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  • Gastritis symptoms

    Gastritis sick in our country children of preschool and school age, youth, adults, elderly people and the elderly. But this is not an epidemic, but the result of neglect of one's health or lack of understanding and lack of knowledge in this area.

    Some people do not trust doctors and believe that they are just waiting for the opportunity to treat someone, to torment them, because they, doctors, are the only ones who know how to do this, in their opinion.

    Others do not trust doctors, books or anyone, considering that nobody can understand them better than their ancestors. .. How to treat this disease with folk remedies, see here.

    Still others do not think about their health at all.

    Fourth, there is simply no time to go to polyclinics, but you really do not want to be ill. Here for them the given information.

    I. In the form:

    1. Simple( banal, catarrhal).

    2. Corrosive.

    3. Fibrinous.

    4. Phlegmonous.

    II.For ethical reasons:

    1. Exogenous( external).

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    2. Endogenous( internal).

    There are several different classifications of gastritis .In 1990, the International Congress of Gastroenterologists in Sydney was adopted the following classification:

    I. For etiology:

    1. Associated with Helicobacter pylori.

    2. Autoimmune.

    3. Chemical-Toxic Induced.

    4. Idiopathic.

    5. Special form( eosinophilic, granulomatous).

    II.By the location of the lesion:

    1. Pangastritis( common).

    2. An antrum gastritis( pyloroduodenitis).

    3. Gastritis of the body of the stomach.

    III.According to the severity of the morphological manifestations of

    1. No change.

    2. Slightly expressed.

    3. Moderate.

    4. Heavy changes.

    IV.By endoscopy( morphological changes)

    1. Eritomatous exudative.

    2. Flat erosive.

    3. Atrophic.

    4. Hemorrhagic.

    5. Hyperplastic.

    V. By the nature of gastric fluid secretion:

    1. With preserved or increased secretion.

    2. With secretory insufficiency.

    Acute gastritis is an inflammatory disorder of the gastric mucosa, which is accompanied by motor and secretion disorders and arises for numerous reasons, this is what is commonly called poisoning or acute inflammation of the gastric mucosa. First, there is usually a feeling of pressure and heaviness in the stomach, combined with nausea, drooling, unpleasant taste in the mouth. At the same time, there are pains in the upper abdomen that are characterized by spasms. There is vomiting, usually recurring, and in severe cases it becomes indomitable. Vomit in the beginning consists of food residues, then from a liquid with an admixture of mucus and bile. Such vomiting is very dangerous, since dehydration of the body may occur.

    But vomiting is a symptom of not only acute gastritis. For example, with appendicitis, cholecystitis( inflammation of the gallbladder), pancreatitis( inflammation of the pancreas) may also be vomiting. However, with these diseases, the pains are of a different nature: thus, with pancreatitis, they seem to encircle the trunk - extend both to the abdomen and back( more in the upper half of the abdomen), and with cholecystitis and appendicitis the pain is more pronounced in the right side of the abdomen.

    However, if you firmly associate the occurrence of gastritis with the reception of something that is of poor quality, then it is better to wash the stomach, and immediately. In light cases, rinsing can be limited by drinking water with subsequent vomiting( salt can be added to the water - a teaspoon of common salt per 1 glass of warm water).And in severe cases, it is necessary to call a doctor and rinse the stomach with plenty of water using a probe.

    Despite the multiplicity and diversity, the causes of inflammation of the stomach can be combined into two large groups:

    1. Exogenous, or irritative( gastritis develops in response to external factors).

    2. Endogenous, or hematogenous, associated with internal effects on the gastric mucosa of pathological irritants emanating from the body itself( acute infections, metabolic disorders, the breakdown of body proteins in burns and irradiation, some mental and neuropathological diseases, etc.)..

    Among the main external causes of gastritis are: the intake of poor quality food, overeating, the use of very sharp, fatty, too hot or excessively cold, hard-to-digest food, strong alcoholic drinks, etc. Gastritis, which develops due to the factors listed above, is called"Alimentary gastritis."

    Each of us knows the expression "to fill the stomach" and the unpleasant feeling of heaviness and discomfort in the epigastric region that occurs after a fast, hasty meal. Here to you and one of the reasons of a gastritis. From this point of view, the wisdom of the Tibetan lamas, striking us with longevity and extremely long youth, is understandable - after all, they chew even ordinary drinking water!

    Good chewing food requires strong, healthy teeth. Hence the need for careful care for them, regular visits to the dentist and timely prosthetics, which in our difficult time of economic instability, alas, is not always and not everyone is available.

    The cause of gastritis may be a violation of diet( overeating, especially after a long break between meals) and eating dry. Abuse of alcohol and smoking can also cause inflammation of the stomach.

    Among the causes of gastritis, it should be especially noted the reception of poor-quality, infected food, the so-called food-borne diseases: colitis, salmonella, botulism, staphylococcal toxic infections, iersiniosis, etc.

    Severe inflammatory lesions of the gastric mucosa can be triggered by prolonged intake of a number of medications. In a number of similar drugs, salicylic preparations, quinine, digitalis, atopan, arsenic, sulfonamides, antibiotics, iodine, bromine, steroid hormones, butadione, insulin, etc. should be mentioned.

    Severe allergic gastritis occurs with individual hypersensitivity to certain tablets, powders,medicines, etc.

    It should be emphasized that the individual immunity of the gastric mucosa plays an important role in the origin of gastritis. Well-known fact of the existence of so-called tinned stomachs, capable of digesting any food. Along with them, there are stomachs sensitive to the most common dishes, such as milk, eggs, strawberries, smoked fish, melons, tomatoes, caviar, mushrooms, etc.

    All of the above external causes cause gastritis in direct contact with the mucous membrane of the stomach orwhen irritants enter the mucosa through the circulatory system. In the latter case, the stimulus first enters the blood, in the composition of which it is delivered to the mucous membrane of the stomach and causes its inflammation.

    Among the exogenous causes of severe gastritis, it should be noted poisoning some toxic substances. Among them - strong acids( sulfuric, hydrochloric, nitric, chromic, acetic, phosphoric, carbolic, formic, etc.), caustic alkali( ammonia, caustic soda, caustic potassium, caustic soda), mercuric chloride, potassium cyanide, arsenic,chloroform, lysol, high alcohol concentrations and high doses of medications. These substances can be mistaken. The aforementioned toxic substances not only cause severe irritation of the gastric mucosa, but at a certain concentration they have a pronounced necrotizing( necrosis factor) effect. With the action of concentrated acids, a cortical degeneration of the tissues of the gastric mucosa develops;When contact with caustic alkalis, the formation of dead tissue occurs in the form of a loose crust. The extent and extent of the lesion depends on the concentration and residence time of the poison in the stomach. In mild cases, the mucous membrane can regenerate, in severe cases develop rough cicatricial changes.

    With endogenous gastritis, both poison agents and metabolic products have a damaging effect on the gastric mucosa.

    In healthy people, the immunity of the gastric mucosa to the action of toxic substances is very high. It even exceeds the resistance of the skin. Under the influence of a number of predisposing factors that reduce the immunity of the patient, the stability of the gastric mucosa to the action of irritating chemical or protein compounds is significantly reduced. Among such factors include: mental and physical fatigue, lack of proper rest, occupational hazards, physical development and hereditary characteristics of the organism, as well as the diseases that have been transferred.

    The causes of gastritis development include acute and chronic infectious diseases( measles, scarlet fever, diphtheria, typhoid fever, flu, typhus, pulmonary abscess, tuberculosis, etc.).In the emergence of this group of gastritis, the leading role is played by hematogenous entry into the gastric wall of pathogenic microbes and toxic substances released by them. In addition, with infectious diseases, a significant amount of protein products of vital activity of microorganisms harmful to the body is formed. These harmful substances, together with bacterial poisons, enter the stomach wall with blood and cause its inflammation.

    The cause of gastritis may be uremia( absorption of urine into the blood), burns, frostbites. These pathological conditions are accompanied by serious circulatory disorders, hypoxia of the gastric mucosa and the introduction of toxic substances into the bloodstream, which is the pathogenetic basis of gastritis development in these diseases.

    Endogenous factors of gastric inflammation play a prominent role in diseases of endocrine glands and metabolic disorders: diabetes mellitus, gout, hyperthyroidism, etc., in which there is also a thrombotic pathological effect of toxic substances( metabolic products) on the mucosastomach.

    In the development of gastritis, which arise under the influence of mental disorders, negative emotions and states of prolonged exposure to the conditions of psychological discomfort, the leading role is played by circulatory disturbances in the stomach. This leads to a lack of supply of oxygen to the gastric mucosa and some other functional disorders. For example, to the violation of the excretory function of the gastric glands and the contractile function of the muscles of the stomach.

    A decrease in appetite observed in a number of patients is most often due to stasis and reverse peristalsis of the stomach muscles and a decrease in its secretory function.

    Insufficient secretion of pepsin( a digestive enzyme that breaks down proteins) and hydrochloric acid by the glands of the stomach, as well as excessive peristaltic activity due to increased contractions of the stomach muscles, underlies pain or discomfort in the epigastric region. All this is also characteristic of inflammation of the stomach.

    Difficulty in swallowing leads to reflux( casting) into the esophagus of acidic stomach contents, which causes irritation of the nerve endings of the predominantly distal( output) section of the esophagus. As a consequence, the patient has heartburn, that is, a burning sensation behind the sternum.

    Gastritis is often accompanied by a clinical symptom, such as eructation - sudden, involuntary exit through the mouth of gases from the stomach into the esophagus. Its occurrence is associated with strains and a slight anti-peristaltic movement of the esophagus and stomach. This is accompanied by short-term or prolonged symptoms of difficulty swallowing.

    Delayed removal of digested food from the stomach is a consequence of its inflammation. And can lead to the appearance of regurgitation - throwing into the pharynx or oral cavity a small amount of esophageal or gastric contents. In this case, the masses emitted from the stomach contain hydrochloric acid, which gives them an acidic taste.

    The basis of diarrhea, often observed with gastritis, is the violation of intestinal peristalsis and impaired absorption of food and water, as well as inflammatory processes in the wall of the intestine. This prevents the full digestion of food and the natural formation of stool in the intestine.

    A frequent symptom of gastritis is nausea( an unpleasant sensation in the abdominal cavity, which can be accompanied by faintness, drooling, pale skin, sweating, dizziness and even a fainting condition).The emergence of vomiting is caused by irritation of the vagus and celiac nerves with subsequent transfer of impulses to the vomiting center and in the opposite direction, provokes a difficulty in the patency of the upper parts of the digestive tract.

    Vomiting in gastritis is a complex reflex act associated with irritation of the emetic located in the medulla oblongata with pathological impulses emanating from the receptor apparatus of the mucous membrane of the inflamed stomach and toxic substances entering the bloodstream. The irritation of the emetic center causes nerve impulses that cause the development of a number of successive processes: the descent of the diaphragm, the closure of the glottis, the reduction of certain parts of the stomach, the relaxation of the body of the stomach and its cardiac sphincter, the emergence of anti-peristaltic waves. Due to the contraction of the diaphragm and abdominal muscles, intra-abdominal and intragastric pressure increases. The result of these processes is a rapid release of the contents of the stomach into the mouth through the esophagus.

    The occurrence of pain in acute gastritis is associated with mechanical irritation of the contents of the stretched stomach of pathologically sensitive receptors located in its mucosa. Inflamed hyperemic gastric mucosa becomes a source of pain already with any mechanical irritation, being devoid of protective mucus, for example, under the influence of cauterizing action of a gastric juice rich in hydrochloric acid.

    Symptoms of the disease appear 4-8 hours after eating( poor quality foods, strong alcoholic beverages, abundant, fatty foods, excessively hot or too cold foods, etc.).

    The disease develops rapidly or gradually, depending on the nature, extent and duration of the etiological factor, as well as on the level of individual sensitivity of the patient's body.

    There is an increasing general weakness unpleasant taste in the mouth, nausea, belching stagnant, decomposed food. Disturb the feeling of heaviness, raspiranie and pain in the epigastric region, headache. Sometimes as a result of a spasm in the stomach area there are cramping pains in the abdomen. Appetite is absent. There may be an elective need for salt, acidic or cold( water, ice slices) food.

    Soon, vomiting is eaten by food. Often, vomiting is repeated, accompanied by pain in the abdomen and brings temporary relief. Vomit has an unpleasant sour smell. They contain undigested food particles, impurities of mucus and bile. Sometimes there is blood in the vomit. After repeated vomiting and liberation of the stomach from the contents in the vomit, a viscous mucus mixed with bile appears. Vomiting is usually accompanied by pallor of the skin, increased sweating, severe weakness, lower blood pressure.

    In some patients, the general condition suffers little, others suffer a general condition.

    Pale skin and damp skin are noted. Language is surrounded by gray or grayish-yellow coating. There is an unpleasant smell from the mouth of the patient. There may appear herpetic( similar to herpes) rashes on the lips. The abdomen is swollen( flatulence), palpation is painful, especially in the stomach. In a number of patients, body temperature rises. Sometimes there is diarrhea.

    There is an aversion to food, one mention of which can cause a sick nausea and vomiting.

    In a number of cases, especially with the allergic nature of the disease, gastritis acquires a severe course, often accompanied by the formation of multiple surface erosions on the gastric mucosa. At the same time, symptoms of intoxication are added to the sensations of severity in the abdomen, vomiting, flatulence, diarrhea and other disorders: headache, dizziness, adynamia, high fever. There are tachycardia, deafness of cardiac tones. Blood pressure is reduced. Abundant multiple vomiting causes a sharp decrease in body fluid and salt content. In this case, convulsions appear in the calf muscles. A significant loss of fluid( due to vomiting and diarrhea) leads to a so-called blood thickening, which is manifested by an increased content of hemoglobin and erythrocytes.

    At the onset of acute gastritis, there is an increase in gastric secretion and acidity in the contents of the stomach. Further, increased excretory activity is replaced by oppression of the functions of the gastric glands.

    Acute, caused by mechanical influences of external origin, gastritis usually has a short, favorable course. Its duration rarely exceeds 4-5 days. With proper, timely treatment, the symptoms of the disease quickly subsides, and clinical recovery begins.

    On average, acute simple gastritis lasts 5 days. However, pathomorphological changes in the wall of the stomach persist for a longer time. Sometimes after the clinical recovery, a patient is worried for a long time with increased sensitivity to rough food. Often there is a transition of the disease into a chronic form.

    Acute simple gastritis often develops as a complication of infectious diseases. Another cause may be the decay of the body's own proteins, triggered by extensive burns and the effects of ultraviolet or X-ray irradiation. In this case, inflammation of the stomach is a response to the hematogenous drift into its wall of pathogenic microbes and toxic products of protein destruction. With this form of endogenous gastritis in the clinical picture, the symptomatology of the disease that caused its development comes to the forefront. Similar prevalence in the clinical picture of the signs of the underlying disease is observed in gastritis caused by painful changes that occur inside the body. These pathological changes can be triggered by a metabolic disorder. The most typical causes of metabolic disorders in the body are diabetes, gout, thyrotoxicosis( a consequence of the pathology of the thyroid gland), uremia( self-poisoning of the body caused by urine entering the blood), cholemia( self-poisoning of the body with bile acids, accumulating in the blood during bile congestion and impaired functionliver, etc.).

    One of the types of acute exogenous gastritis is erosive gastritis. Its clinical picture has some differences from acute simple gastritis, characteristic only for this form of the disease. The occurrence of erosive acute gastritis is also associated with the intake of poor-quality foods( salted, sharp, overcooked or stale) or medications( eg, large doses of aspirin).But the disease begins with the appearance of dyspeptic disorders( nausea, vomiting, heaviness in the stomach, diarrhea, etc.), pain in the epigastric region and gastric bleeding. Sometimes the onset of the disease is marked by gastric bleeding without other symptoms of gastritis. Bleeding is due to the presence of multiple erosions on the gastric mucosa. The tendency to gastric bleeding distinguishes erosive gastritis from other varieties of acute gastritis due to a multitude of bleeding erosions.

    This rare form of acute gastritis is characterized by extreme severity of the course and very often leads to death, therefore it is necessary to know about it and remember the most important characteristics of this disease. Phlegmonous gastritis is most common in alcoholic men.

    Primary phlegmonous gastritis occurs in case of infection( streptococcus, Escherichia coli, Staphylococcus, pneumococcus) through a defect in the gastric mucosa, which can occur in ulcers, stomach cancer, traumatic injury, the consequences of transferred operations, etc.

    Whenthe secondary phlegmon of the stomach, pathogenic bacteria penetrate into its wall from neighboring organs or are entered with the blood flow, ie, by metastasis. Secondary phlegmonous gastritis occurs in such septic( infectious) diseases as erysipelas, endocarditis, sepsis, as well as with furunculosis, typhoid fever, smallpox, after removal of the infected tooth and surgical interventions on the stomach.

    An important role in the emergence of this form of gastritis is played by predisposing factors: alcoholism, prolonged malnutrition, traumas, acute infectious diseases transferred, foci of chronic infections in the body, chronic gastritis with secretory insufficiency.

    Phlegmonous gastritis is characterized by the development of bacterial damage and suppuration of the stomach wall. In this case, there is a predominant distribution of pus under the mucous membrane. Bacterial agents that cause purulent process in the stomach are hemolytic streptococcus, staphylococcus, Escherichia coli, Proteus, pneumococcus, causative agent of gas gangrene and other pathogenic microorganisms.

    The process can develop gradually, but more often has a violent course and features an acute infectious disease. There is a high fever with a shaking chill, the temperature rises and again drops to a normal level, so it can be repeated in periods, accompanied by a profuse sweating. The patient is disturbed by nausea, vomiting. In vomit masses contain an admixture of bile, less often - blood and pus. Gastric bleeding may develop. The patient is restless or in prostration. Its condition is heavy, with a tendency to progressive deterioration. There is thirst, intense diffuse pain in the abdomen, diarrhea. There is bloating, his palpation causes pain. Muscular tension is determined in the epigastric region palpation. Sometimes in the stomach area it is possible to probe a painful tumor of elastic consistency.

    Later, the phenomena of peritonitis and sepsis are added. The toxic cardiovascular insufficiency develops.

    In a number of cases, phlegmon of the stomach is complicated by the development of purulent flebititis of the veins of the portal system, the formation of multiple purulent liver lesions, gastric bleeding, purulent pleurisy, liver abscess.

    In the patient's blood, a severe complicated leukocytosis with toxic granularity of leukocytes is determined( as one of the types of blood infection is determined).

    Diagnosis of the disease is very difficult. Often mistakenly diagnosed with pancreatitis, liver abscess, penetration of the stomach or duodenal ulcer into other organs, or other acute diseases of the abdominal cavity, characterized by a clinical picture of an abdominal catastrophe.

    In case of ingestion of strong acids, caustic alkalis and other toxic substances listed above, the patient immediately after swallowing has a phenomenon of acute obstruction of the gastrointestinal tract. There are pains and a burning sensation in the mouth, diffuse pain along the esophagus, difficulty swallowing, excessive salivation with the release of viscous saliva.

    Symptoms of acute gastrointestinal obstruction quickly signs of severe stomach damage. There are strong, painful pains in the stomach, combined with a sharp thirst and the inability to swallow the liquid. The patient is disturbed by nausea and repeated vomiting by bloody masses containing a large amount of mucus and food remnants. The smell of vomit can help determine the type of poisonous substance taken to the patient.

    To establish the quality of the poison, also the appearance of characteristic spots on the mucous membrane of the lips, corners of the mouth, cheeks, tongue, throat, soft palate, larynx. On the mucous membrane of the mouth, esophagus, stomach, there are extensive areas of burns and inflammatory changes of varying severity: hyperemia, edema, erosion, ulceration;in severe cases - the transition of the disease to other organs of the abdominal cavity. There is edema of the larynx, as a result of which the voice disappears or becomes hoarse.

    Palpation of the abdomen causes severe pain, especially pronounced in the epigastric region. Poisoning in some cases is accompanied by an oppressed psychogenic state and adynamia, in others - signs of excitation of the nervous system.

    In severe cases, a state of deep shock develops rapidly, caused by sharp pain, poisoning with toxic products of protein breakdown in one's own body, loss of blood and fluid. There is a collaptoid( characteristic for collapse) condition, accompanied by a sharp drop in arterial and venous pressure and a change in the volume of circulating blood.

    The amount of daily urine decreases. In the urine, protein, erythrocytes, cylinders, hemoglobin degradation products, urobilin are found. In a number of cases, diffuse kidney lesions develop. The feces determine the latent blood.

    Sometimes a black tar unformed stool with a fetid odor is observed, which is caused by bleeding from the stomach or esophagus affected by the poisonous substance.

    Severe corrosive gastritis is accompanied by deep lesions of the stomach wall and destruction of its glandular apparatus, as a result of which the stomach completely stops releasing gastric juice and other digestive substances, ie, substances that have entered the stomach simply corrode the stomach wall.

    In severe cases, patients die within the next few hours and days. Critical are the first 2-3 days from the onset of the disease. Death can come from shock, acute esophageal or gastric bleeding, laryngeal edema, aspiration pneumonia;acute, severe damage to the walls of the stomach( in severe forms - purulent), which developed due to the penetration of the disease into the esophagus, as well as peritonitis due to severe pathological changes in the stomach.

    Serious consequences should be taken seriously. They are heavily dependent on timely and proper therapy. Complete recovery is possible only in mild cases. Restoration of the morphological structure and functions of the gastric mucosa occurs rarely.

    If the death of a patient does not occur in the next few days after poisoning, his condition begins to gradually improve. The disease leads to extensive cicatricial changes in the esophagus and stomach, due to which esophageal stenosis, swallowing disorders( dysphagia), narrowing of the middle and cardial parts of the stomach, scarring of the stomach, motor and secretory gastric insufficiency, chronic atrophic gastritis, achilles.

    If part of the gastric glands persists or gradually restores the function, hydrochloric acid and enzymes of gastric juice reappear in the gastric juice. However, such regeneration refers to rare phenomena and is possible only with shallow lesions of the gastric mucosa that are not accompanied by its gross morphological changes. It should be noted that the reception of weak solutions of acids and alkalis does not cause the development of corrosive gastritis. In these cases, a clinical picture of the usual acute gastritis is observed.

    Chronic gastritis is one of the most common diseases that occupy a prominent place among the processes of painful changes in the gastrointestinal tract. Chronic gastritis is more common in men than in women. The disease is characterized by an inflammatory process in the mucous membrane of the stomach, accompanied by morphological changes of the stomach( atrophy, impaired ability to restore), a violation of peristalsis and excretory function of the gastric glands.

    Chronic gastritis, unlike acute, develops gradually. No one can say: "I fell ill with a chronic gastritis on such and such a day."The exact date for this disease is not and can not be. Moreover, a person who easily agrees with the diagnosis of "acute gastritis", stubbornly does not want to admit gastritis chronic, does not want to accept the idea that this sore will now always bother him. How, when, at what stage does acute gastritis become chronic?

    For a long time a person can not pay attention to some unusual, unpleasant sensations in the stomach area - often this inattention is associated with hard work, with a lot of urgent matters, etc., in general, people have no time to think about their health. At the same time, the person notes with surprise that some foods that he had previously eaten calmly and which were easily digested, now the stomach for some reason does not tolerate the stomach. But a single-minded person, who can not be prevented by anything, attributes all these strange manifestations to the characteristics of the aging organism and does not attach importance to them. He gradually restricts his diet, knowing that some of his food can no longer absorb his stomach.

    It's strange, but a person remembers that he has a stomach, and begins to feel his work only when he gets sick. This is similar to how a team usually does not notice a good employee. It works without failures, it performs its work on time and qualitatively, and it seems to everyone that this should be so. But suddenly the employee became inattentive, began to make mistakes or became ill - he would immediately be shown increased attention, realizing that he was the very cog, without which the machine would not work. The same happens with the work of the stomach.

    Simultaneously with inflammation of the stomach with chronic gastritis other internal organs are affected, i.e. the disease is not local, but general.

    Similarly to acute inflammation of the stomach, a chronic process can cause both exogenous and endogenous factors. In some cases, chronic gastritis develops after acute acute inflammation of the stomach. In other cases, it is an independent disease and develops in response to prolonged exposure to irritant factors. Among them, an important role is played by: overeating, the use of rough, spicy, indigestible food, the abuse of spices, smoked foods, fatty foods. Contribute to the emergence of the disease, as well as eating dry food, hasty food with poor chewing food, disturbed rhythm and diet( a long break between meals, long starvation, abundant food before bedtime), the systematic reception of strong alcoholic beverages, smoking( the action of nicotine increases the excretory function of the stomach glands).

    To a great extent, the cause of chronic gastritis can be the quality of food consumed: its low caloric content, the overwhelming predominance of one or several foods, insufficient protein and vitamin composition, lack of ascorbic and nicotinic acids, thiamine, riboflavin, pyridoxine, vitamin A. Absencein the diet of high-grade proteins leads to atrophic processes in the mucous membrane of the stomach. The temperature of the food and the fluid taken is important. It is established that a very hot tea or soup causes damage to the mucous membrane of the stomach, similar to defects caused by the action of strong alcoholic beverages.

    The important exogenous( external) factors include occupational hazards. The disease often develops in workers in hot shops, as well as in workers in soap, margarine, candle plants as a result of a constant irritant effect on the gastric mucosa of alkali and fatty acid vapors. Chronic inflammation of the stomach can be the result of prolonged lead poisoning, ingestion of metal, cotton and coal dust.

    Professional chronic gastritis is often found in food industry workers, in canneries workers. The development of chronic inflammation of the stomach in these categories of workers is associated with the use of a large amount of spiced meat, fish, etc.

    Long-term use of a number of drugs( salicylates, sodium bicarbonate, digitalis, euphyllin, diuretin, laxatives, sulfonamides, atophane, mercury preparations, etc.) can provoke the development of chronic gastritis as a result of their irritating effect on the mucous membrane of the stomach and changes in its excretory function.

    In the development of exacerbations of chronic gastritis, an important role belongs to a disease characterized by the manifestation of an increased sensitivity of the body to food intake( food allergy), as well as defects in neurohumoral regulation of gastric functions.

    An important role in the origin of chronic gastritis is played by reflex effects that emanate from diseased internal organs, i.e., diseases of other organs can cause gastritis. There are cases of chronic gastritis caused by diseases of the pancreas, gall bladder, intestine, and helminth diseases( ascariasis, opisthorchiasis, trichocephalus, etc.).That is, in the case of chronic gastritis, we are faced with the fact that this disease is capable of causing other diseases, as well as arise due to painful disorders in our body.

    Chronic gastritis can develop due to circulatory disorders or hypoxia( insufficient oxygen supply) of stomach tissues in diseases of the cardiovascular system. The development of chronic gastritis is promoted by uremia, pneumosclerosis( a disease associated with changes in the structure of lung tissue), emphysema, i.e., diseases that can cause a decrease in the supply of oxygen to our body. In addition, chronic gastritis can be caused by diseases of the kidneys, liver, circulatory system, diseases of the endocrine glands( pituitary gland, thyroid, adrenal glands), as well as metabolic disorders caused by obesity, gout, diabetes, iron deficiency. The secretory activity of the stomach is also disturbed by diseases of the adrenal and thyroid gland.

    Chronic infections can become the causes of chronic gastritis development: tonsillitis, sinusitis, adnexitis, cholecystitis, carious teeth, chronic appendicitis, syphilis, tuberculosis, malaria. No less important are acute infections: influenza, diphtheria, paratyphoid, enterocolitis, infection with pyloric Helicobacter.

    The causes of chronic gastritis include allergic diseases, which lead to an increase in the excretory function of the gastric glands.

    Thus, chronic gastritis is caused by many factors, each of which determines certain features of the course of this disease. However, despite the differences in the mechanisms of the development of the pathological process, the basis of all forms of chronic inflammation of the stomach is structural damage to its mucous membrane. The damaging agent can act on it directly, or its action is mediated by the flow through the bloodstream.

    Exogenous toxic( poisonous) substances entering the stomach, destroy its protective mucous barrier and then cause structural damage to the mucous membrane.

    The atrophy of the gastric mucosa lies at the basis of the development of chronic gastritis in diseases accompanied by tissue hypoxia( circulatory insufficiency, difficulty in accessing oxygen, iron deficiency anemia( a violation of the ability of hemoglobin to bind and deliver oxygen to the organs and tissues of the body), pneumosclerosis, etc.)violation of tissue respiration and oxygen starvation of cellular elements of the glandular apparatus of the stomach.

    The development of a lack of a large number of vitamins and avitaminosis( A, B, C, etc.) is a consequence of the violation of the secretory and absorption functions of the stomach and dysbacteriosis, which are observed in chronic gastritis. The emergence of the latter is also promoted by long-term diets and the use of a number of medications, in particular, sulfonamides, which destroy vitamins. The violation of the absorption process of iron supplied with food causes the development of anemia. When a foci of the disease forms in the lower part of the stomach, the cells that produce gastromucoprotein( a protein associated with the release of B vitamins) die, which leads to the development of hypochromic anemia( low hemoglobin content in the blood).

    Symptoms of chronic gastritis are very diverse and often do not depend on the extent and prevalence of the inflammatory process in the stomach. The intensity and abundance of complaints are to some extent influenced by neurotic manifestations, stress, because gastritis often occurs in people whose life-pace is on the verge of possible.

    Chronic gastritis has very diverse symptoms. Disease for a long time can go unnoticed, so it is usually difficult to accurately determine the time of its onset. Regardless of the form of chronic gastritis, the clinical picture of all its varieties has similarities. The first include complaints of a violation of appetite, belching air or rotten egg, heartburn, nausea, vomiting, burning sensation, overflow and pain in the epigastric region associated with eating;diarrhea or constipation, bloating and his rumbling, sometimes tenesmus( painful, false urge to defecate).These complaints are part of the so-called gastric and intestinal dyspepsia( decay of food in the stomach and intestines due to violations of its digestion).Symptoms of gastric malaise( nausea, vomiting, etc.) may have varying degrees of severity. Their occurrence is associated with a decrease in the level of gastric secretion and loss of bactericidal properties of gastric juice.

    After eating, the patient experiences unpleasant sensations in the stomach area in the form of gravity and pressure. An unpleasant metallic taste is felt in the mouth. An eructation can have the smell of eaten food. Heartburn occurs in varying degrees of intensity, more often it is manifested by a burning sensation in the upper part of the abdomen( epigastrium) and behind the breastbone. A common symptom of chronic gastritis is nausea that occurs after eating. Vomiting is not permanent, it is observed sporadically. If the morphological changes with gastritis are superficial, the appetite is preserved. With pronounced atrophic lesions of the gastric mucosa, the appetite is reduced or absent altogether.

    Many patients develop intestinal dyspepsia, which manifests itself in the form of diarrhea, less often - constipation. Diarrhea is caused by a violation of the quality of gastric juice, which affects the process of gastric digestion, reduces the bactericidal activity of gastric juice, resulting in the colony of the stomach, there are colonies of bacteria that cause the rotting of poorly digested food. Developed intestinal dysbiosis, because of what putrefaction occurs in the intestine. The constipation is based on a violation of the rhythm of contractions of the muscles of the intestine and a tendency to spasms.

    Pain in chronic gastritis has a different degree of severity: from a feeling of pressure and raspiraniya in the abdominal cavity to real pain. Pains usually appear right after eating and last for several hours. In this case, they can increase or decrease. Pain can be permanent. They are usually stupid, aching, moderate strength, but sometimes they become intense. Pain in the stomach is associated with irritation of the inflamed receptors of the gastric mucosa during its extension, as well as spasm of the musculature of the stomach.

    The general condition of patients is most often not disturbed. If gastric secretion is retained or reduced slightly, the processes of gastric digestion and digestion of food are not violated, the patient does not lose weight. With significant morphological( atrophic) changes in the mucosa, a pronounced secretory insufficiency develops( up to the Achilles).As a result of these pathological changes, the patient loses appetite, up to a prolonged restriction of food intake, lethargy, hypodynamia, hypotension develop. Because of insufficient secretory function of the stomach develops hypoproteinemia( protein deficiency), the patient loses weight. Sometimes there is a progressive decrease in the body weight of the patient. In chronic gastritis, there are often symptoms of polyhypovitaminosis( lack of a large number of vitamins) and beriberi, whose development mechanisms have been described above.

    Clinically, they are manifested by dry skin, redness, friability and bleeding gums, changes in the tongue( thickened, with the prints of the teeth, can become smooth, atrophic, shiny).In a number of patients, the phenomena of cheilitis are observed, i.e., inflammation of the lips: their blanching, the presence of cracked cracks, maceration in the corners of the mouth. Such signs, in particular, are characterized by angular stomatitis.

    Patients with chronic gastritis often have a significantly lower hemoglobin content in the blood, accompanied by the appearance of a corresponding clinical symptomatology.

    Inspection of the abdomen with chronic gastritis sometimes does not reveal any pathological changes. Palpation of the abdomen often does not cause painful sensations in the patient. Sometimes it is a pain in the stomach or in the solar plexus.

    In chronic gastritis, the liver and the biliary system are often involved in the pathological process. In this case, the development of cholecystitis and hepatitis is due to the arrival of microbial agents and toxic products of their decay into the portal vein system, followed by hematogenous migration of bacteria, as well as the spread of the process along the biliary tract. If chronic gastritis is complicated by the development of the abovementioned complications, palpation of the abdomen often reveals the soreness of the gallbladder and the dense, painless edge of the liver.

    Objective symptoms of chronic gastritis include changes in acidity and volume of gastric secretion, as well as in the quantitative content of pepsin in gastric juice, substances with the participation of the synthesis of B vitamins, proteins and other impurities of protein nature in the urine. The change in these parameters depends on the degree of disruption of the gastric secretion process and will be discussed in the following sections of the book. Objective symptoms of chronic inflammation of the stomach are also established with its fibrogastroscopic, roentgenologic, cytological examination and will be discussed below.

    There is a definite correlation between the secretory function of the stomach and the degree of morphological changes in its mucous, and consequently, clinical manifestations of chronic gastritis. Each of the forms listed in this classification has its own characteristic clinical, morphological and functional features, which it is advisable to consider separately.

    The disease is more common in people of mature and advanced age. In some cases, the disease from the outset develops as a gastritis with a decreased acidity and lack of free hydrochloric acid. In other cases, it is the final stage of gastritis with high acidity.

    The most pronounced clinical symptomatology is observed in patients suffering from a stomach disorder. In such patients, the sensations of severity and discomfort in the epigastric region are at the forefront. They are bothered by belching with air or a rotten egg. Often there is nausea and heaviness in the stomach. Pain is not a characteristic symptom. Sometimes 1-2 hours after a meal, mild aching pains occur, depending on the quantity and quality of the food( spicy, spicy, canned, etc.).When localizing the process in the upper stomach, as well as gastroduodenitis, the pain symptom is more pronounced. The appetite is lowered.

    In gastritis caused by irritating effects of food, patients feel unpleasant taste in the mouth. In some cases, vomiting is noted on an empty stomach. A frequent symptom of the disease is diarrhea associated with the loss of secretory function of the gastric glands and the creation of favorable conditions for the development of dysbiosis, with a predominance of microflora in the intestine that causes decay and fermentation processes. This is the so-called diarrhea associated with impaired digestive function of the stomach. In their development, the functional pancreatic insufficiency, which in a number of cases complicates the course of chronic gastritis, provoked by poor-quality or acute food products, also assumes definite significance.

    Disorder of the functional activity of the intestine, characteristic of this form of gastritis, is manifested by the alternation of diarrhea and constipation, flatulence, a violation of digestion of food.

    Disease, as a rule, is complicated by the development of duodenal lesions( duodenitis), liver( chronic hepatitis, expressed by the formation of cells of a different nature).Lesions are also affected by bile ducts( angiocholecystitis), functional pancreatic insufficiency develops. In addition, protein and vitamin deficiency( polyhypovitaminosis A, B, C, PP) are often developed in the patient's body, violations of hematopoiesis( iron deficiency and B12 deficiency anemia).Patients may experience neuropsychic disorders.

    Chronic gastritis with secretory insufficiency belongs to the group of precancerous diseases of the stomach. It proceeds in several variants, each of which has the characteristic features of the symptomatology:

    1. Chronic rigorous( antral) gastritis.

    This disease has a dystrophic process, concentrated in the lower part of the stomach. It is accompanied by spasms followed by the development of a sclerotic process in the wall of the stomach and a violation of its normal mobility.

    The lower part of the stomach is deformed and takes the form of a narrow tube.

    Rigid gastritis occurs as a severe form of chronic gastritis with secretory insufficiency. The disease is characterized by severe pain syndrome, long-term persistent dyspepsia. Transition to the cancer process is observed in about 10-40% of patients.

    The disease has a characteristic morphological and radiographic picture. Microscopically, weakening of functions and atrophy of the main glands of the stomach, proliferation of the covering epithelium of the mucous membrane, hypertrophy of the muscle fibers and proliferation of connective tissue.

    2. Chronic hypertrophic organic gastritis, Menentry's disease.

    Medical science identified two forms of giant hypertrophic gastritis:

    1. Individual flat polyadenomas( outgrowths) of hypertrophied gastric mucosa.

    2. Multiple polyposis polyadenomas of the gastric mucosa.

    The disease is characterized by local hyperplasia of the mucosa, localized in the body, sinus or cardiac( pericardial) stomach. Men and women get sick with the same frequency. Usually the age of patients is from 30 to 70 years, but sometimes children become ill.

    The clinical picture is diverse, has no characteristic features. The disease has a chronic course.

    Patients are concerned about the phenomena of gastrointestinal dyspepsia, a feeling of discomfort, pressure, spasm and pain in the stomach. Sometimes there are no pains. But more often the pain syndrome resembles that of a peptic ulcer. The attack of pain is relieved after vomiting, food intake and alkaline solutions. Gastric indigestion manifests itself in the form of nausea and vomiting. Vomit can contain an admixture of blood.

    Very often, patients lose weight. They develop iron deficiency anemia and protein deficiency of the body. Often there is swelling of the hands and feet. Diagnosis is based on data from gastroscopy and radiology.

    Fibrogastroscopy reveals the presence of hypertrophied, sinuous, edematous folds of the gastric mucosa, the surface of which is covered with mucus. Sometimes erosion is detected. A number of patients on the surface of the mucous membrane of the stomach can see warty or papillary growths( a kind of cobblestone pavement or gyrus).

    Histological examination reveals structural changes in the gastric glands, their hypertrophy;metaplasia of the main and lining cells, multiple mucous cysts;sometimes typical epithelial growths, resembling malignant growth.

    3. Polyposis gastritis, polyposis of the stomach.

    Gastric polyps are seals( papilloma) or swelling( adenoma) of the gastrointestinal tissue. They have a foot or a wide base. Polyps are often located on the anterior and posterior walls of the upper stomach.

    Polyposis gastritis, as a rule, is a complication of chronic gastritis with secretory insufficiency. The age of patients is often from 40 to 50 years.

    The clinical picture of polyposis gastritis does not differ significantly from usual atrophic gastritis with secretory insufficiency. The disease is often combined with a rigid gastritis. There is a tendency to bleeding. A poly-pose transition into a cancerous tumor is often observed.

    When the polyp is located on the border of the stomach and duodenum, this polyp may fall into the duodenum, resulting in a disease such as obstruction at the border of the stomach and duodenum. It is accompanied by pain and vomiting. When cancer degeneration or prolapse of the polyp in the duodenum is possible bleeding.

    Because of the constant change in cellular nature, polyposis gastritis can in many cases turn into a cancer. Therefore, it is necessary to take the most drastic measures to cure this ailment.

    Chronic gastritis with normal and increased secretion is usually seen in young and middle-aged people. Often this variety of gastritis precedes the development of peptic ulcer of the stomach and duodenum.

    Is manifested in two forms:

    a) dyspeptic( with digestive disorders);B) painful.

    Characteristic symptoms of dyspeptic form: heartburn, acidic eructation, regurgitation of sour, feeling of heaviness, burning and raspiraniya in the stomach, constipation. The appetite is saved or promoted.

    With this form of the disease, pain occurs after eating and is removed by taking bicarbonate sodium. Dyspeptic phenomena often appear after the intake of fatty, carbohydrate foods, as well as alcoholic beverages.

    The painful form of the disease is characterized by a marked pain syndrome, alternating with digestive disorders. The patient is concerned about moderately expressed late and hungry, dull, aching pains in the stomach that occur 2-3 hours after eating, as well as night and morning pain. Pain syndrome decreases after eating. It is caused by a pyloric spasm, increased gastric motility and active release of gastric juice and enzymes. Sometimes in the origin of the pain, the accompanying diseases of the gastrointestinal tract play a role. In this case, the pain syndrome increases with shaking and walking. Seasonality of pain is not as pronounced as with peptic ulcer.

    Sometimes, with pain gastritis, erosion occurs on the gastric mucosa with the development of erosive gastritis.

    As with dyspepsia, and with painful forms of chronic gastritis with normal and increased secretion, a prolonged pathological constipation is observed;

    is often involved in the inflammatory process of the liver, bile ducts;develop hypovitaminosis, neurasthenic syndrome.

    A characteristic complication of these forms of gastritis is the development of cicatrical changes in the lower stomach or in the bulb of the duodenum. Often there is a spasm of the gatekeeper( the border of the stomach and duodenum).

    There may be hypoglycemic conditions( a sharp decrease in the sugar content in the blood), manifested by the weakness of the patient, trembling of the hands, pale face, hunger and cold sticky sweat. This condition can be accompanied by the occurrence of pain in the abdominal cavity.

    Acute forms of gastritis and gastric ulcer, as well as chronic forms of these diseases, often originate in preschool and school age. The causes of damage to the mucous membrane of the stomach are nervous disorders, diseases of the cardiovascular system, kidneys, blood diseases, endocrine system diseases( diabetes, adrenal insufficiency, etc.).Untimely prevention and treatment of diseases leads to pronounced anatomical changes in the body and in the future to loss of ability to work, and in the future, at the age of an adult, disability can occur.

    In the last 10 years, children often have an increase in the incidence of severe forms of gastritis and gastroduodenitis. These lesions lead to the development of peptic ulcer, multiple erosions and subatrophy, atrophy of the gastroduodenal mucosa.

    The peptic ulcer disease in children at the present stage is also characterized by an unfavorable course with the formation of multiple and chronic ulcers that can not be treated in an ordinary way and require surgical intervention.

    Chronic duodenal diseases and peptic ulcer are mutually complementary diseases that promote the development of other severe ailments.

    Peptic ulcer is more common in children with a hereditary predisposition to the disease of organs located in the abdominal cavity. A peptic ulcer develops in a child, if the general state of his health is weakened due to somatic and infectious diseases that were transferred earlier, the body's ability to restore weakened protective functions is upset. In children born from mothers with pathology of pregnancy and with difficult births who were on artificial feeding and have signs of severe allergic disease, the risk of developing peptic ulcer, gastritis, symptomatic ulcers, etc., increases many times when infected with pyloric Helicobacter.

    The decisive factors in the occurrence of acute and chronic forms of gastritis and peptic ulcer in children are hereditary predisposition, as well as features of the physical structure of the body. Hereditary predisposition often occurs in a child whose father has a peptic ulcer. At the same time predisposition to an early disease peptic ulcer is more often transmitted on the paternal line.

    By inheritance from the father to the son the organism predisposition can be transferred to produce insufficient quantity of hormones and other biologically active substances providing protection and normal development of the gastric mucosa.

    The neuropsychic stress caused by the school load in the school provokes disruptions in the normal functioning of the children's organism and is the cause of the development of the disease.

    From the earliest years the child( especially in the conditions of a large megalopolis) is faced with an incredible number of factors provoking the occurrence of acute lesions of the gastric mucosa. Such factors include: exhaust gases( 0.5 hours standing in a "stopper", and, at least, painful sensations in the abdominal cavity are provided), a system of fast-food establishments, calls to visit which are associated with insolent speculation on the feelings of the child. Uncontrolled use of low-alcohol drinks, as well as soft drinks of questionable technology in early adolescence, an early addiction to tobacco and many other "signs of freedom" also provoke stomach damage in adolescence.

    Naturally, the background that contributes to the development of almost all diseases of the gastrointestinal tract, especially in childhood and adolescence, is the intestinal dysbiosis. This dangerous phenomenon should be known in detail, since our body, its ability to digest proteins, fats, minerals, trace elements, amino acids depends on the state of the intestinal microflora.

    Modern fundamental and clinical studies clearly demonstrate that intestinal dysbacteriosis is not an independent disease, but a clinical and laboratory syndrome that occurs with a variety of diseases of the gastrointestinal tract, other organs and endocrine glands involved in the digestive process. This syndrome is characterized by a change in the qualitative and quantitative composition of microorganisms inhabiting the intestine, the transition of their various species to an uncharacteristic state, or their excess growth. Also a dysbacteriosis can arise because of weakening of vital forces of microorganisms of our intestines, decrease in their resistibility to external influence. In some patients, dysbacteriosis is accompanied by clinical symptoms of diseases of the stomach and intestines, ie, signs of peptic ulcer, acute or chronic gastritis.

    The human gastrointestinal tract is inhabited by a huge number of microorganisms( about 500 different species) with a total mass of 1-1.5 kg, which in number( 1010) approach the number of cells in the human body, 1013. Normal microflora is the qualitative and quantitative ratio of variousmicrobes of individual organs and systems, supporting the biochemical, immune balance and equilibrium of the metabolism of the human body, necessary for the preservation of his health.

    In the human gastrointestinal tract many bacteria live, which, in fact, are the "cohabitants" of their "master," that is, they are not found anywhere in nature. These microorganisms participate in the digestion of food, contribute to easy digestion of various proteins, carbohydrates, amino acids, vitamins, microelements by the intestine. Some types of bacteria that inhabit our intestines take part in the provision of immune and restorative processes in the body, that is, through the allocation of special biochemical products to the human body, they contribute to the preservation of the robust health of their host. Strange as it sounds, the organism of the "master" also needs microbial inhabitants, as well as they in its support. And if the qualitative composition of these microorganisms changes, some species disappear, and others - will have the possibility of excessive quantitative increase, then the body will cease to receive the necessary substances in natural proportions, and this in turn will cause numerous diseases.

    In the normal microflora of the gastrointestinal tract more than 400 species of non-pathogenic aerobic( capable of developing in the atmosphere) and facultatively anaerobic( capable of developing without access to oxygen) bacteria are isolated.

    Intestinal biocoenosis also includes a small number of conditionally pathogenic organisms that form the so-called "residual colony": staphylococci, fungi, proteus, etc.

    The composition of the microflora is not the same throughout the gastrointestinal tract. In the upper and middle sections of the small intestine, the population of microorganisms is relatively small( at the beginning of the jejunum their content is not more than 100 microorganisms per 1 ml of contents) and includes predominantly gram-positive aerobic bacteria, a small amount of anaerobic bacteria, yeasts and fungi.

    The greatest content of microorganisms is observed in the large intestine. Here their concentration reaches 1010-1011 and more per 1 g of content.

    In the large intestine, the bulk of anaerobic microorganisms live. The "main population"( about 70%) is anaerobic bacteria - bifidobacteria and bacteroides. As "accompanying" are lactobacilli, E. coli, enterococci.

    Bacteria that inhabit the lumen of the gastrointestinal tract perform a number of functions that are very important for the host organism.

    The main representative of anaerobic intestinal microflora - bifidobacteria - produce amino acids, proteins, vitamins B1, B2, B6, B12, Vikasol, nicotinic and folic acids. It has been suggested that certain substances produced by bifidobacteria have special properties and contribute to reducing the risk of cancer of the colon.

    The most important role in the processes of protein splitting belongs to the E. coli, which possesses large and diverse properties. Thus, one of the types of Escherichia coli produces several vitamins( thiamin, riboflavin, pyridoxine, vitamins B12, K, nicotinic, folic, pantothenic acids), participates in the exchange of cholesterol, bilirubin, choline, bile and fatty acids and also affects the absorption of iron andcalcium.

    Lactic acid, acetic, succinic, formic acids are the products of vital activity of lactic acid bacteria( bifidobacteria, lactobacilli) and bacteroids. This ensures that the intestinal acidity index is maintained at pH 4.0-3.8, thereby inhibiting the growth and multiplication of pathogens and putrefactive microorganisms in the gastrointestinal tract.

    If to abuse strong spirits or to be engaged in a selftreatment of some diseases with application of antibiotics which dosage is established by the patient at will, it is easy to exterminate useful microorganisms of an intestine. The consequences can be the most unpleasant. For example, a metabolic disorder in the body, a decrease in the body's ability to resist infectious and many other diseases. And, most unpleasant, the imbalance of normal microflora causes prolonged constipation, i.e., the normal patency of the gastrointestinal tract is disturbed, which creates conditions for the occurrence of peptic ulcer and gastritis.