Peptic ulcer disease PUD
المرحلة الرابعة/د.خلدون العبايجي- Includes commonly ulcers in the stomach and duodenum, but may occur in the lower esophagus in GERD, in jejunum after stomach anastomosis and in Meckles diverticulum.
- acute and chronic ulcers penetrate muscularis mucosa but in acute ulcer no fibrosis.
- erosions do not penetrate muscularis mucosa.
Gastric and duodenal ulcers
- chronic GU usually single, 90% in the lesser curve within the antrum.
- chronic DU usually in the first part of the duodenum, 50% on the anterior wall.
- both DU and GU coexist in 10% of patients.
- DU is multiple in 10% of patients.
Pathophysiology
- strongly associated with H.pylori infection in 90% of patient with DU and 70% of GU.
- In the west 30% of PUD is due to NSAIDs.
- prevalence of H.pylori infection increases with age, in developing countries it affects 90% of population.
- majority of infected persons are a symptomatic and only minority develop disease.
- it is flagellated gram negative bacteria, produce urease which buffers acid by ammonia production.
- H.pylori colonizes only gastric mucosa and is found in duodenum in association with gastric metaplasia.
- it causes chronic gastritis and some develop gastric atrophy and is associated with gastric cancer.
- in most people it causes antral gastritis associated with somatostatin D cells depletion and increased gastrin release from G cells.
- gastrin stimulates parietal cells to secrete acid and subsequent DU.
- pathogenesis of GU is less clear but probably H.pylori reduces mucosal resistance and make it vulnerable to attack from acid and pepsin.
- in 1% H.pylori leads to pangastritis and later gastric mucosal atrophy and hypochlorhydria allowing bacterial growth which change nitrates in food to mutagenic nitrites predisposing to gastric cancer.
- pathogenecity of H.pylori is due to cag A, vac A genes expression and Bab A adhesion molecules.
- smoking and NSAIDs are also risk factors for PUD.
Clinical features
-chronic condition with relapse and remission.
- recurrent epigastric pain with seasonal variations, symptoms recurs in cold seasons and complications are more frequent.
- in DU food relieves pain. Patient may awake at late night with severe pain. Pain may radiate to back. Patient may gain weight due to increased food intake.
- in GU pain may increase after meals and patient may vomit so weight loss may occur.
- persistent vomiting suggests gastric outlet obstruction.
- in elderly patients symptoms are less prominent with little or no pain.
- in some the ulcer is silent and the patient may present with anemia or peptic ulcer complications e.g bleeding or perforation.
- history of the patient is a poor predictor of the presence of ulcer.
Investigations
Endoscopy: Diagnose ulcer accurately, in GU biopsy is taken to exclude cancer.
Diagnosis of H.pylori infection
A. Non invasive tests
1. serology: can not differentiate between recent and past infection.
2. 13C-urea breath test: the best. Highly specific and sensitive.
3. fecal antigen test: cheap and specific but uncomfortable.
B. Invasive tests: Antral biopsy.
1. Histology: sensitive and specific, needs time.
2. Rapid urease test: quick, 95%specific, 85% sensitive.
3. Culture: gold standard, identify antibiotic sensitivity.
Management
H.pylori eradication prevent relapse and avoid long term treatment in majority of patients.
All patients with acute and chronic DU and GU should be offered eradication therapy.
First line therapy: proton pump inhibitor+clarithromycin 500 mg twice daily+amoxicillin 1gm twice daily or metronidazole 400mg twice daily for 7 days. Success is 90%.
If patient remain infected after First line therapy 2nd attempt may be tried.
Second line therapy for patients not responding to First line therapy use: PPI+bismuth+two antibiotics or long term acid suppression.
Patients on NSAIDs with ulcer risk especially elderly, ppi use may be necessary.
H.pylori eradication is also indicated in H.pylori positive dyspepsia and mucosa associated lymphoid tumor but not in gastroesophageal reflux.
General measures:stop smoking, avoid aspirin and NSAIDs, alcohol in moderation.
Minority of patients need maintenance on low dose PPI.
Surgery for PUD (Billroth one and two) indicated in : perforation, bleeding, pyloric obstruction, recurrent ulcer after initial PUD surgery.
Complication of surgery: dumping, biliary gastritis, diarrhea, weight loss, anemia, metabolic bone disease due to malabsorption, gastric cancer.
Complications of peptic ulcers
1. bleeding: manifested as hematemesis and melena, if severe leads to hypotension and shock, if uncorrected results in acute renal failure, it may occur spontaneously in untreated ulcer or after intake of aspirin and NSAIDs, it may be the first presentation of PUD.
Investigations: Full blood count, urea and electrolytes, liver functions, PT, cross matching.
Management:
i.v access, assess pulse, BP,urine output,
Investigations: Full blood count, urea and electrolytes, liver functions, PT, cross matching.
Seek evidence of liver disease e.g jaundice and ascites.
Identify comorbidity: cardiovascular, CVA, renal disease.
Resuscitation: i.v crystalloid fluids or colloid, blood transfusion, monitor CVP.
O2
Endoscopy: for diagnosis and treatment by diathermy, laser, adrenaline injection, metallic clips. Give i.v PPI.
Surgical treatment after failure of endoscopic hemostasis especially in elderly.
2. Perforation
- May occur in untreated ulcer and may be the first sign of ulcer especially after use of NSAIDs.
- sudden severe epigastric pain and later diffuse abdominal pain due to peritonitis.
- if treatment is delayed leads to septic shock.
- rigid abdomen and absent bowel sounds.
- CXR reveals air under diaphragm.
- water soluble contrast barium meal shows leak.
- treated by surgery, H.pylori should be eradicated.
3. Gastric outlet obstruction
- Usually patient have longstanding history of peptic ulcer.
- Presented as repeated nausea and vomiting with abdominal distension, later weight loss, dehydration, succussion splash 4 hours after eating with visible gastric peristalsis.
- low CL, K, increase urea and bicarbonate.
- Barium meal show hugely dilated stomach with gas bubbles and food particles.
- Endoscopy after wide bore nasogastric tube emptying show a dilated stomach with very narrow pyloric opening.
- Treatment: correct fluid and electrolyte imbalance by normal saline and potassium, in some patients PPI heal the ulcer and relieves pyloric ring edema without need for surgery. Other wise patients may need endoscopic balloon dilatation or surgical procedure. Eradicate H.pylori and give PPI.
Non-ulcer dyspepsia
Chronic upper GIT disorder in the absence of organic cause like ulcer or tumor.
Causes: mucosal disorder, motility defects, psychiatric disorder.
It occurs in adults and elderly and both sexes.
Upper abdominal pain, nausea, vomiting mainly at morning, bloating, early satiety, fullness, stagnation of food in the stomach, hyperacidity, heart burn.
Absent physical signs apart from mild epigastric tenderness, patient looks well.
May merge with irritable bowel syndrome.
Exclude: peptic ulcer, drug intake , malignancy, depression, pregnancy, alcohol misuse.
Alarm features: weight loss, anemia, vomiting, GIT bleeding, dysphagia, palpable abdominal mass.
Investigations: most patients need no investigations, endoscopy to exclude ulcer, tumor, sonography to exclude gall stones.
Management :
Explanation, reassurance, psychological support .
Advice about healthy dietary habits.
Antacids, antispasmodic drugs, prokinetic drugs (domperidone), ranitidine, low dose amitryptyline, simethicone.
If patient has H.pylori infecton give eradication therapy.
Some need psychotherapy and behavioral therapy.