Peptic ulcer disease is characterized by erosion of the GI mucosa due to gastric acid and pepsin. Ulcers most commonly form in the lower esophagus, stomach, and duodenum. The development of ulcers involves disruption of the mucosal barrier that normally protects the GI tract from acid. Common complications include hemorrhage, perforation, and gastric outlet obstruction. Diagnosis involves endoscopy to identify ulcers and tests for H. pylori infection.

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. 40-13

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. 40-14

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. 40-15

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