Gastric peptic ulcer

Associated with duodenal and gastric peptic ulcers... 

Chemical changes in the cellular environment include inactivation of cellular functions or the alteration of the chemical components of body fluid, such as a change in the pH. For example, antacids neutralize gastric acidity in patients with peptic ulcers. 

Use peptic ulcer therapeutic, gastric acid secretion inhibitor... 

Histamine receptors were first divided into two subclasses Hi and H2 by Ash and Schild (1966) on the basis that the then known antihistamines did not inhibit histamine-induced gastric acid secretion. The justification for this subdivision was established some years later when Black (see Black et al. 1972) developed drugs, like cimetidine, that affected only the histamine stimulation of gastric acid secretion and had such a dramatic impact on the treatment of peptic ulcers. A recently developed H2 antagonist zolantidine is the first, however, to show significant brain penetration. A further H3 receptor has now been established. It is predominantly an autoreceptor on histamine nerves but is also found on the terminals of aminergic, cholinergic and peptide neurons. All three receptors are G-protein-coupled but little is known of the intracellular pathway linked to the H3 receptor and unlike Hi and H2 receptors it still remains to be cloned. Activation of Hi receptors stimulates IP3 formation while the H2 receptor is linked to activation of adenylate cyclase. 

Helicobacter pylori is associated with chronic gastritis, peptic ulceration and possibly involved in the pathogenesis of gastric carcinoma (Correa and Ruiz, 1992 Dixon,... 

Kishi, A., Yoshikawa, T., Naito, Y., Ando, T., Yasuda, M., Tsujigiwa, M., Tomii, T., Takahashi, S., Tas i, M., Takano, H. and Kondo, M. (1990). Evaluation of superoxide dismu-tase activity in the gastric mucosa of chronic peptic ulcer patients. Gastroenterology 98, A68. 

Less common causes of peptic ulceration include Zollinger-Ellison syndrome (ZES), cancer chemotherapy, radiation, and vascular insufficiency. ZES is caused by a gastrin-producing tumor called a gastrinoma and results in gastric acid hypersecretion. High-dose oral proton pump inhibitor (PPI) therapy is the initial treatment of choice for ZES intermittent intravenous PPI therapy may be required for any patient in whom oral therapy is contraindicated.1... 

Dietary factors such as coffee, tea, cola, beer, and a highly-spiced diet may cause dyspepsia, but they have not been shown to independently increase PUD risk. Although caffeine increases gastric acid secretion and alcohol ingestion causes acute gastritis, there is inconclusive evidence to confirm that either of these substances are independent risk factors for peptic ulcers. 

Prostaglandins, one of the most important epithelial growth factors, inhibit gastric acid secretion and have numerous mucosal protective effects, the most important of which include the stimulation of both mucus and phospholipid production, promotion of bicarbonate secretion, and increased mucosal cell turnover. Damage to the mucosal defense system is the primary method by which HP or NSAIDs cause peptic ulcers. 

Superior mesenteric artery syndrome Enteric infections Inflammatory bowel diseases Pancreatitis Appendicitis Cholecystitis Biliary colic Gastroparesis Postvagotomy syndrome Intestinal pseudo-obstruction Functional dyspepsia Gastroesophageal reflux Peptic ulcer disease Hepatitis Peritonitis Gastric malignancy Liver failure... 

A 48-year-old man with a history of hypertension, peptic ulcer disease (gastric ulcer 1 year ago), and morbid obesity presents to the emergency department complaining of excruciating pain in his left big toe and both ankles. This is similar to a painful episode he had with his left toe and ankle 6 months ago. On examination, his left great toe and both ankles are red, swollen, and warm to the touch. He describes the pain as throbbing and rates it as a 1 0 of 1 0 (where 1 0 is the worse pain he has ever experienced). He admits to drinking a six-pack of beer on weekends. 

Brunton, L., Agents for control of gastric acidity and treatment of peptic ulcers, in Goodman and Gilman s The Pharmacological Basis of Therapeutics, 9th ed., Hardman, J.G. and Limbird, L.E., Eds., McGraw-Hill, New York, 1996, chap. 37. 

The anti-ulcer agents omeprazole, lanzoprazole, and pantoprazole have been introduced during the past decade for the treatment of peptic ulcers. Gastric acid secretion is efficiently reduced by prazole inhibition of H+K+-ATPase in the parietal cells of the gastrointestinal mucosa [75]. The prazoles themselves are not active inhibitors of the enzyme, but are transformed to cyclic sulfenamides in the intracellular acidic compartment of parietal cells [76]. The active inhibitors are permanent cations at pH < 4, with limited possibilities of leaving the parietal cells, and thus are retained and activated at the site of action. In the neutral body compartments the prazoles are stable, and only trace amounts are converted to the active drugs. (For a review on omeprazole, see Ref. [77].)... 

Helicobacter pylori 1.66/1578 (68) Peptic ulcer, gastric cancer, gastric lymphoma (MALT)... 

Concurrent colonization by Gram-negative bacilli occurs in some patients with failure of the gastric acid barrier, suggesting additional deficiencies of host defense abnormal oral flora, malnutrition, general illness, or diseases or medication interfering with intestinal peristalsis and clearance. This type of microflora is also seen in 10-30% of patients on acid inhibitors, for which mucosal injury and functional changes related to peptic ulcer and reflux disease may be responsible. 

Peptic ulcers Ulcer of the digestive tract, caused by digestion of the mucosa by acid and pepsin. May occur in, for example, the duodenum (duodenal ulcer) or the stomach (gastric ulcer)... 

H. pylori is one of the main causes of human chronic gastritis, resulting in various diseases including peptic ulcers, gastric adenocarcinomas, and mucosa-associated lymphoid tissue (MALT) lymphomas (Williams... 

Prostaglandins inhibit the secretion of protons by the parietal cells in the stomach, which is normally increased in response to food and the hormone gastrin. Consequently, inhibition of prostaglandin synthesis by aspirin or other similar drugs results in increased secretion of protons by the stomach, which can result in considerable gastric discomfort and can, if chronic, lead to the development of a peptic ulcer. Consequently, there is some conflict between the use of such inhibitors to relieve chronic pain (see below), in diseases such as arthritis, and the risk of development of ulcers. 

---