Pathophysiology · MU Sofia

141. Peptic ulcer disease - classification, etiology, pathogenesis, clinical manifestations.

Inside: 4 sections · 2 tables · 15 flashcards · 2 min

Topic 141 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 4 sections, about 248 words (2 min of reading), with 15 flashcards.

In this note

  1. Peptic ulcer disease - classification, etiology, pathogenesis, and clinical manifestations.
  2. Classification
  3. Etiology
  4. Pathogenesis

Peptic ulcer disease - classification, etiology, pathogenesis, and clinical manifestations.

Peptic ulcer disease (PUD)

Peptic ulcer disease refers to chronic mucosal ulcers in areas exposed to gastric acid and pepsin, most commonly in the stomach and proximal duodenum.

Classification

By location

By number

  • Single.
  • Multiple.

Etiology

Helicobacter pylori infection (most common)

  • Especially in duodenal ulcers (~90% cases).

Nonsteroidal anti- inflammatory drugs (NSAIDs)

  • Inhibit prostaglandin synthesis → reduced mucosal protection.

Other factors

  • Smoking.
  • Excessive alcohol use.
  • Corticosteroids.
  • Zollinger-Ellison syndrome (gastrinoma → excess acid).
  • Severe stress (e.g., ICU patients → "stress ulcers").

Pathogenesis

Balance disturbance

  • PUD arises from an imbalance between mucosal protective factors and damaging factors.

Damaging factors

  • Gastric acid and pepsin.
  • H. pylori toxins.
  • NSAIDs (via prostaglandin inhibition).

Protective factors

  • Mucus- bicarbonate barrier.
  • Prostaglandins.
  • Adequate mucosal blood flow.
  • Epithelial regeneration.

Mechanism

  1. H. pylori infection → produces urease → local ammonia production → mucosal damage.
  2. Induces chronic gastritis → increased gastrin → increased acid secretion (especially in duodenal ulcers).
  3. NSAIDs reduce prostaglandins → impaired mucus and bicarbonate production → higher susceptibility to acid injury.
  4. Acid and pepsin digest mucosa → ulcer formation.

Clinical manifestations

General features

  • Epigastric burning or gnawing pain.

Gastric ulcer

  • Pain worsens with meals (due to acid secretion stimulating ulcer).
  • Possible weight loss (patients avoid eating).

Duodenal ulcer

  • Pain improves with meals, recurs 2–3 hours after eating ("hunger pain").
  • Possible weight gain (patients eat to relieve pain).

Other symptoms

  • Nausea, bloating.
  • Belching.

Complications

  • Gastrointestinal bleeding (hematemesis, melena).
  • Perforation → peritonitis → sudden severe abdominal pain.
  • Gastric outlet obstruction (due to scarring, edema ).
  • Penetration into adjacent organs (e.g., pancreas).

Read the full note free

The whole note, all 4 sections, is free with an AceMed account, with its 15 flashcards. Premium adds flashcard recall, highlights and Ask AI.