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Updated: Dec 11 2021

Peptic Ulcer Disease

  • Snapshot
    • A 45-year-old male presents to the clinic for black stool for the past day. He reports intermittent epigastric pain that is worse with food intake for the past 4 months. The pain is described as dull, 6/10, nonradiating and improves with antacids. He reports a 5-lb. unintended weight loss but denies diarrhea, constipation, cancer history, or fevers. A physical examination is unremarkable.
  • Introduction
    • Clinical definition
      • characterized by erosion and defects in the mucosal lining of the stomach, duodenum, and sometimes the lower esophagus that persist as a function of the acid or peptic activity in gastric juice
        • gastric ulcers describe ulcers occurring at the stomach
        • duodenal ulcers describe ulcers occurring at the duodenum
      • duodenal ulcers
        • abdominal pain is relieved with food intake
        • the majority (90%) of cases are secondary to Helicobacter pylori
      • gastric ulcers
        • abdominal pain is exacerbated with food intake
        • the leading causes are H. pylori followed by nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Associated conditions
      • Zollinger-Ellison syndrome
        • suspect in patients with refractory duodenal ulcers
      • Behcet disease
      • Crohn disease
  • Epidemiology
    • Demographics
      • ulcer incidence increases with age
      • H. pylori is the predominant cause of peptic ulcer disease (PUD) worldwide
      • increasing prevalence of NSAID-related PUD due to widespread use of aspirin and NSAID
    • Risk factors
      • NSAIDs
      • smoking
      • stress
      • age
    • Pathogenesis
      • development of ulcers is secondary to the disruption of normal protective mechanisms of the gastric mucosa (e.g., bicarbonate)
      • H. pylori
        • secretion of urease creates an alkaline environment which allows for the survival of the bacteria
        • inflammatory cytokines inhibit parietal cell acid secretion causing gastric ulcers
        • at the pyloric antrum, somatostatin production is reduced and gastric production is increased, leading to metaplasia of the duodenal cells and causing duodenal ulcers
      • NSAIDs
        • mechanism of action blocks the function of cyclooxygenase-1 (COX-1), which is essential for the production of prostaglandins that stimulates the secretion of mucous that protects the gastric mucosa
        • also inhibits stomach mucosa cell proliferation and mucosal blood flow
      • other causes
        • stress from serious illness
        • gastric ischemia
        • metabolic disturbances
        • vasculitis
        • gastrinoma (Zollinger-Ellison syndrome)
  • Presentation
    • Symptoms
      • abdominal pain
        • most commonly at the upper quadrants
      • belching
      • vomiting
      • weight loss
      • poor appetite
      • bloating
      • hematemesis
      • melena
    • Physical exam
      • abdominal tenderness
      • peritoneal signs if perforation
  • Evaluation
    • Diagnostic testing
      • diagnostic approach
        • diagnosis is primarily based on clinical presentation and preemptive treatment, confirmation of the diagnosis is made via endoscopy
      • imaging
        • esophagogastroduodenoscopy (EGD)
          • gold standard of diagnosis
          • indicated in patients who show no symptom improvement following few weeks of treatment
          • allows for direct visual identification and allows for evaluation of the location and severity of the disease
          • biopsy is important for the differentiation between benign ulcers and malignancy
        • abdominal and chest radiographs
          • may be useful in detecting pneumoperitoneum secondary to perforation
          • positive findings include air-fluid levels with bowel dilation or free air
      • studies
        • urease breath test
          • best initial test
          • noninvasive and allows for the detection of H. pylori infection
        • complete blood count
          • often normal
        • serum gastrin
          • can be used to evaluate Zollinger-Ellison syndrome
  • Differential
    • Gastric malignancy
      • differentiating factors
        • lesions will appear different on endoscopy and will be confirmed via biopsy
    • Chronic pancreatitis
      • differentiating factors
        • may have characteristic disease history and will present with calcifications on abdominal imaging
  • Treatment
    • Management depends on disease etiology and severity
    • H. pylori-induced PUD
      • clarithromycin, amoxicillin, and pantoprazole for 7-14 days
      • clarithromycin, amoxicillin, pantoprazole, and metronidazole for 7-14 days
    • NSAID-induced PUD
      • stop NSAID use
      • introduce proton pump inhibitor (PPI) use
    • Bleeding ulcers
      • resuscitation with IV fluids and/or blood products
      • IV PPI
      • endoscopic therapy with either cautery, endoclip or epinephrine injection
    • Surgery
      • indicated in patients with perforated ulcer and/or hemorrhage
        • requires IV antibiotics and PPI prior to repair
      • other indications include PUD refractory to medical therapy and Zollinger-Ellison syndrome
  • Complications
    • Bleeding
    • Perforation
      • manage with broad spectrum antibitoics, PPI, and emergency surgery
    • Obstruction
    • Malignancy
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