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L8 peptic ulcer
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 acid-peptic 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. Ulcers are caused by loss of balance between
Mucosal defence & acid attack.
Loss of balance between
Attack& Defence
H.pylori
NSAIDs
Ulcers are caused by loss of balance
Between protective & Hostile factors.
13. Ulcers are caused by loss of balance
Between protective & Hostile factors.
Loss of balance
between
Attack& Defence
14. Pathogenesis
• H. Pylori plays crucial role in
pathogenesis.
• 10-fold higher risk (antral atrophy 12-fold
higher risk)
• Corpus atrophy decreases the risk
when complete atrophy)
(to zero
15. Pathogenesis of
DU
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.
16. 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.
17. 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.
18. 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).
19. 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.
20. 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
21.
22. 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 &
23.
24. Remitting & relapsing lesions
Once a peptic ulcer patient, always a peptic ulcer patient .
Age: DU- 5th decade, GU- 6th decade
People at risk: DU-StressExecutives, 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
25. 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.
28. 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.
29. 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.
31. Gross Morphology
• The proximal margin tends
to have overhanging
edges, whereas the distal
margin usually has sloping
borders.
32. Whole mount view of chronic peptic ulcer. The external muscle layer
has been totally destroyed. Note the overhanging mucosa on one edge
and the sloping mucosa on the other.
33. • On section, there is
undermining of the edges
(especially on the proximal
side) and complete
replacement of the muscle
wall by grayish white fibrous
tissue.
34. Morphology
On the serosal side, there
may be subserosal fibrosis
and inflammatory
enlargement of the
regional lymph nodes.
35. Morphology
• Prominent marginal nodularity about the ulcer
should suggest the presence of carcinoma;
however, it should be remembered that it may be
impossible to distinguish grossly a peptic ulcer from
an ulcerated carcinoma. As a matter of fact,
approximately 10–15% of gastric carcinomas
appear, grossly, to be benign ulcers.
36. MICROSCOPY
•
Four histological zones
Chr. Peptic ulcer have 4 histological zones. From within outside, these are as
under:
• 1. Nicrotic zone— lies in the floor of the ulcer & is
composed of fibrinous exudate containing necrotic
debris & a few leukocytes.
• 2. Superficial exudative zone –lies underneath the
necrotic zone. The tissue elements here show
coagulative necrosis giving eosinophilic, smudgy
appearance with nuclear debris.
• 3. Granulation tissue zone– is seen merging into
the necrotic zone. It is composed of nonspecific
inflammatory infiltrate & proliferative capillaries.
37. • 4. Zone of Cicatrization– is seen merging into
thick layer of granulation tissue. It is composed of
dense fibrocollagenic scar tissue over
which granulation tissue rests. Thrombosed or
sclerotic arteries may cross the ulcer which on
erosion may result in haemorrhage.
38.
39. • Other common features in the ulcer bed include:
1)Thickening of vessels (caused by
subendothelial fibrous proliferation) and
2)Hypertrophy of nerve bundles;
both of these changes are probably secondary events.
• The necrotic surface may show superimposed
infection by Candida albicans.
40. • The mucosa surrounding the ulcer is of pyloric
type, including a component of gastrin (and
somatostatin) immunoreactive cells.
• In cases infected with H. pylori, a typical
constellation of morphologic changes
•
(loss of the apical portion and
dropout of epithelial cells,
epithelial pits, erosions, and cellular
tufts) is seen at the ulcer edge.
41. Classification of Peptic Ulcer
• DU & GU
• Acute, Subacute & Chronic
Peptic ulcers can be classified according to their
• shape and size (round-oval, giant, linear),
• activity (open ulcers or ulcer scars),
• depth of penetration (submucosa, muscularis
externa, or beyond), or
• a combination of these criteria.
45. 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
46. Chronic, larger & deeper ulcers cause complications.
Duodenal stenosis,’hour glass’ deformity.
Cancers ulcerate but ulcers rarely cancerate
47.
48. Zollinger–Ellison Syndrome (ZES)
caused by a non–beta islet cell, gastrin-secreting
tumor of the pancreas that stimulates the acidsecreting cells of the stomach to maximal activity,
with consequent gastrointestinal mucosal
ulceration.
ZES may occur sporadically or as part of an autosomal
dominant familial syndrome called multiple
endocrine neoplasia type 1 (MEN 1). The primary
tumor is usually located in the pancreas, duodenum
or abdominal lymph nodes, but ectopic locations
have also been described (e.g., heart, ovary,
gallbladder, liver, kidney).
