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Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
Peptic Ulcer Disease Ppt   April 2005
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Peptic Ulcer Disease Ppt April 2005

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  • 1. Peptic Ulcer Disease
  • 2. Peptic Ulcer Disease
    • Condition characterized by
      • Erosion of GI mucosa resulting from the digestive action of HCl and pepsin
      • Any portion of GI tract that comes in contact with gastric secretions is susceptible to ulcer development including lower esophagus, stomach, & duodenum
      • Includes gastric and duodena l ulcers
  • 3. Types
    • Acute
      • Superficial erosion
      • Minimal inflammation
      • Resolves quickly when cause is identified & removed
    • Chronic
      • Muscular wall erosion with formation of fibrous tissue
      • Present continuously for many months or intermittently
      • 4 times more common than acute ulcers
  • 4. Peptic Ulcers
  • 5. Peptic Ulcer Disease Etiology and Pathophysiology
    • Develop only in presence of acid environment
    • Excess of gastric acid not necessary for ulcer development
    • Person with a gastric ulcer has normal to less than normal gastric acidity compared with person with a duodenal ulcer
  • 6. Peptic Ulcer Disease Etiology and Pathophysiology
    • Some acid does seem to be essential for a gastric ulcer to occur
    • Under specific circumstances the mucosal barrier can be broken and HCL freely enters the mucosa & injury to tissues occurs
    • This results in cellular destruction & inflammation
    • Histamine is released
      • Vasodilation, ↑ capillary permeability
      • Further secretion of acid and pepsin
  • 7. Peptic Ulcers
    • Agents known to to destroy the mucosal barrier include:
    • H. Pylori - causes chronic inflammation making mucosa more vulnerable to noxious agents
    • drugs (aspirin, NSAIDs, corticosteroids) – cause abnormal permeability
  • 8. Gastric Ulcers
    • Commonly found on lesser curvature in close proximity to antral junction
    • Less common than duodenal ulcers
    • Prevalent in women, older adults, persons from lower socioeconomic class
  • 9. Gastric Ulcers
    • Characterized by a normal to low secretion of gastric acid
    • Back diffusion of acid is greater (chronic)
    • The ability of the gastric acid to penetrate the mucosal barrier is more important than the amount of gastric acid produced
  • 10. Gastric Ulcers
    • Critical pathologic process is amount of acid able to penetrate mucosal barrier
    • H. pylori is present in 50% to 70%
    • H. pylori is thought to be more destructive when noxious agents are used e.g.. drugs or smoking
  • 11. Gastric Ulcers
    • Drugs can cause acute and chronic gastric ulcers
      • Aspirin, corticosteroids, and NSAIDs
      • Other known causative factors are:
        • Chronic alcohol abuse, chronic gastritis
        • Cigarette smoking is positively linked with gastric ulcers
        • Ingestion of hot, spicy foods may be a cause but no evidence to support this
  • 12. Duodenal Ulcers
    • Occur at any age and in anyone
    • Incidence is high between ages of 35 to 45 years
    • Affect more men than women
    • Account for 80% of all peptic ulcers
  • 13. Duodenal Ulcers
    • Associated with ↑ HCl acid secretion
    • H. pylori is found in 90-95% of patients
      • Direct relationship has not been proven
  • 14. Duodenal Ulcers
    • Diseases with ↑ risk of duodenal ulcers -
      • COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal failure
    • Treatments used for these conditions may promote ulcer development
  • 15. Duodenal Ulcer
  • 16. Psychological Stress Ulcers
    • Acute ulcers that develop following a major physiologic insult such as trauma or surgery
    • A form of erosive gastritis
  • 17. Psychological Stress Ulcers
    • Gastric mucosa of body of stomach undergoes a period of transient ischaemia in association with
      • Hypotension
      • Severe injury
      • Extensive burns
      • Complicated surgery
  • 18. Peptic Ulcer Pain
    • Gastric
    • Burning or gaseous
    • Can occur when stomach empty or immediately after food
    • Located high in epigastrium
    • Not necessarily relieved by food
    • Duodenal
    • Burning or cramp-like
    • Occurs 2-4 hrs after meals
    • Located in mid-epigastrium
    • Usually relieved by food or antacids
  • 19. Peptic Ulcer Disease Complications
    • 3 major complications
      • Hemorrhage
      • Perforation
      • Gastric outlet obstruction
    • Initially treated conservatively
    • May require surgery at any time during course of therapy
  • 20. Peptic Ulcer Disease Hemorrhage
    • Most common complication of peptic ulcer disease
    • Develops from erosion of
      • Granulation tissue found at base of ulcer during healing
      • Ulcer through a major blood vessel
  • 21. Peptic Ulcer Disease Perforation
    • Most lethal complication of peptic ulcer
    • Commonly seen in large penetrating duodenal ulcers that have not healed and are located on posterior mucosal wall
    • Perforated gastric ulcers often located on lesser curvature of stomach
  • 22. Peptic Ulcer Disease Perforation Fig. 40-15

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