Helicobacter pylori infection is the leading cause of peptic ulcers, occurring in 80-95% of cases. Peptic ulcers develop when there is an imbalance between gastric acid and the protective mucus layer of the stomach and duodenum. Common symptoms of peptic ulcer disease include abdominal pain, nausea, vomiting, and loss of appetite. H. pylori infection impairs the stomach's protective mechanisms, allowing gastric acid and enzymes to damage the mucosa and cause ulceration. Stress, smoking, excess acid production, and NSAID use can also increase the risk of developing peptic ulcers.
2. It is defined as an autoimmune disorder which is caused by
disruption of normal balance between corrosive effect of
gastric juice and protective effect of mucus on gastric
epithelial cells and most often caused by Helicobacter pylori
infection. Types of peptic ulcer :
Gastric ulcer : the ulcer that occurs in the stomach lining
some of them may be malignant.
Duodenal ulcer : most often seen in first portion of
duodenum.
6. Infection with the bacteria Helicobacter pylori occurs in 80 to 95% of
patients with peptic ulcer disease. H. pylori infection impairs the
protective mechanisms of the G.I. tract against low pH and digestive
enzymes and leads to ulceration of the mucosa.
Stress — Emotional, trauma, surgical.
Injury or death of mucus-producing cells.
Cigarette smoking.
Excess acid production in the stomach. The hormone gastrin stimulates
the production of acid in the stomach; therefore, any factors that increase
gastrin production will in turn increase the production of stomach acid.
Drugs: Chronic use of aspirin and NSAIDs drugs.
7. PATHOGENESIS OF H. PYLORI
1. H.pylori infection is a major factor in the pathogenesis of peptic ulcer.
2. H.pylori does not enter into the tissue system ,it induces an inflammation &
immune response which is due to increased production of cytokine which
activates the neutrophils & causes ulceration.
3. H.pylori secretes urease & also produce phospholipase which damage surface
epithelial cells.
4. A bacterial platelet-activating factor promotes thrombotic occlusion of
surface capillaries.
5. Mucosal damage allows leakage of tissue nutrients in the surface
microenvironment , sustaining the bacillus.
6. Damage of the protective mucosal layer. The epithelial cells are exposed to the
damaging effect of acid-peptic digestion. Inflammation of the gastric mucosa
occurs.
8.
9. • Anne Waugh, Allison Grant, Ross and Wilson Anatomy and Physiology in
health and illness(11th edition),Churchill livingstone elsevier ltd,
reprint(2010),chapter 12:The Digestive System, page no.(277-328).
• Fantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September 4th,
2006, from www.emedicine.com/med/topic1776.htm