Peptic ulcer

Lecture 8

H Pylori HELICOBACTER

PYLORI

H 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.

Campylobacter Pylori

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.

Acid peptic digestion is the ultimate cause forUlceration.

DU: GU= 4:1

Reflux of Bile & Pancreatic Juices

Hurry, worry & Curry

Genetic Factors:Blood group: O & AMonozygotic twins,association with HLA-B5 gene

Work, worry, weather

Bile Reflux

L Ulcers are caused by loss of balanceBetween protective & Hostile factors.

Loss of balance betweenAttack& Defence

DefensiveForces

Damaging Forces

Ulcers are caused by loss of balance betweenMucosal defence & acid attack

Ulcers are caused by loss of balanceBetween protective & Hostile factors.

Loss of balance betweenAttack& Defence

Pathogenesis of DUDuodenal 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.

•

Pathogenesis of gastric ulcerGU: 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.

• 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).

Mucosal erosion (loss of continuity of the epithelial lining) is a common feature of acute gastritis.

Pathogenesis• 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.

ACID ? Hyperacidity? Role of hyperacidity in acute gastritis?

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 acute gastritis.

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, leadersGU—Labouring groups

Periodicity: attacks—2-6 weeks,Interval of freedom-1-6 weeks

Attacks worsened by

‘work, worry, weather

Vomiting, Hematemesis, melena,Appetite, Diet, Weight loss,deep tenderness

Indigestion

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 neverGU 1%-carcinoma• Malignant GU are larger, bowl-shaped with elevated &

indurated mucosa at the margins

Endoscopic gastric biopsy

The radiographic diagnosis is approximately 95%

Fiberoptic gastroscopy

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

Seems to be decreasing

Seems to be decreasing

Associated with acid HypersecretionMucosal Injury

80% 19%

secrete either low normal or below normal amounts of acid.