Peptic ulcer disease Notes

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Access comprehensive Peptic Ulcer Disease (PUD) Notes PDF. These notes provide a detailed understanding of PUD, a condition characterized by sores or ulcers in the lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer). The PDF covers the etiology (including Helicobacter pylori infection and NSAID use), pathophysiology, clinical manifestations, diagnostic approaches, and pharmacological and non-pharmacological management strategies. Essential for students of medicine, gastroenterology, pharmacology, nursing, and related health sciences. You can download these "Peptic Ulcer Disease Notes PDF" for free for offline study or view them directly online. Slides By DuloMix offers these valuable educational resources to aid your learning.

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Why Download These Peptic Ulcer Disease Notes?

• Common Gastrointestinal Disorder: PUD is a prevalent condition with significant clinical impact.
• In-Depth Pathophysiology and Treatment: The notes explain the causes and the rationale behind various treatment modalities.
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• Convenient Study Resource: Download for offline access or view online to fit your study schedule.
• Clinically Relevant Information: Key for understanding diagnosis and management of patients with PUD.

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Peptic Ulcer Disease (PUD): Pathophysiology, Causes, and Management

Peptic Ulcer Disease (PUD) refers to the development of open sores, or ulcers, in the mucosal lining of the gastrointestinal (GI) tract that are exposed to gastric acid and pepsin. These ulcers most commonly occur in the stomach (gastric ulcers) or the duodenum (duodenal ulcers), the first part of the small intestine. PUD arises from an imbalance between aggressive factors that damage the mucosa and protective mechanisms that defend it.

Pathophysiology of Peptic Ulcer Disease

The gastroduodenal mucosa is normally protected by several defense mechanisms:

• Mucus Layer: A thick, adherent layer that forms a physical barrier.
• Bicarbonate Secretion: Neutralizes gastric acid at the mucosal surface.
• Prostaglandins: Stimulate mucus and bicarbonate secretion, inhibit acid secretion, and promote mucosal blood flow and epithelial cell restitution.
• Adequate Mucosal Blood Flow: Delivers oxygen and nutrients, removes toxic metabolites.
• Epithelial Cell Integrity and Rapid Regeneration: Tight junctions between cells and quick repair of minor damage.

Ulcers develop when these protective mechanisms are overwhelmed or impaired by aggressive factors:

• Gastric Acid and Pepsin: Essential for ulcer formation but usually not the primary cause in a healthy mucosa. Pepsin is a proteolytic enzyme activated by acid.
• Helicobacter pylori (H. pylori) Infection: A spiral-shaped bacterium that colonizes the gastric mucosa.
• Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Including aspirin.
• Other Factors: Smoking, excessive alcohol consumption, severe physiological stress (e.g., in critically ill patients - stress ulcers), Zollinger-Ellison syndrome (gastrin-producing tumor).

Major Etiological Factors

1. Helicobacter pylori Infection

• The most common cause of PUD worldwide.
• H. pylori produces several virulence factors:
  • Urease: Converts urea to ammonia, which neutralizes gastric acid locally, allowing the bacteria to survive. Ammonia can also be toxic to epithelial cells.
  • Adhesins: Allow bacteria to bind to gastric epithelial cells.
  • Toxins: E.g., CagA (cytotoxin-associated gene A) and VacA (vacuolating cytotoxin A) contribute to inflammation and mucosal damage.
• Induces a chronic inflammatory response (gastritis) in the stomach, which can disrupt mucosal integrity, alter acid secretion (can increase or decrease depending on location of gastritis), and predispose to ulceration.
• Associated with both duodenal and gastric ulcers, as well as gastric cancer and MALT lymphoma.

2. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

• The second most common cause of PUD.
• Mechanism of Damage:
  • Systemic Effect: Inhibition of cyclooxygenase (COX) enzymes (COX-1 and COX-2), leading to decreased synthesis of prostaglandins. COX-1 is constitutively expressed and produces prostaglandins vital for mucosal protection.
  • Topical Effect: NSAIDs are weak acids and can directly irritate the gastric mucosa in their non-ionized form, especially if trapped within epithelial cells.
• Risk factors for NSAID-induced ulcers include older age, history of PUD, concomitant use of corticosteroids or anticoagulants, high NSAID dosage, and long duration of use. COX-2 selective inhibitors have a lower risk of GI toxicity than non-selective NSAIDs but do not eliminate it entirely.

Clinical Features

• Epigastric Pain: The most common symptom. Often described as burning, gnawing, or aching.
  • Duodenal Ulcer Pain: Typically occurs 1-3 hours after meals, often relieved by food or antacids. May awaken the patient at night.
  • Gastric Ulcer Pain: More variable; may be precipitated or worsened by food.
• Nausea, vomiting.
• Dyspepsia (indigestion), bloating, belching.
• Loss of appetite, weight loss (more common with gastric ulcers or if pain is food-related).
• Many patients, especially elderly or those on NSAIDs, may be asymptomatic until a complication occurs.

Diagnosis

• Endoscopy (Esophagogastroduodenoscopy - EGD): The gold standard for diagnosing PUD. Allows direct visualization of the ulcer, biopsy for histology (to rule out malignancy in gastric ulcers), and testing for H. pylori.
• Testing for H. pylori Infection:
  • Invasive (Endoscopy-based): Rapid urease test (RUT), histology, culture.
  • Non-invasive: Urea breath test (UBT), stool antigen test, serology (detects antibodies, indicates exposure but not necessarily active infection).
• Barium Upper GI Series: Less sensitive than endoscopy, used if endoscopy is contraindicated or unavailable.

Complications of PUD

• Bleeding (Hemorrhage): Most common complication. Manifests as hematemesis (vomiting blood), melena (black, tarry stools), or iron deficiency anemia.
• Perforation: Ulcer erodes through the entire wall of the stomach or duodenum, leading to peritonitis. A surgical emergency.
• Penetration: Ulcer erodes into an adjacent organ (e.g., pancreas, liver).
• Gastric Outlet Obstruction (GOO): Scarring and edema from ulcers near the pylorus can obstruct gastric emptying. Manifests as persistent vomiting, abdominal distension.

Management of Peptic Ulcer Disease

Goals of treatment are to relieve pain, heal the ulcer, prevent recurrence, and manage complications.

1. Eradication of H. pylori (if present)

• Significantly reduces ulcer recurrence.
• Requires combination therapy, typically for 10-14 days.
  • Triple Therapy (standard first-line): A Proton Pump Inhibitor (PPI) + Clarithromycin + Amoxicillin (or Metronidazole if penicillin allergic).
  • Quadruple Therapy (used if high clarithromycin resistance, or after failed triple therapy):
    • Bismuth-based: PPI + Bismuth subsalicylate + Tetracycline + Metronidazole.
    • Non-bismuth (Concomitant): PPI + Clarithromycin + Amoxicillin + Metronidazole.
• Confirmation of eradication is recommended (e.g., UBT or stool antigen test) 4 weeks after completing therapy and off PPIs.

2. Acid Suppression Therapy

• Proton Pump Inhibitors (PPIs): (e.g., Omeprazole, Lansoprazole, Esomeprazole, Pantoprazole, Rabeprazole)
  • Most potent acid suppressors. Irreversibly inhibit the H⁺/K⁺-ATPase (proton pump) in gastric parietal cells.
  • Promote ulcer healing and symptom relief. Usually given for 4-8 weeks.
• Histamine H₂-Receptor Antagonists (H₂RAs): (e.g., Ranitidine - though largely withdrawn due to NDMA concerns, Famotidine, Cimetidine)
  • Block histamine H₂ receptors on parietal cells, reducing acid secretion. Less potent than PPIs.
  • Used for ulcer healing, especially if PPIs are not tolerated, or for maintenance therapy in some cases.

3. Mucosal Protective Agents

• Sucralfate: Forms a protective coating over the ulcer crater in an acidic environment. Minimal systemic absorption.
• Bismuth Compounds (e.g., Bismuth subsalicylate): Have coating effects, antimicrobial activity against H. pylori, and may stimulate prostaglandin synthesis.
• Prostaglandin Analogues (e.g., Misoprostol): Stimulate mucus and bicarbonate secretion, inhibit acid secretion. Used primarily for preventing NSAID-induced ulcers, but limited by side effects (diarrhea, abdominal cramping, abortifacient).

4. Management of NSAID-Induced Ulcers

• Discontinue NSAID if possible.
• If NSAID must be continued, use the lowest effective dose, consider switching to a COX-2 selective inhibitor (if appropriate and no cardiovascular contraindications), and co-prescribe a PPI or misoprostol for gastroprotection.
• Heal ulcer with PPI therapy. Test for and treat H. pylori if present, as co-infection increases risk.

5. Lifestyle Modifications

• Smoking cessation (smoking impairs ulcer healing and increases recurrence).
• Avoidance of excessive alcohol.
• Avoidance of foods and beverages that trigger symptoms (individualized).
• Stress management (though direct causality to common PUD is less clear than for stress ulcers in critical illness).

6. Management of Complications

• Bleeding: Endoscopic therapy (e.g., injection, cautery, clips), PPI infusion, and sometimes surgery.
• Perforation: Surgical repair.
• Gastric Outlet Obstruction: Nasogastric decompression, endoscopic balloon dilation, or surgery.

Peptic ulcer disease is a manageable condition with modern therapeutic approaches, particularly with the focus on H. pylori eradication and effective acid suppression. These notes provide a comprehensive outline for understanding and approaching PUD.

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