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Peptic ulcer st f n
1. H Pylori HELICOBACTER
Campylobacter Pylori
PYLORI
H. pylori has been found in 90% of patients with chronic
gastritis, 95% with duodenal ulcer disease, 70%
with gastric ulcer, and 50% with gastric carcinoma.
H Pylori
PePtic
ulcer
Lecture 8
2. Definition
• Ulcer of the GIT (Peptic ulcer) is defined
histologically as
a breach in the mucosa
that extends through the muscularis
mucosea into the submucosa or deeper.
The areas of degeneration & necrosis of
gastrointestinal mucosa exposed to acidpeptic secretions.
10. L Ulcers are caused by loss of balance
Between protective & Hostile factors.
Loss of balance
between
Attack& Defence
11. Damagin
g
Forces
Defensive
Forces
Ulcers are caused by loss of balance
between
Mucosal defence & acid attack
Loss of balance
between
Attack& Defence
Ulcers are caused by loss of balance
Between protective & Hostile factors.
12. Pathogenesis of
Duodenal Ulcer: High acid-pepsin secretions
•
•
•
•
•
•
1. Hypersecretion of gastric acid into the fasting stomach at night (vagal
stimulation).
2. Rapid emptying of the stomach exposing the duodenal mucosa to the
aggressive action of HCl.
3. H. pylori:
i) Mucosal defence is broken by bacterial elaboration of urease, protease,&
phospholipase.
ii) Host factors: H. pylori infected mucosal epithelium releases proinflammatory
cytokines such as IL-1, IL-6, IL-8 & TNF-incite inflammatory reaction.
iii) Bacterial factors: Epithelial injury is also induced by cytotoxic-associated
gene protein (Cag A), while vacuolating cytotoxin (Vac A) induces
elaboration of cytokines.
•
DU
13. Pathogenesis of gastric ulcer
GU: Impaired gastric mucosal defences against
acid-pepsin secretions.
Other features in pathogenesis:
• 1. Hyperacidity due to increased serum gastrin
levels in response to ingested food in an atonic
stomach.
• 2.In case of Low to Normal HCl: Damaging influence
of gastritis, bile reflux, smoking.
• 3. Disorder of protective gastric mucus ‘barrier’ by
H. pylori.
14. DU & GU
• Gastric & duodenal ulcers
represent two diseases as far as
their etiology, pathogenesis &
clinical features are concerned
• but morphological findings in
both are similar.
15. Acute Peptic(Stress) Ulcer
• Multiple, small mucosal erosions, seen most
commonly in the stomach but may occur in the
duodenum. Mucosal erosion (loss of continuity of the
epithelial lining) is a common feature of acute
gastritis.
• Etiology:
• I. Psychological Stress
• II. Physiological stress: Shock, trauma, septicaemia, Extensive burns
•
•
•
(curling’s ulcer )
Intracranial lesions (Cushing’s ulcers developing from hyperacidity following
excessive vagal stimulation).
Drug intake (Aspirin, steroids)
Local irritants (alcohol, smocking, coffee).
16. ACID ?
Pathogenesis
Hyperacidity? Role of hyperacidity in acute gastritis?
• 1. Ischaemic hypoxic injury to the
mucosal cells.
• 2. Depletion of the gastric mucus
barrier rendering the mucosa
susceptible to attack by acid-peptic
secretions.
Mucosal erosion (loss of continuity of the epithelial lining) is a common feature of acute
gastritis. If the defect is severe enough to penetrate the muscularis mucosae to involve the
submucosa, this becomes—by definition—an ulcer.
Acute ulcers can be distinguished morphologically from
chronic gastritis by the lack of fibrosis in the former.
17. Morphology of Acute Peptic Ulcer
• Gross: Multiple, more common in stomach, oval
or circular, small (<1cm).
• Microscopically, shallow, do not invade the
muscular layer. The margins & base may show
some inflammatory reaction. Heal without any
scar.
• Complications: Hemorrhage, Perforation.
Mucosal erosion (loss of
continuity of the epithelial
lining) is a common feature of
18.
19. Chronic Peptic Ulcer
• Always occurs in an achlorhydric zone of mucosa
( an area of stomach lined by pyloric type mucosa).
Up to 95% of the ulcers are located on the lesser
curvature (Magenstrasse) near the incisura
angularis.
• Can be found anywhere in the stomach.
Pyloric antrum & lesser curvature of the stomach are the sites most exposed
for longer periods to local irritants & thus are the common sites for occurrence of
gastric ulcers.
Local Irritants: Heavily spiced foods,
alcohol, smoking & aspirin,coffee.
20.
21. Remitting & relapsing lesions
Once a peptic ulcer patient, always a peptic ulcer patient.
Age: DU- 5th decade, GU- 6th decade
People at risk: DU-Stress-Executives,
leaders
GU—Labouring groups
Vomiting, Hematemesis, melena,
Appetite, Diet, Weight loss
,deep tenderness
Periodicity: attacks—2-6 weeks,
Interval of freedom-1-6 weeks
Attacks worsened by
Indigestion
‘work,
worry,
weather
22. Morphology of Chronic gastritis
• Morphology of GU & Du are similar.
• Location: GU –along the Lesser curvature in the the
pyloric antrum on the posterior wall.
• Du: in the first part of the duodenum, immediately
post pyloric on the anterior wall.
• Number: Solitary (80%)
• Size: Small (1-2.5cm)
• Shape: Round to oval
• Punched out: Rounded, sharply circumscribed,
with sharply demarcated vertical margins.
25. A, Typical gross appearance of chronic peptic ulcer of stomach. B,
Sharply delimited chronic peptic ulcer with converging folds of mucosa
in the upper half. The ulcer bed is covered by fibrinopurulent exudate.
Punched Out Ulcer: rounded, sharply circumscribed, often multiple lesions with sharply
demarcated vertical margins.
26. Morphology of Chronic Gastritis
• Benign ulcers usually have flat margins in level with
the surrounding mucosa. The mucosal folds
converge towards the ulcer.
• Depth: The ulcers may vary in depth from being
superficial (confined to mucosa) to deep ulcers
( penetrating into the muscular layer).
• Coexistence: GU+DU in 10-20% cases
• Malignant transformation: DU never
GU 1%-carcinoma
• Malignant GU are larger, bowl-shaped with elevated &
indurated mucosa at the margins
30. Chronic, larger & deeper ulcers cause complications.
Duodenal stenosis,’hour glass’ deformity.
Cancers ulcerate but ulcers rarely cancerate
31.
32. 80%
19%
Seems to be decreasing
Seems to be
decreasing
secrete either low normal or below
normal amounts of acid.
Associated with acid Hypersecretion
Mucosal Injury