PEPTIC ULCER DISEASE
DEFINITION:
A chronic inflammatory disorder of the stomach or duodenum
resulting in ulceration of the gastric or duodenal mucosa.
EPIDEMIOLOGY:
- incidence: ?
- age of onset:
- gastric ulcers - before age 6
- duodenal ulcers - after age 10 with mean age of diagnosis at
11.3 years (46% symptomatic before 10 years and 15% symptomatic
before age 6 years)
- risk factors:
PATHOGENESIS:
- exposure to a triggering agent -> acute or chronic
inflammation
- ulcer formation
- ulcers tend to occur whenever there is an imbalance between
the protective mechanisms of the mucosa (mucous layer,
bicarbonate layer, epithelial layer, submucosal layer,
prostaglandin metabolism, vasculature) and harmful mechanisms to
the mucosa (hyperacidity, increased pepsin, cytotoxic agents)
- the triggering agents outlined below have been identified in
precipitating this imbalance
2. Helicobacter Pylori
- probably the most common cause of acute and chronic
gastritis and duodenitis leading to pepetic ulcer disease
- found in 90-100% of those with duodenal ulcers
- found in 66-77% of those with gastric ulcers
- a spiral urease-producing organism specific for gastric and
duodenal mucosa
- resides in the boundary between the epithelial cell surface
and the overlying mucous gel where the urease degrades gastric
mucin (part of the protective barrier) and a cytotoxin is
produced
- incidence of H. pylori infection increases with age:
- this shows that not everyone with a H. pylori infection
develops peptic ulcer disease
- H. pylori has also been associated with gastritis, gastric
carcinomas, and gastric mucoid-associated lymphoid-tissue (MALT)
lymphoma
- try to rule out other causes of peptic ulcer disease
(stress, drugs, diseases) before considering H. pylori infection
3. Stress-Induced Ulcers
- can develop within minutes to hours after the initial insult
- due to ischemic damage -> decreased mucosal blood flow ->
injury to the mucosa -> ulcer formation
CLINICAL FEATURES:
- abdominal pain
- abdominal tenderness
- melena
- nausea/vomiting
- hematemesis
- complications:
- perforation +/- peritonitis
- gastric cancer (with longstanding H. pylori infection)
2. Abdominal Pain
- onset usually an hour after meals
- made worse after ingestion of pop (pH 2.8-3.2), pickles,
vinegar, tomatoes, alcohol, spices
- made better after eating or antacids
- epigastric or RUQ in older children and adolescents
- periumbilical, RLQ, or poorly localized in younger children
- associated symptoms include nocturnal or early morning pain
and feeding problems (in younger children)
3. Types of Peptic Ulcer Disease
- more prevelent in those under 6 years of age
- M = F
2. Duodenal Ulcer
- more prevelent in those older than 10 years of age
- M > F
INVESTIGATIONS:
- diagnostic for peptic ulcer disease in 85% of children
- endoscopic biopsy with culture or histology (Giemsa, Warthin-Starry
stain, hematoxylineosin) is the gold standard for H. pylori
infection
2. Imaging Studies
3. Screening Tests for H. pylori
- serology for IgG antibodies to H. pylori
- breath tests of urease activity
MANAGEMENT:
- has a 80-90% eradication rate
- give therapy for 14 days
- Bismuth Compound (Pepto Bismol)
- contains salicylate (watch for Reye's Syndrome if
recent varicella or influenzae infection)
- Metronidazole
- Tetracycline or Amoxicillin
- used in the first line treatment of MALT lymphoma and
can lead to regression of low-grade MALT lymphomas
2. Double Combination
2. Stress-Induced
- IV or po cimetidine or ranitidine
- antisecretory agents which directly inhibit gastric
secretion
- see below
2. Sucralfate
3. Drug-Induced
- magnesium and aluminum-containing antacids
- dose depends on age and size of patient
- avoid calcium carbonate (Tums)
2. H2-Receptor Antagonists
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