1- Definition and comparison between UD and UG:
• gastric or duodenal substance loss of non-tumor origin
• Chronic Disease (MUGD) evolving by recurrent acute attacks
– Duodenal ulcer (DU)
– Gastric ulcer (UG)
• Elderly often asymptomatic ulcers revealed by a complication (bleeding or perforation). Promoting the role of NSAIDs in the over 65 year old patient.
2- Etiology:
• imbalance between aggressive factors (gastric acid, pepsin, bile acids, pancreatic enzymes) and protective factors of gastric mucosa (mucus, bicarbonate, blood flow, prostaglandins, growth factors, cell renewal)
• Helicobacter pylori is found in 90% of drug users (70% for UG). It is a major factor in the ulcérogenèse, in addition to gastric acid secretion.
• The Gastrotoxic treatments such as NSAIDs or aspirin can be responsible for ulcers, more often than gastric duodenal, or aggravate preexisting ulcers.
Risk factors:
• Demonstrated: acid hypersecretion (especially during Zollinger-Ellison syndrome), H. pylori infection (UD for UG), smoking, taking gastro-toxic drugs (NSAIDs, aspirin), family history of MUGD, pancreatitis Chronic (UD), cirrhosis
• Possible: corticosteroids (prolonged high doses), blood group O
• Very little or not probable: spices, alcohol, caffeine, paracetamol
3- Clinical signs:
• Pain
– Usually, epigastric cramps or burning occurring 1-3 hours after meals, relieved by food, antacids or anti-secretory, willingly waking the patient before morning. These pains gladly have a recurrent one.
– Sometimes vague pains, type of digestive discomfort, cramps, painful hunger
• Dyspepsia, heartburn
• Vomiting postprandial (unusual, should be investigated, pyloroduodenal stenosis)
• Signs of complications (greater frequency of asymptomatic forms revealed by a complication in patients taking an NSAID)
– Perforation (severe abdominal pain quickly diffuse)
– Bleeding (haematemesis, melena, more rarely iron deficiency anemia)
4- Diagnostic tests:
Laboratory tests:
• Iron deficiency anemia (first eliminate colic because before assigning the ulcer)
• Identification of H. pylori infection (culture of biopsies, fast urea test, serology)
• Study of gastric secretion and assay of gastrin (only looking for a ZE)
Esophageal-gastroduodenal endoscopy, the ulcer can locate and biopsies
Pathology:
• Loss of mucous substance reaching the muscular
• Diameter frequently ulcer> 5 mm
• H. pylori present (antral biopsies) in 90% of drug users, and over 75% of UG
5- Diagnosis:
+ Diagnosis:
• Endoscopy (sensitivity> 95%)
• Biopsies perendoscopic
– In the den in search of H. pylori
– On the banks of the ulcer in case of UG (++, differential diagnosis of ulcerative cancer)
Differential diagnosis:
• Cancer shape if ulcerated UG. The repeat endoscopy and biopsies after medical treatment is imperative.
• Gastroesophageal reflux disease
• Non-ulcer Dyspepsia
• Acute Gastritis (drug, allergy, infectious …)
• Cholelithiasis
• Pancreatitis
• Angina => posterolateral diaphragmatic infarction: vagal signs.
• Achievement of gastric Crohn’s disease