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Peptic ulcer

NANIA ™ "2 ^ 51BGTOLEZNYA (YAB) ~ CHR ° nicheskuyu, recurrent disease with ^ i ™ ™ m ™ ^ ROGRE ° SYRONIC" m ° RFological substrate of which SSi ^ 3? CONSTRUCTIVE ulcer of the duodenum or duodenum,

S ™? R VIL ° 'On F ° Not gastritis; caused by HP infection. docinpay tl! arises from neurohumoral and en-SZET disorders of the septal and motor processes, and also

Yakv? T! G mechanisms of the mucous membrane of these organs, it ^^? P1p.TSYYA ^ YDeI Any age, but more often at the age of 30-40 years, YAB Sennrnf% of the adult population. The urban population suffers VDNER2TIU ° rural> men suffer 6-7 times more often than women (especially duodenal ulcer ulcer).


It should be strictly separated YAB and symptomatic ulcers - ulceration of the mucous membrane of the stomach and duodenum, occurring in various diseases and conditions. These are ulcers in endocrine pathology, stress, acute and chronic circulatory disorders, taking NSAIDs.

Etiology. The causes of the disease are not well understood. Currently, it is believed that the factors contributing to its occurrence are the following:

• prolonged or often repeated neuro-emotional overstrain (stress);

• genetic predisposition, including a persistent increase in the acidity of the gastric juice of a constitutional nature;

• other hereditary constitutional features (blood group 0; HbA-B3 antigen; decrease in antitrypsin activity);

• the presence of chronic gastritis, duodenitis (associated with HP), functional disorders of the stomach and duodenum (pre-ulcer state);

• violation of the diet;

• smoking and drinking spirits;

• use of certain drugs with ulcerogenic properties (acetylsalicylic acid, butadione, indometacin, etc.).

Pathogenesis. The mechanism of development of ulcer is still not well understood. Damage to the mucous membrane with the formation of ulcers, erosions and inflammation is associated with the predominance of aggression factors over the protection factors of the mucous membrane of the stomach and / or duodenum. Local protection factors include the secretion of mucus, the ability to quickly regenerate the epithelium, a good blood supply to the mucous membrane, local synthesis of prostaglandins, etc. Hydrochloric acid, pepsin, bile acids are considered aggressive factors. However, the normal mucous membrane of the stomach and duodenum is resistant to aggressive factors of gastric and duodenal contents in normal (normal) concentrations.

In recent years, the role of HP infection in the pathogenesis of PUD has been clarified.

So, due to the peculiarities of the structure and functioning of the gastric mucosa, some people are genetically immune to HP. In this category of people, HP, once in the body, is not capable of adhesion (sticking) to the epithelium and therefore does not damage it. Other individuals (who subsequently develop ulcer) HP, entering the body, settle mainly in the antrum of the stomach, which leads to the development of active chronic inflammation (neutrophilic infiltration of the epithelium and its own mucosal plate), as well as mononuclear infiltration.

The cytokines of inflammatory cell infiltrates play a significant role in mucosal damage. Upon adhesion of HP to epithelial cells, the latter respond with the production of a whole range of cytokines (primarily IL-8). Leukocytes and macrophages secreting TNF-a and interferon migrate to the focus of inflammation, which attracts the next cells involved in inflammation. Metabolites of reactive oxygen species produced by neutrophils also damage the mucous membrane. The colonization of the mucous membrane of the duodenum and the disease is possible after the formation in it of foci of gastric metaplasia in response to acidic aggression. HP is closely associated with aggression factors


I WOULD. It is believed that HP directly, as well as indirectly through the cytokines of the inflammatory infiltrate, leads to disharmony between the G-cells (producing gastrin) and D-cells (producing, somatostatin and playing a role in the functioning of the parietal ketetok). Hypergastrinemia is accompanied by an increase in the number of parietal cells and an increase in the production of hydrochloric acid. The role of HP in the development of ulcer is confirmed by the fact that successful eradication of these microorganisms causes a sharp decrease in the frequency of relapses (no more than 5%), whereas in the absence of successful eradication, relapses of ulcer occur during the year in 50-80% of cases.

At the same time, a peculiar violation of gastric motility develops, at which an early discharge of acidic gastric contents into the duodenum occurs, which leads to “acidification” of the contents of the duodenal bulb.

Thus, HP is the main cause supporting aggravation in the gastroduodenal region.

HP is found in 100% of cases when the ulcer is localized in the anthroporoduodenal zone and in 70% of cases - with a stomach ulcer.

Depending on the location of the ulcer, some pathogenetic features of ulcer are distinguished. Thus, in the development of ulcer with localization of the ulcerative defect in the body of the stomach, a significant role is played by the reduction of the local protective mechanisms of the mucous barrier as a result of inflammation of the mucous membrane, impaired mucin formation, regeneration of the pathogenic epithelium, impaired blood flow and local synthesis of prostaglandins. In addition, a significant role is played by duodenogastric reflux with regurgitation of bile acids and isolecitins, which destroy the mucous barrier and cause retrodiffusion of H + ions and the formation of an ulcer defect under the influence of pepsin.

Ulceration in the pyloroduodenal zone of the mucous membrane is associated with prolonged hyperchlorhydria and peptic proteolysis, caused by hypervigraphy, hypergastrinemia and hyperplasia of the main glands of the stomach, as well as gastroduodenal dysmotoria. In addition, an ineffective neutralization of the stomach contents with mucoid substances and the alkaline component of the duodenum, with prolonged acidification of the pyloroduodenal environment, also plays a role. The pathogenesis of ulcer is presented in Figure 15.

Classification. YAB subdivide:

• by clinical and morphological signs - on gastric ulcer and duodenal ulcer;

• by the form of the disease - for the first time revealed and recurrent;

• localization secrete a lesion of the cardiac part; lesser curvature of the stomach; the prepyloric part of the stomach; duodenal bulb; non-onionics (postbulbar ulcers);

• on the phases of the flow: aggravation; subsiding exacerbation; remission;

• by severity: benign; protracted (stable); progressive. With a benign course, the ulcerative defect is small and shallow, relapses are rare, there are no complications. Conservative treatment gives a clear effect in about a month. For a protracted course is characterized by incomplete effect of treatment, its long terms; possible relapses during the first year. The progressive course is characterized by a minimal effect of treatment, the development of complications; D "Cydives are frequent;


• by the presence of complications: complicated; uncomplicated. Complications of ulcer manifest as bleeding, penetration, perforation, malignancy, pyloric stenosis and bulb, perivisceritis.

Clinical picture. Clinical manifestations of ulcer are diverse and depend on the phase of the course (exacerbation or remission), clinical and morphological variant (ulcer of the stomach or duodenum) and the presence of complications.

During exacerbation of ulcer, regardless of its clinical variant, the following main syndromes are expressed: 1) pain (it has certain patterns depending on the localization of the ulcer); 2) gastric dyspepsia; 3) intestinal dyspepsia; 4) asthenovegetative; 5) local changes; 6) complications.

Stomach ulcer. YAB of the stomach occurs, as a rule, in people of mature age, more often in men. The defect is localized predominantly on the gastrointestinal tract of the lesser curvature or in the antrum, but can be found in the cardiac and pyloric regions.

At stage I of the diagnostic search, complaints related to the manifestation of the ulcer itself, the presence of complications, and the involvement of other organs of the digestive system in the process are detected.

During exacerbation of gastric ulcer, the main complaint is pain in the upper half of the epigastric region. Although the localization of pain is not absolute, it is believed that in case of ulcers of the cardiac part and ulcers, on the back wall of the stomach, pain is localized behind the sternum, may radiate to the left shoulder (resembling pain in angina).

For ulcers of the lesser curvature of the stomach, a clear rhythm of pain is characteristic: they occur 15–60 minutes after eating, especially if the diet is not followed. Sra-


After eating, pain occurs if the ulcer is localized in the cardial part or on the back wall of the stomach.

The "hungry", nocturnal, late (2-3 hours after eating) pains resembling pains in duodenal ulcer indicate an antral ulcer of the stomach. In ulcers of the pyloric part, pain is intense, not associated with eating.

Attaching pains of the shingles nature or irradiating them in the back, the intense nature of the pain requires research of the pancreas at subsequent stages of the diagnostic search (reactive pancreatitis, penetration into the pancreas).

The syndrome of gastric dyspepsia is less pronounced, manifested by belching with air, food, regurgitation; nausea and vomiting are often noted with ulcers of the pyloric canal.

Vomiting is a frequent complaint of ulcer, vomit consists mainly of food impurities. Frequent vomiting, worse in the evening, containing long-eaten foods, combined with a feeling of fullness in the stomach, weight loss, may indicate stenosis of the output section of the stomach.

Intestinal and asthenovegetative syndromes are less pronounced in gastric ulcer than in duodenal ulcer. Some patients complain of constipation, combined with pain along the colon and abdominal distention.

Bleeding tendency is characteristic of antral ulcer in young; Bleeding in elderly patients is alarming with respect to malignancy (development of gastric ulcer).

At this stage of the survey, the effectiveness of previous treatment is evaluated, the frequency of relapses is ascertained, i.e. clarify the nature of the flow of the process - benign or progressive.

At stage II of the diagnostic search reveal: a) symptoms of local changes; b) complications; c) involvement in the process of other parts of the digestive system.

Physical signs of ulcer in uncomplicated course are few. As a rule, moderate local muscle protection in the epigastrium and pinpoint pain in various parts of this area are noted. In cardiac ulcers, pinpoint pain is revealed under the xiphoid process; for ulcers of the pyloric part - in the pyloroduodenal zone.

Spilled pain in the epigastrium with simultaneous local pain is a sign of exacerbation of chronic hepatitis (chronic hepatitis accompanied by ulcer) or perigastritis (complication of ulcer). Physical examination can be obtained data on the development of other complications. Thus, the appearance of splashing noise 5–6 hours after fluid intake indicates the development of pyloric stenosis.

Pallor and moisture of the skin, low-grade body temperature, tachycardia, a decrease in blood pressure, the disappearance of pain in the epigastric region during palpation of the abdomen are signs of ulcerative bleeding.

At the third stage of the diagnostic search, it is possible: 1) to determine the nature of the impaired gastric secretion; 2) to clarify the nature and location of ulcerative lesions; 3) to identify or clarify the complications.

The study of gastric secretion reveals its violations in the direction of a decrease or a moderate increase, i.e. characteristic violation of secretion in gastric ulcer does not exist.


X-ray examination of the stomach in approximately 3/4 of patients allows detecting the main symptom of ulcer - “niche”. Superficial ulcers that are not accompanied by an inflammatory reaction of the surrounding mucous membrane, can not be detected radiographically.

In the absence of a direct radiological sign (“niche”), indirect signs are taken into account: “finger” retraction, delayed barium sulfate in the stomach for more than 6 hours after it has been taken, local tenderness during palpation during the study. X-rays can reveal cicatricial narrowing of the pylorus, a stomach tumor (polyps, cancer, etc.).

The most valuable information about the “niche”, its localization, depth, character (presence of a kaleznaya ulcer) and to clarify the complications (malignania, penetration, bleeding, etc.) give the results of gastroduodenal fibrosis


Gastroscopy in combination with targeted biopsy facilitates the identification

malignant ulcers.

In the presence of anemia and a positive reaction of Weber in the study of feces, we can confidently talk about recurrent bleeding.

Duodenal ulcer. Duodenal ulcer disease occurs predominantly in young males; in women there is an increase in the incidence during menopause.

In most cases, the defect is localized in the duodenal bulb, often on the back wall; there are so-called kissing ulcers, affecting both the back and the front wall of the bulb.

At the first stage of the diagnostic search for a set of complaints, it is likely that the possibility of exacerbation of the duodenal ulcer may be suggested.

The main symptom is pain that occurs 1.5–3 hours after a meal (the so-called late pains), often on an empty stomach (hungry pains) and at night (night pains), disappears after meals and alkalis.
The seasonality of pain is clearly manifested (exacerbation in spring and autumn).

The structure of the pain syndrome can be represented as follows: hunger - pain - food - relief - hunger - pain, etc. There is no clear localization of pain: they can be in the pit of the stomach, right upper quadrant of the abdomen, near the navel, etc.

The change in the nature of the pain indicates the possibility of the development of a complication: when penetrating into the pancreas, pain appears in the left upper quadrant of the abdomen, they radiate into the spine. For penetra-cia ulcers in the gallbladder are characterized by dominant pain in the right hypochondrium with irradiation under the right scapula, in the back.

The second important symptom is vomiting, usually occurring at the height of pain, especially in complicated forms of the disease. Vomiting, as a rule, brings relief (pain decreases).

The earliest and most frequent symptom is heartburn (a symptom of "Acid-Dism"). Belching sour is less likely to bother patients, usually occurs after meals.

Characterized by constipation due to changes in intestinal motility, Pathognomonic for duodenal ulcer.

This disease is also distinguished by the severity of asteno-vegetative manifestations (irritability, sleep disturbance, decreased Efficiency, etc.).


At stage II of the diagnostic search data is less informative. Physical examination reveals the symptoms: 1) autonomic dysfunction (excessive sweating, red and white dermographism, dishydrosis); 2) local pain and muscle tension in the epigastrium and pyloroduodenal zone; 3) enhancement of the motor function of the stomach and colon (hyperperistalsis, spastic condition); 4) involvement in the process of other organs of the digestive system (pancreas, gall bladder).

The data of the third stage of the diagnostic search allow: a) to make a final diagnosis; b) clarify the development of complications; c) detect involvement in the pathological process of other organs.

For duodenal ulcer is characterized by increased secretory function of the stomach. In the study of gastric juice revealed an increase in basal and stimulated secretion of hydrochloric acid and pepsin 1 / 2-2 times compared with the secretion of healthy people.

A direct sign of ulcer is the discovery of a “niche”, which is most often localized in the duodenal bulb, less often outside it (postbulbar). The main diagnostic methods are radiological and endoscopic (fibrogastroduodenoscopy).

X-ray examination reveals: 1) direct signs: a) a “niche” with radial convergence of folds; b) typical onion deformation; 2) indirect signs: a) spasm of the gatekeeper; b) dyskinesia of the bulb, increasing the tone and strengthening the duodenal motility; c) the jagged contours of the mucous membrane of the bulb; d) hypersecretion of the stomach.

Stenosis of the bulb and the degree of severity is also detected radiographically.

For the diagnosis of post-bulbar ulcers using radiopaque duodenography, it is carried out in case of hypotension of the duodenum.

When fibrogastroduodenoscopy revealed ulcers of the mucous membrane.

A blood test that reveals anemia makes it possible to suspect massive or recurrent bleeding.

A serial study of fecal occult blood helps to detect latent bleeding.

Diagnostics. Для постановки правильного диагноза необходимо учитывать ряд признаков.

• Основные: 1) характерные жалобы и типичный язвенный анамнез; 2) обнаружение язвенного дефекта при гастродуоденоскопии; 3) выявление симптома «ниши» при рентгенологическом исследовании.

• Дополнительные: 1) локальные симптомы (болевые точки, локальное мышечное напряжение в эпигастрии); 2) изменения баз&тьной и стимулированной секреции; 3) «косвенные» симптомы при рентгенологическом исследовании; 4) скрытые кровотечения из пищеварительного тракта.

Формулировка развернутого клинического диагноза учитывает: 1) клинический вариант (ЯБ желудка или двенадцатиперстной кишки); 2) форму заболевания (впервые выявленное, рецидивирующее); 3) локализацию язвы: малая кривизна, антральный отдел, канал привратника; внелукович-ная язва и сочетанные язвы (на основании данных эндоскопического и рентгенологического исследований); 4) фазу течения: обострение, стихающее обострение, ремиссия; 5) наличие осложнений: желудочно-кишечное


кровотечение, перфорация, пенетрация, стенозирование, перивисцерит, развитие рака, реактивного панкреатита.

Treatment. Консервативное лечение ЯБ всегда комплексное, дифференцированное с учетом факторов, способствующих заболеванию, патогенеза, покализации язвенного дефекта, характера клинических проявлений, степени нарушения функций гастродуоденальной системы, осложнений и сопутствующих заболеваний.

В период обострения больных необходимо госпитализировать возможно паньше, так как установлено, что при одной и той же методике лечения длительность ремиссий выше у больных, лечившихся в стационаре. Лечение в стационаре должно проводиться до полного рубцевания язвы. Однако к этому времени все еще сохраняются гастрит и дуоденит, в связи с чем следует продолжить лечение еще в течение 3 мес в амбулаторных условиях.

Противоязвенный курс: 1) устранение факторов, способствующих рецидиву болезни; 2) лечебное питание; 3) лекарственная терапия; 4) физические методы лечения (физиолечение, гипербарическая оксигенация — ГБО, иглорефлексотерапия, лазеротерапия, магнитотерапия).

• Устранение факторов, способствующих рецидиву болезни, преду сматривает организацию регулярного питания, оптимизацию условий труда и быта, категорическое запрещение курения и употребления алкоголя, за прещение приема лекарственных препаратов, обладающих ульцерогенным


• Лечебное питание обеспечивается назначением диеты, которая должна содержать физиологическую норму белка, жира, углеводов и витаминов. Предусматривается соблюдение принципов механического, термического и химического щажения.

• Лекарственная терапия имеет своей целью:

а) эрадикацию HP;

б) подавление избыточной продукции соляной кислоты и пепсина или их нейтрализацию и адсорбцию;

в) восстановление моторно-эвакуаторной функции желудка и двена дцатиперстной кишки;

г) защиту слизистой оболочки желудка и двенадцатиперстной кишки;

д) стимуляцию процессов регенерации клеточных элементов слизистой оболочки и купирование воспалительно-дистрофических изменений в


• Эрадикация HP достигается проведением недельного курса «трех- компонентной» схемы (терапия первой линии):

омепразол 20 мг, амоксициллин 1000 мг, кларитромицин

250 мг (2 раза в день), или:

омепразол 20 мг, тинидазол 500 мг, кларитромицин 250 мг

(2 раза в день), или:

ранитидин висмута цитрат (пилорид) 400 мг 2 раза в день в

конце еды, кларитромицин 250 мг или тетрациклин 500 мг

или амоксициллин 1000 мг (2 раза в день), тинидазол 500 мг

2 раза в день во время еды.


При неэффективности эрадикации назначают на 7 дней резервную че-тырехкомпонентную схему (терапия второй линии), состоящую из ингибитора протоновой помпы, препарата солей висмута и двух антимикробных Препаратов: омепразол 20мг2 раза в день (утром и вечером, не поздне-^ 20 ч), коллоидный субцитрат висмута 120 мг 3 раза в день за •эО мин до еды и 4-й раз через 2 ч после еды перед сном, метронида-30л 250 мг 4 раза в день после еды или тинидазол 500 мг 2 раза в день

после еды, тетрациклин или амоксициллин по 500 мг 4 раза в день после еды.

После окончания комбинированной эрадикаиионной терапии следует продолжить лечение еще в течение 5 нед при ЯБ двенадцатиперстной кищ, ки и 7 нед при ЯБ желудка с использованием одного из следующих препаратов: ранитидин (300 мг в 19—20 ч) или фамотидин (40 мг в 19—20 ч) или ранитидин висмута цитрат (пилорид — 400 мг утром и вечером).

• Подавление избыточной секреции желудка достигается с помощью селективных м-холиноблокаторов — пирензепин (гастроцепин) в суточной дозе 75—100 мг (по 25—50 мг утром за 30 мин до завтрака и 50 мг перед сном).

Для снижения секреции используют также блокаторы Н2-рецепторы (фамотидин, ранитидин). Эти препараты, блокируя Н2-рецепторы, находящиеся в обкладочных клетках желудка, тормозят базальную и стимулированную гистамином и пентагастрином секрецию соляной кислоты. Используют также блокаторы «протонового насоса» — омепразол, применяемый 2 раза в день по 20 мг.

При лечении антисекреторными препаратами (омепразолом, блокатора-ми Н2-рецепторов и в меньшей степени гастроцепином) в слизистой оболочке желудка развивается гиперплазия гастрин- и гистаминобразующих клеток. В связи с этим необходимы постепенная отмена этих препаратов после рубцевания язвы и обязательное сочетание их приема с нерастворимыми антацидами (алмагель, фосфалюгель, гелюсил лак), которые принимают только в промежутке между приемом пищи (через 1,5—2 ч после еды и на ночь) до наступления полной ремиссии.

• Для нормализации моторно-эвакуаторной функции желудка и двенадцатиперстной кишки назначают метоклопрамид (церукал) по 10 мг 3—4 раза в день или сульпирид (эглонил) по 50 мг 3 раза в день или дом-перидон (10 мг).

• Для защиты слизистой оболочки желудка и двенадцатиперстной кишки применяют коллоидный субцитрат висмута (де-нол), который, соединяясь с белками, освобождающимися в язвенном и эрозивном дефектах, образует вокруг них нерастворимый преципитат, покрывающий слизистую оболочку белково-висмутовой пленкой, Де-нол назначают по 1—2 таблетки за 30 мин до еды 3—4 раза в день. Другой препарат, образующий на поверхности слизистой оболочки защитный слой, резистентный к деструктивному действию соляной кислоты и пепсина — сукральфат (по 1 таблетке 3 раза в день за 30—40 мин до еды и 4-й раз — перед сном).

Де-нол и сукральфат особенно показаны больным, которые не могут самостоятельно прекратить курение, поскольку курение в несколько раз снижает эффективность блокаторов Н2-рецепторов.

В клиническую практику в последние годы введены новые препараты — синтетические аналоги простагландинов. Синтетический аналог простагландина Е, — риопростил — обладает выраженным антисекреторным эффектом, высокоэффективен также энпростил (аналог простагландина Е2).

• Физические методы лечения — тепловые процедуры в период стихания обострения (аппликации парафина, озокерита) при неосложненном течении заболевания и отсутствии признаков скрытого кровотечения.

При длительно нерубцующихся язвах, особенно у больных пожилого и старческого возраста, применяют в комплексной терапии ГБО, позволяющую уменьшить гипоксию слизистой оболочки выраженного органа. Наконец, имеется положительный опыт применения облучения язвенного де-


фекта лазером (через фиброгастроскоп); 7—10 сеансов облучения в существенной степени укорачивают сроки рубцевания.

В ряде случаев возникает необходимость в хирургическом лечении. Оперативное лечение показано больным ЯБ с частыми рецидивами при непрерывной терапии поддерживающими дозами противоязвенных препа-

Операпия безусловно показана в случаях пенетрации, перфорации язвы, стеноза пилородуоденального отдела с выраженными эвакуаторными нарушениями и при профузном желудочно-кишечном кровотечении.

В период ремиссии ЯБ необходимо:

1) исключение ульцерогенных факторов (прекращение курения, упот ребления алкоголя, крепкого чая и кофе, лекарственных препаратов —


2) соблюдение режима труда и отдыха, соблюдение диеты;

3) санаторно-курортное лечение;

4) диспансерное наблюдение с проведением поддерживающей терапии.

Непрерывная поддерживающая терапия проводится в течение нескольких месяцев (и даже лет) антисекреторным препаратом в половинной дозе (например, принимать ежедневно вечером ранитидин по 150 мг или фамотидин по 20 мг).

Показаниями для непрерывной поддерживающей терапии являются:

• неэффективность проведенной эрадикационной терапии;

• осложнения (кровотечение или перфорация в анамнезе);

• наличие сопутствующих заболеваний, требующих приема НПВП;

• сопутствующий эрозивно-язвенный рефлюкс-эзофагит;

• возраст старше 60 лет в случае ежегодного обострения ЯБ, несмотря

на адекватную терапию.

Forecast. Для неосложненных форм ЯБ прогноз благоприятный, он ухудшается при часто рецидивирующих формах, серьезный при осложнениях.

Prevention. В целях профилактики ЯБ рекомендуются устранение нервного напряжения, отрицательных эмоций, интоксикаций; прекращение курения, злоупотребления алкоголем; нормализация питания; соответствующее трудоустройство, активная лекарственная терапия хеликобактер-ной инфекции у больных ХГ.

Профилактическую терапию «по требованию» назначают при появлении симптомов, характерных для обострения ЯБ; она включает прием одного из антисекреторных препаратов (ранитидин, фамотидин, омепразол) в полной суточной дозе в течение 2—3 дней, а затем в половинной дозе — в течение 2 нед.
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Язвенная болезнь

  1. Peptic ulcer
    Epidemiology Accurate epidemiological data on the frequency and prevalence of peptic ulcer are not available. According to various studies, in the United States every 10th man and every 20th woman has a peptic ulcer. Most likely, the prevalence and frequency of the disease tend to decrease. Previously, peptic ulcer disease was more common in men than in women (4: 1).
  2. Peptic ulcer
    Peptic ulcer is a chronic recurrent disease, characterized by a defect in the mucous membrane area and ulceration in the stomach and / or duodenum. Along with peptic ulcer as an independent nosological form, it is now customary to distinguish secondary, symptomatic ulcers and gastroduodenal ulcers that occur when exposed to a known etiological
  3. Peptic ulcer
    Peptic ulcer is a group of heterogeneous diseases, a common manifestation of which is a local defect or erosion in the mucous membrane of the stomach and / or duodenum. This is a very common pathology, which, for example, in the United States for life endure about 10% of men and 5% of women. It should be noted that the prevalence of gastrointestinal
  4. Bowel disease. Infectious enterocolitis (dysentery, typhoid fever, cholera). Nonspecific ulcerative colitis. Crohn's disease. Ischemic bowel disease. Appendicitis. Colon cancer.
    1. Macroscopic characteristics of the small intestine with cholera enteritis 1. gray-yellow film tightly soldered to the wall 2. ulceration of the mucous membrane 3. multiple hemorrhages 4. wall sclerosis 2. Elements of the pathogenesis of typhoid fever 1. bacteremia 2. bacteriochemia 3. cerebral swelling 4. exudative inflammation 5. hypersensitivity reaction in the lymphoid apparatus 3. Modern
  5. Inflammatory bowel disease (ulcerative colitis, Crohn's disease)
    Inflammatory bowel disease (ulcerative colitis, disease
  6. Peptic ulcer disease.
    Peptic ulcer is a chronic, cyclically current disease, the main morphological expression of which is a chronic recurrent gastric or duodenal ulcer. In addition to the ulcer, as manifestations of gastric ulcer and duodenal ulcer, there are so-called symptomatic ulcers, i.e. ulcerations of the stomach and duodenum, which occur with
  7. Stomach ulcer
    Peptic ulcer is a chronic recurrent disease, characterized by the development of the ulcer of the mucous membrane of the stomach or duodenum. The prevalence of peptic ulcer in the structure of gastroenterological pathology ranges from 3.6 to 14.8%. Boys and girls get sick equally often, only after 14 years the number of patients among young people is greater.
  8. Ulcerative disease
    - chronic disease of the stomach or duodenum, characterized by the occurrence of an ulcer defect in the mucous membrane, flowing cyclically and prone to progression. The main clinical manifestations of pain associated with eating and characterized by periodicity and seasonality; dyspeptic syndrome, manifested nausea, vomiting, bringing
  9. Peptic ulcer and 12 duodenal ulcer
    Questions for repetition: 1. Methods of examination of children with diseases of the stomach and duodenum. 2. Fractional study of gastric secretion in children. Test questions: 1. Modern views on the etiopathogenesis of peptic ulcer. 2. Classification of peptic ulcer. 3. Clinical manifestations of duodenal ulcer: 3.1. pain syndrome 3.2. dyspeptic syndrome 3.3.
  10. Peptic ulcer
    Peptic ulcer or duodenal ulcer is a chronic disease, the main symptom of which is the formation of ulcers in the digestive tract during an exacerbation of ulcers. The main etiological factor is Helicobacter Pilori infection. A major role in the formation of pathology is played by psychosocial factors, toxic-allergic factors, hereditary constitutional
  11. Peptic ulcer and its features
    Statistics show that peptic ulcer is the most common disease of the digestive system. More often it affects men than women. People of working age mostly get sick. With improper behavior (smoking, alcohol abuse, disregard for the diet, etc.), peptic ulcer disease can be difficult, gives complications (bleeding, perforation
  12. 5.2. Ulcerative disease
    Цели лечения: 1. ликвидация болей и диспепсических проявлений 2. эрадикация Helicobacter pylori (HP) 3. заживление язвы 4. нормализация гастродуоденальной моторики 5. предупреждение обострений и осложнений Фармакотерапия ЯБ, ассоциированной с Helicobacter pylori: Терапия первой линии (тройная терапия) в течение 7-10 дней до 14 дней: 1. Ингибитор протонной помпы
  13. Ulcerative Disease of Stomach and Twelfth Intestinal Disease
    Since about 200 years ago, Cruveilier attracted the attention of doctors to a stomach ulcer, interest in this disease has been increasing progressively. Much the same applies to the duodenal ulcer, described in detail much later (Moynihan, 1913). Under peptic ulcer now understand the common, chronic, relapsing, cyclically flowing disease in which
  14. Examination of peptic ulcer
    Laboratory tests Although routine laboratory tests do not provide important information for peptic ulcer disease, it is imperative that you perform a blood test and determine the levels of calcium and creatinine in the blood to rule out blood loss, hypercalcemia and renal failure, respectively. Special laboratory tests should be carried out in those patients in whom
  15. Peptic ulcer and 12 duodenal ulcer (codes C 25; C 26)
    Definition Peptic ulcer and (or) duodenal ulcer (essential mediogastralny and duodenal ulcer) - a heterogeneous disease with a lot? actor's aetiology, complex pathogenesis, chronic recurrent course, morphological equivalent in the form of a defect in the mucous and submucosal layers with an outcome in the connective tissue scar. Statistics. At different age periods
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