This document discusses peptic ulcer disease (PUD), including its definition, types, causes, pathogenesis, clinical features, investigations, and management. PUD is defined as ulceration of the gastrointestinal tract exposed to gastric acid. The main types are acute and chronic ulcers. Common causes include H. pylori infection, NSAIDs, smoking, and stress. H. pylori is present in most duodenal and 70% of gastric ulcers. Investigations include endoscopy, biopsy, and tests for H. pylori. Management involves eradicating H. pylori, acid suppression, enhancing mucosal defenses, and surgery for complications.

1. PEPTIC ULCER disease (PUD)PEPTIC ULCER disease (PUD)
Sara Elzeiny

2. * Definition:
Ulceration of any part of the G.I.T exposed to
the gastric juice.

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

5. I.I. ACUTE PEPTIC ULCERSACUTE PEPTIC ULCERS
(STRESS ULCERS)(STRESS ULCERS)

6. * Etiology:
I. Infective: Salmonellosis & staph. Food poisoning.
II. Non infective:
•Drugs; NSAI, cytotoxic drugs and cortisone.
•Alcoholism.
•Cigarette smoking.
•Uremia.
•Severe stress.
•Chemical irritation: by strong alkalis, acids.
•Mechanical trauma; during endoscopic examination.

7. * Sites: stomach & 1st
part of duodenum.
* Pathology: hemorrhagic inflammation and
superficial ulceration.
* Fate: usually heal by regeneration.

8. Chronic peptic ulcer diseaseChronic peptic ulcer disease

9. * Sites of peptic ulcer:
• Duodenum: (25 times more commoner than
gastric ulcer ) usually toward the anterior wall is
more often affected.
• Stomach: Usually antrum toward the Lesser
curvature.
• At the margins of a gastroenterostomy (stomal
ulcer)
• In the duodenum, stomach or jejunum of
patients with Zollinger-Ellison syndrome.
• Within Meckel’s diverticulum that contains
ectopic gastric mucosa.

13. Duodenal ulcerDuodenal ulcer

14. * Pathogenesis of Duodenal ulcer:Duodenal ulcer:
•Due to increased gastric juice secretion + Rapid
emptying of stomach into duodenum
* Causes:
•Increased vagus nerve stimulation.
•Increased number of parietal cell (as in tall thin patient).
•Increase hormonal stimulation (Z.E syndrome)
Gastrinoma → Gastrin.
•Increase the responsiveness of parietal cells to
secretory stimuli.
•↑ psychosomatic stimuli.

15. Duodenal ulcerDuodenal ulcer

16. Gastric ulcerGastric ulcer

17. Types

18. * Pathogenesis of Gastric ulcer.Gastric ulcer.
•Due to decreased mucosal defense mechanisms or
increasing damaging forces…

19. Causes of decrease mucosal
resistant

21. H. Pylori infection
• H. pylori is the etiologic factor in most patients with
peptic ulcer disease and may predispose individuals to
the development of gastric carcinoma. H. pylori
colonizes in the human stomach.
• H. pylori infection is present in almost all patients with
duodenal ulcers and 70% of cases with gastric ulcers.

22. * Mechanism:
1. H. pylori secretes urease (generates ammonia),
protease (breaks down glycoprotein in the gastric
mucus) and phospholipases.
2. Bacterial lipopolysaccharide attracts inflammatory
cells to the mucosa. Chronically inflamed mucosa are
susceptible to injury.
3. A bacterial platelet-activating factor promotes
thrombotic occlusion of surface capillaries.

24. * Gross features:* Gross features:
• Site: Gastric ulcers are located at the antrum
toward the lesser curvature. The duodenal ulcer
is usually located at the 1st
part anteriorly.
• Shape: Round, oval.
• Size: Usually less than 4 cm in diameter.
PATHOLOGY OF PUD

25. • Edge:
- Sharp edge.
• Floor:
- Clean
• Base of ulcer:
- Firm (formed of bundles of muscles and fibrous tissue).
• Margin (Surrounding gastric mucosa):
- Edematous and reddened due to gastritis.

26. • Depth of the ulcer:
- Superficial ulcer penetrate the mucosa reaching up to
the muscularis mucosa.
- Deeply excavated ulcers having their bases on the
muscularis propria.
- When the entire wall is penetrated, the base of the
ulcer may be formed by adherent pancreas, omental
fat, or liver. Free perforation into the peritoneal
cavity may occur.

27. GU

28. Gastric ulcerGastric ulcer

29. Biopsy of peptic ulcerBiopsy of peptic ulcer
• Biopsy is necessary to distinguish between benign and
malignant ulcers.
• Biopsy should be taken from the ulcer edge, at least from
each quadrant.
• Up to 10-12 biopsies may be taken to exclude cancer.
* Microscopic features:
• Active peptic ulcer shows;
1. Superficial zone: fibrinoid necrosis & neutrophils.
2. Intermediate zone: chronic inflammatory cells & granulation tissue.
3. Deep zone: fibrous tissue, muscle remnants.

31. *SYMPYOMS OF PUD

33. * Complications of PUD :
1. Hemorrhage: hematemesis or melena.
2. Perforation
3. Healing by fibrosis causing gastric or duodenal
obstruction.
4. Malignant transformation: rare (0.5% of gastric
peptic ulcer).

34.  Functional dyspepsia:
By Endoscopy
 Zollinger Ellison Syndrome (Gastrinoma)
 Gastric Malignant Ulcer:
Endoscopy + Biopsy
 Biliary or pancreatic diseases:
Ultrosonography, MRCP, ERCP
*Differential Diagnosis

36. INVISTIGATION OF PUD

37. *Laboratory analysis
CBC : chronic blood lose
Urinalysis
Liver enzyme studies
Serum amylase determination
Stool examination : occult blood
*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

38.  *Tests for H. pylori*Tests for H. pylori
Noninvasive testsNoninvasive tests
 Serum or whole blood antibody testsSerum or whole blood antibody tests
 Immunoglobin G (IgG)Immunoglobin G (IgG)
 Urea breath testUrea breath test
Invasive testsInvasive tests
 Biopsy of stomachBiopsy of stomach
 Rapid urease testRapid urease test

39. *RADIOLOGICAL
 Barium contrast studiesBarium contrast studies
Widely usedWidely used
 X-ray studiesX-ray studies
Ineffective in differentiating a pepticIneffective in differentiating a peptic
ulcer from a malignant tumorulcer from a malignant tumor

41. TREATMENT

42. CONSERVATIVE TREATMENT*
GENERAL MEASURE
-Rest
-Diet: -small frequent meals -avoid irritant food,drugs
&smoking -milk give some relief
DRUG THERAPY

57. Establish the diagnosis
(endoscopy or UGI)
Gastric ulcer
biopsy, R/O cancer
Duodenal ulcer
Assess pathogenesis:
H.pylori
NSAIDs
Smoking
Family history
Serum gastrin
Therapy:
Treat H.pylori
Acid suppression
Enhance mucosa defense
Document H.pylori eradication
Complications -Surgery
(obstruction, perforation, intractable bleeding, malignant transformation)
Endoscopic follow-up
to healing

58. References:
Robbins and Cotran’s:
Pathologic Basis of
Disease. Seventh
edition.