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Peptic injury

The equine stomach is lined dorsally by a stratified squamous epithelium and ventrally by a glandular epithelium, which have different functions and susceptibility to peptic injury. The squamous portion of the stomach has no secretory or absorptive function and appears to serve as a reservoir for ingesta. The gastric glandular mucosa has an array of secretory and endocrine functions. [Pg.97]

In addition to their acid-neutralizing properties, antacids containing aluminum appear to have properties that can protect the gastric mucosa from peptic injury. These antacids have been shown to protect the mucosa against NSAID- or ethanol-induced injury by a mechanism that involves the production of NO, which promotes mucosal blood flow (Konturek et al 1992). [Pg.106]

Polysaccharide extracted from Hizikia fusiformis (Hf-PS-1) exhibited protective effects against ethanol-induced peptic injury. In in vivo assay, the ethanol group exhibited decrease of total glutathione (GSH) and increase of jun N-terminal kinase (JNK) phosphorylation relative to the control group, whereas levels were significantly increased and decreased, respectively, in the Hf-PS-1 group. Hf-PS-1... [Pg.143]

Goldenseal Hydrastis canadens s Antiseptic for skin (topical), astringent for mucous membranes (mouthwash), wash for inflamed eyes, sinus infections, peptic ulcers, colitis, gastritis Large doses may cause dry or irritated mucous membranes and injury to the gastrointestinal system may reduce the beneficial bacteria in the intestines. Siould not be taken for more than 3-7 days. [Pg.660]

Salim (1992d) has performed several studies using reser-pine to produce a chronic model of peptic ulceration in rats. Administration of allopurinol, DMSO, cysteine or methionine-S-methylsulphonium chloride protected against injury. In addition allopurinol and DMSO were found to stimulate healing in this model. In an acute model of duodenal ulceration induced by pentagastrin and carbachol allopurinol, DMSO, cysteine or methionine-S-methylsulphonium chloride all protected against injury. [Pg.146]

Patients with peptic ulcer disease have mucosal injury and may develop fibrosis in the antroduodenal region and... [Pg.6]

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. [Pg.8]

The physical condition determines the psychic disposition and vice versa. Consider gravely wounded combatants in war, oblivious to their injuries while fighting to survive, only to experience severe pain in the safety of the field hospital, or the patient with a peptic ulcer caused by emotional stress. [Pg.76]

Prophylactic and therapeutic administration of Enterosgel to rats with experimental peptic ulcer and ulcerative colitis, significantly decreased the number and surface area of lesions on gastro-intestinal tract (GIT) mucosa and reduced the severity of the syndrome of endogenous intoxication that accompanied these injuries [21, 22]. The first evidence of clinical use of Enterosgel in combined therapy of peptic gastric ulcer and duodenum was reported by S.M. Tkach, who had noted that enterosorp-tion significantly reduced the number of side effects of treatment, and the rate of Helicobacter eradication increased from 83.3 to 93.3% [23]. [Pg.207]

The normal gastroduodenal mucosa has the following three defense mechanisms for resisting injury arising from the acid and peptic activity in gastric juice. [Pg.591]

Smoking is especially harmful to diabetics who are already at an increased risk of cardiovascular disease, stroke, and kidney disease. The habit also negatively affects joints and interferes with the healing of wounds. Healing of fractures is delayed because smoking impairs the formation of new bone. Smokers are more likely to develop degenerative disorders and injuries of the spine. The risk for peptic ulcers is increased. Smoking also may upset thyroid function. [Pg.372]

Yeoh et al. (1995) demonstrated that chilli could protect humans against aspirin-induced gastroduodenal mucosal injury. A survey conducted by Kang et al. (1995) established the protective effect of chilli against peptic ulcer. Red pepper and natural and synthetic capsaicin in the diet significantly decreased cholesterol in the liver (Sambaiah and Satyanarayana, 1980). [Pg.279]

Physicians may consciously or unconsciously communicate to the patient whether or not they are concerned about the patient s problem, or are certain about the diagnosis and about the value of prescribed therapeutic measures. In the care of a physician who projects personal warmth, competence, and confidence, the patient in turn feels comfort and less anxiety and optimistically anticipates recovery. The physical condition determines the psychic disposition and vice versa. Consider gravely wounded combatants in war, oblivious to their injuries while fighting to survive, only to experience severe pain in the safety of the field hospital or the patient with a peptic ulcer caused by emotional stress. [Pg.80]

Gastric ulceration induced by NSAIDs is a neutrophil-dependent process (78) and the association of H. pylori infection with neutrophil infiltration has also been well documented. Gastric injury by NSAIDs is minimal in neutropenic animals, and the cumulative incidence of peptic ulcers in long-term NSAID users is increased in the presence of neutrophil infiltration in the mucosa of patients who are H. py/on-positive, suggesting a possible link between NSAIDs and H. pylori in the pathogenesis of peptic ulcers (79,80). [Pg.2562]

The pathophysiology of peptic ulcer disease is best viewed as an imbalance between mucosal defense factors (bicarbonate, mucin, prostaglandin, nitric oxide, and other peptides and growth factors) and injurious factors (acid and pepsin). On average, patients with duodenal ulcers produce more acid... [Pg.629]

NSAlDs also are very frequently associated with peptic ulcers (in up to 60% of patients, particularly those with complications such as bleeding). Topical injury by the luminal presence of the dmg appears to play a minor role in the pathogenesis of these ulcers, as evidenced by the fact that ulcers can occur with very low doses of aspirin (10 mg) or with parenteral administration of NSAlDs. The effects of these drugs are instead mediated systemicaUy the critical element is suppression of COX-1 in the mucosa and decreased production of the cytoprotective prostaglandins PGE and PGI. ... [Pg.630]

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]

Perforation of Peptic Ulcer 217 Acute Gastric Volvulus 218 Proximal Small Bowel Volvulus Emphysematous Gastritis 222 Injuries to the Stomach and Duodenum 224 Rupture of the Stomach 224 Intramural Haematoma of the Duodenum 224 Retroperitoneal Rupture of the Duodenum 226 Diaphragmatic Rupture 226 References 228... [Pg.217]


See other pages where Peptic injury is mentioned: [Pg.98]    [Pg.98]    [Pg.105]    [Pg.106]    [Pg.145]    [Pg.157]    [Pg.98]    [Pg.98]    [Pg.105]    [Pg.106]    [Pg.145]    [Pg.157]    [Pg.146]    [Pg.200]    [Pg.319]    [Pg.205]    [Pg.1309]    [Pg.319]    [Pg.598]    [Pg.1469]    [Pg.431]    [Pg.327]    [Pg.633]    [Pg.17]    [Pg.702]    [Pg.630]    [Pg.1477]    [Pg.4529]    [Pg.265]    [Pg.318]    [Pg.368]    [Pg.194]    [Pg.201]   
See also in sourсe #XX -- [ Pg.98 ]




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