for resistant strains include bismuth quadruple therapy, concomitant therapy, sequential therapy, etc. Confirm eradication with breath test or stool antigen test ≥ 4 weeks after treatment.
- • NSAID ulcers: Remove offending agent if possible. Maximize PPI prophylaxis (omeprazole 20-40 mg BD or equivalent). Can add misoprostol 200 mcg QID.
- • ZES: High dose PPI (omeprazole 40-60 mg TID). H2 blockers and antacids for breakthrough acid breakthrough. Octreotide may help suppress gastrin and acid secretion. Chemotherapy (streptozocin, 5-FU, doxorubicin) or surgical resection for refractory disease or tumor complications.
- • Other causes: Treat underlying condition. Provide acid suppression with PPIs or H2 blockers to promote ulcer healing.
- • Lifestyle changes: Avoid NSAIDs, smoking, alcohol. Reduce stress.
- Surgical management: Indicated for medically unresponsive or complicated PUD (perforation, refractory bleeding, gastric outlet obstruction, etc.). Options include:
- • Vagotomy (truncal, selective, proximal) – denervates parietal cells reducing acid secretion. Rarely done alone now due to side effects.Healing rate 60-90% for duodenal ulcers.
- • Partial gastrectomy – removes part of stomach, usually acid-secreting areas. Preserves gastric function but still significant side effects. Very effective but can cause “dumping syndrome”. Should only be done in elderly or high-risk patients.
- • Antrectomy: Removes distal stomach and duodenal bulb to reduce acid secretion. Higher risk of side effects like diarrhea but >95% healing rate. •
- • Perforated ulcer: Emergency surgery to close perforation and wash abdominal cavity. Definitive surgery can be done electively.
- • Gastric resection: For bleeding ulcers unresponsive to endoscopic therapy. Removes portion of stomach to control bleeding.
- Points to highlight:
- • PPIs are the cornerstone of treatment for peptic ulcers due to their superior acid suppression.
- • Eradicating H. pylori is key to preventing ulcer recurrence.
- • Lifestyle changes and avoiding medications that irritate the stomach can help.
- • Endoscopy is the best method to diagnose the underlying cause of ulcers.
- • Anemia and gastrointestinal bleeding can be signs of serious ulcer complications requiring surgery.
- • The type of surgery depends on ulcer location, severity of complications and patient condition.
