Peptic Ulcer Disease

Overview

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