Diseases of the digestive system - a common pathology of childhood. The prevalence of these diseases has no regional characteristics and currently exceeds 100 cases per 1000 children. In recent years, the possibilities of early diagnosis and treatment of gastrointestinal diseases have significantly expanded. This was facilitated by the development and widespread introduction into practice of endoscopic and new radiation diagnostic methods, which began in the 70-80s. XX century. Role Revealing Helicobacter pylori in the etiology and pathogenesis of chronic gastritis, gastroduodenitis and peptic ulcer of the stomach and duodenum has made it possible to develop the most rational ways to treat these diseases. In children, the peak incidence of diseases of the digestive system falls on 5-6 and 9-12 years. At the same time, with age, the frequency of functional disorders of the digestive system decreases and the proportion of organic diseases increases.
DISEASES OF THE STOMACH AND DUODENUM
Acute gastritis
Acute gastritis is an acute inflammation of the gastric mucosa, caused by exposure to a strong irritant that enters (enters) the stomach cavity.
Etiology
The development of acute gastritis may be due to exogenous or endogenous factors. There are the following types of acute gastritis.
Acute primary (exogenous) gastritis: - alimentary;
Toxic-infectious.
Acute secondary gastritis, complicating severe infectious and somatic diseases.
Corrosive gastritis that occurs when concentrated acids, alkalis and other caustic substances enter the stomach.
Acute phlegmonous gastritis (purulent inflammation of the stomach). The causes of acute exogenous and endogenous gastritis are presented in Table 16-1.
Table 16-1.Etiological factors causing acute gastritis
Pathogenesis
With exogenous gastritis of alimentary origin, poor-quality food has a direct irritating effect on the gastric mucosa, disrupting the processes of digestion, the secretion of enzymes that make up the gastric juice. With food poisoning (PTI), the pathogen itself (for example, salmonella) and its toxins act on the gastric mucosa. With endogenous gastritis, the inflammatory process in the gastric mucosa develops due to the penetration of the etiological agent by the hematogenous route.
Clinical picture
The clinical picture of acute gastritis depends on its form and etiology.
The first symptoms of acute exogenous gastritis of alimentary origin appear a few hours after exposure to a pathological agent. The duration of the disease is on average 2-5 days. The main clinical manifestations are as follows. - Anxiety of the child, general malaise, profuse salivation, nausea, loss of appetite, feeling of "fullness" in the epigastric region.
Chills are possible, then subfebrile fever.
Subsequently, pain in the abdomen intensifies, repeated vomiting occurs, in the vomit - the remains of food eaten 4-6 hours ago.
Pallor of the skin, coating of the tongue with a white-yellow coating, flatulence, palpation of the abdomen - pain in the epigastric region are objectively noted.
Possible diarrhea.
Clinical manifestations of toxic-infectious acute exogenous gastritis resemble those of alimentary gastritis. The features of toxic-infectious gastritis include:
The possibility of developing dehydration due to more frequent vomiting;
Localization of pain in the epigastric and paraumbilical regions;
Severe diarrhea;
Moderate neutrophilic leukocytosis in the analysis of peripheral blood.
Acute phlegmonous gastritis is very difficult, accompanied by purulent fusion of the stomach wall and the spread of pus along the submucosa. Phlegmonous gastritis can develop with injuries of the stomach or as a complication of peptic ulcer. It is characterized by high fever, severe abdominal pain, rapid deterioration of the child's condition, repeated vomiting, sometimes with an admixture of pus. In the blood, neutrophilic leukocytosis with a shift of the leukocyte formula to the left is detected, in the analysis of urine - leukocyturia and albuminuria.
Diagnostics
Diagnosis is usually based on history and clinical presentation. In doubtful and severe cases, FEGDS is indicated.
Treatment
Bed rest for 2-3 days. Hunger in the first 8-12 hours from the onset of the disease. Plentiful frequent drinking in small portions is shown (tea, a mixture of 0.9% sodium chloride solution with 5% glucose solution). After 12 hours, fractional dietary nutrition is prescribed: mashed mucous soups, low-fat broths, crackers, kissels, cereals. By the 5-7th day of illness, the child is usually transferred to a regular table. According to indications (in the first hours of the disease), gastric lavage is prescribed through a gastric tube with warm 0.5-1% sodium bicarbonate solution or 0.9% sodium chloride solution. With toxic-infectious gastritis, anti-inflammatory therapy, enzymes
(pancreatin), antispasmodics (papaverine, drotaverine). Phlegmonous gastritis is treated in a surgical hospital.
Prevention
It is necessary to properly organize the nutrition of the child in accordance with his age, avoid overeating, avoid fatty, fried and spicy foods. When taking certain drugs (for example, acetylsalicylic acid, glucocorticoids), it is necessary to monitor the condition of the gastric mucosa, use antacids.
Forecast
The prognosis of acute gastritis in most cases is favorable - complete recovery.
Chronic gastritis
Chronic gastritis is a long-term inflammation of the gastric mucosa of a diffuse or focal nature with the gradual development of its atrophy and secretory insufficiency, leading to indigestion.
Epidemiological studies indicate an extreme prevalence of this disease, increasing with age. It should be noted that in children, chronic gastritis occurs as an isolated disease only in 10-15% of cases. Much more often, chronic gastritis (usually antral) is combined with damage to the duodenum, biliary tract, and pancreas.
Etiology and pathogenesis
Chronic gastritis most often develops as a result of constantly existing violations of rational nutrition (both quantitatively and qualitatively): non-compliance with the diet, constant use of dry, poorly chewed, too hot or cold, fried, spicy food, etc. Chronic gastritis may develop with prolonged use of certain drugs (eg, glucocorticoids, NSAIDs, antibiotics, sulfonamides). In recent years, importance has also been attached to hereditary predisposition, since chronic gastritis is more often detected in children with a family history aggravated by gastrointestinal diseases.
Plays a significant role in the development of chronic gastritis Helicobacter pylori. This microorganism is often found in other
family members of a sick child. Helicobacter pylori is able to break down urea (with the help of the urease enzyme), the resulting ammonia affects the surface epithelium of the stomach and destroys the protective barrier, opening gastric juice access to the tissues, which contributes to the development of gastritis and ulcerative defect of the stomach wall.
Classification
The modern classification of chronic gastritis ("Sydney system") is based on the morphological features and etiology of chronic gastritis (Table 16-2).
Table 16-2.Modern classification of chronic gastritis*
Clinical picture
The main symptom of chronic gastritis is pain in the epigastric region: on an empty stomach, 1.5-2 hours after a meal, at night, often associated with an error in the diet. Decreased appetite, heartburn, belching with air or sour, nausea, and a tendency to constipation are also characteristic. When examining a patient, palpation determines pain in the epigastric region and the pyloroduodenal zone. Subsequently, flatulence, rumbling and a feeling of "transfusion" in the abdomen appear.
Diagnostics
The diagnosis is made on the basis of a characteristic clinical picture, objective examination data and special research methods. Of the latter, FEGDS is especially informative, allowing to detect several types of changes in the gastric mucosa: hypertrophic, subatrophic, erosive, and sometimes hemorrhagic gastritis. Functional study of gastric juice allows you to evaluate the secretory, acid and enzyme-forming function of the stomach. As an irritant of the glandular apparatus, pentagastrin, a 0.1% solution of histamine, is used. This evaluates the pH and proteolytic activity of gastric juice, the amount of released hydrochloric acid (debit-hour).
Treatment
Treatment of chronic gastritis should be differentiated, complex and individual, depending on the etiology, morphological changes, the course of the process and the age of the child. The main components of the treatment of chronic gastritis are listed below.
With severe exacerbation, inpatient treatment is necessary.
Diet: food should be mechanically and chemically sparing (slimy soups, mashed vegetables and meat, kissels, cereals, mashed cottage cheese). Everything must be consumed warm every 3 hours (except for the night break).
With increased gastric secretion, antisecretory drugs are prescribed - blockers of H 2 -histamine receptors (for example, ranitidine). The inhibitor of H +, K + -ATPase omeprazole is prescribed for 4-5 weeks.
Given the frequent presence Helicobacter pylori, prescribe the so-called three-component therapy: bismuth tripotassium dicitrate for 2-3 weeks, amoxicillin for 1 week and metronidazole for 1 week, in age doses.
With hypermotor dyskinesia in the gastroduodenal zone, myotropic antispasmodics (papaverine, drotaverine), as well as metoclopramide and domperidone are used.
Polyenzymatic preparations are shown (for example, pancreatin - "Pancitrate", "Creon").
Outside of exacerbation, patients need sanatorium treatment.
Chronic gastroduodenitis
Chronic gastroduodenitis is characterized by nonspecific inflammatory restructuring of the mucous membrane of the stomach and duodenum, as well as secretory and motor-evacuation disorders.
In children, unlike adults, an isolated lesion of the stomach or duodenum is observed relatively rarely - in 10-15% of cases. A combined lesion of these departments is observed much more often. The duodenum, being a hormonally active organ, has a regulatory effect on the functional and evacuation activity of the stomach, pancreas and biliary tract.
Etiology and pathogenesis
The leading etiological role belongs to alimentary (irregular and malnutrition, abuse of spicy food, dry food) and psychogenic factors. The significance of these factors increases in the presence of a hereditary predisposition to diseases of the gastroduodenal zone. Psychotraumatic situations in the family, school, social circle are often realized in the form of SVD, which affects secretion, motility, blood supply, regenerative processes and the synthesis of gastrointestinal hormones. Also, long-term use of drugs (glucocorticoids, NSAIDs), food allergies and other factors that reduce local specific and nonspecific protection of the mucous membrane are also important.
One of the main causes of chronic gastroduodenitis is infection Helicobacter pylori. Duodenitis develops against the background of gastritis caused by Helicobacter pylori, and metaplasia of the epithelium of the duodenum into the gastric, which develops as a result of the discharge of acidic gastric contents into the duodenum. Helicobacter pylori settles in areas of metaplastic epithelium and causes the same changes in them as in the stomach. Foci of gastric metaplasia are unstable to the effects of the contents
duodenum, which leads to erosion. Therefore, gastroduodenitis associated with Helicobacter pylori, more often erosive.
The above etiological factors have a toxic-allergic effect and cause morphological changes in the duodenal mucosa. Under these conditions, the role of acid-peptic damage to the mucous membrane increases in the occurrence of evacuation-motor disorders and a decrease in intraduodenal pH. Damaging factors first cause irritation of the mucous membrane, and later - dystrophic and atrophic changes in it. At the same time, local immunity changes, autoimmune aggression develops, and the synthesis of hormones that regulate the motor-secretory function of the pancreatobiliary system is disrupted. In the latter, inflammatory changes also occur. This leads to a decrease in secretin synthesis and saturation of pancreatic juice with bicarbonates, which, in turn, reduces the alkalinization of the intestinal contents and contributes to the development of atrophic changes.
Classification
There is no generally accepted classification of chronic gastroduodenitis. They are subdivided as follows:
Depending on the etiological factor - primary and secondary gastroduodenitis (concomitant);
According to the endoscopic picture - superficial, erosive, atrophic and hyperplastic;
According to histological data - gastroduodenitis with mild, moderate and severe inflammation, atrophy, gastric metaplasia;
Based on the clinical manifestations, phases of exacerbation, incomplete and complete remission are distinguished.
Clinical picture
Chronic gastroduodenitis is characterized by polymorphism of symptoms and is often combined with other diseases of the digestive system, and therefore it is not always possible to distinguish the manifestations caused by gastroduodenitis itself from the symptoms caused by concomitant pathology.
Gastroduodenitis in the acute phase is manifested by aching cramping pains in the epigastric region that occur 1-2 hours after eating and often radiate to the hypochondrium (usually the right one) and the umbilical region. Eating or taking antacids reduces or stops the pain. The pain syndrome may be accompanied by
heaviness, bursting in the epigastric region, nausea, salivation. In the mechanism of development of pain syndrome and dyspeptic phenomena, the main role belongs to duodenal dyskinesia. As a result, duodenogastric reflux increases, causing bitter belching, sometimes vomiting with an admixture of bile, less often heartburn.
When examining patients, attention is drawn to the pallor of the skin, as well as low body weight. The tongue is coated with white and yellowish-white coating, often with imprints of teeth on the lateral surface. On palpation of the abdomen, pain is determined in the pyloroduodenal region, less often around the navel, in the epigastric region and hypochondria. The symptom of Mendel is characteristic. Many patients have symptoms of Ortner and Ker.
In children with chronic duodenitis, vegetative and psycho-emotional disorders are often noted: recurrent headaches, dizziness, sleep disturbance, fatigue, which is associated with a violation of the endocrine function of the duodenum. Vegetative disorders can be manifested by the clinical picture of dumping syndrome: weakness, sweating, drowsiness, increased intestinal motility, occurring 2-3 hours after eating. With a long break between meals, there may also be signs of hypoglycemia in the form of muscle weakness, trembling in the body, and a sharply increased appetite.
Chronic gastroduodenitis has a cyclic course: the exacerbation phase is replaced by remission. Exacerbations often occur in spring and autumn, are associated with a violation of the diet, overload at school, various stressful situations, infectious and somatic diseases. The severity of the exacerbation depends on the severity and duration of the pain syndrome, dyspeptic symptoms, and violations of the general condition. Spontaneous pain disappears on average after 7-10 days, palpation pain persists for 2-3 weeks. In general, exacerbation of chronic duodenitis lasts 1-2 months. Incomplete remission is characterized by the absence of complaints in the presence of moderate objective, endoscopic and morphological signs of duodenitis. In the remission stage, neither clinical, nor endoscopic, nor morphological manifestations of inflammation in the duodenum are found.
Diagnostics
The diagnosis of chronic gastroduodenitis is based on data from clinical observation, the study of the functional state of the duodenum, endoscopic and histological (biopsy specimens of the mucous membrane) studies.
With functional duodenal sounding, changes characteristic of duodenitis are revealed: dystonia of the sphincter of Oddi, pain and nausea at the time of introduction of the irritant into the intestine, reverse leakage of magnesium sulfate solution through the probe due to spasm of the duodenum. Microscopy of duodenal contents reveals desquamated intestinal epithelium, and vegetative forms of lamblia are not uncommon. To assess the functional state of the duodenum, the activity of enterokinase and alkaline phosphatase enzymes in the duodenal contents is determined. The activity of these enzymes is increased in the early stages of the disease and decreases as the severity of the pathological process worsens.
The study of gastric secretion is also important. Its indicators in acidopeptic duodenitis (bulbitis) are usually elevated, and when duodenitis is combined with atrophic gastritis and enteritis, they are reduced.
The most informative method for diagnosing gastroduodenitis is FEGDS (see the section "Chronic gastritis").
X-ray examination of the duodenum is not of great importance in the diagnosis of chronic duodenitis, but allows you to identify various motor-evacuation disorders that accompany the disease or are its cause.
Treatment
Treatment for chronic gastroduodenitis is carried out according to the same principles as for chronic gastritis.
In the acute period of the disease, bed rest is indicated for 7-8 days.
Diet matters a lot. Is a table recommended in the first days of illness? 1, subsequently - a table? 5. During the period of remission, good nutrition is shown.
For eradication Helicobacter pylori carry out three-component therapy: bismuth tripotassium dicitrate in combination with amoxicillin or macrolides and metronidazole for 7-10 days.
With increased acidity of the stomach, H 2 blockers of histamine receptors are recommended, as well as omeprazole for 3-4 weeks.
According to indications, motility-regulating agents (metoclopramide, domperidone, drotaverine) are used.
In the process of rehabilitation, physiotherapy, exercise therapy, spa treatment are prescribed.
Prevention
With a disease of the gastroduodenal zone, it is very important to follow the principles of age-related nutrition, to protect the child from physical and
emotional overload. Secondary prevention includes adequate and timely therapy, observation and regular consultations with a pediatric gastroenterologist.
Forecast
With irregular and ineffective treatment, chronic gastritis and gastroduodenitis recur and become the main pathology of adults, which reduces the quality of life of the patient, his ability to work.
Peptic ulcer of the stomach and duodenum
Peptic ulcer is a chronic relapsing disease accompanied by the formation of a peptic ulcer in the stomach and / or duodenum, due to an imbalance between the factors of aggression and protection of the gastroduodenal zone.
In recent years, cases of peptic ulcer in children have become more frequent, at present the disease is registered with a frequency of 1 case per 600 children (according to A.G. Zakomerny, 1996). Also noted is the “rejuvenation” of the disease, an increase in the proportion of pathology with a severe course and a decrease in the effectiveness of therapy. In this regard, peptic ulcer of the stomach and duodenum in children is a serious problem in clinical medicine.
ETIOLOGY
The disease develops as a result of several unfavorable factors affecting the body, including hereditary predisposition and emotional overload, combined with permanent alimentary errors (irregular meals, abuse of spicy foods, dry food, etc.). The main reasons are considered to be a disorder of the nervous and hormonal mechanisms of the activity of the stomach and duodenum, an imbalance between aggression factors (hydrochloric acid, pepsins, pancreatic enzymes, bile acids) and defense factors (mucus, bicarbonates, cellular regeneration, PG synthesis). Ulceration is associated with prolonged hyperchlorhydria and peptic proteolysis caused by vagotonia, hypergastrinemia and hyperplasia of the main gastric glands, as well as with gastroduodenal dysmotility and prolonged acidification of the antrobulbar zone.
plays an important role in the development of peptic ulcer Helicobacter pylori, found in 90-100% of patients in the mucous membrane of the antrum of the stomach.
PATHOGENESIS
There are several mechanisms that lead to an increase in the secretion of hydrochloric acid and pepsins, a decrease in the production of mucous substances and a violation of the motor regulation of the gastroduodenal zone. An important role in this process is assigned to the central nervous system, which has a dual effect on the secretion and motility of the stomach and duodenum (Fig. 16-1).
Rice. 16-1.Influence of the central nervous system on the secretion and motility of the stomach and duodenum.
Pathological changes in the central and autonomic nervous system play an important role in imbalance between protective and aggressive factors, contributing to the formation of an ulcer.
CLASSIFICATION
Classification of peptic ulcer of the stomach and duodenum is given in table. 16-3.
Table 16-3.Classification of peptic ulcer in children*
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
CLINICAL PICTURE
The clinical picture depends on the localization of the process and the clinical endoscopic stage of the disease.
Stage I (fresh ulcer)
The leading clinical symptom is pain in the epigastric region and to the right of the midline, closer to the navel, pain occurs on an empty stomach or 2-3 hours after eating (late pain). Half of the children report night pain. A clear “Moynigam” rhythm of pain is noted: hunger-pain-eating-relief. Expressed dyspeptic syndrome: heartburn (an early and most common symptom), belching, nausea, constipation. Superficial palpation of the abdomen is painful, deep and difficult due to the protective tension of the muscles of the anterior abdominal wall.
Endoscopic examination against the background of pronounced inflammatory changes in the mucous membrane of the gastroduodenal zone reveals a defect (defects) of a round or oval shape, surrounded by an inflammatory ridge, with a bottom covered with gray-yellow or white fibrin overlays.
In the stomach, ulcers are located mainly in the pyloroanthral region (found more often in boys).
In the duodenum, ulcers are localized on the anterior wall of the bulb, as well as in the zone of the bulboduodenal junction. Motor-
evacuation disorders include duodeno-gastric reflux and spastic bulb deformity.
II stage (the beginning of the epithelialization of the ulcer)
Most children have late pains in the epigastric region, but they occur mainly during the day, and after eating there is a lasting relief. Pains become more dull, aching. The abdomen is well accessible to superficial palpation, but with deep muscle protection is preserved. Dyspeptic manifestations are less pronounced.
In endoscopic examination, the hyperemia of the mucous membrane is less pronounced, the edema around the ulcer is reduced, and the inflammatory shaft disappears. The bottom of the defect begins to clear of fibrin, the convergence of the folds to the ulcer is outlined, which reflects the healing process.
III stage (healing ulcer)
Pain in this stage persists only on an empty stomach, at night their equivalent may be a feeling of hunger. The abdomen becomes accessible to deep palpation, soreness is preserved. Dyspeptic disorders are practically not expressed.
During endoscopy at the site of the defect, traces of repair are determined in the form of red scars that have a different shape - linear, circular, stellate. Possible deformation of the wall of the stomach or duodenum. Signs of the inflammatory process of the mucous membrane of the stomach and duodenum, as well as motor-evacuation disorders, persist.
IV stage (remission)
The general condition is satisfactory. There are no complaints. Palpation of the abdomen is painless. Endoscopically, the mucous membrane of the stomach and duodenum is not changed. However, in 70-80% of cases, a persistent increase in the acid-forming function of the stomach is detected.
Complications
Complications of peptic ulcer are recorded in 8-9% of children. In boys, complications occur 2 times more often than in girls.
The structure of complications is dominated by bleeding, and with a duodenal ulcer they develop much more often than with a stomach ulcer.
Perforation of the ulcer in children often occurs with a stomach ulcer. This complication is accompanied by acute "dagger" pain in the epigastric region, often a shock condition develops.
The disappearance of hepatic dullness during percussion of the abdomen due to the ingress of air into the abdominal cavity is characteristic.
Penetration (penetration of an ulcer into neighboring organs) occurs rarely, against the background of a long difficult process and inadequate therapy. Clinically, penetration is characterized by sudden pain radiating to the back and repeated vomiting. The diagnosis is clarified with the help of FEGDS.
DIAGNOSTICS
The diagnosis of peptic ulcer, in addition to the above clinical and endoscopic substantiation, is confirmed by the following methods:
Fractional probing of the stomach with the determination of the acidity of gastric juice, debit-hour of hydrochloric acid and pepsins. Characterized by an increase in the pH of gastric juice on an empty stomach and with the use of specific stimuli, an increase in the content of pepsins.
X-ray examination of the stomach and duodenum with barium contrast. Direct signs of an ulcer are a symptom of a niche and a typical deformity of the duodenal bulb, indirect signs are pyloric spasm, dyskinesia of the duodenal bulb, hypersecretion of the stomach, etc.
Identification Helicobacter pylori.
Repeated determination of occult blood in the feces (Gregersen reaction).
TREATMENT
Treatment of patients with peptic ulcer of the stomach and duodenum should be complex, it is carried out in stages, taking into account the clinical and endoscopic phase of the disease.
Stage I - the phase of exacerbation. Treatment in a hospital.
Stage II - the phase of subsiding manifestations, the beginning of clinical remission. Dispensary observation and seasonal prophylaxis.
Stage III - the phase of complete clinical and endoscopic remission. Sanatorium treatment.
I stage
Conservative treatment of peptic ulcer begins immediately after diagnosis. In many patients, the ulcer heals within 12-15 weeks.
Bed rest for 2-3 weeks.
Diet: chemically, thermally and mechanically sparing food. Treatment tables according to Pevzner? 1a (1-2 weeks), ? 1b (3-4 weeks), ? 1 (during remission). Meals should be fractional (5-6 times a day).
Reducing the damaging effect of hydrochloric acid and pepsins.
Non-absorbable antacids: algeldrate + magnesium hydroxide, aluminum phosphate, simaldrate, etc .;
Antisecretory drugs: antagonists of histamine H 2 receptors (for example, ranitidine) for 2-3 weeks; inhibitor of H + -, K + - ATPase omeprazole for 40 days.
Elimination of hypermotor dyskinesia in the gastroduodenal zone (papaverine, drotaverine, domperidone, metoclopramide).
In the presence of Helicobacter pylori- three-component treatment for 1-3 weeks (bismuth tripotassium dicitrate, amoxicillin, metronidazole).
Taking into account the presence of digestive and absorption disorders - polyenzymatic preparations (pancreatin).
II stage
The treatment is carried out by the local pediatrician. He examines the child once every 2 months and conducts anti-relapse treatment in the autumn-winter and spring-winter periods (table? 1b, antacid therapy, vitamins for 1-2 weeks).
Stage III
Sanatorium treatment is indicated 3-4 months after discharge from the hospital in local gastroenterological sanatoriums and drinking balneological resorts (Zheleznovodsk, Essentuki).
PREVENTION
Exacerbations of peptic ulcer disease are usually seasonal, therefore, secondary prevention requires regular examination by a pediatrician and the appointment of preventive therapy (antacids), if necessary, diet, restriction of school load (1-2 unloading days per week in the form of home schooling). Providing a favorable psycho-emotional environment at home and at school is of great importance.
FORECAST
The course of peptic ulcer disease and long-term prognosis depend on the timing of the primary diagnosis, timely and adequate therapy. To a large extent, the success of treatment depends on the position of the parents, their understanding of the seriousness of the situation. Constant monitoring of the patient by a pediatric gastroenterologist, compliance with the rules of seasonal exacerbation prevention, hospitalization in a specialized department during an exacerbation significantly improve the prognosis of the disease.
DISEASES OF THE SMALL AND LARGE INTESTINE
Chronic non-communicable diseases of the small and large intestines develop quite often, especially in preschool children. They represent a serious medical and social problem due to the high prevalence, difficulties in diagnosis and the severity of the consequences that disrupt the growth and development of the child. Intestinal diseases can be based on both functional and morphological changes, but it is rarely possible to differentiate them in the early period of the disease.
In young children, due to the anatomical and physiological features of the digestive system, the small and large intestines (enterocolitis) are more often simultaneously involved in the pathological process. For school-age children, more isolated lesions of the intestines are characteristic.
Chronic enteritis
Chronic enteritis is a chronic recurrent inflammatory-dystrophic disease of the small intestine, accompanied by a violation of its main functions (digestion, absorption) and, as a result, a violation of all types of metabolism.
In the structure of the pathology of the digestive system, chronic enteritis as the main disease is recorded in 4-5% of cases.
Etiology
Chronic enteritis is a polyetiological disease that can be both primary and secondary.
Great importance is attached to nutritional factors: dry eating, overeating, excess carbohydrates and fats in food with a lack of protein, vitamins and trace elements, early transfer to artificial feeding, etc.
In recent years, such etiological factors as exposure to poisons, salts of heavy metals (lead, phosphorus, cadmium, etc.), drugs (salicylates, glucocorticoids, NSAIDs, immunosuppressants, cytostatics, some anti-
biotics, especially with long-term use), ionizing radiation (for example, with x-ray therapy).
The occurrence of diseases of the small intestine is promoted by congenital and acquired enzymopathies, malformations of the intestines, impaired immunity (both local and general), food allergies, surgical interventions on the intestines, diseases of other digestive organs (primarily the duodenum, pancreas, biliary tract). ), etc. With the development of chronic enteritis in a child, it is usually difficult to single out one etiological factor. Most often, a combination of a number of factors, both exogenous and endogenous, is detected.
Pathogenesis
Under the influence of any of the above factors or their combination, an inflammatory process develops in the mucous membrane of the small intestine, acquiring a chronic course due to the insufficiency of immune and compensatory-adaptive reactions. The enzymatic activity of the intestinal glands is disturbed, the passage of chyme is accelerated or slowed down, conditions are created for the proliferation of microbial flora, the digestion and absorption of essential nutrients are disturbed.
Clinical picture
The clinical picture of chronic enteritis is polymorphic and depends on the duration and phase of the disease, the degree of change in the functional state of the small intestine, and comorbidities. There are two main clinical syndromes - local and general.
Local intestinal (enteric) syndrome is caused by a violation of parietal (membrane) and cavity digestion. Flatulence, rumbling, abdominal pain, diarrhea are observed. The stools are usually profuse, with bits of undigested food and mucus. Diarrhea and constipation may alternate. On palpation of the abdomen, pain is determined mainly in the umbilical region, the symptoms of Obraztsov and Porges are positive. In severe cases, the phenomenon of "pseudoascites" is possible. Intestinal symptoms often occur when taking milk, raw vegetables and fruits, confectionery.
General intestinal (enteral) syndrome is associated with water-electrolyte imbalance, malabsorption of macro- and micronutrients, and involvement of other organs in the pathological process (malabsorption syndrome). Characteristic: increased fatigue, irritability, headache, weakness, weight loss of varying severity. Dry skin, change
nails, glossitis, gingivitis, seizures, hair loss, impaired twilight vision, increased fragility of blood vessels, bleeding. The above symptoms are due to polyhypovitaminosis and trophic disorders. In young children (up to 3 years old), anemia and metabolic disorders are often detected, manifested by osteoporosis and bone fragility, seizures. The severity of general and local enteric syndromes determines the severity of the disease.
Diagnosis is based on anamnesis data, clinical manifestations, results of laboratory and instrumental methods of examination. Carry out differentiated carbohydrate loads with mono- and disaccharides, a test with d-xylose. Endoscopy with targeted biopsy and subsequent histological examination of the biopsy is also informative. Creatorrhoea, steatorrhea, amylorrhea are revealed in the coprogram.
Differential diagnosis is carried out with the most frequently developing hereditary and acquired diseases that occur with malabsorption syndrome - acute enteritis, intestinal form of cystic fibrosis, gastrointestinal form of food allergy, celiac disease, disaccharidase deficiency, etc.
Treatment
See section "Chronic enterocolitis".
Chronic enterocolitis
Chronic enterocolitis is a polyetiological inflammatory-dystrophic disease in which the small and large intestines are affected simultaneously.
Etiology
The disease occurs most often after acute intestinal infections (salmonellosis, dysentery, escherichiosis, typhoid fever, viral diarrhea), helminthiases, diseases caused by protozoa, errors in the diet (prolonged irregular, insufficient or excessive nutrition), food allergic reactions. The development of the disease is facilitated by congenital and acquired enzymopathies, immunity defects, diseases of the stomach, liver, biliary tract and pancreas, abnormalities in the development of the intestine, dysbacteriosis, vitamin deficiency, neurogenic, hormonal disorders, radiation exposure, irrational use of drugs, in particular antibiotics, etc. .
Pathogenesis
The pathogenesis is not completely clear. It is believed, for example, that infectious agents can cause a violation of the integrity of the cells of the tissues of the digestive tract, contributing to their destruction or morphological metaplasia. As a result, antigens are formed that are genetically alien to the body, causing the development of autoimmune reactions. There is an accumulation of clones of cytotoxic lymphocytes and the production of antibodies directed against antigen structures of autologous tissues of the digestive tract. They attach importance to the deficiency of secretory IgA, which prevents the invasion of bacteria and allergens. Changes in the normal intestinal microflora contribute to the formation of chronic enterocolitis, secondarily increasing the permeability of the intestinal mucosa for microbial allergens. On the other hand, dysbacteriosis always accompanies this disease. Chronic enterocolitis can also be secondary, with diseases of other digestive organs.
Clinical picture
Chronic enterocolitis is characterized by an undulating course: exacerbation of the disease is replaced by remission. During the period of exacerbation, the leading clinical symptoms are abdominal pain and stool disorders.
The nature and intensity of pain can be different. Children often complain of pain in the navel, in the lower abdomen with right-sided or left-sided localization. Pain occurs at any time of the day, but more often in the second half of the day, sometimes 2 hours after eating, intensifies before defecation, when running, jumping, driving, etc. Dull pulling pains are more characteristic of lesions of the small intestine, intense - of the large intestine. Pain equivalents: loosening of stool after eating or, especially in young children, refusal to eat, taste selectivity.
Another major symptom of chronic enterocolitis is a stool disorder in the form of alternating diarrhea (with a predominant lesion of the small intestine) and constipation (with the lesion of the large intestine). Frequent urge to defecate (5-7 times a day) with small portions of feces of different consistency (liquid with an admixture of undigested food, with mucus; gray, shiny, frothy, fetid - with a predominance of putrefactive processes) predominates. Often there is a "sheep" or ribbon-like feces. The passage of solid feces can cause the formation of cracks in the anus. In this case, a small amount of scarlet blood appears on the surface of the feces.
The constant symptoms of chronic enterocolitis in children also include bloating and a feeling of fullness in the abdomen, rumbling and transfusion in the intestines, increased gas discharge, etc. Sometimes the psychovegetative syndrome dominates in the clinical picture of the disease: weakness, fatigue, poor sleep, irritability, and headache develop. Complaints about bowel dysfunction fade into the background. With a long course of the disease, there is a delay in the increase in body weight, less often in growth, anemia, signs of hypovitaminosis, metabolic disorders (protein, mineral).
Diagnosis and differential diagnosis
Chronic enterocolitis is diagnosed on the basis of anamnestic data, a clinical picture (long-term intestinal dysfunction, accompanied by the development of dystrophy), laboratory examination results (anemia, hypo- and dysproteinemia, hypoalbuminemia, a decrease in the concentration of cholesterol, total lipids, β-lipoproteins, calcium, potassium, sodium in the blood serum, detection of mucus, leukocytes, steatorrhea, creatorrhea, amylorrhea in the feces), the results of instrumental research methods (sigmoidoscopy, colonofibroscopy, X-ray and morphological studies).
Chronic enterocolitis should be differentiated from protracted dysentery (see the chapter "Acute intestinal infections"), congenital enzymopathies [cystic fibrosis, celiac disease, disaccharidase deficiency, exudative enteropathy syndrome (see the section "Congenital enzymopathies and exudative enteropathy")], etc.
Treatment
Treatment for chronic enteritis and chronic enterocolitis is aimed at restoring impaired bowel functions and preventing exacerbations of the disease. The basis of the ongoing therapeutic measures is therapeutic nutrition (they prescribe a table? 4 according to Pevzner). Multivitamins, enzyme preparations (pancreatin), pre- and probiotics [bifidobacteria bifidum + activated charcoal (Probifor), Lineks, lactobacilli acidophilus + kefir fungi (Acipol), Hilak-forte], enterosorbents ( dioctahedral smectite), prokinetics (trimebutine, loperamide, mebeverine, etc.). According to strict indications, antibacterial drugs are prescribed: "Intetrix", nitrofurans, nalidixic acid, metronidazole, etc. Phytotherapy, symptomatic agents, physiotherapy, exercise therapy are used. Sanatorium treatment is indicated no earlier than 3-6 months after the exacerbation.
Forecast
With timely and adequate treatment at all stages of rehabilitation, the prognosis is favorable.
irritable bowel syndrome
Irritable bowel syndrome is a functional disorder of the gastrointestinal tract, manifested by a combination of violations of the act of defecation with pain in the absence of organic changes in the intestine.
At an international workshop of experts in Rome (1988), a single definition of irritable bowel syndrome ("Rome criteria") was developed - a complex of functional disorders lasting more than 3 months, including abdominal pain (usually decreasing after defecation) and dyspeptic disorders (flatulence rumbling, diarrhea, constipation or their alternation, feeling of incomplete emptying of the bowels, imperative urge to defecate).
In developed countries, in the adult population, irritable bowel syndrome develops with a frequency of 14 to 48%. Women suffer from this disease 2 times more often than men. It is believed that 30-33% of children suffer from functional disorders of the intestine.
Etiology and pathogenesis
Irritable bowel syndrome is a polyetiological disease. An important place in its development is given to neuropsychic factors. It has been established that the evacuation function of both the small and large intestines is impaired in irritable bowel syndrome. Changes in the motor function of the intestine may be due to the fact that in these patients the sensitivity of the intestinal wall receptors to stretching is increased, as a result of which pain and dyspeptic disorders occur in them at a lower threshold of excitability than in healthy people. A certain role in the formation of irritable bowel syndrome in children is played by the peculiarities of nutrition, in particular, insufficient intake of vegetable fiber. Significant importance is also attached to the loss of a conditioned reflex to the act of defecation and asynergy of the muscular structures of the pelvic diaphragm, leading to violations of the evacuation function of the intestine.
Irritable bowel syndrome can develop secondarily with other diseases of the digestive system: gastritis, duodenitis, peptic ulcer of the stomach and duodenum, pancreatitis, etc. A certain role can be played by past acute intestinal infections, gynecological diseases in girls, pathology of the urinary system.
Clinical picture
Depending on the clinical manifestations, 3 variants of irritable bowel syndrome are distinguished: mainly with diarrhea, constipation and abdominal pain and flatulence.
In patients with a predominance of diarrhea, the main symptom is loose stools, sometimes mixed with mucus and undigested food, usually 4 times a day, more often in the morning, after breakfast, especially with emotional stress. Sometimes there are imperative urges to defecate, flatulence.
In the second variant of irritable bowel syndrome, stool retention is noted (up to 1-2 times a week). In a number of children, the act of defecation is regular, but is accompanied by prolonged straining, a feeling of incomplete emptying of the intestines, a change in the shape and nature of the stool (hard, dry, like sheep, etc.). In some children, prolonged constipation is replaced by diarrhea, followed by recurrence of constipation.
In patients with the third variant of irritable bowel syndrome, cramping or dull, pressing, bursting pains in the abdomen, combined with its swelling, predominate. Pain occurs or increases after eating, during stress, before defecation and disappear after passing gases.
In addition to local manifestations, patients experience frequent headaches, a sensation of a lump in the throat when swallowing, vasomotor reactions, nausea, heartburn, belching, heaviness in the epigastric region, etc. A distinctive feature of irritable bowel syndrome is the variety of complaints. Attention is drawn to the discrepancy between the duration of the disease, the variety of complaints and the good appearance of sick children, physically normally developed.
Diagnosis and differential diagnosis
Diagnosis of irritable bowel syndrome is based on the principle of excluding other intestinal diseases, often using functional, instrumental and morphological examination methods.
Differential diagnosis is carried out with endocrine diseases (hypothyroidism, hyperthyroidism - with constipation; with vipoma, gastrinoma - with diarrhea), impaired intestinal absorption syndrome (lactase deficiency, celiac disease, etc.), gastrointestinal allergies, acute and chronic constipation, etc.
Treatment
Treatment of patients with irritable bowel syndrome is based on the normalization of the regimen and nature of nutrition, psychotherapy, prescription
medicines. In order to normalize the state of the central and autonomic nervous system, as well as intestinal motility, exercise therapy, massage, physiotherapy and reflexology are prescribed. The drugs of choice among drugs are cisapride, loperamide, pinaverium bromide, mebeverine, etc.
In irritable bowel syndrome with diarrhea, a positive effect is exerted by dioctahedral smectite, which has pronounced adsorption and cytoprotective properties. Pre- and probiotics are also used to restore normal microflora ["Enterol", bifidobacteria bifidum, bifidobacteria bifidum + activated carbon ("Probifor"), lactobacilli acidophilus + kefir fungi ("Acipol"), "Hilak-forte", "Lineks" and etc.], antibacterial agents (“Intetrix”, nifuroxazide, furazolidone, metronidazole, etc.), herbal preparations [lingonberry leaves + St. + a series of grass + sage leaves + eucalyptus rod-shaped leaf (“Elekasol”)], reducing bloating, rumbling in the abdomen, the amount of mucus in the stool.
With irritable bowel syndrome, which occurs with constipation, ballast substances are prescribed (bran, flax seed, lactulose, etc.).
According to the indications, they are prescribed: antispasmodics (drotaverine, papaverine), anticholinergics (hyoscine butyl bromide, prifinium bromide), drugs that normalize the state of the central and autonomic nervous system (the choice of the drug depends on the affective disorders identified in the patient); tranquilizers (diazepam, oxazepam), antidepressants (amitriptyline, pipofezin), antipsychotics (thioridazine) in combination with nootropics and B vitamins. Optimal treatment results can be obtained with the joint observation of a patient by a pediatrician and a neuropsychiatrist.
Forecast
The prognosis is favorable.
Congenital enzymopathies and exudative enteropathy
The most common congenital enzymopathies of the gastrointestinal tract are celiac disease and disaccharidase deficiency.
PATHOGENESIS AND CLINICAL PICTURE Celiac disease
Celiac enteropathy is a congenital disease caused by a lack of enzymes that break down gluten (cereal protein)
to amino acids, and the accumulation in the body of toxic products of its incomplete hydrolysis. The disease manifests itself more often from the moment of the introduction of complementary foods (semolina and oatmeal) in the form of abundant foamy stools. Then anorexia, vomiting, symptoms of dehydration, a picture of false ascites join. Severe dystrophy develops.
An x-ray examination of the intestine with the addition of flour to a barium suspension shows a sharp hypersecretion, accelerated peristalsis, a change in the tone of the intestine and the relief of the mucous membrane (a symptom of a "snow blizzard").
Disaccharidase deficiency
In young children, it is more often primary, due to a genetic defect (ρ) in the synthesis of enzymes that break down lactose and sucrose. In this case, lactose intolerance is manifested by diarrhea after the first breast milk feedings, sucrose intolerance - from the moment sugar is introduced into the child's diet (sweet water, supplementary feeding). Characterized by flatulence, watery stools with a sour smell, the gradual development of persistent malnutrition. The chair, as a rule, quickly normalizes after the cancellation of the corresponding disaccharide.
Syndrome of exudative enteropathy
It is characterized by the loss of large amounts of plasma proteins through the intestinal wall. As a result, children develop persistent hypoproteinemia, and a tendency to edema appears. The primary syndrome of exudative enteropathy is associated with a congenital defect of the lymphatic vessels of the intestinal wall with the development of lymphangiectasias, detected by morphological examination. The secondary syndrome of exudative enteropathy is observed in celiac disease, cystic fibrosis, Crohn's disease, ulcerative colitis, cirrhosis of the liver and a number of other diseases.
DIAGNOSTICS
Diagnosis is based on a combination of clinical and laboratory data, the results of endoscopic and morphological studies. In the diagnosis, stress tests are used (for example, the d-xylose absorption test, etc.), immunological methods (determination of agliadin antibodies, etc.), as well as methods to determine the content of protein, carbohydrates, lipids in feces, blood.
DIFFERENTIAL DIAGNOSIS
When conducting differential diagnosis, it is important to take into account the age of the patient, in which the first symptoms of the disease appeared.
During the neonatal period, congenital lactase deficiency (alactasia) is manifested; congenital glucose-galactose malabsorption, congenital enterokinase deficiency, intolerance to cow's milk protein, soy, etc.
TREATMENT
Of decisive importance is the organization of individual therapeutic nutrition, in particular the appointment of elimination diets depending on the period of the disease, the general condition and age of the patient, the nature of the enzyme deficiency. With celiac disease, the diet should be gluten-free (exclude foods rich in gluten - rye, wheat, barley, oatmeal) with milk restriction. With disaccharidase deficiency, it is necessary to exclude the use of sugar, starch or fresh milk (with lactose intolerance). With exudative enteropathy, a diet rich in proteins is prescribed, with fat restriction (medium chain triglycerides are used). According to indications, parenteral nutrition is prescribed in severe cases. Enzyme preparations, probiotics, vitamins, symptomatic therapy are shown.
FORECAST
The prognosis with strict observance of the elimination diet and careful prevention of relapses in patients with celiac disease, some enteropathies is generally favorable, with exudative enteropathy it is only possible to achieve clinical remission.
Prevention of diseases of the small and large intestine
Secondary prevention includes: careful adherence to a diet that is complete in composition; repeated courses of treatment with vitamins, enzymes (under the control of the state of the stool), enterosorbents, prokinetics, herbs, probiotics, as well as mi-
mineral water (with a tendency to diarrhea, "Essentuki 4" is prescribed, heated to 40-50? C); therapeutic exercises and abdominal massage; protecting the child from intercurrent diseases and injuries; exclusion of swimming in open water.
In chronic enteritis and chronic enterocolitis during the period of stable remission, physical education and preventive vaccinations are allowed.
Observation of children and their treatment during the period of remission is carried out by district pediatricians and gastroenterologists of the polyclinic in the first year of discharge from the hospital on a quarterly basis. Sanatorium treatment is indicated no earlier than 3-6 months after the exacerbation. The sanatorium-therapeutic complex includes: a sparing training regimen, dietary nutrition, according to indications - drinking heated low-mineralized waters, mud applications on the stomach and lower back, radon baths, oxygen cocktails, etc. The duration of the course of sanatorium treatment is 40-60 days.
Crohn's disease
Crohn's disease is a chronic nonspecific progressive transmural granulomatous inflammation of the gastrointestinal tract.
The terminal part of the small intestine is more often affected, therefore, there are such synonyms for this disease as terminal ileitis, granulomatous ileitis, etc. Any part of the digestive tract from the root of the tongue to the anus can be involved in the pathological process. The frequency of damage to the intestines decreases in the following order: terminal ileitis, colitis, ileocolitis, anorectal form, etc. There are also focal, multifocal and diffuse forms. The course of Crohn's disease is undulating, with exacerbations and remissions.
Crohn's disease is found in children of all age groups. The peak incidence occurs at 13-20 years of age. Among the sick, the ratio of boys and girls is 1:1.1.
Etiology and pathogenesis
The etiology and pathogenesis of the disease are unknown. Discuss the role of infection (mycobacteria, viruses), toxins, food, some drugs considered as a starting point for the development of acute inflammation. Great importance is attached to immunological, dysbiotic, genetic factors. An association has been established between the HLA histocompatibility system and Crohn's disease, in which the DR1 and DRw5 loci are often detected.
Clinical picture
The clinical picture of the disease is very diverse. The onset of the disease is usually gradual, with a long-term course with periodic exacerbations. Sharp forms are also possible.
The main clinical symptom in children is persistent diarrhea (up to 10 times a day). The volume and frequency of stools depend on the level of damage to the small intestine: the higher it is, the more frequent the stools, and, accordingly, the more severe the disease. The defeat of the small intestine is accompanied by malabsorption syndrome. In the stool, blood impurities periodically appear.
Abdominal pain is a common symptom in all children. The intensity of pain varies from minor (at the beginning of the disease) to intense cramping associated with eating and defecation. When the stomach is affected, they are accompanied by a feeling of heaviness in the epigastric region, nausea, and vomiting. In the later stages, the pain is very intense, accompanied by bloating.
General symptoms of the disease: general weakness, weight loss, fever. With a significant lesion of the small intestine, the absorption and metabolism of proteins, carbohydrates, fats, vitamin B 12, folic acid, electrolytes, iron, magnesium, zinc, etc. are disturbed. Hypoproteinemia is clinically manifested by edema. Delayed growth and sexual development are characteristic.
The most common extraintestinal manifestations of Crohn's disease: arthralgia, monoarthritis, sacroiliitis, erythema nodosum, aphthous stomatitis, iridocyclitis, uveitis, episcleritis, pericholangitis, cholestasis, vascular disorders.
Complicationsin Crohn's disease, they are most often associated with the formation of fistulas and abscesses of various localization, intestinal perforation, and peritonitis. Possible intestinal obstruction, acute toxic dilatation of the colon.
In the general blood test, anemia is detected (decrease in erythrocytes, Hb, hematocrit), reticulocytosis, leukocytosis, and an increase in ESR. A biochemical blood test reveals hypoproteinemia, hypoalbuminemia, hypokalemia, a decrease in the content of trace elements, an increase in the level of alkaline phosphatase, and 2-globulin and C-reactive protein. The severity of biochemical changes correlates with the severity of the disease.
The endoscopic picture in Crohn's disease is highly polymorphic and depends on the stage and extent of the inflammatory process. Endoscopically, 3 phases of the disease are distinguished: infiltration, ulcers-cracks, scarring.
In the infiltration phase (the process is localized in the submucosa), the mucous membrane looks like a “quilt” with a matte surface, the vascular pattern is not visible. In the future, erosions appear according to the type of aphthae with separate superficial ulcerations and fibrinous overlays.
In the phase of ulcers-cracks, individual or multiple deep longitudinal ulcerative defects are detected, affecting the muscular layer of the intestinal wall. The intersection of the cracks gives the mucous membrane the appearance of a "cobblestone pavement". Due to significant edema of the submucosa, as well as damage to the deep layers of the intestinal wall, the intestinal lumen narrows.
In the scarring phase, areas of irreversible intestinal stenosis are found.
Characteristic radiological signs (the study is usually carried out with double contrast): segmental lesions, wavy and uneven contours of the intestine. In the colon, irregularities and ulcerations are determined along the upper edge of the segment, while haustration is preserved along the lower one. In the stage of ulcers-cracks - a kind of "cobblestone pavement".
Diagnosis and differential diagnosis
The diagnosis is established on the basis of clinical and anamnestic data and the results of laboratory, instrumental, morphological studies.
Differential diagnosis of Crohn's disease is carried out with acute and prolonged intestinal infections of bacterial and viral etiology, diseases caused by protozoa, worms, malabsorption syndrome, tumors, ulcerative colitis (Table 16-4), etc.
Table 16-4.Differential Diagnosis of Inflammatory Bowel Disease*
* According to Kanshina O.A., 1999.
Treatment
The regimen during the period of exacerbation is bed, then sparing. Medical nutrition - a table? 4 according to Pevzner. The nature of the diet largely depends on the localization and extent of the intestinal lesion, the phase of the course of the disease.
The most effective drugs are aminosalicylic acid preparations (mesalazine), sulfasalazine. At the same time, it is necessary to take folic acid and multivitamins with microelements according to the age dose. In the acute phase of the disease and with severe complications (anemia, cachexia, joint damage, erythema, etc.), glucocorticoids (hydrocortisone, prednisolone, dexamethasone) are prescribed, less often immunosuppressants (azathioprine, cyclosporine).
In addition, broad-spectrum antibiotics, metronidazole, probiotics, enzymes (pancreatin), enterosorbents (dioctahedral smectite), antidiarrheal drugs (eg, loperamide), and symptomatic agents are used to treat patients with Crohn's disease. In severe cases of the disease, with the development of hypoproteinemia, electrolyte disturbances, intravenous infusions of solutions of amino acids, albumin, plasma, and electrolytes are carried out. According to the indications, surgical treatment is carried out - removal of the affected sections of the intestine, excision of fistulas, anastomosis to restore patency.
Prevention
Forecast
The prognosis for recovery is unfavorable, the prognosis for life depends on the severity of the disease, the nature of its course, and the presence of complications. It is possible to achieve long-term clinical remission.
Nonspecific ulcerative colitis
Nonspecific ulcerative colitis is a chronic inflammatory disease of the colon with recurrent or continuous course, local and systemic complications.
Nonspecific ulcerative colitis is predominantly common among the population of industrialized countries (common
among adults - 40-117:100,000). In children, it develops relatively rarely, accounting for 8-15% of the incidence of adults. In the last two decades, there has been an increase in the number of patients with ulcerative colitis, both among adults and among children of all age groups. The onset of the disease can occur even in infancy. The gender distribution is 1:1, and at an early age boys are more likely to get sick, in adolescence - girls.
Etiology and pathogenesis
Despite many years of study, the etiology of the disease remains unclear. Among the various theories of the development of nonspecific ulcerative colitis, the infectious, psychogenic and immunological theories are most widely used. The search for any single cause of the ulcerative process in the colon has so far been unsuccessful. As etiological factors, viruses, bacteria, toxins, some food ingredients that can, as triggers, cause the onset of a pathological reaction leading to damage to the intestinal mucosa are assumed. Great importance is attached to the state of the neuroendocrine system, local immune protection of the intestinal mucosa, genetic predisposition, adverse environmental factors, psychological stress, iatrogenic drug effects. In ulcerative colitis, a cascade of self-sustaining pathological processes occurs: first non-specific, then autoimmune, damaging target organs.
Classification
The modern classification of nonspecific ulcerative colitis takes into account the length of the process, the severity of clinical symptoms, the presence of relapses, and endoscopic signs (Table 16-5).
Table 16-5.Working classification of ulcerative colitis*
Extraintestinal manifestations and complications
* Nizhny Novgorod Research Institute of Pediatric Gastroenterology.
Clinical picture
The clinical picture is represented by three leading symptoms: diarrhea, blood in the stool, abdominal pain. In almost half of the cases, the disease begins gradually. With mild colitis, single streaks of blood in the stool are noticeable, with severe - a significant admixture of it. Sometimes the stool takes on the appearance of a foul-smelling liquid bloody mass. Most patients develop diarrhea, stool frequency varies from 4-8 to 16-20 times or more per day. In loose stools, in addition to blood, there is a large amount of mucus and pus. Diarrhea with an admixture of blood is accompanied, and sometimes preceded by it, abdominal pain - more often during meals or before defecation. The pains are cramping, localized in the lower abdomen, in the left iliac region or around the navel. Occasionally, a dysentery-like onset of the disease develops. Quite characteristic of severe ulcerative colitis is fever (usually not higher than 38 °C), loss of appetite, general weakness, weight loss, anemia, and delayed sexual development.
Complicationsnonspecific ulcerative colitis are systemic and local.
Systemic complications are diverse: arthritis and arthralgia, hepatitis, sclerosing cholangitis, pancreatitis, severe lesions of the skin, mucous membranes (erythema nodosum, pyoderma, trophic ulcers, erysipelas, aphthous stomatitis, pneumonia, sepsis) and eyes (uveitis, episcleritis).
Local complications in children are rare. These include: profuse intestinal bleeding, intestinal perforation, acute toxic dilatation or stricture of the colon, damage to the anorectal region (fissures, fistulas, abscesses, hemorrhoids, weakness of the sphincter with incontinence of feces and gases); colon cancer.
Laboratory and instrumental research
A blood test reveals leukocytosis with neutrophilia and a shift of the leukocyte formula to the left, a decrease in the content of erythrocytes, Hb, serum iron, total protein, dysproteinemia with a decrease in albumin concentration and an increase in γ-globulins; possible violations of the electrolyte composition of the blood. According to the severity and phase of the disease, the ESR and the concentration of C-reactive protein increase.
A decisive role in the diagnosis of nonspecific ulcerative colitis is played by endoscopic research methods. During colonoscopy in the initial period of the disease, the mucous membrane is hyperemic, edematous, easily vulnerable. In the future, a picture of a typical
erosive and ulcerative process. During the period of manifest manifestations, the circular folds of the mucous membrane thicken, the activity of the sphincters of the large intestine is disrupted. With a long course of the disease, folding disappears, the intestinal lumen becomes tubular, its walls become rigid, and the anatomical curves are smoothed out. Hyperemia and edema of the mucous membrane increase, its granularity appears. The vascular pattern is not determined, contact bleeding is pronounced, erosions, ulcers, microabscesses, pseudopolyps are found.
X-ray reveals a violation of the gaustral pattern of the intestine: asymmetry, deformation or its complete disappearance. The intestinal lumen looks like a hose, with thickened walls, shortened sections, and smoothed anatomical curves.
Diagnosis and differential diagnosis
The diagnosis is established on the basis of clinical and laboratory data, the results of sigmoidoscopy, sigmoid and colonoscopy, irrigography, as well as histological examination of the biopsy material.
Differential diagnosis is carried out with Crohn's disease, celiac disease, diverticulitis, tumors and polyps of the colon, intestinal tuberculosis, Whipple's disease, etc.
Treatment
Diet is of the utmost importance in the treatment of nonspecific ulcerative colitis in children. Assign a dairy-free table? 4 according to Pevzner, enriched with protein due to meat and fish products, eggs.
The basis of basic drug therapy is sulfasalazine and aminosalicylic acid preparations (mesalazine). They can be taken orally and administered as a medicated enema or suppository into the rectum. The dose of drugs and the duration of treatment is determined individually. In severe cases of nonspecific ulcerative colitis, glucocorticoids are additionally prescribed. According to strict indications, immunosuppressants (azathioprine) are used. Symptomatic therapy and local treatment (microclysters) are also carried out.
An alternative to conservative treatment is surgical - subtotal resection of the intestine with the imposition of an ileorectal anastomosis.
Prevention
Prevention is aimed primarily at preventing relapse. After discharge from the hospital, all patients should be recommended
recommend courses of maintenance and anti-relapse treatment, including basic drug therapy, diet, and a protective and restorative regimen. Patients with nonspecific ulcerative colitis are subject to mandatory dispensary observation. Preventive vaccination is carried out only according to epidemiological indications, weakened by vaccine preparations. Children are exempted from exams, physical activities (physical education classes, labor camps, etc.). It is desirable to conduct training at home.
Forecast
The prognosis for recovery is unfavorable, for life it depends on the severity of the disease, the nature of the course, and the presence of complications. Regular monitoring of changes in the mucous membrane of the colon is shown due to the possibility of its dysplasia.
DISEASES OF THE BILIOLOGICAL SYSTEM
Etiology and pathogenesis
The formation of the pathology of the biliary system in children is facilitated by qualitative and quantitative violations of the diet: an increase in the intervals between meals, the early introduction of fatty and spicy foods into the diet, overeating, an excess of sweets, and a sedentary lifestyle. Psycho-emotional disorders, previous perinatal encephalopathy, SVD, stressful situations predispose to the development of the pathology of the biliary system in children. A significant role is played by concomitant diseases of the stomach and duodenum, helminthic invasions, giardiasis, anomalies in the development of the gallbladder and biliary system, food
allergies, bacterial infections. Among the bacteria that cause inflammation in the gallbladder and bile ducts, predominate E. coli and various cocci; less commonly, anaerobic microorganisms are the cause. Hereditary predisposition is also of great importance.
Various lesions of the biliary tract are closely related and have much in common at all stages of pathogenesis. The disease usually begins with the development of biliary dyskinesia, i.e. functional disorders of the motility of the gallbladder, bile ducts, sphincters of Lutkens, Oddi and Mirizzi. Against this background, there is a change in the physicochemical properties of bile, leading to the formation of crystals of bilirubin, cholesterol, etc. As a result, the development of organic inflammatory lesions of the gallbladder and bile ducts, as well as the formation of gallstone disease, is possible.
Biliary dyskinesia
In the occurrence of biliary dyskinesia, the functional state of the stomach and duodenum plays an important role. Violation of the activity of sphincters, duodenostasis, edema and spasm of the major duodenal papilla lead to hypertension in the biliary system and impaired bile secretion. There are different mechanisms leading to impaired bile passage. Two possible variants of such mechanisms are shown in Fig. 16-2.
CLINICAL PICTURE AND DIAGNOSIS
There are hypotonic (hypokinetic) and hypertonic (hyperkinetic) types of dyskinesias. A mixed form is also possible.
Dyskinesia hypotonic type
The main signs of dyskinesia of the hypotonic type are: a decrease in the tone of the muscles of the gallbladder, its weak contraction, and an increase in the volume of the gallbladder. Clinically, this option is accompanied by aching pain in the right hypochondrium or around the navel, general weakness, and fatigue. Sometimes it is possible to palpate a large atonic gallbladder. Ultrasound reveals an enlarged, sometimes elongated gallbladder with normal or delayed emptying. When taking an irritant (egg yolk), the transverse size of the gallbladder usually decreases by less than 40% (normally by 50%). Fractional duodenal sounding reveals an increase in the volume of portion B at normal or high
Rice. 16-2.Mechanisms of violation of the passage of bile.
how fast is the outflow of gallbladder bile, if the tone of the bladder is still preserved. A decrease in tone is accompanied by a decrease in the volume of this portion.
Hypertensive type dyskinesia
The main signs of hypertonic dyskinesia are: reduction in the size of the gallbladder, acceleration of its emptying. Clinically, this variant is characterized by short-term, but more intense bouts of pain localized in the right hypochondrium or around the navel, sometimes there is dyspepsia. With ultrasound, a decrease in the transverse size of the gallbladder after a choleretic breakfast is determined by more than 50%. Fractional duodenal sounding reveals a decrease in the volume of portion B with an increase in the rate of bile outflow.
TREATMENT
Treatment can be carried out both in the hospital and at home. When prescribing treatment, the type of dyskinesia should be taken into account.
Medical nutrition:
Table? 5 with a full content of proteins, fats and carbohydrates;
Unloading days, for example, fruit-sugar and kefir-curd (for the purpose of detoxification);
Fruit and vegetable juices, vegetable oil, eggs (for a natural increase in the outflow of bile).
Choleretic agents. Cholagogue therapy should be carried out for a long time, intermittent courses.
Choleretics (stimulating the formation of bile) - bile + garlic + nettle leaves + activated charcoal ("Allochol"), bile + powder from the pancreas and mucous membrane of the small intestine ("Holenzim"), hydroxymethylnicotinamide, osalmide, cyclovalone, rosehip fruit extract ( "Holosas"); plants (mint, nettle, chamomile, St. John's wort, etc.).
Cholekinetics (promoting the release of bile) - increasing the tone of the gallbladder (for example, ordinary barberry preparations, sorbitol, xylitol, egg yolk), reducing the tone of the biliary tract (for example, papaverine, platifillin, belladonna extract).
To eliminate cholestasis, a tubage according to G.S. is recommended. Demyanov with mineral water or sorbitol. In the morning, the patient is given a glass of mineral water (warm, without gas) to drink on an empty stomach, then for 20-40 minutes the patient lies on his right side on a warm heating pad without a pillow. Tubage is carried out 1-2 times a week for 3-6 months. Another variant of tubage: after taking a glass of mineral water, the patient takes 15 deep breaths with the participation of the diaphragm (the body position is vertical). The procedure is carried out daily for a month.
Acute cholecystitis
Acute cholecystitis is an acute inflammation of the gallbladder wall.
Pathogenesis.Enzymes of microorganisms affect the dehydroxylation of bile acids, increase the desquamation of the epithelium,
yat on the neuromuscular apparatus and sphincters of the gallbladder and biliary tract.
clinical picture. Acute catarrhal cholecystitis is usually manifested by pain, dyspeptic disorders and intoxication.
The pains are paroxysmal in nature with localization in the right hypochondrium, epigastric region and around the navel, the duration of the pain syndrome varies from several minutes to several hours. Occasionally, pain radiates to the region of the lower angle of the right shoulder blade, the right supraclavicular region, or the right half of the neck. More often, pain occurs after taking fatty, spicy or spicy foods, as well as emotional experiences.
Dyspeptic syndrome is manifested by nausea and vomiting, sometimes constipation.
The main manifestations of the intoxication syndrome are febrile fever, chills, weakness, sweating, etc.
On palpation of the abdomen, tension of the anterior abdominal wall, positive symptoms of Kerr, Murphy, Ortner and de Mussy-Georgievsky (phrenicus symptom) are determined. Possible enlargement of the liver. Less often, jaundice is possible due to obstruction of the common bile duct (due to edema or stones).
Diagnostics.The diagnosis is made on the basis of the clinical picture and ultrasound data (thickening and heterogeneity of the walls of the gallbladder, inhomogeneity of the contents of its cavity).
Treatment.Catarrhal acute cholecystitis is usually treated conservatively in a hospital or at home.
Bed rest (duration depends on the condition of the patient).
Diet - a table? 5. Unloading days: fruit-sugar, kefir-curd, apple - to relieve intoxication.
A large amount of liquid (1-1.5 l / day) in the form of tea, fruit drinks, rosehip broth.
Natural choleretic agents (fruit and vegetable juices, vegetable oil, eggs).
Antispasmodic drugs.
Antibiotics to suppress infection (semi-synthetic penicillins, erythromycin in a course of 7-10 days).
Forecast.In most cases, the prognosis is favorable. However, in approximately 1/3 of patients, acute cholecystitis transforms into a chronic form.
Chronic non-calculous cholecystitis
Chronic cholecystitis is a chronic polyetiological inflammatory disease of the gallbladder, accompanied by
changes in the outflow of bile and changes in its physicochemical and biochemical properties.
Etiology.The etiology of chronic cholecystitis is complex and largely associated with the state of the biliary system, duodenum and stomach. Violation of the activity of the sphincter apparatus, duodenostasis, edema and spasm of the major duodenal papilla lead to hypertension in the biliary system, impaired passage of bile and hypomotor dyskinesia of the gallbladder. Just as in the development of acute cholecystitis, an infectious process (usually bacterial) plays a certain role, contributing to the formation of cholesterol crystals.
Pathogenesis.Allergic factors play a certain role in the formation of chronic cholecystitis. Bacterial toxins, chemical and medicinal influences exacerbate dyskinetic disorders. The role of intestinal dysbacteriosis is noted. Simplified pathogenesis of chronic cholecystitis is shown in Fig. 16-3.
clinical picture. The disease is manifested by recurrent paroxysmal pains in the epigastric region, right hypochondrium and around the navel, often radiating to the right shoulder blade. During the period of exacerbation of chronic cholecystitis, the clinical picture consists of several components, caused not only by the pathology of the gallbladder, but also by a secondary violation
Rice. 16-3.The pathogenesis of chronic cholecystitis.
functions of other internal organs. So, insufficiency or complete cessation (acholia) of the flow of bile into the intestine leads to a violation of digestion and intestinal motility, changes in the evacuation-motor and secretory functions of the stomach and duodenum, a decrease in the secretion of pancreatic enzymes, the occurrence of fermentative, and sometimes putrefactive processes in the intestine, the appearance of dyspeptic disorders (nausea, bitterness in the mouth, loss of appetite, flatulence, constipation or loose stools). As a result, signs of chronic intoxication appear: weakness, subfebrile body temperature, dizziness, headache. Body weight decreases, children may lag behind in physical development. The skin and sclera may be somewhat icteric due to cholestasis. The tongue is lined, sometimes swollen, with imprints of the teeth along the edges. Palpation of the abdomen determines pain in the right hypochondrium and epigastric region.
Diagnostics.During the period of exacerbation in the peripheral blood, moderate leukocytosis with neutrophilosis, an increase in ESR, an increase in the concentration of bilirubin and alkaline phosphatase activity (due to cholestasis) are possible. The diagnosis is established on the basis of anamnesis and clinical and instrumental studies. Ultrasound reveals a thickening of the gallbladder wall, an increase in its volume, a thick secret is often determined in the lumen of the bladder, after a test breakfast, the gallbladder is not completely emptied. The bubble may acquire a spherical shape.
Differential diagnosis. Acute and chronic cholecystitis is differentiated from other diseases of the gastroduodenal zone - chronic gastroduodenitis, biliary dyskinesia, hepatitis, chronic pancreatitis, etc.
Treatmentchronic cholecystitis during an exacerbation is built on the same principles as the treatment of acute cholecystitis: bed rest, diet? 5 and? 5a with a ratio of proteins, fats and carbohydrates 1:1:4, a large amount of fruits and vegetables, fractional nutrition. Table? 5 for 2 years is recommended and during remission. After the second year of observation, the diet may be expanded. In severe exacerbation of chronic cholecystitis, detoxification therapy is indicated - intravenous administration of glucose, saline solutions. Otherwise, drug therapy is the same as for acute cholecystitis.
Prevention.With the threat of developing chronic cholecystitis, prevention consists in strict adherence to the diet, the use of choleretic agents, including choleretic tea, limiting physical activity (including physical education at school), and reducing emotional stress.
Forecast.Relapses of the disease can lead to the development of anatomical and functional disorders (for example, thickening of the gallbladder wall, the appearance of parietal stagnation, possible formation of gallstones).
Chronic calculous cholecystitis
Chronic calculous cholecystitis is rarely observed in pediatric practice. But in recent years (apparently due to the use of ultrasound), it is detected in children more often than before, especially in adolescent girls with various types of metabolic disorders.
Etiology and pathogenesis. The formation of cholelithiasis is based on parietal stagnation of bile in hypomotor dyskinesia of the gallbladder, an inflammatory process in the biliary tract and changes in the chemical composition of bile due to metabolic disorders. Under the action of these factors, cholesterol, calcium, bilirubin precipitate, especially in the parietal layer of bile, followed by the formation of stones. In young children, pigment stones (yellow, consisting of bilirubin, a small amount of cholesterol and calcium salts) are more often formed, in older children, cholesterol stones (darkish, consisting of cholesterol crystals) are usually found.
clinical picture. There are two options for the clinical picture of calculous cholecystitis in children. More often, the disease occurs without typical attacks of abdominal pain, only aching pains, heaviness in the upper abdomen, bitterness in the mouth and belching are noted. Less often, a typical course is observed with repeated attacks of acute pain in the right hypochondrium (biliary colic). Pain can be repeated many times at certain intervals. Colic is often accompanied by nausea, vomiting, cold sweat. The passage of a stone can cause temporary obstruction of the bile duct, acute obstructive jaundice, and acholic stools. If the stone is small and has passed through the biliary tract, pain and jaundice stop.
Diagnostics.The diagnosis is established on the basis of clinical data and special research methods: ultrasound and radiological (cholecystography). With ultrasound of the gallbladder and biliary tract, dense formations are found in them. With cholecystography, multiple or single defects in the filling of the gallbladder are fixed.
Treatment.Both medical and surgical treatment is possible. There are drugs that soften and dissolve pigment and cholesterol stones of small diameter (0.2-0.3 cm). But,
given the general metabolic disorders and chronic disorders of the biliary function, re-formation of stones is possible. A radical method should be considered cholecystectomy - removal of the gallbladder. Currently, the endoscopic method - laparoscopic cholecystectomy - is widely used.
DISEASES OF THE PANCREAS
Of all the diseases of the pancreas in children, pancreatitis is most often diagnosed. Pancreatitis is a disease of the pancreas caused by the activation of pancreatic enzymes and enzymatic toxemia.
Acute pancreatitis
Acute pancreatitis can be represented by acute edema of the gland, its hemorrhagic lesion, acute fat necrosis and purulent inflammation.
Etiology
The main etiological factors of acute pancreatitis are as follows.
Acute viral diseases (for example, mumps, viral hepatitis).
Bacterial infections (eg, dysentery, sepsis).
Traumatic lesion of the pancreas.
Pathology of the stomach and duodenum.
Diseases of the biliary tract.
Severe allergic reaction.
Pathogenesis
A simplified diagram of the pathogenesis of acute pancreatitis is shown in Fig. 16-4.
Entering the blood and lymph, pancreatic enzymes, products of enzymatic cleavage of proteins and lipids activate the kinin and plasmin systems and cause toxemia, which affects the functions of the central nervous system, hemodynamics and the state of parenchymal organs. In most children, as a result of exposure to inhibitory systems, the process can be interrupted at the stage of pancreatic edema, then pancreatitis undergoes a reverse development.
Classification
Clinical and morphological classification of acute pancreatitis includes edematous form, fatty pancreonecrosis and hemorrhagic
Rice. 16-4.The mechanism of development of acute pancreatitis.
cue pancreatic necrosis. Depending on the clinical picture, acute edematous (interstitial), hemorrhagic and purulent pancreatitis are isolated.
Clinical picture
The symptoms of the disease largely depend on its clinical form and the age of the child (Table 16-6).
Table 16-6.Clinical picture and treatment of acute pancreatitis*
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
Diagnostics
The diagnosis is established on the basis of the clinical picture and data from laboratory and instrumental studies.
In the general blood test, leukocytosis is detected with a shift of the leukocyte formula to the left, an increase in hematocrit.
In the biochemical analysis, an increased content of amylase is noted. For early diagnosis of the disease, repeated (after 6-12 hours) studies of amylase activity in the blood and urine are used. However, its content does not serve as a criterion for the severity of the process. So, moderately pronounced edematous pancreatitis may be accompanied by a high content of amylase, and severe hemorrhagic - minimal. With pancreatic necrosis, its concentration in the blood falls.
Ultrasound reveals an increase in the size of the pancreas, its compaction and swelling.
Differential Diagnosis
Differential diagnosis of acute pancreatitis is carried out with peptic ulcer of the stomach and duodenum, acute cholecystitis (see the relevant sections), choledocholithiasis, acute appendicitis, etc.
Treatment
Treatment, as well as the clinical picture, depends on the form of the disease and the age of the child (see Table 16-6).
Chronic pancreatitis
Chronic pancreatitis is a polyetiological disease of the pancreas with a progressive course, degenerative and destructive changes in the glandular tissue of a focal or diffuse nature, and a decrease in the exocrine and endocrine functions of the organ.
Etiology
In most children, chronic pancreatitis is secondary and is associated with diseases of other digestive organs (gastroduodenitis, pathology of the biliary system). As a primary disease, chronic pancreatitis develops in children only in 14% of cases, most often due to fermentopathy or acute abdominal trauma. It is impossible to exclude the toxic effect of drugs.
Pathogenesis
The mechanism of the development of the disease can be due to two factors: the obstruction of the outflow of pancreatic enzymes and the causes acting directly on the glandular cells. Just as in acute pancreatitis, the pathological process in the ducts and parenchyma of the pancreas leads to edema, necrosis, and with a long course - to sclerosis and fibrosis of the organ tissue. Powerful inhibitory systems and protective factors of the gland are able to stop the pathological process at the stage of edema, which occurs in most cases of reactive pancreatitis.
Origin | Primary Secondary |
The course of the disease | Recurrent Monotonous |
Severity of flow (form) | Easy Medium heavy |
Disease period | Exacerbation Subsidence of exacerbation Remission |
Functional state of the pancreas | A. Exocrine function: hyposecretory, hypersecretory, obstructive, normal B. Intrasecretory function: hyperfunction or hypofunction of the insular apparatus |
Complications False cyst, pancreolithiasis, diabetes, pleurisy, etc. |
|
Accompanying illnesses | Peptic ulcer, gastroduodenitis, cholecystitis, hepatitis, enterocolitis, colitis, ulcerative colitis |
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
The main clinical manifestation of chronic pancreatitis is pain. Pain is often paroxysmal, localized in the upper abdomen - in the epigastric region, right and left hypochondria. Sometimes they become aching, worse after eating and in the afternoon. Most often, the occurrence of pain is associated with errors in the diet (eating fatty, fried, cold, sweet foods). Sometimes an attack can be triggered by significant physical exertion or an infectious disease. The duration of pain is different - from 1-2 hours to several days. Pain often radiates to the back, the right or left half of the chest, weakens in the sitting position, especially when the torso is tilted forward. The most typical for a patient with chronic pancreatitis is the knee-elbow position (with it, the pancreas is, as it were, in a “suspended” state).
Of the pathological symptoms during the period of exacerbation of the disease, the symptoms of Mayo-Robson, Kach, de MussiGeorgievsky, Grott are often found. In most children, a firm and painful head of the pancreas can be palpated.
Chronic pancreatitis is characterized by dyspeptic disorders: loss of appetite, nausea, vomiting that occurs at altitude
pain attack, belching, heartburn. More than a third of patients have constipation, followed by diarrhea during an exacerbation of the disease.
General symptoms of chronic pancreatitis: weight loss, asthenovegetative disorders (fatigue, emotional instability, irritability).
The severity of clinical symptoms is related to the severity of the disease. The accompanying organic changes in the duodenum (duodenostasis, diverticula) and the biliary system (chronic cholecystitis, cholelithiasis) aggravate the course of the process.
Diagnostics
The diagnosis is based on clinical, laboratory and instrumental data.
In the study of the content of pancreozymin and secretin, pathological types of pancreatic secretion are detected.
Provocative tests with glucose, neostigmine methyl sulfate, pancreozimine reveal changes in the content of amylase, trypsin.
With the help of ultrasound, the structure of the gland is determined. If necessary, CT and endoscopic retrograde cholangiopancreatography are used.
Treatment
The basis of the treatment of chronic pancreatitis is a diet that reduces pancreatic and gastric secretion. The patient's diet should contain a sufficient amount of protein while limiting fats (55-70 g) and carbohydrates (250-300 g). To stop the pain syndrome, drotaverine, papaverine, benziklan are prescribed.
The negative impact of hydrochloric acid exposure is neutralized by the appointment of antisecretory drugs - blockers of histamine H 2 receptors, as well as other drugs of this series (for example, omeprazole). Given the violation of the motility of the duodenum and biliary dyskinesia, prescribe metoclopramide, domperidone.
In the period of exacerbation of chronic pancreatitis, the first 3-4 days are recommended to be hungry, unsweetened tea, alkaline mineral waters, rosehip broth are allowed. Means of pathogenetic therapy are inhibitors of proteolytic enzymes (for example, aprotinin). The preparations are administered by drip intravenously in 200-300 ml of 0.9% sodium chloride solution. Doses are selected individually.
Recently, somatostatin (octreotide) has been proposed to suppress pancreatic secretion. It has a multifaceted effect on the gastrointestinal tract: it reduces abdominal pain, eliminates intestinal paresis, normalizes the activity of amylase, lipase, trypsin in the blood and urine.
Replacement therapy with enzyme preparations (pancreatin, etc.) is also important. The indication for their use is signs of exocrine pancreatic insufficiency. If an exacerbation of chronic pancreatitis is accompanied by an increase in body temperature, an increase in ESR, a neutrophilic shift of the leukocyte formula to the left, broad-spectrum antibiotics are prescribed.
After discharge from the hospital, patients with chronic pancreatitis are subject to dispensary observation, they are given courses of anti-relapse treatment. Sanatorium treatment is recommended in Zheleznovodsk, Essentuki, Borjomi and others.
CHRONIC HEPATITIS
Chronic hepatitis is a diffuse inflammatory process in the liver that proceeds without improvement for at least 6 months.
The classification of chronic hepatitis adopted at the International Congress of Gastroenterologists (Los Angeles, 1994) is presented in Table. 16-8.
Table 16-8.Classification of chronic hepatitis
The prevalence of chronic hepatitis has not been accurately established due to the large number of erased and asymptomatic forms and the lack of population-based studies. Most often, chronic viral hepatitis is detected, caused by the persistence of hepatitis B and C viruses in the body.
Chronic viral hepatitis
Chronic viral hepatitis - chronic infectious diseases caused by hepatotropic viruses and characterized by
with a clinical and morphological picture of diffuse inflammation of the liver lasting more than 6 months and a symptom complex of extrahepatic lesions.
CHRONIC HEPATITIS B Etiology and pathogenesis
The causative agent of the disease is a DNA virus (hepatitis B virus). The main route of transmission is parenteral. It is believed that chronic hepatitis B is a disease that is primarily chronic or that has arisen after an erased or subclinical form of an acute infection. The transition of acute hepatitis B to chronic is noted in 2-10% of cases, mainly in mild or latent forms of the disease. The vast majority of patients with chronic hepatitis have no history of acute hepatitis.
It is believed that the cause of the development of chronic hepatitis B may be a lack of immune response due to genetic causes or the immaturity of the body (infection of the fetus, newborn or young child). Infection of a child in the perinatal period and in the first year of life in 90% of cases ends with the formation of chronic hepatitis B or the carriage of the hepatitis B virus. Chronic hepatitis B and carriage of HB s Ag are often recorded in diseases associated with impaired immune system functions: immunodeficiency states, chronic diseases kidneys, chronic lymphocytic leukemia, etc.
Chronic hepatitis B has several phases: initial (immune tolerance); immune response (replicative), occurring with pronounced clinical and laboratory activity; integrative, carriage of HB s Ag. The process usually remains active for 1-4 years and is replaced by the phase of integration of hepatitis B virus DNA into the hepatocyte genome, which coincides with the clinical remission of the disease. The process may end with the development of carriage or cirrhosis of the liver.
The hepatitis B virus itself does not appear to cause cytolysis. Damage to hepatocytes is associated with immune responses that occur in response to viral (HB s Ag, HB ^ g) and hepatic antigens circulating in the blood. In the phase of virus replication, all three hepatitis B virus Ags are expressed, immune aggression is more pronounced, which causes massive necrosis of the liver parenchyma and virus mutation. As a result of the mutation of the virus, the composition of serum antigens changes, so the replication of the virus and the destruction of hepatocytes take a long time.
Replication of the virus is also possible outside the liver - in the cells of the bone marrow, mononuclear cells, thyroid and salivary glands, which, apparently, is the reason for the extrahepatic manifestations of the disease.
Clinical picture
The clinical picture of chronic hepatitis B is associated with the virus replication phase and is polysyndromic.
Almost all patients have a slight intoxication syndrome with asthenovegetative manifestations (irritability, weakness, fatigue, sleep disturbance, headaches, sweating, subfebrile condition).
Jaundice is possible, although more often patients have subicteric or mild scleral icterus.
Hemorrhagic syndrome, which correlates with the severity of the process, is recorded in approximately 50% of patients; it is expressed in mild nosebleeds, petechial rash on the face and neck, and hemorrhages on the skin of the extremities.
Vascular manifestations (the so-called extrahepatic signs) occur in 70% of patients. They include telangiectasias ("spider veins") on the face, neck, and shoulders, as well as palmar erythema, a symmetrical reddening of the palms ("liver palms") and feet.
Dyspeptic syndrome (bloating, flatulence, nausea, aggravated after eating and taking medications, belching, anorexia, intolerance to fatty foods, a feeling of heaviness in the right hypochondrium and epigastric region, unstable stool) is associated with both functional liver deficiency and concomitant damage biliary tract, pancreas, gastroduodenal zone.
Hepatomegaly is the main and sometimes the only clinical symptom of chronic hepatitis B. The size of both lobes of the liver is enlarged both percussion and palpation. Sometimes the liver protrudes 6-8 cm from under the edge of the costal arch, has a densely elastic consistency, a rounded or pointed edge, and a smooth surface. Palpation is painful. Signs of liver damage are more pronounced with an active process. Patients often complain of constant aching pain in the right hypochondrium, aggravated by physical exertion. With a decrease in activity, a decrease in the size of the liver occurs, palpation becomes less painful, pain in the liver area bothers the child less.
A pronounced enlargement of the spleen is found with high activity of hepatitis.
Endocrine disorders are possible - menstrual disorders in girls, striae on the thighs, acne, hirsutism, etc.
Extrahepatic systemic manifestations include nervous tics, erythematous spots on the skin, urticaria, erythema nodosum, transient arthralgia.
In the general blood test in the active period and in severe chronic hepatitis B, anemia, leukopenia, thrombocytopenia, lymphopenia and an increase in ESR are detected. In the blood serum, an increase in the activity of aminotransferases by 2-5 times or more, hyperbilirubinemia (an increase in the concentration of bound bilirubin), hypoalbuminemia, hypoprothrombinemia, an increase in cholesterol, alkaline phosphatase (3 times or more) and γ-globulins are noted. Using ELISA, RIF, DNA hybridization and PCR, markers of hepatitis B virus replication (HB e Ag, anti-HB e Ag-IgM, viral DNA) are detected.
CHRONIC HEPATITIS C
Etiology.The causative agent of the disease is an RNA virus (hepatitis C virus). The modes of transmission are similar to those of chronic hepatitis B.
Pathogenesis.Chronic viral hepatitis C is the outcome of acute hepatitis C (in 50-80% of cases). The hepatitis C virus has a direct cytopathic effect on hepatocytes. As a result, viral replication and persistence in the body are associated with hepatitis activity and progression.
clinical picture. Clinical manifestations of chronic hepatitis C are usually mild or absent. Patients are concerned about fatigue, weakness, dyspeptic disorders. On examination, hepatomegaly, telangiectasia, palmar erythema are found. The course of the disease is undulating and prolonged. In a biochemical blood test, an increase in the activity of alanine aminotransferase (ALT) is detected. The diagnosis is based on the detection of specific markers of chronic hepatitis C - virus RNA and antibodies to it (in the absence of hepatitis B virus markers).
CHRONIC HEPATITIS DELTA
Etiology.The causative agent is a small defective RNA virus (hepatitis D virus); contagious only when infected with the hepatitis B virus (since, due to the incomplete genome, it uses proteins of the hepatitis B virus for replication). The main route of transmission is parenteral.
Pathogenesis.Chronic viral hepatitis D is always the outcome of its acute form, which proceeded as a superinfection or co-infection in patients with acute or chronic hepatitis B. The hepatitis D virus has a cytopathogenic effect on hepatocytes, maintains activity and promotes the progression of the process in the liver.
clinical picture. Symptoms of liver failure are clinically detected (severe weakness, drowsiness during the day, insomnia at night, bleeding, dystrophy). In most patients, jaundice and pruritus, extrahepatic systemic manifestations, enlargement and hardening of the liver are expressed. Chronic hepatitis D is characterized by a severe course. In the blood, markers of chronic hepatitis D are detected - virus DNA and antibodies to its Ag. Hepatitis B virus replication is suppressed as cirrhosis progresses rapidly.
DIAGNOSTICS
Diagnosis of chronic viral hepatitis is based on anamnestic, clinical (intoxication, hemorrhagic syndrome, liver enlargement and hardening, extrahepatic signs), biochemical (increased ALT, thymol test, dysproteinemia, hyperbilirubinemia, etc.), immunological (signs of immune inflammation, specific markers ) and morphological data.
DIFFERENTIAL DIAGNOSIS
TREATMENT
Treatment of chronic viral hepatitis includes, first of all, basic, then symptomatic and (according to indications) detoxification and antiviral therapy.
The basic therapy includes the regime and diet, the appointment of vitamins.
The mode of patients with chronic hepatitis should be as sparing as possible, in the active period of the disease - half-bed. Limit physical and emotional stress.
When prescribing a diet, individual tastes and habits of the patient, the tolerance of individual products and concomitant diseases of the gastrointestinal tract are taken into account. They use mainly fermented milk and vegetable products, 50% of fats should be of vegetable origin. Exclude fatty, fried, smoked foods, ice cream, coffee, chocolate, carbonated drinks. Limit meat and fish broths, as well as the amount of raw fruit. Meals should be fractional (4-5 times a day).
To normalize metabolic processes and vitamin balance, vitamin C (up to 1000 mg/day), multivitamin preparations are prescribed.
Symptomatic therapy includes the appointment of courses of mineral waters, choleretic and antispasmodic drugs, enzyme preparations and probiotics for the treatment of concomitant dysfunctions of the biliary system and gastrointestinal tract.
With severe intoxication, drip intravenous administration of povidone + sodium chloride + potassium chloride + calcium chloride + magnesium chloride + sodium bicarbonate ("Hemodeza"), 5% glucose solution for 2-3 days is necessary.
In the active phase of the disease (phase of virus replication), interferon preparations are carried out (interferon alfa-2b - subcutaneously 3 times a week for 6 months at a dose of 3 million IU / m 2 of body surface; interferon alfa-2a is also used; interferon alfa-p1 ) and other antiviral drugs. The effectiveness of treatment is 20-60%. Chronic viral hepatitis D is resistant to interferon therapy. If antiviral therapy is ineffective, a combination of interferon alfa with antiviral drugs (for example, ribavirin) is possible. In chronic hepatitis B, lamivudine therapy is also carried out.
PREVENTION
Primary prevention has not been developed. Secondary prevention consists in early recognition and adequate treatment of patients with acute viral hepatitis. Children who have had acute viral hepatitis B, C, D, G must be registered at the dispensary for at least one year. During the follow-up period, it is recommended, in addition to an examination with determining the size of the liver, to conduct a biochemical study of blood serum (total bilirubin, transaminase activity, sedimentary samples, specific markers, etc.). Showing withdrawal from medical vaccinations, limitation of physical activity, strict adherence to diet, spa treatment (without exacerbation). The widespread introduction of vaccination against hepatitis A and B will solve the problem of not only acute, but also chronic hepatitis.
FORECAST
The chance of complete recovery is low. As the process progresses, cirrhosis of the liver and hepatocellular carcinoma develop.
autoimmune hepatitis
Autoimmune hepatitis is a progressive hepatocellular inflammation of unknown etiology, characterized by the presence of periportal hepatitis, hypergammaglobulinemia, liver-associated serum autoantibodies, and the positive effect of immunosuppressive therapy.
The prevalence of autoimmune hepatitis in European countries is 0.69 cases per 100,000 population. In the structure of chronic liver diseases, the proportion of autoimmune hepatitis in adult patients is 10-20%, in children - 2%.
Etiology and pathogenesis
The etiology of autoimmune hepatitis is not known, and the pathogenesis is not well understood. It is believed that autoimmune hepatitis develops as a result of a primary conditioned violation of the immune response. Viruses (Epstein Barr, measles, hepatitis A and C) and some drugs (for example, interferon) are indicated as possible starting (trigger) factors contributing to the onset of the disease.
In the presence of an appropriate genetic predisposition, with or without exposure to trigger factors, an immune dysregulation occurs, manifested by a defect in the function of suppressor T cells, linked by the HLA A1-B8-DR3 haplotype in the white population in Europe and North America, or by the HLA DR4 allele, more common in Japan and other Southeast Asian countries). As a result, there is an uncontrolled synthesis of IgG class antibodies by B cells, which destroy the membranes of normal hepatocytes. Together, DR3 and/or DR4 alleles are detected in 80-85% of patients with autoimmune hepatitis. Currently, autoimmune hepatitis I, II and III types are distinguished.
Type I is the classic variant, accounting for about 90% of all cases of the disease. The role of the main autoantigen in type I autoimmune hepatitis belongs to the liver-specific protein (liver specific protein, LSP). Antinuclear cells are found in the blood serum (antinuclear antibodies, ANA) and/or anti-smooth muscle (smooth muscle antibody, SMA) AT in titer more than 1:80 in adults and more than 1:20 in children. In 65-93% of patients with this type of hepatitis, perinuclear neutrophil cytoplasmic antibodies (pANCA) are also found.
Autoimmune hepatitis type II accounts for about 3-4% of all cases, most of the patients are children from 2 to 14 years old. The main autoantigen in type II autoimmune hepatitis is liver microsome Ag
and type I kidneys (liver kidney microsomes, LKM-1). In autoimmune hepatitis type II, antibodies to microsomes of liver cells and epithelial cells of the glomerular apparatus of the kidneys of type I (anti-LKM-!) are detected in the blood serum.
Type III autoimmune hepatitis is also distinguished, characterized by the presence of AT to soluble hepatic Ag. (soluble liver antigen) anti-SLA in the absence of ANA or anti-KLM-1 Patients with type III disease often have SMA (35%), anti-mitochondrial antibodies (22%), rheumatoid factor (22%), and anti-hepatic membrane anti-Ag (anti-LMA) (26%).
Clinical picture
The clinical picture in children in 50-65% of cases is characterized by the sudden onset of symptoms similar to those in viral hepatitis. In some cases, the disease begins imperceptibly with asthenovegetative disorders, pain in the right hypochondrium, slight jaundice. The latter often appears in the later stages of the disease, is unstable and increases during exacerbations. The appearance of telangiectasias (on the face, neck, hands) and palmar erythema is characteristic. The liver is compacted and protrudes from under the edge of the costal arch by 3-5 cm, the spleen is almost always enlarged. Often, autoimmune hepatitis is accompanied by amenorrhea and infertility; boys may develop gynecomastia. It is possible to develop acute recurrent migratory polyarthritis involving large joints without their deformities. One of the options for the onset of the disease is fever in combination with extrahepatic manifestations.
Laboratory research
A blood test reveals hypergammaglobulinemia, an increase in the concentration of IgG, a decrease in the concentration of total protein, a sharp increase in ESR. Leukopenia and thrombocytopenia are detected in patients with hypersplenism and portal hypertension syndrome. Autoantibodies against liver cells are found in the blood serum.
Diagnosis and differential diagnosis
There are "certain" and "probable" autoimmune hepatitis.
A “definite” diagnosis of autoimmune hepatitis implies the presence of a number of indicators: periportal hepatitis, hypergammaglobulinemia, autoantibodies in the blood serum, increased activity of serum transaminases with normal concentrations of ceruloplasmin, copper and a 1 -antitrypsin. At the same time, the concentration of serum γ-globulins exceeds the upper limit of the norm by more than 1.5 times, and the titers of antibodies (ANA, SMA and anti-LKM-1) do not
less than 1:80 in adults and 1:20 in children. In addition, there are no viral markers in the blood serum, bile duct damage, copper deposition in the liver tissue and other histological changes suggesting a different etiology of the process, and there is no history of blood transfusions and the use of hepatotoxic drugs. A "probable" diagnosis is justified when the presenting symptoms suggest autoimmune hepatitis but are not sufficient to make a "definite" diagnosis.
In the absence of autoantibodies in the blood serum (about 20% of patients), the disease is diagnosed on the basis of an increase in the activity of transaminases in the blood, severe hypergammaglobulinemia, a selective increase in the IgG content in the blood serum, typical histological signs and a certain immunological background (identification of other autoimmune diseases in a sick child or his relatives) with the obligatory exclusion of other possible causes of liver damage. Some diagnostic features of various types of autoimmune hepatitis are given in Table. 16-9.
Table 16-9.Diagnostic criteria for different types of autoimmune hepatitis
Differential diagnosis is carried out with chronic viral hepatitis, insufficiency of a 1 -antitrypsin, Wilson's disease.
Treatment
The basis of treatment is immunosuppressive therapy. Prednisolone, azathioprine, or a combination of both are prescribed. Combination therapy is recommended to reduce the likelihood of adverse reactions from the use of glucocorticoids: in this case, prednisolone is prescribed at a lower dose than with monotherapy. A positive response to such therapy is one of the criteria for the diagnosis of autoimmune hepatitis. However, in the absence of an effect, this diagnosis cannot be completely excluded, since the patient may have a violation of the drug regimen or an insufficient dosage. The goal of treatment is to achieve complete remission. Remission means the absence of biochemical signs of inflammation [the activity of aspartate aminotransferase (AST) is no more than 2 times higher than normal] and histological data indicating the activity of the process.
Therapy with prednisolone or a combination of prednisolone with azathioprine allows achieving clinical, biochemical and histological remission in 65% of patients within 3 years. The average duration of treatment until remission is achieved is 22 months. Patients with histologically confirmed cirrhosis of the liver respond to therapy as well as patients without signs of cirrhosis: the 10-year survival rate of patients with or without cirrhosis during therapy is practically the same and is 89 and 90%, respectively. Prednisolone is prescribed at a dose of 2 mg / kg (maximum dose 60 mg / day) with its subsequent decrease by 5-10 mg every 2 weeks under weekly monitoring of biochemical parameters. With the normalization of transaminases, the dose of prednisolone is reduced to the lowest possible maintenance dose (usually 5 mg / day). If normalization of liver tests does not occur during the first 6-8 weeks of therapy, azathioprine is additionally prescribed at an initial dose of 0.5 mg / kg. In the absence of signs of toxic action, increase the dose of the drug to 2 mg / day. Although a decrease in transaminase activity by 80% of the initial one occurs within the first 6 weeks in most patients, complete normalization of the enzyme concentration occurs only after a few months (after 6 months with type I autoimmune hepatitis, after 9 months with type II). Relapses during therapy occur in 40% of cases, while temporarily increasing the dose of prednisolone. After 1 year from the onset of remission, it is recommended to try to cancel immunosuppressive therapy, but only after a control puncture liver biopsy. In this case, a morphological study should indicate the absence or minimal severity of inflammatory changes. However, it is not possible to completely cancel immunosuppressive therapy in most cases. With repeated recurrence of autoimmune hepatitis after the abolition of immunosuppressive drugs,
lifelong maintenance therapy with prednisolone (5-10 mg/day) or azathioprine (25-50 mg/day). Long-term immunosuppressive therapy causes adverse reactions in 70% of children. With the ineffectiveness of glucocorticoid therapy, cyclosporine, cyclophosphamide are used.
In 5-14% of patients with a confirmed diagnosis of autoimmune hepatitis, primary resistance to treatment is observed. This small group of patients can be clearly identified as early as 14 days after the start of treatment: their liver tests do not improve, and their subjective well-being remains the same or even worsens. Mortality among patients in this group is high. They are subject to mandatory consultation at liver transplantation centers, as are those patients who develop a therapy-resistant relapse during or after treatment. Drug treatment of such patients is usually ineffective, continuing to take high doses of glucocorticoids only leads to the loss of precious time.
Prevention
Primary prevention has not been developed. The secondary consists in regular dispensary observation of patients, periodic determination of the activity of liver enzymes, the content of γ-globulins and autoantibodies for the timely diagnosis of relapse and the strengthening of immunosuppressive therapy. Important points: adherence to the regime of the day, limitation of physical and emotional stress, diet, withdrawal from vaccination, minimal medication. Periodic courses of hepatoprotectors and maintenance therapy with glucocorticoids are shown.
Forecast
The disease without treatment is continuously progressing and does not have spontaneous remissions. Improvements in well-being are short-term, normalization of biochemical parameters does not occur. As a result of autoimmune hepatitis, cirrhosis of the liver of the macronodular or micronodular type is formed. The forecast at children with primary resistance to treatment is unfavorable. If immunosuppressive therapy fails, liver transplantation is indicated for patients. After liver transplantation, the 5-year survival rate in patients with autoimmune hepatitis is more than 90%.
Diseases of the digestive system- this group of diseases occupies one of the leading places among diseases of internal organs. The fact is that the digestive system is constantly affected by various environmental factors - the nature of nutrition, working and living conditions.
In addition to structural changes in the digestive system, functional disorders may also occur. The internal organs of digestion include the esophagus, stomach, intestines, liver, and pancreas. The bile ducts are also involved in digestion.
Diseases of the digestive system are widespread. Most often, these are various inflammatory processes associated with the presence of infection or disruption of the endocrine glands. Any of these diseases in the acute stage requires immediate treatment, since when it becomes chronic, surgery may be required.
Diseases of the digestive system
Diseases of the digestive tract are distinguished by the variety of their clinical and morphological features.
They include independent primary diseases, which are studied by the science called gastroenterology, as well as other, secondary ones, which are a manifestation of a number of diseases of an infectious and non-infectious nature, of an acquired or hereditary origin.
These diseases can be based on various general pathological processes, such as alteration, inflammation, hyper- and dysplastic processes, autoimmune disorders, and, finally, tumors.
Descriptions of diseases of the digestive system
Causes of diseases of the digestive system
The causes of indigestion are:
Exogenous, endogenous, as well as genetic factors can provoke diseases of the digestive system.
exogenous
These primary causes of the disease include:
- dry eating,
- eating very hot foods
- abuse of various spices and spices,
- excessive drinking,
- smoking,
- eating junk food,
- no diet,
- hasty eating,
- defects of the human chewing apparatus,
- uncontrolled medication,
- unfavorable environmental conditions.
Diseases caused by exogenous factors include gastritis and enteritis, colitis, gastric and duodenal ulcers, cholelithiasis, as well as dyskinesia and cirrhosis of the liver.
Endogenous
Secondary (or endogenous) causes of gastrointestinal diseases are diseases such as diabetes mellitus and anemia, obesity and hypovitaminosis, various diseases of the kidneys and lungs, and stress. Diseases provoked by endogenous factors are hepatitis and cholecystitis, pancreatitis and enterobiasis.
genetic
This group includes genetic factors, as well as developmental anomalies, including malformations of the esophagus and benign tumors (both the esophagus and the stomach), diagnosed abnormal development of the pancreas (for example, cystic fibrosis of the pancreas itself), as well as congenital pancreatic hypoplasia .
It should be noted that most often gastrointestinal diseases occur with a combination of both endogenous and exogenous factors.
Symptoms of diseases of the digestive system
The symptoms of diseases of the digestive system are varied, but the main signs of the presence of the disease are always present:
- nausea;
- frequent change of stool;
- belching;
- vomit;
- flatulence;
- loss of appetite;
- fast fatiguability;
- weight loss;
- pain in the abdomen of various locations;
- insomnia.
Other characteristic symptoms are different and depend on the type of disease. In many cases, digestive diseases are accompanied by rashes on the skin.
Diagnosis of diseases of the digestive system
Initially, if you suspect the development of diseases of the digestive system, the doctor must conduct a thorough examination of the patient. During the examination, palpation, percussion, and auscultation are practiced. It is necessary to ask in detail about the complaints, to study the anamnesis.
As a rule, with diseases of this type, the patient is assigned to conduct laboratory tests:
- general and biochemical blood tests,
- general urinalysis,
- stool analysis.
Radiation methods of research are also widely practiced in the diagnostic process. An informative method is an ultrasound examination of the abdominal organs, radiography, fluoroscopy with the use of contrast agents, CT, MRI.
Depending on the disease, procedures can also be prescribed to assess the state of the internal organs of the digestive system and at the same time obtain material for a biopsy:
- colonoscopy,
- esophagogastroduodenoscopy,
- sigmoidoscopy,
- laparoscopy.
In order to examine the stomach, the use of functional tests is practiced, which allow obtaining detailed information about the acid secretion of the stomach, its motor function, as well as the state of the pancreas, small intestine.
Treatment of diseases of the digestive system
The method of treatment is determined after the diagnosis. In infectious and inflammatory pathologies, antibiotic therapy is required. The following drugs are used: m "Ciprofloxacin", "Cefazolin", "Metranidazole".
For the treatment of enzyme deficiency, drugs "Mezim", "Pancreatin" are used. Anti-inflammatory and antisecretory agents are also used. Surgical treatment consists in eliminating intestinal obstruction, removing calculi, tumor formations, suturing an ulcer, etc.
Nutrition for diseases of the digestive system
Nutrition for diseases of the digestive system should be special. In this regard, in our country at one time the Russian Academy of Medical Sciences developed special diets that are suitable not only for diseases of the digestive system, but also for other systems too (diets are indicated in articles on the treatment of certain diseases). A specially selected diet is necessary in the treatment of diseases of the digestive system and is the key to successful treatment.
If normal enteral nutrition is not possible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter the blood immediately, bypassing the digestive system. Indications for the appointment of this food are: complete esophageal dysphagia, intestinal obstruction, acute pancreatitis and a number of other diseases.
The main ingredients of parenteral nutrition are amino acids (polyamine, aminofusin), fats (lipofundin), carbohydrates (glucose solutions). Electrolytes and vitamins are also introduced, taking into account the daily needs of the body.
Prevention of diseases of the digestive system
The main and most important prevention of diseases of the digestive system, and not only them, is maintaining a healthy lifestyle.
This includes the rejection of bad habits (smoking, alcohol, etc.), regular physical education, exclusion of physical inactivity (lead a mobile lifestyle), adherence to work and rest regimes, good sleep, and more.
It is very important to have a complete, balanced, regular diet, which ensures the intake of the necessary substances (proteins, fats, carbohydrates, minerals, trace elements, vitamins), monitoring the body mass index.
Also, preventive measures include annual medical examinations, even if nothing bothers you. After 40 years, it is recommended to conduct an ultrasound examination of the abdominal organs and esophagogastroduodenoscopy annually.
And in no case should you start the disease, if symptoms appear, consult a doctor, and not self-medicate or only traditional medicine.
Questions and answers on the topic "Diseases of the digestive system"
Question:I eat, go to bed and there is bitterness in my throat and mouth.
Answer: Bitterness in the mouth and throat is considered a manifestation of many diseases of various types: from otolaryngological and dental pathologies to disorders in the digestive tract. The most likely cause of a feeling of bitterness in the throat is a violation of the biliary tract. You need an internal consultation with a doctor for examination.
Question:Hello! I'm 52 years old. Somewhere in the year 2000, I was examined by a doctor, the diagnosis was gastritis and a hernia of the esophagus, pancreatitis, cholecystitis, in general, a whole bunch of diseases. There were stones in the gallbladder. I drank various preparations, herbal decoctions, and then stopped my treatment. But for many years I have been suffering from heartburn, there are pains in the stomach and liver. I take various drugs for heartburn, and for a year, after every meal, I feel heaviness in my stomach and after a while I constantly feel sleepy and again frequent heartburn. I almost always save myself with antacids alone. Please tell me why I start to feel sleepy after eating and is it harmful to use Rennie and Almagel A frequently?
Answer: First of all, you need to decide on the stones in the gallbladder. If they are, all your problems will only get worse. An examination by a gastroenterologist is necessary.
To maintain its vital activity, the human body must regularly receive vitamins, trace elements and other nutrients. The digestive system is responsible for this process, the functioning of which depends on the state of many organs. Any failure in their work can disrupt the well-established mechanism, so diseases of the digestive system must be treated in a timely manner.
How does the digestive system work?
When a person sends food to his mouth, he does not think about its further fate. Meanwhile, bypassing the oral cavity, food then passes through the pharynx, esophagus and enters the stomach. In this organ, food is broken down by the action of gastric juice containing hydrochloric acid. Then the primary processed food moves into the initial section of the intestine - the duodenum. Bile is responsible for its splitting in this organ. The final processing of food is carried out by the small intestine, where nutrients are absorbed into the blood. Finally, undigested food residues are sent to the large intestine and, under the influence of its motor functions, are removed from the body. It should be noted that the liver and pancreas are also involved in the process of digestion.
Diseases
If the work of at least one of the above organs is disrupted, the digestive system can no longer function normally. People develop various diseases, and recently this has been happening quite often. There are many diseases of the digestive system. The most common diseases are gastric ulcer and colitis, gastroduodenitis, reflux esophagitis, dyskinesia of the gastrointestinal tract, intestinal obstruction, cholecystitis, pancreatitis, constipation, diarrhea.
Causes
The development of diseases of the digestive system depends on many factors. There are a variety of specific and provoking factors, but doctors identify external and internal causes of these pathologies. First of all, the digestive organs are negatively affected by external causes: the use of poor-quality food, excessive smoking, stressful situations, long-term use of medications.
The internal causes of diseases of the digestive system include autoimmune processes occurring in the human body, malformations of intrauterine development, hereditary predisposition. Sometimes the consequence of the development of any one disease is the presence of two or more predisposing factors.
Symptoms
Pain syndrome of varying severity is the main symptom characteristic of most diseases of the digestive organs. However, pain manifests itself in different ways. It can be aching, or intense and sharp, as with an exacerbation of a stomach ulcer. With pancreatitis, the pain is girdle in nature, gives under the shoulder blades or in the region of the heart. Cholecystitis is accompanied by pain sensations that are localized in the region of the right or left hypochondrium. Food intake plays an important role in the development of pain syndrome. In particular, with peptic ulcer pain occurs mainly on an empty stomach, and with pancreatitis or cholecystitis after eating fatty foods.
Another common symptom that signals problems in the gastrointestinal tract is dyspepsia. It comes in two varieties. Upper dyspepsia is belching, heartburn, loss of appetite, feeling of fullness in the epigastric region, nausea, and vomiting. Lower dyspepsia is manifested in (flatulence), diarrhea or constipation. Manifestations of a particular dyspepsia depend on the specific disease of the digestive organs.
Treatment and prevention
Treatment of diseases of the digestive system consists in taking appropriate medications and following a diet. The main thing is to correctly diagnose the disease that has appeared and try to avoid the transition of the existing disease into a chronic form.
Problems associated with the work of the stomach or intestines cause discomfort in any person. Therefore, the prevention of diseases of the digestive system plays an important role. It is necessary to take care of a balanced diet, be physically active, have a good rest, give up bad habits, and learn how to deal with stress. And upon reaching the age of 40, you should regularly undergo an ultrasound examination of the abdominal organs. Take care of your health!
Causes of diseases of the digestive system
Each disease of the digestive system has its own specific causes, but among them are those that are characteristic of most diseases of the digestive system. All these reasons can be divided into external and internal.
The main ones are, of course, external causes. These, first of all, include food, liquids, medicines:
Unbalanced diet (lack or excess of proteins, fats, carbohydrates) irregular meals (every day at different times), frequent consumption of “aggressive” ingredients (spicy, salty, hot, etc.), the quality of the products themselves (various additives such as preservatives) - all these are the main causes of diseases of the stomach and intestines and often the only cause of such digestive disorders as constipation, diarrhea, increased gas formation and other digestive disorders.
From liquids, first of all, diseases of the digestive system can cause alcohol and its surrogates, carbonated and other drinks containing preservatives and dyes.
And, of course, drugs. Almost all of them, to one degree or another, have a negative effect on the gastric mucosa.
Also, external causes of diseases of the digestive system include microorganisms (viruses, bacteria and protozoa that cause specific and non-specific diseases), worms (flukes, tapeworms, roundworms), which come mainly with food or water.
Smoking, an independent cause of diseases of the stomach and intestines, is rare, but it, together with insufficient oral hygiene, causes diseases of the oral cavity (gingivitis, stomatitis, periodontal disease, lip cancer).
More external causes of diseases of the stomach and intestines include frequent stress, negative emotions, worries for any reason.
The internal causes of diseases of the digestive system include genetic ones - this is a predisposition (that is, the presence of a disease of the digestive system in previous generations), intrauterine development disorders (mutations in the genetic apparatus), autoimmune (when the body for one reason or another begins to attack its organs).
The main symptom in diseases of the digestive system is pain along the digestive tract. This symptom is present in almost every disease of the stomach or intestines, but depending on the disease it will have one or another character. By localization, pain can occur in the right (cholecystitis) or left hypochondrium, girdle (pancreatitis), without specific localization, along the esophagus, often pain can radiate (give) between the shoulder blades (inflammation of the esophagus), to the heart area, etc. Pain can be constant aching or, conversely, at some point very strong (perforation of a stomach ulcer), and eventually disappear, appear on palpation, tapping (cholecystitis). May be associated with meals or not, or when taking a particular food (for example, fatty as in chronic pancreatitis or cholecystitis), or, conversely, when taking some food to pass (for example, dairy in hyperacid gastritis), or occur when you do not eat anything (gastric ulcer). In diseases of the rectum, pain may occur during the act of defecation.
In diseases of the stomach, a symptom such as dyspepsia is often encountered. It can be divided into upper and lower. The upper includes symptoms such as heartburn (a burning sensation behind the sternum or in the upper abdomen with gastritis), belching (sour in stomach diseases, bitter in gallbladder damage), nausea, vomiting (peptic ulcer), a feeling of fullness and pressure in the epigastric areas (with disorders of the evacuation function of the stomach), dysphagia (swallowing disorders in diseases of the esophagus), anorexia (loss of appetite).
Lower dyspepsia includes a feeling of fullness and fullness in the abdomen, flatulence (excessive accumulation of gases in the intestines in violation of the digestive processes), diarrhea (infectious diseases), constipation (irritable bowel syndrome).
Other symptoms include a change in the color of the stool (discoloration in hepatitis, melena - tarry stools in gastric bleeding, "raspberry jelly" in amoebiasis, green in salmonellosis, scarlet blood in the feces).
There are also various changes on the skin, as manifestations of symptoms of various diseases of the digestive system (rash - infectious diseases, spider veins and skin color changes in liver diseases).
Diagnosis of diseases of the digestive system
Prevention of diseases of the stomach and intestines.
The main and most important prevention of diseases of the digestive system, and not only them, is maintaining a healthy lifestyle. This includes the rejection of bad habits (smoking, alcohol, etc.), regular physical education, exclusion of physical inactivity (lead a mobile lifestyle), adherence to work and rest regimes, good sleep, and more. It is very important to have a complete, balanced, regular diet, which ensures the intake of the necessary substances (proteins, fats, carbohydrates, minerals, trace elements, vitamins), monitoring the body mass index.
Also, preventive measures include annual medical examinations, even if nothing bothers you. After 40 years, it is recommended to conduct an ultrasound examination of the abdominal organs and esophagogastroduodenoscopy annually. And in no case should you start the disease, if symptoms appear, consult a doctor, and not self-medicate or only traditional medicine.
Compliance with these measures will help to avoid or timely identify and promptly begin treatment of diseases not only of the digestive system, but of the body as a whole.
Nutrition in diseases of the stomach and intestines.
Nutrition for diseases of the digestive system should be special. In this regard, in our country at one time the Russian Academy of Medical Sciences developed special diets that are suitable not only for diseases of the digestive system, but also for other systems too (diets are indicated in articles on the treatment of certain diseases). A specially selected diet is necessary in the treatment of diseases of the digestive system and is the key to successful treatment.
If normal enteral nutrition is not possible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter the blood immediately, bypassing the digestive system. Indications for the appointment of this food are: complete esophageal dysphagia, intestinal obstruction, acute pancreatitis and a number of other diseases. The main ingredients of parenteral nutrition are amino acids (polyamine, aminofusin), fats (lipofundin), carbohydrates (glucose solutions). Electrolytes and vitamins are also introduced, taking into account the daily needs of the body.
Diseases of the digestive system include:
Diseases of the oral cavity, salivary glands and jaws
Diseases of the esophagus, stomach and duodenum
Diseases of the appendix [vermiform appendix]
Hernias
Noninfectious enteritis and colitis
Other bowel diseases
Diseases of the peritoneum
Liver disease
Diseases of the gallbladder, biliary tract and pancreas
Other diseases of the digestive system
More about diseases of the digestive system:
22.09.2014 10:11
Entry into the body of the proper amount of nutrients is the most important factor in ensuring the normal functioning of a person. The process of intake of vitamins and minerals necessary for the body is provided by the digestive organs. Diseases of the digestive system disrupt the normal supply of nutrients to the body and, as a result, disrupt the functioning of literally all systems and organs. That is why the treatment of diseases affecting the digestive system must be diagnosed and treated in a timely manner.
How are the digestive organs arranged?
Diseases of the digestive system can affect different organs, which anatomy divides into several sections. The process of digestion begins with the pre-processing of food, which is carried out in the oral cavity. From there, food travels down the throat, then into the esophagus, and finally into the main digestive organ, the stomach.
The stomach, consisting of muscles, has in its internal cavity many glands that produce gastric juice and hydrochloric acid. Food broken down by the above liquids begins to move into the duodenum, which is the initial section of the intestine. Here, the digested food is exposed to bile and pancreatic juice.
Of course, a large number of organs contributes to a variety of ailments - diseases of the digestive system are numerous, painful and can significantly reduce the quality of life.
The longest section of the digestive system is the small intestine. In it, food is finally broken down, and nutrients safely penetrate into the blood. The process of digestion in the large intestine is completed - undigested food remains enter it, which are excreted from the body due to the movement of the large intestine.
Diseases of the digestive system can also affect such organs as the liver and pancreas. It is thanks to these two important organs, as well as the salivary and microscopic glands, that the process of digestion occurs. The liver is responsible for the production of bile, and the pancreas is responsible for insulin and the enzymes necessary for the breakdown of proteins, fats, and carbohydrates. The salivary glands are responsible for softening the food eaten.
Only the well-coordinated and clear work of the digestive system allows us to talk about the normal state of the body, the slightest disturbances and failures in this complex biological mechanism provoke certain diseases of the digestive system. We have to admit that today violations in the functioning of the gastrointestinal tract are a very common phenomenon. Improper nutrition, stress, unhealthy food, chronic diseases - all these factors increase the risk of joining the ranks of patients suffering from gastrointestinal diseases. The most common diseases of the digestive system are, first of all, gastritis, dysbacteriosis, duodenitis, peptic ulcer of the duodenum and stomach, reflux esophagitis, erosive bulbitis, food poisoning, intestinal obstruction and many other ailments. Each of the above diseases should be treated competently and in a timely manner. Ignoring the diseases of the digestive system, the patient, due to a violation of the supply of nutrients to the blood, endangers the health of the whole organism.
Causes of diseases of the digestive system
Diseases of the digestive system depend on many specific factors. Doctors, on the other hand, classify all the existing causes that provoke the diseases in question into two categories - internal and external. The fundamental role influencing the occurrence of a particular disease of the digestive system is undoubtedly played by external causes:
. the use of harmful and low-quality food;
. the use of liquids harmful to the body;
. misuse or misuse of medications.
Diseases of the digestive system are often the result of an unbalanced diet. It, in particular, is expressed in excess or, on the contrary, in insufficient consumption of proteins, fats, carbohydrates. Often, diseases of the digestive system become the result of carelessness and a frivolous attitude to the diet and health in general, we are talking, first of all, about the following:
. prolonged neglect of regular nutrition;
. excessive consumption of spicy, salty and very hot foods;
. the presence of preservatives in daily food.
That is why diseases of the digestive system are so dependent on the diet, diet and the quality of the products consumed. The amount of harmful foods in the diet should be minimized, and even better - reduced to zero. At the first symptoms indicating a particular disease of the digestive system, you should immediately review your diet, excluding from it all foods that are undesirable for the body.
No less harm to the digestive system is caused by the thoughtless use of essentially harmful liquids - alcohol and its surrogates, soda, and other drinks with preservatives and dyes.
The next factor that increases the risk of developing any disease of the digestive system is smoking. Stress, experiences are also very common provocateurs of the ailments in question.
Among the internal causes of diseases of the digestive system are:
. malformations of intrauterine development;
. hereditary factors;
. autoimmune processes.
The main symptom that accompanies diseases of the digestive system is the pain that occurs in the digestive tract. The intensity of pain varies, it depends on the specific disease.
1. Cholecystitis. This disease of the digestive system is accompanied by pain spreading along the hypochondrium - right or left.
2. Pancreatitis. It is accompanied by girdle pain of incomprehensible localization. Often the pain radiates between the shoulder blades or in the region of the heart.
3. Gastric ulcer. Perforation of a stomach ulcer causes sharp, intense pain.
The pains can be sharp and aching, weak and intense, they can also depend on the food eaten. So, for example, patients with pancreatitis and cholecystitis, after eating fatty foods, experience unpleasant pain. And with a stomach ulcer, an increase in pain begins if a person does not take food for a long time. But pain in hyperacid gastritis can be removed by drinking milk.
At the first suspicion of the presence of diseases of the gastrointestinal tract, the doctor, conducting a thorough examination, uses the following diagnostic methods:
. palpation;
. auscultation;
. percussion.
The doctor, when diagnosing, is also interested in the patient's complaints in detail, studies the anamnesis.
Usually, diseases of the digestive system require all kinds of laboratory tests:
. general blood analysis;
. blood chemistry;
. stool analysis;
. Analysis of urine.
Also, the following research methods can be used for diagnosis:
. radiation;
. Ultrasound of the abdominal cavity;
. fluoroscopy with contrast agents;
. radiography;
. MRI and CT. 
In addition, some diseases of the digestive system may require the procedures necessary to assess the condition of the internal organs and at the same time obtain material for biopsy. These are the following procedures:
. colonoscopy;
. sigmoidoscopy;
. esophagogastroduodenoscopy;
. laparoscopy.
To examine the stomach in detail, functional tests can be used to obtain information about its motor function and acid secretion. In addition, tests allow you to examine the condition of the small intestine and pancreas.
Treatment of diseases of the digestive system
The scheme according to which treatment is performed depends on the specific ailment diagnosed in the patient. Diseases of the digestive system, like any ailments, require timely and competent treatment in order to prevent, firstly, complications, and, secondly, the transition of an acute stage into a chronic form.
After conducting the necessary research, the doctor, based on the results obtained, draws up a therapy regimen. The most important stage in the treatment of the vast majority of diseases of the gastrointestinal tract is, undoubtedly, a special diet. In the acute form of the disease, the patient can be prescribed parenteral nutrition for a certain time - it provides the supply of all useful substances directly to the blood. Then, the recovering person is prescribed a normal diet, however, foods that can provoke the return of symptoms of the disease are eliminated from the diet.
Diseases of the digestive system are often treated in stages. For example, acute gastritis is treated as follows:
. normalize the excretory functions of the gastrointestinal tract;
. treat the patient with antibiotics;
. prescribe drugs that allow the cells of the gastric mucosa to renew themselves and normalize metabolism.
Diseases of the gastrointestinal tract are often cured in a matter of weeks, and it happens that it takes years to cure them. As a rule, the speed of treatment is affected by the timeliness of diagnosis. So, in particular, it is extremely important to diagnose diseases of the digestive system in children in time - this allows you to minimize the time of treatment.
Often, when gastrointestinal diseases are detected, patients are prescribed complex treatment - it, as a rule, brings the maximum effect. For example, with a stomach ulcer, the patient is first recommended to eliminate the causes that provoke the development of the disease. Then the doctor prescribes a course that includes medication and diet. At the same time, such treatment methods as physiotherapy, magnetotherapy, laser therapy and others can be prescribed.
In order for the treatment to be successful, the patient himself must be aware of the importance of preventing gastrointestinal diseases. He needs, in particular, to change his lifestyle - eat right, get rid of bad habits, observe sleep patterns.
Today, diseases are often diagnosed without any manifestation of clinical symptoms. We are talking about chronic ischemic disease of the digestive system - it is provoked by damage to the visceral arteries of the abdominal aorta. This disease causes a violation of the patency of the above-mentioned arteries. A detailed diagnosis is extremely important here, otherwise the treatment will not be effective. Patients with such a problem are shown a special diet (a ban on foods that cause flatulence; the patient should eat a little, but often). Treatment is carried out by means of antispasmodic drugs, as well as agents that normalize blood circulation.
The lack of effect with conservative therapy forces physicians to resort to surgical intervention. There are two options for operations - low-traumatic and abdominal.
Prevention of gastrointestinal diseases
Diseases of the digestive system require mandatory preventive measures, which consist primarily in organizing proper nutrition and maintaining a healthy lifestyle. To prevent diseases of the gastrointestinal tract, it is necessary to engage in daily physical activity, actively relax and get enough sleep.
A separate preventive measure is regular preventive examinations, which are needed even in the absence of any alarming symptoms. It would be useful to know that people who have crossed the forty-year milestone should have an abdominal ultrasound done annually.
The issue of nutrition is very important in the prevention of gastrointestinal diseases. Nutrition plays almost a key role in the development of the diseases in question. That is why it is so important to eat right - regularly, balanced and varied. Eating should be moderate in nature - overeating is unacceptable. You can not eat until you feel full. You should get up from the table slightly hungry.
For a well-coordinated and accurate work of the digestive system, raw vegetables and fruits should be present in the diet every day. Food must be exceptionally fresh. It should be eaten slowly and chewed thoroughly. You need to eat 4-5 times a day, observing the meal regimen. The diet should not be filled with excessively hot and cold food. Over time, you should stop eating all refined carbohydrates and limit your salt intake.
