gastritis


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gastritis

inflammation of the lining of the stomach

Gastritis

 

an inflammation disease of the mucosa of the stomach. The development of gastritis is caused by exogenous factors (prolonged nutritional imbalance, overeating, insufficiently varied diet, alcohol abuse, nicotine abuse, and other kinds of intoxication and infection) and endogenous factors (functional disorders of the nervous system, neural reflexes from other diseased organs, such as the intestine and the gall bladder). The form of gastritis is determined by the nature, the intensity, and the duration of the exposure to the irritant that caused the gastritis and also by the organism’s resistance and the occurrence of relapses. Types of gastritis include acute and chronic, localized and diffuse, hypertrophic, atrophic, erosive, polypous, and gastritis with a high or low acidity of the gastric mucus.

Severe gastritis develops as a result of overeating, alcohol abuse, poisoning by alkalis or acids, the intake of irritative medicines, or the ingestion of food that is mechanically irritating, spicy, or too cold or too hot or fatty food that is hard to digest; severe gastritis can also be caused by certain microbes (streptococci, staphylococci, salmonellae, etc.), which enter the organism from contaminated food. Sometimes gastritis develops as a result of the endogenous intoxication of the organism, for example, in uremia and also in cases of individual intolerance of certain foods (fish, crayfish, crab, strawberries, eggs, etc.). Acute gastritis usually begins abruptly with the appearance of an unpleasant sensation in the abdomen, burning and heaviness in the epigastrium, headache, loss of appetite, nausea, eructation, and recurrent vomiting (sometimes with bile and mucus) that brings temporary relief; in some cases symptoms include thirst, chills, and fever. As the inflammation spreads to the intestine sharp colicky pain, borborygmus, and diarrhea appear. The sickness lasts for three to five days and, as a rule, ends with recovery. But there may be relapses.

Chronic gastritis is characterized by chronic inflammation of the mucosa of the stomach with gradual atrophy. Chronic gastritis develops either as a result of frequently recurring acute gastritis or as a result of the prolonged effects on the organism of the same causes that bring about acute gastritis. Often, chronic gastritis is caused by a chronic disease (tuberculosis, hepatitis, dental caries, etc.), by a dysfunction of the central nervous system, or by a metabolic disorder; occupational hazards (working in soap factories and hot shops and candle and margarine factories; the swallowing of metallic, cotton, or coal dust) and the prolonged ingestion of certain medicines can also cause gastritis. Chronic gastritis may take its course with insufficient, normal, or increased secretion of gastric juice. In the case of gastritis with decreased secretion patients are disturbed by lack of appetite, an unpleasant astringent or metallic taste in the mouth, eructation of air or with a rotten-egg aftertaste, nausea, a sensation of heaviness in the epigastrium, and occasional vomiting soon after eating. Sharp pains appear when food is ingested into the intestine. Chronic gastritis with normal or increased secretion begins at an early age. It is accompanied by pains and heaviness in the epigastrium, persistent heartburn, acidic eructation, a burning sensation, and a sensation of pressure and bursting that usually occurs two to three hours after eating. After the ingestion of food the pains pass.

Treatment for gastritis includes the elimination of the causes of acute gastritis, regulation of the functions of the central nervous system, treatment of the underlying diseases, the elimination of focal infection, improvement of oral hygiene, and elimination of occupational hazards. Of special importance are the hygienic and sanitary measures and adequate control of the food products for sale and the preparation of food in public catering facilities. Health-resort therapy yields good results (Essentuki, Zheleznovodsk, Borzhomi, Piatigorsk, Arzni, Druskininkai, etc.).

REFERENCES

Gordon, O. L. Khronicheskii gastrit i tak nazyvaemye funktsional’nye zabolevaniia zheludka. Moscow, 1959.
Sobakin, M. A. “Elektrograficheskoe issledovanie motornoi deiatel’nosti zheludka pri pishchevarenii v eksperimente i v klinike.” In the collection Voprosy fiziologii i patologii pishchevareniia. Moscow, 1958. Pages 141-60.

I. S. SAVOSHCHENKO

Gastritis in animals. Gastritis is observed in all animal species; in ruminants the equivalent is inflammation of the abomasum. It is caused by feeding on spoiled feeds, overfeeding, abrupt changes in diet, poisoning by poisonous plants and chemicals, tooth diseases, abnormal wearing down of teeth, and secondarily by certain infectious and parasitic diseases. The clinical aspects of gastritis include a decrease or absence of appetite, apathy, pain during palpation of the stomach, and colic; among carnivores and swine gastritis is accompanied by vomiting. In the diagnosis of gastritis the examination of the contents of the stomach obtained by means of a probe or by a needle puncture (in ruminants) is of great importance. Acute gastritis runs a course of several days and has a favorable outcome; chronic gastritis can effect permanent changes and can persist for months. Treatment focuses on elimination of the causes and prescription of an appropriate diet. In cases of intoxication, lavage of the stomach and laxatives are prescribed; for dogs and swine emetics must be used. In order to improve secretory and motor activity, Karlovy Vary salts, hydrochloric acid, pepsin, bitters, and other medicines are administered orally. Systematic veterinary and sanitary monitoring of the quality of feeds, the condition of pastures, the feed diet, and the watering places is necessary for prevention of gastritis.

N. M. PREOBRAZHENSKII

gastritis

[ga′strīd·əs]
(medicine)
Inflammation of the stomach.
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Dyspepsia--including gastritis and gastric ulcers--was considered to be caused by combinations of spicy foods and stress, leading to overproduction of acid.
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pylori -infected patients, with the progress of atrophic gastritis from the antrum to the corpus mucosa, the amount of PG I is considerably reduced or abolished owing to the damage of principal cells and parietal cells, while the level of serum PG II increases because the infiltration model of neutrophils and mononuclear cells is toward the upper stomach from the antrum.[38],[39] One study concluded that PG II is independently associated with risk of gastric cancer.[42] This evidence indicated that the serum PG level was closely correlated with the progression of atrophic gastritis.[43] Meantime, it indirectly reflected the status of H.
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