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Inflammation of the stomach (gastritis)

Distinguish between acute and chronic gastritis. Most often, gastritis occurs in children aged 5-6 years, 9-12 years, during periods of the most intensive development of all organs and systems. The incidence of girls and boys is the same, but during puberty is more common in girls.

Acute gastritis is an acute inflammation of the gastric mucosa caused by short-term action of strong irritants.

Acute gastritis can be primary and secondary. The causes of primary acute gastritis are most often the effects on the mucous membrane of pathogenic microbes and their toxins, medications, rough and spicy foods, overloading the stomach with large amounts of food, and the use of foods containing food allergens.

The cause of secondary acute gastritis can be diseases such as sepsis, influenza, diphtheria, measles, acute renal failure.

The main factor in the development of the disease is invasion of the mucous membrane by microbes and toxins, which have an irritating effect on the mucous membrane, where an inflammatory process develops that causes a violation of trophic mucosa. All this leads to a violation of the secretion of gastric juice and the digestive process.

The hematogenous pathway of the spread of infection and toxins in secondary acute gastritis also leads to inflammatory changes in the mucous membrane.

In acute gastritis of alimentary origin, inadequate food has a direct effect on the mucous membrane of the stomach, depletes its secretory apparatus, and slows down the digestion of food. Food lingers in the stomach. Products of incomplete breakdown of food irritate the gastric mucosa and cause inflammation. When taking medications, overdosing, prolonged use, mucous membrane irritation also occurs and the inflammatory process develops. Inflammation of the mucous membrane is accompanied by infiltration, hyperemia, as well as dystrophic changes in the epithelium of the mucous membrane.

In acute gastritis, a superficial change in the mucous membrane or deep damage can develop up to its necrosis.

Clinic. The main manifestations of the disease are characterized by a violation of the secretory and motor functions of the stomach, the depth and severity of inflammatory phenomena, as well as the addition of symptoms of damage to other organs and systems to the inflammatory process.

There are clinically simple and catarrhal gastritis, as well as corrosive and phlegmonous gastritis. Catarrhal gastritis develops 4-8 hours after the etiological factor. The main symptoms are:

1) general malaise;

2) nausea;

3) vomiting;

4) salivation or dry mouth.

With gastritis of toxic infectious origin, intoxication, prolonged vomiting, dehydration, febrile or high temperature appear.

Usually the tongue is covered with a grayish-whitish coating. In the epigastric region, pain is noted during palpation. A frequent pulse is noted, blood pressure is slightly reduced. In the contents of the stomach there is a lot of mucus, secretory and acid-forming functions are reduced, motor function is impaired.

Acute corrosive necrotic gastritis is characterized by the severity of the course. It develops when substances irritating and damaging local effects enter the stomach. These include acids, alkalis, salts of heavy metals.

In addition to local effects, symptoms of shock in severe cases may appear in the clinical picture. The severity of damage to the gastric mucosa corresponds to the amount and concentration of substances that enter the stomach. It also matters whether the stomach is full of food or empty. Symptoms also depend on the presence of damage to the mucous membrane of the mouth and esophagus. The child may have pains in the mouth, behind the sternum, in the epigastric region (this symptom is characteristic of all gastritis).

The severity of poisoning is determined by general phenomena, collapse or shock. The abdomen is swollen, symptoms of peritoneal irritation may be noted, and perforation of the wall of the stomach may even occur in the first hours after poisoning, kidney damage, as well as jaundice associated with erythrocyte hemolysis, may occur due to resorptive action.

Complications With a severe course of simple gastritis, general intoxication develops, a violation of the cardiovascular system. With corrosive gastritis, complications can occur in the form of perforation of the wall of the stomach, the development of peritonitis, bleeding.

Diagnostics. Acute gastritis is diagnosed on the basis of an anamnesis, clinical symptoms that occur with the action of factors that disrupt the normal functioning of the stomach.

Treatment. Bed rest is prescribed for 2-3 days. The main thing is to eliminate the cause of gastritis. With vomiting, gastric lavage is prescribed with an isotonic sodium chloride solution, 1% sodium bicarbonate solution, mineral or boiled water. In the first 8-12 hours of the disease, heavy drinking in small portions is indicated, infusion therapy, administration of Ringer's solution, a mixture of isotonic sodium chloride solution with 5% glucose solution are prescribed. After 12 hours, the patient is allowed kefir, mashed soup, low-fat broth, jelly, cereals. By the 5-7th day of illness, cottage cheese, meat soufflé, soft-boiled eggs, and white flour crackers are introduced (table 1a).

With severe pain syndrome, antispasmodics (no-shpa, papaverine) are prescribed in an age-related dose, in the absence of secretory disorders of anticholinergics (belladonna preparations), antacids (almagel, maalox). Adsorbing drugs are prescribed (smecta, polyphenan, cholestyramine). Adsorbents are taken between meals with plenty of water. It should be noted that antacids and adsorbents are not prescribed at the same time, since these drugs are very close in pharmacological functions. To eliminate vomiting, cerucal, motilium are used.

With gastritis of toxic infectious origin, antibiotic therapy is prescribed in a generally accepted dosage, vitamins of group B, enzyme therapy is carried out.

In case of corrosive gastritis, gastric lavage begins with a large amount of water through a probe. The probe is not administered with collapse and severe damage to the esophagus. When acid gets into the stomach, water is added to milk, alkalis, diluted citric or acetic acid, antidotes are introduced. With the collapse, caffeine, cordiamine, mesatone are administered, if necessary, cardiac glycosides. If perforation is suspected, surgical treatment is indicated. A fatal outcome can occur from shock, bleeding, peritonitis.

Prevention The principles of age-related diet and food hygiene apply. Overeating fatty and sweet foods is unacceptable. Long-term use of drugs with an irritating effect on the gastric mucosa is not recommended.

Chronic gastritis is a disease that is prone to progression, recurring, characterized by focal, long-lasting inflammatory changes in the gastric mucosa with the gradual development of atrophy.

Chronic gastritis in childhood usually develops as a result of: a violation of a balanced diet - eating coarse, excessively plentiful food, poorly chewed, too cold, containing many spices, dry food, malnutrition; chronic diseases of the kidneys, cardiovascular system, prolonged use of drugs, focal infection of the mouth. In the occurrence of the disease, hereditary pathology is important. In addition, food allergies, exposure to microorganisms Helicobacter pylori, parasitic infestations such as giardiasis can be factors contributing to the onset of the disease. Among adolescents, the reasons may be the use of coffee, alcohol, smoking and other bad habits.

Internal factors of the development of the disease include: a hereditary predisposition associated with the formation of antibodies to the gastric mucosa, reflux of food into the stomach from the duodenum, and concomitant diseases of the stomach and endocrine system.

Distinguish:

1) chronic gastritis associated with H. pylori;

2) autoimmune;

3) idiopathic (unspecified);

4) special types: reactive - against the background of other diseases,

eosinophilic - against the background of an allergy.

The development of chronic gastritis varies depending on the cause that caused it.

Gastritis associated with H. pylori is triggered by a spiral gram-negative microorganism. Infection can occur if personal hygiene is violated through contaminated objects, products, poorly crafted endoscopes, and probes. The causative agent multiplies on the epithelium of the antrum, secrete virulence factors, one of which is urease. It breaks down urea to carbon dioxide and ammonia, which damages the epithelium of the gastric mucosa. The formation of an alkaline environment creates favorable conditions for the life of bacteria. Alkalization of the antrum epithelium leads to an increase in gastrin secretion and an increase in gastric secretion. The resulting inflammatory process leads to the formation of erosion. The acidic contents of the stomach are rapidly evacuated. Acidification of the duodenum occurs, which leads to the death of the mucous epithelium. The altered epithelium of the duodenum is populated by NeisoCet pyloru. An inflammatory process develops in the mucous membrane of the duodenum, exacerbating violations of the motor and secretory functions of the digestive tract.

Against the background of some systemic diseases, autoimmune chronic gastritis can develop, which is characterized by the formation of autoantibodies to the lining cells of the stomach.
As a result of autoimmune processes, atrophy of the mucous membrane develops. The secretory function of the stomach decreases. This leads to a violation of the digestion of food. The function of the digestive organs is impaired.

Antibodies can be produced to Castle's internal factor, this leads to impaired absorption of vitamin B12 and, as a result, B12-deficient anemia.

Reactive gastritis is usually associated with the use of medications or with the duodeno-gastric reflex.

Clinic. Symptoms of chronic gastritis are associated with a violation of the secretory and motor functions of the stomach. There are two types of disease:

1) ulcer-like (associated with N. pyloru);

2) gastritis-like (autoimmune).

In the period of exacerbation, pain, dyspeptic and asthenic syndromes are characteristic.

Clinical manifestations of peptic ulcer-like gastritis are similar to peptic ulcer and are manifested by acute paroxysmal pains in the epigastric region, which occur 1.5 hours after a meal, but are sometimes detected on an empty stomach.

In addition, belching appears with acidic contents, constipation is noted.

Fatigue, weakness, headaches, emotional lability are characteristic of the asthenic syndrome.

Autoimmune chronic gastritis is characterized by pain that occurs 15-20 minutes after a meal. They appear in the navel and epigastric region, pass through 1.5-2 hours on their own.

When dyspeptic syndrome appears, a feeling of heaviness appears in the stomach, belching of air, nausea, loss of appetite appear. There is an aversion to fatty foods, cereals, dairy products. Diarrhea, weight loss, and anemia may develop. Pallor, dry skin, jams in the corners of the mouth, and brittle nails are characteristic.

An objective examination reveals moderate pain on palpation in the epigastric region.

Diagnosis is based on clinical data and additional examination methods. The most significant are fibrogastroscopy, fractional examination of the gastric contents, ultrasound of the abdominal cavity, coprological examination of feces.

An endoscopic examination can determine common or focal edema and hyperemia, superficial defects of the mucous membrane, erosion in the antrum and duodenal bulb. With endoscopy, an inflammatory process is detected in the region of the body of the stomach or in all its parts.

When examining the secretory function of the stomach, the amount of hydrochloric acid, pH level, and proteolytic activity of gastric juice are evaluated - the latter is usually reduced.

An X-ray examination reveals a change in the relief of the mucous membrane and a violation of its motor function.

In some cases, a biopsy is performed during gastroscopy and a histological examination, in which changes in the gastric mucosa, and violations of the regeneration of the epithelium are detected. Surface gastritis with or without atrophy of the glands is usually distinguished.

Treatment. The main thing in treatment is dieting, which can lead to recovery.

Table Recommendations for dietary nutrition for chronic gastritis and gastroduodenitis ("Children's Diseases" edited by V. N. Samarina, 2004)
Food & Dishes Allowed Are forbidden
Bread Yesterday's white bread and roll, white crackers Brown bread, fresh white bread and rolls
Flour products Well-boiled pasta made from premium flour, home-made noodles, puddings made from wheat crackers, semolina and vermicelli Poorly cooked durum wheat pasta, pancakes, pancakes, cheesecakes
Soups and broths Vegetarian without cabbage, mashed, with cereals, with the addition of milk, milk soups Soups from strong meat, fish, vegetable and mushroom broths and cabbage broths, borscht and cabbage soup with fresh and pickled cabbage
Meat dishes Steam cutlets, dumplings, soufflé from lean beef, veal, chicken, turkey, rabbit, 1-2 times a week, you can give a piece of well-boiled beef meat or white chicken meat All fatty varieties of meat and poultry, lamb, pork, smoked meats, all sausages, stew, canned meat products
Sauces Butter and Egg, Dairy and Sour Cream -
Fats Butter and vegetable oil Ghee and lard, internal fat
Fish dishes Boiled or steamed white low-fat fish, fish cakes, rolls, dumplings Canned fish, all fatty fish, dried, smoked fish, salted fish roe
Eggs Soft-boiled or bagged eggs, scrambled eggs, souffle Hard boiled eggs, fried scrambled eggs, fried omelet, drachan
Dairy Milk, cream, condensed milk, fresh sour cream and cottage cheese, curd mass, steamed and baked cottage cheese dishes, non-acid kefir (with caution), mild and low-fat varieties of fresh cheese Fried dishes with cottage cheese, cheesecakes, curd cookies, spicy and fat cheeses


Food & Dishes Allowed Are forbidden
Dishes from cereals Porridge-smears from various cereals Crumbly dry cereals, side dishes and fried foods with cereals
Vegetables Potatoes, carrots, pumpkin, cauliflower, boiled beets, mashed in the form of vegetable purees and puddings, a salad of finely chopped ripe tomatoes and peeled and grated cucumbers with the addition of leafy greens. Dressing with cream, non-acidic sour cream or vegetable oil White cabbage, all salted and pickled vegetables, unpeeled cucumbers, radish, radishes, fresh onions and garlic, horseradish, fried vegetables
Fruits and berries Sweet varieties of ripe fruit without peel, peeled off tangerines, delicate grapes, bananas, melon, watermelon, sweet ripe berries Sour fruits and berries and dishes thereof
Sweet foods and drinks Jelly, stewed fruit, mousse, jelly, milkshakes with non-sour berries and fruits, sugar, honey, jam, jam. Weak tea with milk or cream, weak cocoa or surrogate coffee in milk, mineral water without gas in the form of heat Dishes from sour and unripe berries and fruits, ice cream
Sample menu for chronic gastritis and gastroduodenitis

First breakfast. Milk porridge, a sandwich with mild cheese, butter, tea or surrogate coffee with milk.

Lunch. Grated apple with cream; sweet, natural water diluted with water; cookies.

Dinner. Soup from mashed vegetables, milk jelly.

An afternoon snack. Surrogate tea or coffee with milk, white crackers or inedible cookies.

Dinner. A piece of boiled soft meat or fish with mashed vegetables, pudding, tea.

Before bedtime. A glass of milk, kefir or fermented baked milk, cottage cheese with cream and sugar.

Diet therapy is based on the principle of mechanical, chemical and thermal sparing, treatment tables 1b, 5 are prescribed.

Table 1b is assigned in the first 5-10 days, food is given in a puree or mushy form. When the condition improves, diet No. 1 is prescribed for up to 6 months, then table No. 5.

With reduced secretion, diets No. 2 and No. 5 are prescribed. From drug therapy are prescribed depending on the symptoms:

1) antacid therapy (magnesium oxide, almagel, vicalin, maalox, gastal);

2) antispatic drugs (papaverine, no-spa);

3) mineral waters (Truskavets, Borjomi, Essentuki);

4) to eliminate dyspeptic phenomena - cerucal, motilium;

5) for the destruction of helicobacteria, complex therapy with antibacterial drugs is prescribed;

6) with increased secretion - H2-histamine receptor blockers (cimetidine, ranitidine), bismuth preparations - denol, vicalin;

7) with severe pain syndrome - antispasmodics. To increase appetite, shamrock juice, aralia tincture, etc. are prescribed.

Of the physical methods of treatment, diatherapy, electro and hydrotherapy are used.

Санаторно-курортное лечение при хроническом гастрите назначается не ранее, чем через 3 месяца после клинической ремиссии. При гастрите с повышенной секреторной функцией желудка показано лечение в санаториях Ессентуков, Железноводска, Кисловодска или в санаториях местной климатической зоны.

При хроническом гастрите с пониженной секреторной функцией желудка рекомендуется лечение, включающее назначение хлоридно-натриевых или гидрокарбонатно-хлоридно-натриевых вод («Ессентуки» и др.).

Прогноз для выздоровления сомнительный.

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Воспаление желудка (гастрит)

  1. Болезни желудка. Гастрит. Язвенная болезнь. Опухоли желудка.
    1. При остром гастрите в слизистой оболочке желудка развивается 1. энтеролизация 2. коагуляционный некроз 3. продуктивное воспаление 4. экссудативное воспаление 5. пролиферация покровного эпителия 2. Кишечная метаплазия эпителия может развиться при хроническом гастрите 1. поверхностном 3. атрофическом 2. продуктивном 4. катаральном 3. Макроскопическая характеристика острой язвы желудка 1. края
  2. Питание при сахарном диабете с заболеваниями желудочно-кишечного тракта (гастрит, язвенная болезнь желудка или двенадцатиперстной кишки)
    В питании при сахарном диабете с заболеваниями желудочно- кишечного тракта необходимо соблюдать все требования, которые предъявляются к питанию диабетика. Вместе с тем необходимо щадить слизистую желудка. Для того чтобы избежать механического, химического и термического ее раздражения, все блюда готовят в отварном протертом виде и на пару. Режим питания дробный - 5-6 раз в день. РЕКОМЕНДУЕМЫЕ
  3. Роль воспаления в возникновении рака желудка
    Хронический атрофический гастрит и Helicobacter pylori Кишечная метаплазия эпителия желудка (замена нормального эпителия желудка на абсорбционные и бокаловидные клетки) встречается более чем у 70 % больных раком желудка, но также и при отсутствии онкологического процесса. Кишечный тип рака желудка тесно связан с наличием кишечной метаплазии и часто развивается на ее фоне. У 80—90 % больных
  4. INFLAMMATION: DEFINITION, ESSENCE, BIOLOGICAL SIGNIFICANCE. MEDIATORS OF INFLAMMATION. LOCAL AND GENERAL MANIFESTATIONS OF INFLAMMATION. ACUTE INFLAMMATION: ETIOLOGY, PATHOGENESIS. MORPHOLOGICAL MANIFESTATION OF EXUSDATIVE INFLAMMATION. RESULTS OF ACUTE INFLAMMATION
    Inflammation is a biological, and at the same time a key, general pathological process, the appropriateness of which is determined by its protective and adaptive function aimed at eliminating the damaging agent and repairing damaged tissue. In medicine, to indicate inflammation, the term "um" is added to the name of the organ in which the inflammatory process develops - myocarditis, bronchitis,
  5. Питание при гастрите с пониженной кислотностью (гипоацидный гастрит)
    При понижении кислотности, т. е. при недостаточном выделении желудочного сока, лечебное питание имеет следующие цели: 1. Щадить больной орган; 2. Стимулировать активную выработку желудочного сока. В связи с уменьшением количества соляной кислоты в желудке, следует поднимать для улучшения переваривания белков выделительную способность больного органа приготовленной пищей. Большое значение
  6. Inflammation. Definition, essence, mediators of inflammation. Local and general manifestations of exudative inflammation, morphological manifestations of exudative inflammation. The answer is the acute phase. Ulcerative necrotic reactions with inflammation.
    1. The main processes that develop in the body in response to tissue damage are 1. amyloidosis 2. inflammation 3. regeneration 4. formation of granulomas 5. hyperplasia of cell ultrastructures 2. Inflammation is 1. hyperplasia of cell ultrastructures 2. restoration of lost structures 3 uncontrolled growth of cellular elements 4. exudative-proliferative response to damage 5. cellular
  7. Строение и функции желудка в норме. Врожденные аномалии желудка
    Как один из важнейших пищеварительных органов, выполняющих секреторную и эндокринную функции, желудок подразделяется на 5 главных анатомических зон: кардию, дно, тело, преддверие и привратник. Кардия (cardia) — узкая часть желудка, окружающая зону пищеводно-желудочного соединения. Дно (fundus) — часть желудка, несколько возвышающаяся слева над кардией и составляющая около */3 органа. Body
  8. 32. ОСМОТР ЖИВОТА, ПАЛЬПАЦИЯ, ПЕРКУССИЯ ЖЕЛУДКА, ПАТОЛОГИЧЕСКИЕ СИМПТОМЫ. DIAGNOSTIC VALUE. МЕТОДЫ ИССЛЕДОВАНИЯ ФУНКЦИОНАЛЬНОГО СОСТОЯНИЯ ЖЕЛУДКА. ОСНОВНЫЕ ПОКАЗАТЕЛИ.
    При осмотре необходимо обращать внимание на его величину, форму, симметричность, дыхательные движения, перистальтику, состояние брюшной стенки. Перкуссия желудка: обычно определяется низкий тимпанический звук, а над кишечником высокий. Перкутируют по срединной линии от области кишечного тимпанита вверх и измеряют расстояние от пупка. Аускультативная пальпация: раструб ставят в эпигастральный
  9. ЗЛОКАЧЕСТВЕННЫЕ ОПУХОЛИ ЖЕЛУДКА РАК ЖЕЛУДКА
    занимает первое место и составляет около 40 % всех раковых поражений. Морфологически различают: экзофитные опухоли (растут в просвет желудка и отграничены от здоровых тканей); эндофитные опухоли (обладают инфильтративным ростом и злокачественным течением). Международная классификация рака желудка Желудок разделяется на три примерно равные части: верхнюю (проксимальный отдел), среднюю
  10. Gastritis
    Гастрит - это воспаление слизистой оболочки желудка, поэтому см. статью ЖЕЛУДОК (ПРОБЛЕМЫ), с тем дополнением, что человек, заболевший гастритом, переживает или пережил какой-то сильный гнев. См. также объяснение на стр.
  11. Хронический гастрит (шифры К 29.3 - 6)
    Definition Хронический гастрит - клиникоморфологическое понятие, характеризующееся нарушением физиологической регенерации эпителия с исходом в атрофию, нарушениями секреторной функции желудка, его моторной и отчасти инкреторной деятельности. Statistics. Хронический гастрит - самое распространенное заболевание системы пищеварения, поражающее около 50% взрослого населения. В структуре
  12. Вопрос 20 ГАСТРИТ
    - воспаление слизистой оболочки желудка. Различаются острый и хронический гастрит. Острый гастрит - полиэтиологическое воспаление слизистой оболочки желудка, вызываемое рядом раздражителей как извне, так и изнутри. Этиологияи патогенез.Среди экзогенных факторов выделяются: алиментарные погрешности питания (качество и количество съеденной пищи, особенно обильная еда на ночь, употребление
  13. Хронический гастрит
    ХРОНИЧЕСКИЙ ГАСТРИТ (ХГ) — заболевание желудка, характеризующееся хроническим воспалительным процессом его слизистой оболочки, выражающимся в уменьшении количества железистых клеток, нарушении физиологической регенерации, дисплазии слизистой оболочки (при прогресси-ровании — развитии атрофии и кишечной метаплазии), расстройстве секреторной, моторной и нередко инкреторной функций желудка.
  14. ХРОНИЧЕСКИЙ ГАСТРИТ И ГАСТРОДУОДЕНИТ
    Хронический гастрит (ХГ) – хроническое рецидивирующее очаговое или диффузное воспаление слизистой (подслизистой) оболочки желудка с нарушением процессов физиологической регенерации, со склонностью к прогрессированию, развитию атрофии, секреторной недостаточности, лежащих в основе нарушения пищеварения и обмена веществ. Хронический гастродуоденит (ХГД) – хроническое воспаление со структурной
  15. Гастрит.
    Гастрит — воспаление слизистой оболочки желудка. По характеру течения делится на острый и хронический. Острый гастрит — это кратковременное заболевание, которое в зависимости от тяжести течения протекает чаще всего бессимптомно, реже сопровождается болями в эпигастрии, тошнотой, рвотой, иногда с различными признаками желудочного кровотечения. Причины острого гастрита разнообразны:
  16. Productive and chronic inflammation. Granulomatosis. The morphology of specific and non-specific inflammation.
    1. Chronic inflammation is manifested by a simultaneous combination of 1. failed repair 2. angiogenesis, scarring 3. reactive changes 4. tissue damage 5. embolism 2. Causes of chronic inflammation 1. acute infection 2. persistent infection 3. prolonged exposure to toxic substances 3. Chronic inflammation characterized by 1. deposition of amyloid 2. mononuclear infiltration
  17. Лечебный режим при болях в желудке, при слабости желудка и при различных состояниях аппетита
    Боли в желудке Боли в желудке возникают либо от расстройства натуры без материи, особенно - горячей, жгучей, либо от [расстройства] при наличии материи, особенно - горячей и жгучей, либо от нарушения непрерывности, причиной которого являются [либо] ветры, распирающие или жгучие, либо нечто объединяющее в себе оба эти качества, как бывает при горячих опухолях; иногда [нарушение непрерывности]
  18. Хронический гастрит
    — хроническое воспаление слизистой оболочки желудка (диффузное или очаговое), сопровождающееся нарушением физиологической регенерации эпителия, его атрофией, функциональной недостаточностью желудка, расстройством секреторной, моторной и нередко инкреторной функций желудка Основные клинические проявления хронического гастрита Местно появление болей (тупые, без иррадиации), тяжести и
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