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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
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.
Acid peptic digestion is the
ultimate cause for
Ulceration.

DU: GU= 4:1
Hurry, worry & Curry
Genetic Factors:
Blood group: O & A
Monozygotic
twins,association
with HLA-B5 gene

Work, worry, weather

Reflux of Bile & Pancreatic Juices
Bile Reflux
L Ulcers are caused by loss of balance

Between protective & Hostile factors.

Loss of balance
between
Attack& Defence
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.
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
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.
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.
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).
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.
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
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.
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
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.
>3 cm
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.
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
Fiberoptic gastroscopy

The radiographic
diagnosis is
approximately 95%

Endoscopic gastric biopsy

multiple (about 10) biopsies are
recommended for the standard-size
ulcer.
Chronic, larger & deeper ulcers cause complications.

Duodenal stenosis,’hour glass’ deformity.

Cancers ulcerate but ulcers rarely cancerate
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
Peptic ulcer st f n

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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.
  • 3. Acid peptic digestion is the ultimate cause for Ulceration. DU: GU= 4:1
  • 4.
  • 5. Hurry, worry & Curry Genetic Factors: Blood group: O & A Monozygotic twins,association with HLA-B5 gene Work, worry, weather Reflux of Bile & Pancreatic Juices
  • 7.
  • 8.
  • 9.
  • 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.
  • 23. >3 cm
  • 24.
  • 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
  • 27.
  • 28. Fiberoptic gastroscopy The radiographic diagnosis is approximately 95% Endoscopic gastric biopsy multiple (about 10) biopsies are recommended for the standard-size ulcer.
  • 29.
  • 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