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Acid peptic attack

Studies in laboratory animals and humans suggest that there is a second component of injury in which acid peptic attack deepens erosions resulting from compromised mucosal defence with development of deep erosions and ulcers [9, 10]. These studies also suggest that relatively powerful acid... [Pg.193]

The term peptic ulcer refers to an> ulcer in an area where the niucusa is bathed in the hydrochloric add and pepsin of gastric juice (i.e. the stomach and upper part of the duodenum). Drugs that are effective in the treulmcnt of peptic ulcer cither reduce gastric acid secretion (left centre and righO or increase mucosat resistance to acid-pepsin attack (bottom left). [Pg.30]

In the area of a gastric or duodenal peptic ulcer, the mucosa has been attacked by digestive juices to such an extent as to expose the subjacent connective tissue layer (submucosa). This self-digestion occurs when the equilibrium between the corrosive hydrochloric acid and acid-neutralizing mucus, which forms a protective cover on the mucosal surface, is shifted in favor of hydrochloric acid. Mucosal damage can be promoted by Helicobacter pylori bacteria that colonize the gastric mucus. [Pg.166]

A 55-year-old man presents with complaints of an acute gouty arthritis attack. His left big toe is red, swollen, and tender to the touch. This is his first attack. He has no history of peptic ulcer disease. His uric acid level is 8 mg/dL. Which of the following agents would you recommend for treatment ... [Pg.91]

When it attacks proteins, pepsin liberates tyrosine bound by central bonds at the carboxyl end of the peptide chain, as well as tyrosine at the amino terminal end. At the Rockefeller Institute, M. L. Anson and A. E. Mirsky made liberation of tyrosine the basis of their method for estimating pepsin. They added a pepsin solution to a standard solution of hemoglobin in 0.6 N HCl. Hemoglobin is a substrate easily prepared in large quantities it can be stored without deterioration and it is uniform from one batch to another. The acidity chosen by Anson and Mirsky is well on the acid side of the pH where small variations in pH cause large changes in peptic activity. Anson and Mirsky stopped the reaction with trichloracetic acid and measured the tyrosine in the filtrate by means of the Ciocalteu-Folin phenol reagent. The method was universally adopted. ... [Pg.89]

As in the stomach, chronic inflammation follows colonization of islands of duodenal gastric metaplasia by K pylori and the inflamed duodenal mucosa becomes increasingly vulnerable to peptic acid attack and exposed to subsequent ulceration [31] (Fig. 1). Although H. pylori infection can be eradicated successfully, gastric metaplasia may persist or regress only partially [28, 32]. There is no continued increased risk for further duodenal ulcer relapse once H. pylori is eradicated. [Pg.177]

Peptic ulcers are sores in the stomach lining that expose it to acid attack. These sores result from infection by the bacterium Helicobacter pylori. H. pylori is susceptible to antibiotics such as amoxicillin, but the acid content of the stomach causes rapid destruction of the antibiotic. Thus the successful eradication of H. pylori infection and the cure of peptic ulcers relies on administration of the antibiotic... [Pg.61]


See other pages where Acid peptic attack is mentioned: [Pg.48]    [Pg.118]    [Pg.139]    [Pg.11]    [Pg.49]    [Pg.278]    [Pg.298]    [Pg.490]    [Pg.180]    [Pg.251]    [Pg.20]   
See also in sourсe #XX -- [ Pg.193 ]




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