Gastric ulcer and duodenal ulcer represent limited interruptions, unique or multiple of the gastro-duodenal wall continuity, accompanied by a fibrous reaction, penetrating through the mucosa, submucosa and even to the serosa.
Peptic ulcer epidemiology
The clinical prevalence is 5-10% of the population. The real prevalence, based on necroptic studies, is 20-30% in men and 10-20% in women. Nowadays there is an important decreasing tendency of the disease prevalence.
Gastro-duodenal ulcer etiopathogenesis
Approximately 10% of the adult population suffers or have suffered from gastro-duodenal ulcer. Helicobacter Pylori-this germ affecting over 2 billions of people! The infection is produced via faecal-oral or possibly oral-oral.
The Helicobacter Pylori acute infection manifests it self like an acute gastroduodenitis, with self-limited evolution. There remains a chronic gastritis, which will be involved in the ulcer genesis. In case of antral gastritis(inflammation), this will lead to the increase of gastrin secretion and implicitly to acid hypersecretion. As a response to the acid secretory excess, which will get into the duoden, a gastric metaplasia will appear into the duodenum, a compulsory stage in the duodenal ulcerogenesis. In case of gastric body gastritis, this will lower the mucosal resistance to the aggressive factors, thus generating gastric ulcer. The prevalence of Helicobacter Pylori infection in duodenal ulcer is 90-95% and approximately 70-80% in the gastric ulcer.
Gastric and duodenal ulcer physiopathology
A. Aggressive factors.
They are increased in the peptic ulcer genesis. There are three important aggressive factors.
1. The Helicobacter Pylori infection
The most probable mechanism of transmission is faecal-oral, the source of infection in the underdeveloped countries being the water. Its location in the stomach is between the apical membrane and the mucus layer, thus it is well adapted to the acid stomach environment. Its pathogenetic factors are the enzymes and cytotoxines secreted:urease(eliminating ammonia, which creates an alkaline pH, phospholipase and protease(digest the mucus and gastric and duodenal apical mucosa), the vacuolising cytotoxin.
Ulcerogenesis induced by Helicobacter Pylori is by direct action on the gastroduodenal mucosa and indirectly by increasing the clorhidropeptic secretion. The direct mechanism is determined by the inflammatory process initiated by Helicobacter Pylori toxins, which induces an acute gastritis that becomes chronic subsequently. Helicobacter Pylori does not grow on the duodenal mucosa, but only on the islands of gastric metaplasia in the duoden; these appear as a protection mucosal reaction to the increasing acid secretion. The indirect mechanism of Helicobacter Pylori is realized by the urease secretion which creates an alkaline environment around the gastrin secretory cells, thus stimulating the gastrin secretion and so the hypersecretion.2. The clorhydropeptic hypersecretion
Neither gastric ulcer nor duodenal ulcer can appear without acid secretion, with a higher role in duodenal ulcer. The most importante causes of HCl hypersecretion are: the increasing in number of secretory parietal cells by a genetic mechanism or by hypergastrinemia; the vagal hipertony; the hypersensitivity of parietal cells to vagal stimuli; gastric motility disorders(grown up in duodenal ulcer; with a permanent flux of acid into the duoden, and low in gastric ulcer with gastric stasis).
In addition to the increasing of HCl secretion, pepsin.
3. Billiary acids
They represent another aggressive factor, with ulcerogenous effect by the detergent mechanism on the lipids in the mucosal cells.
B.Defensive factors.
They are low in the ulcer disease, especially in gastric ulcer.Didactically, they are topographically grouped in three:
1. Preepithelial, represented by:
- surface mucus,important in gastric and duodenal mucosal defense,forming a viscous “unshaken” insolubre mucus gel layer, opposed to the retro diffusion of H ions, and lubricating the mucosa;
- bicarbonate ions secreted, which create a neutral pH gradient (7) compared to the acid pH (1-2)in the gastric lumen.
2. Epithelial, represented by the integrity of apical membrane of gastroduodenal mucosa.
3. Postepithelial – vascular, the capillaries having a nutritive role (they bring bicarbonate ions and take away H+ ions).
C. Environmental and individual factors:
Environmental factors, which are considered ulcerogeneous, are:
cigarette smoking by lowering the pancreatic alkaline secretion and canceling the inhibiting mechanisms of acid secretion;
drugs with ulcerogenous potential: aspirin and NSAIDS
other factors: stress, chronic alcohol intake and different alimentary diets.
Individual factors are genetic; there is definite proof of familial aggregation and the existence of genetic markers.
Diagnosis of gastro-duodenal ulcer
The clinical diagnosis. The characteristic pain, linked to food intake (“painful hunger” in duodenal ulcer), the apparition of pain mostly in spring and autumn are typical signs that may suggest an ulcer. However, lately, ulcers discovered endoscopically in the absence of typical symptoms have been reported more and more frequently. Other times, the onset may be dramatic, by a superior digestive hemorrhage (hematemesis and/or melena) or an ulcerous perforation.
Pain is the cardinal symptom in ulcer.
Other symptoms :
- vomiting
- abdominal indigestion
- weight loss
- fatigue
Paraclinic diagnosis is established by endoscopy (gastroduodenoscopy). In the same time, endoscopy allows the biopsy in gastric ulcer, which will show the benign or malignant character of the ulcerous crater. It also evaluates the healing of the ulcer, by proving the scar.
The X-ray
Helicobacter Pylori detection - causal agent in most gastroduodenal ulcers, is a compulsory diagnostic element in the strategy of ulcer evaluation, having as a purpose a subsequent therapeutic attitude. The Helicobacter Pylori detection is made by direct and methods:
- direct methods require endoscopy with obtaining a series of gastric biopsies from which Helicobacter Pylori is histological determined by urease test (based on the changing of a pH indicator color in the presence of Helicobacter Pylori which produces a high quantity of urease), or by culture on special media-in microaerophile medium).
- indirect methods: determination of antibodies anti Helicobacter Pylori in serum or blood or the respiratory tests. The anti Helicobacter Pylori antibodies may be determined also in the saliva and the eradication of Helicobacter Pylori infection may be more recently determined by the bacteria detection in stool.
Differential diagnosis
Based on the clinical symptomatology, the differential diagnosis of gastroduodenal ulcer must be done with other sufferings of the upper abdomen, such as gastric neoplasia, gastric lymphoma (diagnosed compulsory by endoscopy with biopsy), gallstones (diagnosed by ultrasonography), chronic pancreatitis or functional dyspepsia – (“ulcer-like”).
The endoscopic differentiation of a gastric ulcer must be done with an ulcerated neoplasm, which makes the prelevation of biopsies compulsory in every gastric ulcer, at diagnosis and at healing check-out.
Evolution of gastro-duodenal ulcer
The evolution of gastroduodenal ulcer has sensitively improved, thanks to the apparition of new antisecretory drugs extremely potent (H2 blockers or H+ K+ ATP-ase pump blockers); the evolution is favorable in most cases, the complications have been reduced, and the cases requiring surgery are relatively rare. In addition the introduction of anti-Helicobacter Pylori therapy has brought to a maximal decreasing of ulcerous recurrences.
Complications
- superior digestive hemorrhage (hematemesis and/or melena).
- ulcerous perforation with acute abdomen picture. Penetration is a covered perforation in the neighbor organs.
- pyloric stenosis
- ulcer malignization (possible in gastric ulcer, but never in the duodenal ulcer).
Ulcerous disease prognosis has improved a lot in the last decades, and mostly in the last decade,when, by a correct therapy of Helicobacter Pylori eradication, the risk of ulcerous recurrence has decreased fewer that 10% / year,compared to an annual recurrence of over 70% in the absence of Helicobacter Pylori eradication. The, mortality in ulcerous disease is increased mostly in the patients aged over 75 years with superior digestive hemorrhage.
0 comentarii:
Post a Comment