Peptic Ulcer disease

Contents

Peptic Ulcer disease

• Etiology

• Risk factor

• Pathogenesis

• Symptoms

• Treatment

Objectives

At the end of this lecture, student will be able to

• Define peptic ulcer disease

• Explain the etiology of peptic ulcer disease

• Describe the pathophysiology of peptic ulcer disease

Peptic Ulcer

• Breach in the mucosa of the alimentary tract, which extends through the muscularis mucosa into the submucosa or deeper

• Chronic and most often solitary, lesions

• Any portion of gastrointestinal tract exposed to the aggressive action of acid-peptic juices

• Erosion of GI mucosa resulting from digestive action of HCl and pepsin

Duodenal vs gastric ulcers

	DUODENAL	GASTRIC
INCIDENCE	More common	Less common
ANATOMY	First part of duodenum – anterior wall	Lesser curvature of stomach
DURATION	Acute or chronic	Chronic
MALIGNANCY	Rare	Benign or malignant

Peptic ulcer

Imbalance between aggressive & protective factors

Aggressive factors

• Gastric acid

• Proteolytic enzyme

Protective factors

• Mucosal layer

• Bicarbonate secretion

• Prostaglandins

Risk factors of peptic ulcers

• Helicobacter pylori

• Non Steroidal Anti-inflammatory Drugs

• Steroid therapy

• Smoking and Excess alcohol intake

• Genetic factors

• Zollinger Ellison syndrome – rare syndrome caused by gastrin-secreting tumour

• Blood group O and Hyperparathyroidism

Pathophysiology of peptic ulcers

Gastric acid and pepsin

• Potential for producing mucosal damage is related to the secretion of gastric (hydrochloric) acid and pepsin

• Hydrochloric acid - parietal cells - receptors for histamine, gastrin, and acetylcholine

• Increased acid secretion - duodenal ulcers - HP infection

• Patients with ZES have gastric acid hypersecretion resulting from a gastrin-producing tumor

• Patients with gastric ulcer - normal or reduced rates of acid secretion

Mucosal defense mechanisms

• Protect the gastroduodenal mucosa from noxious endogenous and exogenous substances

• Bicarbonate barrier protect the stomach from the acidic contents

• Epithelial cell restitution, growth, and regeneration

• Maintenance of mucosal integrity and repair is mediated by the production of endogenous prostaglandins

H. pylori infection

Mechanisms include:

1) Direct mucosal damage

2) (b) Alterations in the host immune/inflammatory response

3) Hypergastrinemia leading to increased acid secretion

• Virulence factors (vacuolating cytotoxin, cytotoxin-associated gene protein, and growth inhibitory factor)

• Elaborating bacterial enzymes (lipases, proteases, and urease), and adherence

• Lipases and proteases degrade gastric mucus

• Ammonia produced by urease - toxic to epithelial cells

• Bacterial adherence enhances uptake of toxins into gastric epithelial cells

NSAID Induced

• Direct or topical irritation of the gastric epithelium and

• Systemic inhibition of endogenous mucosal prostaglandin synthesis

• Inhibit both COX-1 and COX-2 to varying degrees

• Neutrophil adherence may damage the vascular endothelium

• Lead to a reduction in mucosal blood flow

• Liberate oxygen-derived free radicals and proteases

Symptoms of peptic ulcers

• Abdominal pain that is often epigastric - burning - vague discomfort, abdominal fullness, or cramping

• A typical nocturnal pain that awakens the patient from sleep

• Severity of ulcer pain varies from patient to patient

• May be seasonal, occurring more frequently in the spring or fall

• Episodes of discomfort usually occur in clusters lasting up to a few weeks followed by a pain-free period or remission lasting from weeks to years

• Heartburn, belching, and bloating often accompany the pain

• Nausea, vomiting, and anorexia

Complications of peptic ulcers

• Obstruction – pyloric stenosis and duodenal stenosis

• Hemorrhage – blood in stools; if chronic – leads to anemia

• Perforation

• Malignant transformation to carcinoma

Summary

• Ulcers are defined as a breach in the mucosa of the alimentary tract, which extends through the muscularis mucosa into the submucosa or deeper

• Etiological factors are helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, critical illness, hypersecretion of gastric acid , viral infections ,vascular insufficiency

• HP infection alters host inflammatory response and damages epithelial cells directly by cell-mediated immune system whereas NSAID cause direct irritation to epithelium and decrease PGE2