PEPTIC ULCER DISEASE (PUD)

1
PEPTIC ULCER DISEASE (PUD)

• By
• Dr. Abdelaty Shawky
• Assistant professor of pathology

2

• Ulcer is defined as a breach in the mucosa ,
  which extends through the muscularis mucosa into
  the submucosa or deeper.
• Erosion differs from an ulcer in being more
  superficial and partially affecting the surface
  epithelium).

3
Definition of peptic ulcer

• Peptic ulcers are chronic most often solitary,
  lesions that occur in any portion of the
  gastrointestinal tract exposed to the aggressive
  action of acidic-peptic secretion.

4
Sites of peptic ulcer

• Duodenum (DU) First portion. Anterior wall is
  more often affected.
• Stomach (GU) Usually antrum. Lesser curvature
  (common) .
• At the margins of a gastroenterostomy (stomal
  ulcer)
• In the duodenum, stomach or jejunum of patients
  with Zollinger-Ellison syndrome.
• Within Meckels diverticulum that contains
  ectopic gastric mucosa.

5
Pathogenesis of peptic ulcer

• Peptic ulcers are produced by an imbalance
  between the gastro-duodenal mucosal defense
  mechanisms and damaging forces.

6
(No Transcript)
7
Mucosal defense mechanisms

• Surface mucous secretion.
• Bicarbonate secretion into mucous.
• Tight adherence between epithelial cells to
  prevent any acid leakage to the inside.
• Good blood supply to the mucosa
• Renewal of damaged epithelial cells.
• Elaboration of prostaglandins.

8
Damaging agents

• H. pylori
• NSAIDs.
• Aspirin.
• Cigarette smoking.
• Alcoholism.
• Gastric hyperacidity.
• Duodenal-gastric reflux..

9
Role of H. Pylori infection in the pathogenesis
of peptic ulcer

• H. pylori infection is present in almost all
  patients with duodenal ulcers and 70 of cases
  with gastric ulcers.
• Mechanism
• H. pylori secretes damaging enzymes
• Urease breaks down urea to toxic compounds e.g.
  ammonium chloride.
• Protease breaks down glycoprotein in the gastric
  mucus).
• Phospholipases. Damage the cell membranes of
  surface epithelial cells.

10

• 2. Bacterial lipopolysaccharide stimulate the
  surface epithelial cells to release
  pro-inflammatory cytokines e.g. IL-1, IL-6 and
  TNF. These attracts inflammatory cells
  (Neutrophils) to the mucosa and promote the
  inflammatory reaction
• 3. H. pylori release bacterial platelet-activating
  factor promotes thrombotic occlusion of surface
  capillaries.

11

• 4. H. pylori enhances gastric acid secretion and
  impairs duodenal bicarbonate production, thus
  reducing luminal pH in the duodenum. This altered
  milieu seems to favor gastric metaplasia (the
  presence of gastric epithelium) in the first part
  of the duodenum.
• - Such metaplastic foci provide areas for H.
  pylori colonization.

12
(No Transcript)
13
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 2cm in diameter.
• Lesions less than 0.3 cm are likely to be
  shallow erosions.
• Giant ulcers are usually greater than 3cm in
  diameter.
• Size does not differentiate benign from malignant
  ulcer.

14

• Base of ulcer
• Firm (formed of bundles of muscles and fibrous
  tissue).
• Floor
• Clean (gastric juice digest any food particles at
  the floor.
• Margin (Surrounding gastric mucosa)
• Edematous and reddened due to gastritis.
• 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.

15
GU
16
Gastric ulcer
17
Duodenal ulcer
18
Microscopic features

• - Four distinct layers are present in a peptic
  ulcer in the same sequence starting from the
  luminal side
• 1. Necrotic debris.
• 2. Non-specific acute inflammatory reaction.
• 3. Granulation tissue.
• 4. Fibrosis replacing the muscle wall and
  extending into subserosa.

19
Microscopic picture of peptic ulcer
20
Complications of PUD

• 1. Hemorrhage hematemesis or melena.
• 2. Perforation.
• 3. Healing by fibrosis causing obstruction.
• 4. Malignant transformation rare (0.5 of
  gastric peptic ulcer).

21
Clinical presentation

• A chronic, recurring lesion.
• Age Most often diagnosed in middle aged to older
  adults.
• Pain
• - Epigastric burning or aching pain.
• Pain worse at night and 1 to 3 hours after meal
  during the day specially in duodenal ulcer.
• Classically, the pain is relieved by alkalis or
  food (DU) or vomiting (GU).

22

• Nausea, vomiting, bloating, and significant
  weight loss (raising the possibility of some
  hidden malignancy) are additional manifestations.
  
• With penetrating ulcers, the pain is occasionally
  referred to the back, the left upper quadrant, or
  chest. This type of pain may be misinterpreted as
  being of cardiac origin.

23
Thanks
References Robbins and Cotrans Pathologic
Basis of Disease. Seventh edition.