can be defined as the rupture of the integrity of the mucosa of the stomach and duodenum due to active inflammation caused by acid and pepsin, which extends at least to the muscularis-mucosa. 
Histological Classification of injuries Gastroduodenal Mucosa
Histological Classification of injuries Gastroduodenal Mucosa
Acute-chronic ulcer.
Erosion superficial lesions are rounded, less than 5 mm in diameter, margins slightly raised, brown or red background, multiple. Histologically, the loss of substance is limited to the mucosa, where there are necrotic debris, fibrin, neutrophils and red cells with infiltration by polymorphonuclear cells in the periphery. These erosions usually heal completely without scarring.
Acute ulcer. single or multiple lesions similar in appearance but larger than erosions. It extiense to musc mucosa. At the bottom of the ulcer may be seen some granulation tissue with little fibroblastic reaction. The lining and glandular epithelia show peripheral active aspect because from them there is regeneration.
chronic ulcers.
- Fibrosis in the base
- Healing
area - prevents regeneration total. Abarca mucosa, submucosa, musc, muc.4 CPAs from outside to inside
- Layer fibroleucocitario exudate
- Tej. eosinophilic necrotic
- Tej granulation
- Cel inflammatory.
Etiopathogenesis
defensive mechanisms of the mucosal barrier
The gastroduodenal mucosa has a number defensive mechanisms that contribute to the maintenance of mucosal integrity in the acidic environment of the stomach. The factors involved in this process is the secretion of mucus and bicarbonate, blood flow and gastric mucosal cell regeneration capacity against damage to the mucosa (see Chap. Anatomy, Physiology and exploration disease).
The importance of each of these factors has been well characterized in experimental models of acute injury of gastric mucosa, but their exact involvement in the pathogenesis of chronic ulcers is less well known.
Pathogenic Factors
infection H. pylori and NSAIDs are the most common factors that compromise the strength of the mucosal barrier against peptic activity of gastric juice and are independent factors in the pathogenesis of ulcer disease.
Other factors
Smoking slows healing of ulcers, promotes recurrence and increases the risk of complications, but not a primary pathogenic factor. The mechanisms involved in the effect of smoking on ulcer disease have been attributed to increased basal and stimulated acid secretion, alteration in mucosal blood flow and gastric motility and reduced pancreatic secretion of bicarbonate. Although alcohol at high concentrations or stress can trigger the development of acute lesions of the mucosa, has not been shown to be risk factors for development chronic ulcers.
Clinic
- abdominal pain, localized in the epigastrium and is often described as burning, corrosive pain or painful sensation of hunger.
- The pain is usually related to a rate schedule intake.
- Anorexia and weight loss are not uncommon, and only 20% of duodenal ulcer patients referred increased appetite.
- Nausea and vomiting may occur in the absence of pyloric stenosis.
- dyspeptic symptoms such as belching, bloating, intolerance to fat or heartburn.
The physical examination in uncomplicated ulcer is usually normal or may show pain on deep palpation in the epigastrium, a finding which is completely nonspecific. However, the physical examination may reflect the occurrence of complications.
Thus, the presence of cutaneous and mucosal pallor suggests hemorrhage, palpation of abdomen table with signs of peritoneal irritation reflect the existence of a perforation and the presence of fasting gastric pigeage will suspect pyloric stenosis.
The physical examination should also look for signs of associated diseases, especially cardiac, respiratory or liver that increase the risk of surgical complications in these patients.
Regarding the natural history of ulcer disease, it is noteworthy that this is a relatively benign condition, chronic relapsing course with spontaneous remissions and exacerbations.
80% duodenal ulcers and 50% of gastric will relapse during the 12 months of healing.
Approximately 20% of patients suffer some complication in the course of their disease. Overall mortality is 2.5% and is due to the complications and surgery.
GASTRIC ULCER
pain after meals.
is more difficult to settle down with.
antacids or eating food.
Less Frequent Night Awakenings
Frequent weight loss
DUODENAL ULCER
-Two-Three hours after eating. He
mitigated by Antacids and Food.
-Night Awakenings. Avoid prolonged periods of fasting, weight loss
not
Frequent
Diagnosis
-Anamnesis Diagnosis
-Physical Exam-Endoscopy
-Rx-chemical characteristics
Gastric serum pepsinogen Determinations I and gastrin (see Chap. Anatomy, Physiology and exploration disease)
-Diagnosis of Helicobacter pylori infection
H. Diagnostic Methods pylori
Direct (invasive) endoscopic
-Histology-Farming
-urease test.
Indirect (Non-Invasive) Serology
-breath-test (C13 C14)
treatment and eradication of H. pylori
IBP + Amoxicillin + Clarithromycin
Blogalaxia Tags: peptic ulcer + erosion acute ulcer + ulcer + + and + chronic + gastric ulcer + duodenal ulcer clinical + + of + peptic ulcer diagnosis + of + peptic + ulcer + Helicobacter pylori
0 comments:
Post a Comment