1. Peptic Ulcer Disease

2. Peptic Ulcer Disease Condition characterized by
Erosion of GI mucosa resulting from digestive action of HCl and pepsin

3. Peptic Ulcer Disease Ulcer development Lower esophagus Stomach
Duodenum
10% of men, 4% of women

4. Types Acute Superficial erosion Minimal erosion Chronic
Muscular wall erosion with formation of fibrous tissue
Present continuously for many months or intermittently

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 intraluminal acid does seem to be essential for a gastric ulcer to occur
Pepsinogen is activated to pepsin in presence of HCl and a pH of 2 to 3
Secretion of HCl by parietal cells has a pH of 0.8
pH reaches 2 to 3 after mixing with stomach contents

7. Peptic Ulcer Disease Etiology and Pathophysiology
At pH level 3.5 or more, stomach acid is neutralized
Pepsin has little or no proteolytic activity
Surface mucosa of stomach is renewed about every 3 days
Mucosa can continually repair itself except in extreme instances

8. Peptic Ulcer Disease Etiology and Pathophysiology
Mucosal barrier prevents back diffusion of acid from gastric lumen through mucosal layers to underlying tissue
Mucosal barrier can be impaired and back diffusion can occur

9. Back-Diffusion of Acids
Fig

10. Peptic Ulcer Disease Etiology and Pathophysiology
HCl freely enters mucosa when barrier is broken
Injury to tissue occurs
Result: cellular destruction and inflammation

11. Peptic Ulcer Disease Etiology and Pathophysiology
Histamine is released
Vasodilation, ↑ capillary permeability
Further secretion of acid and pepsin

12. Peptic Ulcer Disease Etiology and Pathophysiology
Ulcerogenic drugs inhibit synthesis of prostaglandins and cause abnormal permeability
Corticosteroids ↓ rate of mucosal cell renewal thereby ↓ protective effects

13. Peptic Ulcer Disease Etiology and Pathophysiology
When mucosal barrier is disrupted, there is a compensatory ↑ in blood flow
Prostaglandin-like substances, histamines act as vasodilators
Hydrogen ions are rapidly removed
Buffers are delivered
Nutrients arrive
↑ Mucosal cell replication

14. Disruption of Gastric Mucosal Barrier
Fig

15. Peptic Ulcer Disease Etiology and Pathophysiology
When blood flow is not sufficient, tissue injury results

16. Peptic Ulcer Disease Etiology and Pathophysiology
Two mechanisms that protect
Mucus forms a layer that entraps or slows diffusion of hydrogen ions across mucosal barrier
Bicarbonate is secreted
Neutralizes HCl acid in lumen of GI tract

17. Peptic Ulcer Disease Etiology and Pathophysiology
↑ Vagal nerve stimulation results in hypersecretion of HCl acid
↑ HCl acid can alter mucosal barrier
Duodenal ulcers are associated with ↑ acid

18. 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

19. Gastric Ulcers Characterized by
A normal to low secretion of gastric acid
Back diffusion of acid is greater (chronic)

20. Gastric Ulcers
Critical pathologic process is amount of acid able to penetrate mucosal barrier
H. pylori is present in 50% to 70%

21. Gastric Ulcers
H. pylori is thought to be more destructive when noxious agents are used, or patient smokes

22. Gastric Ulcers Drugs can cause acute gastric ulcers
Aspirin, corticosteroids, NSAIDs, reserpine
Or known causative factors
Chronic alcohol abuse, chronic gastritis

23. Duodenal Ulcers Occur at any age and in anyone
↑ Between ages of 35 to 45 years
Account for ~80% of all peptic ulcers

24. Duodenal Ulcers Associated with ↑ HCl acid secretion
H. pylori is found in 90-95% of patients
Direct relationship has not been found

25. 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

26. Psychological Stress Ulcers
Acute ulcers that develop following a major physiologic insult such as trauma or surgery
A form of erosive gastritis

27. Psychological Stress Ulcers
Gastric mucosa of body of stomach undergoes a period of transient ischemia in association with
Hypotension
Severe injury
Extensive burns
Complicated surgery

28. Psychological Stress Ulcers
Ischemia due to ↓ capillary blood flow or shunting of blood away from GI tract so that blood flow bypasses gastric mucosa
Imbalance between destructive properties of HCl acid and pepsin, and protective factors of stomach’s mucosal barrier

29. Peptic Ulcer Disease Clinical Manifestations
Common to have no pain or other symptoms
Gastric and duodenal mucosa not rich in sensory pain fibers
Duodenal ulcer pain
Burning, cramplike
Gastric ulcer pain
Burning, gaseous

30. 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

31. 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

32. 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

33. Peptic Ulcer Disease Perforation
Perforated gastric ulcers often located on lesser curvature of stomach

34. Peptic Ulcer Disease Perforation
Fig

35. Peptic Ulcer Disease Perforation
Occurs when ulcer penetrates serosal surface
Spillage of their gastric or duodenal contents into peritoneal cavity
Size of perforation directly proportional to length of time patient has had ulcer
Sudden, dramatic onset

36. Peptic Ulcer Disease Gastric Outlet Obstruction
Ulcers located in antrum and prepyloric and pyloric areas of stomach
Duodenum can predispose to gastric outlet obstruction
↑ contractile force needed to empty stomach results in hypertrophy of stomach wall

37. Peptic Ulcer Disease Gastric Outlet Obstruction
After longstanding obstruction stomach enters decompensated phase
Results in dilation and atony

38. Peptic Ulcer Disease Gastric Outlet Obstruction
Obstruction is not totally due to fibrous scar tissue
Active ulcer formation is associated with edema, inflammation, pylorospasm
All contribute to narrowing of pylorus

39. Peptic Ulcer Disease Gastric Outlet Obstruction
Usually has a history of ulcer pain
Short duration or absence of pain indicative of a malignant obstruction

40. Peptic Ulcer Disease Gastric Outlet Obstruction
Vomiting is common
Constipation is a common complaint
Dehydration, lack of roughage in diet
May show swelling in upper abdomen

41. Peptic Ulcer Disease Diagnostic Studies
Endoscopy procedure most often used
Determines degree of ulcer healing after treatment
Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer

42. Peptic Ulcer Disease Diagnostic Studies
Tests for H. pylori
Noninvasive tests
Serum or whole blood antibody tests
Immunoglobin G (IgG)
Urea breath test
Invasive tests
Biopsy of stomach
Rapid urease test

43. Peptic Ulcer Disease Diagnostic Studies
Barium contrast studies
Widely used
X-ray studies
Ineffective in differentiating a peptic ulcer from a malignant tumor

44. Peptic Ulcer Disease Diagnostic Studies
Gastric analysis
Identifying a possible gastrinoma
Determining degree of gastric hyperacidity
Evaluating results of therapy

45. Peptic Ulcer Disease Diagnostic Studies
Laboratory analysis
CBC
Urinalysis
Liver enzyme studies
Serum amylase determination
Stool examination