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Chronic gastritis

Table of contents
Chronic gastritis
Clinical picture, diagnosis
Verification of the diagnosis
Treatment, prevention

Chronic gastritis — concept the collective, integrating inflammatory and disregeneratorny damages of a mucous membrane of a stomach, various on a morphological structure, an etiology and a pathogeny. The disease is characterized by morphological changes of a mucous membrane of a stomach — a nonspecific chronic inflammation (focal and diffusion) and the phenomena of a degeneration, restructuring with the progressing cover atrophy.

Morphological changes are followed various secretory and motor evakuatornymi by disturbances and various clinical signs.

Epidemiology
Chronic gastritis belongs to eurysynusic diseases, affects more than 40 — 50% of adult population of the globe. Among diseases of the digestive system it makes about 35%, and among stomach diseases —
60 — 85%. Frequency of gastritichesky changes of a mucous membrane and their expressiveness increase the patient with age. L. Demling notes that the frequency of chronic gastritis among the population of life increases every year for 1,4%.

Etiology and pathogeny
The reasons leading to development of chronic gastritis are various. Etiological factors are divided into exogenous and endogenous, and chronic gastritises respectively on primary and secondary.

Long disturbances of quality and diet, bad chewing of food at fast food and defects of the chewing device belong to the exogenous reasons, systematic reception of some medicines, alcohol intake, smoking and some professional harm. Chronic gastritis of this type can be a consequence of a duodenogastralny reflux, and also influence of the infectious agent of Helicobacter pylori (HP), triple to a superficial epithelium of a mucous membrane of antral department of a stomach. This microorganism was found in 1983 J. Marshall and J. R. Warren. HP is located under a slime layer, ureazny activity allows it to decompose urea, surrounding itself with ammonia, protection against pernicious influence of NSL thereby is provided. Ability of HP to cause antral gastritis in connection with production of substances by it with direct cytotoxic effect is proved.

At exogenous gastritis the protective mucous barrier and apical membranes of a cover epithelium are broken in the beginning that leads to damage of blankets of a mucous membrane, first of all peloric department of a stomach. At this stage of change have mainly inflammatory character. Further pathological process extends to deeper layers of a mucous membrane, disregeneratorny and degenerative disturbances with development of an atrophy of the ferruterous device join inflammatory changes. Similar damages of a mucous membrane of a stomach can be referred to gastritis of type B. In process of progressing of a disease the tendency to involvement in process of proximal departments of a stomach and increase of a mucosal atrophy is observed. According to M. Siurala and soavt., for transformation of superficial antral gastritis in widespread atrophic it is required about 19 flyings.

The reflux-gastita is feature early defeat of fundal department of a stomach because of cytotoxic influence of the bile acids and lysolecithin which got into a stomach at a duodenogastralny reflux. Process at the same time in fundal department of a stomach has focal character.

Endogenous gastritis develops against various other diseases owing to the damaging action on a mucous membrane of a stomach of a number of factors (neurodystrophic, toksiko-metabolic, allergic, etc.). At endogenous gastritis unlike exogenous first of all the ferruterous office of fundal department of a stomach suffers. Braking of cellular updating with disturbance of a differentiation of epithelial cells is the cornerstone of an adenosis. From an onset of the illness process has diffusion character and is aimed at the development of a mucosal atrophy of a stomach. Along with an atrophy the disregeneratorny phenomena in the form of "pilorieation" of fundal glands and an intestinal metaplasia are observed. Chronic endogenous gastritis progresses much quicker, than exogenous. Diffusion atrophic gastritis at this option forms for only 4 — 5 years.

Now allocate a special form of chronic atrophic fundal gastritis in which forming autoimmune mechanisms (gastritis of type A) participate. Identification of antibodies to covering cells and an internal factor, and also the high level of serumal gastrin is characteristic of it.

Classification
The fullest and standard classification of chronic gastritises was offered in 1966 by S. M. Ryss. However this classification is difficult for practical use and not completely reflects modern views on essence of an illness.
Abroad the classification offered R. G. Strickland and J. R. Mackay was widely adopted. Authors on the basis of morphological, functional and pathogenetic features allocated 2 types of chronic gastritis: gastritis of type A and type B. Gastritis of type A is characterized by preferential damage of a body of a stomach, existence of the circulating antibodies to covering cells and the high level of gastrin in blood serum. At type gastritis In changes in the basic are localized in antral department, there are no immune disturbances, gastrin level in blood serum is normal or even reduced. Besides, the reflux gastritis is considered as an independent form.

Also a number of domestic authors adheres to similar division of chronic gastritis into 3 types.

However the big group of secondary endogenous gastritises at which, as well as at gastritis of type A, the fundal department of a stomach mainly is surprised drops out of this classification, but there are no antibodies to debugging cells. For practical use the following classification is offered.

Classification of chronic gastritises

I. Main types of chronic gastritis

1. Antral gastritis (gastritis of type B)
2. Fundal gastritis:
a) secondary (endogenous) gastritis;
b) primary autoimmune (gastritis of type A)
3. Reflux gastritis

II. Additional characteristic
1. On a gastroscopic picture:
a) superficial;
b) hypertrophic;
c) atrophic
2. On a histologic picture:
a) superficial;
b) atrophic (moderated, expressed, with the reorganization phenomena on intestinal and peloric type);
c) atrophic - hyperplastic.

3. On a condition of secretory function of a stomach:
a) with the increased secretory function;
b) with normal secretory function; c) with secretory insufficiency (subacid, anacid).

III. Disease phase

1. Aggravation
2. Remission

Separately it is necessary to consider a special form which can only conditionally be carried to chronic gastritises — huge hypertrophic gastritis (Menetriye's illness).

In MKB IX gastritis is included in a heading 535 with division on: 1) atrophic gastritis; 2) hyperplasia of a mucous membrane of a stomach; 3) alcoholic gastritis; 4) other gastritises.

Approximate formulation of the diagnosis:
1. Chronic atrophic gastritis mainly stomach bodies (gastritis of type A) with the expressed secretory insufficiency (an anacid state), B12-scarce anemia.
2. Chronic and trawl superficial gastritis (gastritis of type B) with the increased secretory function of a stomach, an aggravation phase.
3. Arteriomesenteric compression of a duodenum, reflux gastritis


 
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