- HCI is secreted in the stomach by the parietal cells through the action of the Hydrogen-potassium ATPase (proton pump).
- Secretion of HCI is under neural and hormonal control. Both stimulate acid secretion through the direct release of histamine stimulating the parietal cells. Acetylcholine and gastrin also release histamine.
- Somatostatin inhibits both histamine and gastrin release decreasing acid secretion.
- Gastrin is secreted by G cells in the antrum, it stimulates HCI secretion.
A. Helicobacter Pylori (H.Pylori) :
H. pylori is a spiral-shaped, gram negative, urease producing organism.
The organism is found under the mucus layers in close to gastric epithelial cells.
It is transmitted by faeco-oral or oral-oral (saliva) routes.
30-60% of western populations are affected and the prevalence is higher in underdeveloped countries. The older populations are more liable.
Pathogenetic factors of H.pylori infection :
Increase gastrin release.
Increase pepsinogen secretion.
Cytotoxin release.
An alteration in the mucus protective layer.
Decrease in somatostatin from the antral cells (somatostatin inhibits both histamine and gastrin release).
The organism produces urease enzyme. which splits urea producing ammonia which raises the pH around it to protect itself.
B. Non-Steroidal anti-inflammatory drugs (NSAIDs)
Prostaglandins have important several mechanisms to protect gastric mucosa. They stimulate bicarbonate & mucus secretion from the gastric mucosa. Also they increase the microvasculature of the mucosa. All these mechanisms are called the mucosal barrier.
NSAIDs act by inhibiting cyclo-oxygenase enzyme (COX) leading to decrease prostaglandins at the site of inflammation.
NSAIDs decrease gastric and duodenal prostaglandins, so mucosal erosions & ulcerations will occur.
The cyclo-oxygenase enzyme (COX) has 2 types, COX-2, which is present at sites of inflammation and COX-1, which is present in the stomach.So COX-2 inhibitors will not affect the gastrointestinal mucosa .
C. Smoking
D. Other factors :
Reflux is responsible for ulcers at lower esophagus.
Gastrinoma (Zollinger-Ellison syndrome).
Peptic ulcer (PU) is more common in men than women .
Familial incidence especially in duodenal ulcer (DU).
Peptic ulcer is more common with blood group O .
- Secretion of HCI is under neural and hormonal control. Both stimulate acid secretion through the direct release of histamine stimulating the parietal cells. Acetylcholine and gastrin also release histamine.
- Somatostatin inhibits both histamine and gastrin release decreasing acid secretion.
- Gastrin is secreted by G cells in the antrum, it stimulates HCI secretion.
Definition of Peptic Ulcer
It is an ulcer in the duodenum, stomach, lower esophagus or in the Jejunum after gastrojejunostomy with exposure to acid-peptic juices with a defect in the mucosa that extends through the muscularis mucosa into the submucosa or deeper.Aetiology of Peptic ulcer
The proteolytic enzyme pepsin and gastric acid were initially identified as the key factors involved in the pathogenesis of peptic ulcer. So the concept of no acid, no ulcer has been widely used and accepted for many years, recently,the role of factors other than acid and pepsin in the pathogenesis of peptic ulcer has been recognized. e.g. :A. Helicobacter Pylori (H.Pylori) :
H. pylori is a spiral-shaped, gram negative, urease producing organism.
The organism is found under the mucus layers in close to gastric epithelial cells.
It is transmitted by faeco-oral or oral-oral (saliva) routes.
30-60% of western populations are affected and the prevalence is higher in underdeveloped countries. The older populations are more liable.
Pathogenetic factors of H.pylori infection :
Increase gastrin release.
Increase pepsinogen secretion.
Cytotoxin release.
An alteration in the mucus protective layer.
Decrease in somatostatin from the antral cells (somatostatin inhibits both histamine and gastrin release).
The organism produces urease enzyme. which splits urea producing ammonia which raises the pH around it to protect itself.
B. Non-Steroidal anti-inflammatory drugs (NSAIDs)
Prostaglandins have important several mechanisms to protect gastric mucosa. They stimulate bicarbonate & mucus secretion from the gastric mucosa. Also they increase the microvasculature of the mucosa. All these mechanisms are called the mucosal barrier.
NSAIDs act by inhibiting cyclo-oxygenase enzyme (COX) leading to decrease prostaglandins at the site of inflammation.
NSAIDs decrease gastric and duodenal prostaglandins, so mucosal erosions & ulcerations will occur.
The cyclo-oxygenase enzyme (COX) has 2 types, COX-2, which is present at sites of inflammation and COX-1, which is present in the stomach.So COX-2 inhibitors will not affect the gastrointestinal mucosa .
C. Smoking
D. Other factors :
Reflux is responsible for ulcers at lower esophagus.
Gastrinoma (Zollinger-Ellison syndrome).
Peptic ulcer (PU) is more common in men than women .
Familial incidence especially in duodenal ulcer (DU).
Peptic ulcer is more common with blood group O .
