Acute Early acute superficial gastritis: Marked neutrophilic infiltrates appear in the mucous neck region and lamina with a pit microabscess. This<unk>  was<unk> d by Helicobacter pylori. Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming. Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis. Additionally, severe physiologic stress ("stress ulcers") from sepsis, hypoxia, trauma, or surgery is also a common etiology for acute erosive gastritis. This form of gastritis can occur in more than 5% of hospitalized patients. Also, note that alcohol consumption does not<unk>  chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid. Chronic Chronic gastritis refers to a wide range of problems of the gastric tissues. The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining. In some<unk> s bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis. Gastritis may also be<unk> d by other<unk>  conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, and liver or kidney failure. Since 1992, chronic gastritis lesions are classified according to the Sydney system. Metaplasia Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the<unk> s or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.
medical cause of Dysphagia
symptom of Esophageal cancer
symptom of Stomach cancer
complications of Dysphagia
symptom of Gastroesophageal reflux disease
symptom of Hiatal hernia
symptom of Hirschsprung's disease
symptom of Klippel–Feil syndrome