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Peptic Ulcer Disease • A 52-year-old male presents with epigastric pain that improves with meals. Endoscopy demonstrates a 2 Cm ulcerated area located 3 cm distal to the pyloric junction. Which of the following is most likely to have made the strongest contribution to the development of this disease? A. Aspirin use B. Chronic antacid use C. Drinking alcohol D. Helicobacter pylori infection E. Smoking Ulcer 1. Peptic ulcer 2. Stress ulcers (acute gastric ulcers) Ulcer: a breach in the mucosa of the alimentary tract extending through muscularis mucosa into submucosa or deeper. Pathophysiology Aggressive Factors Defensive Factors Pathophysiology imbalance Defensive Factors Aggressive Factors H. pylori Drugs (NSAIDs) Acid pepsin Bile salts Aggressive Factors Defensive Factors Mucus bicarbonate Blood flow, cell renewal Prostaglandins Phospholipid Pathophysiology imbalance Defensive Factors Aggressive Factors H. pylori Drugs (NSAIDs) Acid pepsin Bile salts Aggressive Factors Defensive Factors Mucus bicarbonate Blood flow, cell renewal Prostaglandins Phospholipid Acute peptic ulcers Pathophysiology • As part of an acute gastritis • As a complication of a severe stress response • As a result of extreme hyperacidity. Pathophysiology Acute peptic ulcers • As part of an acute gastritis (acute response to an irritant 'chemical' injury by drugs or alcohol • As a complication of a severe stress response (severe burns (Curling's ulcer), major trauma or cerebrovascular accidents ) • As a result of extreme hyperacidity (ZollingerEllison syndrome). Chronic peptic ulcer Peptic Ulcer Disease Locations • May occur in any portion of the GI tract exposed to acidic gastric juices • 98% located in first portion of duodenum or stomach, ratio = 4:1 • Esophagus……. as a result of GERD or acid secretion by ectopic gastric mucosa. • Gastric mucosa within a Meckel diverticulum can result in peptic ulceration of adjacent mucosa. Peptic Ulcer Disease Gastric ulcers Pathophysiology The mucosal defences against acid attack consist of: 1. Mucus-bicarbonate barrier 2. The surface epithelium. Peptic Ulcer Disease Gastric ulcers Pathophysiology The mucosal defences against acid attack consist of: 1. Mucus-bicarbonate barrier Duodeno-gastric reflux ( bile ) 2. The surface epithelium. 1. NSAIDs (blocking the synthesis of the prostaglandins) 2. H. pylori infection, ( cytotoxins and ammonia) Thus peptic ulcers in the stomach, breakdown of mucosal defence is much more important than excessive acid production. Peptic Ulcer Disease Duodenal ulcers Pathophysiology Increased production of acid assumes more importance in the pathogenesis of duodenal ulceration H. pylori-infected individuals secrete 2-6 times as much acid as non-infected controls Helicobacter Pylori does not colonise normal duodenal epithelium Helicobacter is involved in duodenal ulceration because there is gastric metaplasia in response to excess acid. Gastric metaplasia paves the way for colonisation by Helicobacter + Increased production of acid Helicobacter P = Duodenal ulcers Peptic Ulcer Disease Pathophysiology Duodeno-gastric reflux ( bile ) Gastric ulcers Hyperacidity H. pylori Duodenal ulcers NSAIDs H pylori infection of the pyloric antrum is present in nearly all patients with chronic duodenal ulcer and approximately 75% of patients with chronic gastric ulcer. Although more than 70% of individuals with PUD are infected by H. pylori, fewer than 20% of H. pylori–infected individuals develop peptic ulcer. Morphology • Gross • usually less than 20 mm in diameter but they may > 100 mm in diameter. • The classic peptic ulcer is a round to oval, sharply punched-out defect • In contrast, heaped-up margins are more characteristic of cancers • Microscopy • the base consists of necrotic tissue and polymorph exudate overlying inflamed granulation tissue which merges with mature fibrous (scar) tissue. Clinical features • Epigastric pain (the most common symptom) – Gnawing or burning sensation – Occurs 2-3 hours after meals – Relieved by food or antacids – Patient awakens with pain at night. Some present with complications such as iron deficiency anemia, frank hemorrhage, or perforation. Therapy Current therapies for PUD are aimed at 1. H. pylori eradication 2. Neutralization of gastric acid, primarily with proton pump inhibitors • A 52-year-old male presents with epigastric pain that improves with meals. Endoscopy demonstrates a 2 Cm ulcerated area located 3 cm distal to the pyloric junction. Which of the following is most likely to have made the strongest contribution to the development of this disease? A. Aspirin use B. Chronic antacid use C. Drinking alcohol D. Helicobacter pylori infection E. Smoking • The correct answer is D. The patient has a duodenal peptic ulcer. The strongest risk factor for duodenal peptic ulcer is Helicobacter pylori infection, which is found in almost 100% of these cases (contrast to 70% Infection rate in gastric peptic ulcer). • Aspirin use (choice A) and ethanol use (choice C) are more strongly implicated in gastric ulcer disease than duodenal ulcer disease. • Chronic antacid use (choice B) is seen as a result of peptic ulcer disease, not as a cause of it. • Smoking (choice E) may also be a lesser contributing factor to the development of peptic ulcer. • All of the following are causes of acute peptic ulcer except 1. Severe burns 2. Helicobacter pylori infection 3. Major trauma 4. Zollinger-Ellison syndrome • All of the following are Defensive Factors against gastric ulcer development except A. Mucus B. Bicarbonate C. Bile salts D. Prostaglandins E. Phospholipid A 1) 2) 3) 4) 5) 6) 7) 8) 9) 10) 11) H. pylori Phospholipid Drugs (NSAIDs) Mucus bicarbonate Blood flow Acid pepsin Bile salts cell renewal Prostaglandins B A. Aggressive Factors B. Defensive Factors Scenario • 72-year-old man had multiple episodes hematemesis. He was admitted to the hospital with complaints of syncope, and abdominal pain. • On admission, the patient's blood pressure was 96/72. His conjunctivae were pale. The abdominal examination revealed mild epigastric tenderness. The rectal and prostate examinations were unremarkable; however, black stool, which tested positive for fecal blood, was present. • Hemoglobin : 4.1 gm/dL • The patient was admitted to the Medical Intensive Care Unit, where a nasogastric tube lavage produced coffee-ground gastric contents that tested positive for blood. • He was transfused with six units of packed red blood cells, What is your next step? • An upper GI tract endoscopy was performed, which demonstrated a 5x5 cm gastric ulcer in the antrum along the lesser curvature. Biopsies were taken of the ulcers and surrounding mucosa. • The biopsy specimens showed necrotic debris consistent with an ulcer, and the surrounding mucosa showed acute and chronic inflammation and organisms consistent with Helicobacter pylori. • The patient was treated with acid-suppressive therapy and antibiotics, and was discharged five days after admission. He was given instructions not to take aspirin or drink alcohol.