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Updated: Oct 4 2021

Peptic Ulcer Disease

  • Snapshot
    • A 65-year-old-male presents with complaints of epigastric pain and belching, which improves when he eats food but gets worse within a few hours after his meal. The pain is described as stabbing, intermittent, and concentrated at the epigastric region. He noticed a 5-lb. weight loss over the past 3 months and a dark color to his stools. Calcium carbonate seems to help with the pain.
  • Introduction
    • Clinical definition
      • characterized by erosion and defects in the mucosal lining of the stomach, duodenum, and sometimes the lower esophagus that persists 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
        • lower risk of malignancy
      • gastric ulcers
        • abdominal pain is exacerbated with food intake
        • the leading causes are H. pylori followed by nonsteroidal anti-inflammatory drugs (NSAIDs) use
        • higher risk of malignancy
    • 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)
    • Associated conditions
      • Zollinger-Ellison syndrome
        • suspect in patients with refractory duodenal ulcers
      • Behcet disease
      • Crohn disease
    • Painful sores or ulcers in the lining of the stomach or duodenum
      • breach in the mucosa with extension into the submucosa or deeper
    • Occurs when gastric acid secretion outweighs mucosal defenses
      • most commonly due to decreased mucosal barrier
        • NSAIDs
        • H. pylori
        • smoking
      • less commonly due to acid hypersecretion
        • such as 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 of perforation
  • 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
  • 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
    • Lifestyle
      • discontinue smoking and NSAIDs
    • 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
      • perforated gastric ulcers may erode the left gastric artery
      • perforated duodenal ulcers may erode the gastroduodenal artery
    • Obstruction
    • Malignancy
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