Causes of diseases of the digestive system
Each disease of the digestive system has its own specific causes, but among them one can distinguish 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 reasons. These include, first of all, food, liquids, drugs:
Unbalanced nutrition (lack or excess of proteins, fats, carbohydrates) irregular nutrition (every day at different times), frequent eating of “aggressive” components (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 are often the only cause of digestive disorders such as constipation, diarrhea, gas and other digestive disorders.
Among liquids, primarily diseases of the digestive system can cause alcohol and its substitutes, carbonated and other drinks containing preservatives and dyes.
And, of course, medicines. 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 stomach and intestinal diseases, is rare, but together with insufficient oral hygiene, it 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), disorders of intrauterine development (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, encircling (pancreatitis), without a specific localization, along the esophagus, often pain can radiate (give) between the shoulder blades (inflammation of the esophagus), to the region of the heart, etc. Pain can be constant aching or, conversely, at some point very strong (perforation of a stomach ulcer), and eventually pass, appear on palpation, tapping (cholecystitis). It may be associated with meals or not, or with the intake of a specific food (for example, fatty as in chronic pancreatitis or cholecystitis), or, conversely, while taking some food to pass (for example, milk with hyperacid gastritis), or occur when you do not eat anything (stomach ulcer). In diseases of the rectum, pain can occur during the act of defecation.
With diseases of the stomach, a symptom such as dyspepsia is often found. It can be divided into top and bottom. The top includes symptoms such as heartburn (a burning sensation behind the breastbone or in the upper abdomen with gastritis), belching (sour with stomach diseases, bitter with damage to the gallbladder), 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 gas in the intestines in case of digestive disorders), diarrhea (infectious diseases), constipation (irritable bowel syndrome).
Other symptoms include a change in stool color (discoloration with hepatitis, melena - tarry stools with stomach bleeding, “raspberry jelly” with amoebiasis, green with salmonellosis, red blood in the stool).
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 changes in skin color 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 to maintain a healthy lifestyle. This includes giving up bad habits (smoking, alcohol and others), regular physical education, exclusion of physical inactivity (leading an active lifestyle), compliance with 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 annual ultrasound examination of the abdominal organs and esophagogastroduodenoscopy. And in no case should the disease be started, if symptoms appear, consult a doctor, and not self-medicate or only traditional medicine.
Compliance with these measures will help to avoid or identify and timely begin treatment of diseases not only of the digestive system, but also of the body as a whole.
Nutrition for 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 the articles on the treatment of certain diseases). A specially selected diet is essential in the treatment of diseases of the digestive system and is the key to successful treatment.
If usual enteral nutrition is impossible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter the blood immediately, I bypass 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, aminofusine), fats (lipofundin), carbohydrates (glucose solutions). Also, electrolytes and vitamins are introduced, taking into account the daily needs of the body.
Diseases of the digestive system include:
Diseases of the mouth, salivary glands and jaws
Diseases of the esophagus, stomach and duodenum
Diseases of the appendix [appendix]
Hernia
Non-infectious 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:
Diseases of the digestive system are determined by many specific factors. Nevertheless, doctors identify a number of reasons that are characteristic of most ailments of this type. They are divided into external and internal.
External reasons play a decisive role in this case. Basically, these are the effects on the body of poor-quality food, liquids, medications.
Diseases of the digestive system can be a consequence of an unbalanced diet, in which there is an excess or lack of intake of fats, proteins, carbohydrates. Sometimes diseases of these organs are also manifested as a result of prolonged irregular nutrition, too frequent inclusion in the diet of salty, very spicy, hot dishes that negatively affect the state of the digestive system. The presence of preservatives in those foods that a person eats every day can provoke symptoms of gastrointestinal diseases. That is why the prevention of this type of disease in children and adults provides for the minimum amount of such foods in the diet. And at the slightest manifestation of symptoms of diseases of the digestive system, the list of unwanted foods increases.
Some liquids also have a negative effect. Ailments of the digestive system are provoked, mainly, by alcoholic beverages and their surrogates, soda and other drinks containing a large amount of dyes and preservatives.
The provoking factor is tobacco smoking, as well as regular stressful situations and experiences.
Internal causes of diseases of the digestive system are genetic factors, intrauterine malformations, the development of autoimmune processes in the body.
Symptoms and diagnosis of diseases of the digestive system
With the development of diseases of the digestive system in a person, the main symptom that indicates their manifestation is pain sensations of varying intensity, which arise along the digestive tract. A similar symptom is determined in almost all diseases, however, its nature, depending on what kind of disease of the digestive system develops, may differ.
In particular, with cholecystitis, pain develops in the hypochondrium, left or right. Pancreatitis is manifested by girdle pain that does not have precise localization, sometimes it can radiate to the region of the heart or between the shoulder blades. In some diseases, the pain is aching, in other cases, for example, with perforation of a stomach ulcer, the pain is very sharp and intense. Sometimes the pain is related to food intake. Patients with cholecystitis or pancreatitis suffer after taking fatty foods. With stomach ulcers, the pain increases when a person does not eat for a long time. With hyperacid gastritis, the pain, on the contrary, subsides after the patient has consumed milk.
Dyspepsia is one of the most common symptoms of gastrointestinal diseases. Doctors define upper and lower dyspepsia. Upper dyspepsia manifests itself in a patient with heartburn, constant belching, recurrent vomiting and nausea. There is also discomfort and a feeling of overcrowding in the epigastric region, dysphagia, loss of appetite.
The manifestations of lower dyspepsia are a feeling of fullness inside the abdomen, flatulence, constipation, diarrhea. In addition, with diseases of the digestive system, a person may change the color of the stool, develop rashes and other changes on the skin. More precisely, you can talk about the symptoms when considering a specific disease of the human digestive system.
Initially, if you suspect the development of diseases of the digestive system, the doctor will certainly 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.
Usually, with diseases of this type, the patient is assigned to conduct laboratory tests (general and biochemical blood tests, general urine analysis, feces analysis). Radiation research methods are also widely practiced in the diagnostic process. An informative method is an ultrasound examination of the abdominal organs, radiography, fluoroscopy using contrast agents, CT, MRI. Depending on the disease, procedures can also be prescribed that allow you to assess the state of the internal organs of the digestive system and at the same time obtain material for biopsy. These are colonoscopy, esophagogastroduodenoscopy, sigmoidoscopy, laparoscopy.
For the purpose of examining 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 and small intestine.
Diseases of the digestive system are a common pathology in childhood. The prevalence of these diseases has no regional characteristics and currently exceeds 100 cases per 1000 child population. 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. Revealing the role Helicobacter pylori in the etiology and pathogenesis of chronic gastritis, gastroduodenitis and peptic ulcer of the stomach and duodenum made it possible to develop the most rational methods of treating these diseases. In children, the peak incidence of diseases of the digestive system occurs at 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 entering (received) into the stomach cavity.
Etiology
The development of acute gastritis can be caused by 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 corrosive 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 digestion processes, the secretion of enzymes that make up the gastric juice. With foodborne infection (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 several 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. - Child's anxiety, general malaise, profuse salivation, nausea, loss of appetite, feeling of "fullness" in the epigastric region.
Chills are possible, then subfebrile fever.
Subsequently, abdominal pain intensifies, repeated vomiting occurs, in the vomit - the remains of food eaten 4-6 hours ago.
Objectively, pallor of the skin, lining of the tongue with white-yellow plaque, flatulence, and palpation of the abdomen - pain in the epigastric region are noted.
Diarrhea is possible.
The 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 stomach injuries or as a complication of peptic ulcer disease. It is characterized by high fever, severe abdominal pain, rapid deterioration of the child's condition, repeated vomiting, sometimes mixed with pus. In the blood, neutrophilic leukocytosis is detected with a shift of the leukocyte formula to the left, 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. Shown abundant frequent drinking in small portions (tea, a mixture of 0.9% sodium chloride solution with 5% glucose solution). After 12 hours, a fractional dietary meal is prescribed: mucous pureed soups, low-fat broths, crackers, jelly, porridge. 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 a warm 0.5-1% sodium bicarbonate solution or 0.9% sodium chloride solution. With toxic-infectious gastritis, anti-inflammatory therapy is prescribed, enzymes
(pancreatin), antispasmodic drugs (papaverine, drotaverine). Phlegmonous gastritis is treated in a surgical hospital.
Prophylaxis
It is necessary to properly organize the child's nutrition in accordance with his age, avoid overeating, avoid fatty, fried and spicy foods. When taking certain medications (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 the extreme prevalence of this disease, which increases with age. It should be noted that in children, chronic gastritis only in 10-15% of cases proceeds as an isolated disease. 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 a balanced diet (both quantitatively and qualitatively): non-observance of the food intake, constant consumption of dry, poorly chewed, too hot or cold, fried, spicy foods, etc. Chronic gastritis can develop with prolonged use of certain drugs (for example, glucocorticoids, NSAIDs, antibiotics, sulfonamides). In recent years, they attach importance to hereditary predisposition, since chronic gastritis is more often detected in children with a family history of gastrointestinal diseases.
A significant role in the development of chronic gastritis is played by Helicobacter pylori. This microorganism is often detected in others.
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 the gastric juice access to the tissue, 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 eating, at night, often associated with an error in the diet. Also characteristic are decreased appetite, heartburn, belching with air or sour, nausea, and a tendency to constipation. When examining the patient, tenderness is determined by palpation 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, physical examination data and special research methods. Of the latter, FEGDS is especially informative, which makes it possible 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 assess the secretory, acid- and enzyme-forming function of the stomach. As an irritant to the glandular apparatus, pentagastrin, a 0.1% solution of histamine, is used. At the same time, the pH and proteolytic activity of gastric juice, the amount of hydrochloric acid released (debit-hour) are assessed.
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 chronic gastritis therapy are listed below.
In case of severe exacerbation, inpatient treatment is necessary.
Diet: food should be mechanically and chemically sparing (slimy soups, mashed vegetables and meat, jelly, cereals, grated cottage cheese). Everything should be consumed warm every 3 hours (with the exception of the night break).
With increased gastric secretion, antisecretory drugs are prescribed - blockers of H 2 histamine receptors (for example, ranitidine). An inhibitor of H +, K + -ATPase omeprazole is prescribed for 4-5 weeks.
Given the frequent presence Helicobacter pylori, the so-called three-component therapy is prescribed: 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) are used, as well as metoclopramide and domperidone.
Shown are polyenzyme drugs (for example, pancreatin - "Pancitrate", "Creon").
Outside of exacerbation, patients need spa 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, in contrast to adults, isolated lesions of the stomach or duodenum are observed relatively rarely - in 10-15% of cases. The combined lesion of these departments is much more often observed. 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. Psycho-traumatic 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. Long-term use of drugs (glucocorticoids, NSAIDs), food allergies and other factors that reduce local specific and nonspecific mucosal protection are also important.
One of the main reasons for the development 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. The foci of gastric metaplasia are unstable to the effects of the contents
the 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 mucous membrane of the duodenum. Under these conditions, the role of acid-peptic damage to the mucous membrane in the occurrence of evacuator-motor disorders and a decrease in intraduodenal pH increases. 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, 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 the synthesis of secretin and saturation with bicarbonates of pancreatic juice, which, in turn, reduces alkalization 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;
On the basis of 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 manifestations caused by gastroduodenitis itself from symptoms caused by concomitant pathology.
Gastroduodenitis in the exacerbation phase is manifested by aching cramping pains in the epigastric region, arising 1-2 hours after eating and often radiating to the hypochondrium (usually the right) and the umbilical region. Eating food or antacids can relieve or control pain. Pain syndrome may be accompanied by a feeling
schenia of severity, distention 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 mixed with 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 a white and yellowish-white coating, often with teeth imprints on the lateral surface. On palpation of the abdomen, tenderness is determined in the pyloroduodenal region, less often around the navel, in the epigastric region and hypochondria. Mendel's symptom is characteristic. Many patients have symptoms of Ortner and Kera.
In children with chronic duodenitis, autonomic and psychoemotional disorders are often noted: periodic headaches, dizziness, sleep disturbances, fatigue, which is associated with a violation of the endocrine function of the duodenum. Vegetative disorders can manifest themselves as a clinical picture of dumping syndrome: weakness, sweating, drowsiness, increased intestinal motility, arising 2-3 hours after eating. With a long break between meals, there may be signs of hypoglycemia in the form of muscle weakness, tremors in the body, and a sharp increase in appetite.
Chronic gastroduodenitis has a cyclical course: the exacerbation phase is replaced by remission. Exacerbations more 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 disorders of the general condition. Spontaneous pain disappears on average after 7-10 days, palpation pain persists for 2-3 weeks. In general, the 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 stage of remission, neither clinical, nor endoscopic, nor morphological manifestations of inflammation in the duodenum are found.
Diagnostics
The diagnosis of chronic gastroduodenitis is based on clinical observation data, study of the functional state of the duodenum, endoscopic and histological (mucosal biopsy) studies.
With functional duodenal intubation, changes characteristic of duodenitis are revealed: dystonia of the sphincter of Oddi, pain and nausea at the time of the introduction of the irritant into the intestine, backflow of magnesium sulfate solution through the probe due to duodenal spasm. Microscopy of the duodenal contents reveals a 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 for acidopeptic duodenitis (bulbitis) are usually increased, and when duodenitis is combined with atrophic gastritis and enteritis, they are lowered.
The most informative method for diagnosing gastroduodenitis is FEGDS (see section "Chronic gastritis").
X-ray examination of the duodenum is not of great importance in the diagnosis of chronic duodenitis, but it allows one to identify various motor-evacuation disorders accompanying the disease or causing it.
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 shown for 7 to 8 days.
Diet is of great importance. 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, H2-histamine receptor blockers are recommended, as well as omeprazole for 3-4 weeks.
According to the indications, the means that regulate motility are used (metoclopramide, domperidone, drotaverine).
In the process of rehabilitation, physiotherapy, exercise therapy, and spa treatment are prescribed.
Prophylaxis
With a disease of the gastroduodenal zone, it is very important to observe 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 patient's quality of life, his ability to work.
Peptic ulcer and duodenal ulcer
Peptic ulcer is a chronic recurrent disease, accompanied by the formation of a peptic ulcer in the stomach and / or duodenum, caused by an imbalance between the factors of aggression and protection of the gastroduodenal zone.
In recent years, cases of peptic ulcer disease in children have become more frequent, at present the disease is recorded 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, gastric ulcer and duodenal ulcer in children is a serious problem in clinical medicine.
ETIOLOGY
The disease develops as a result of exposure to the body of several adverse factors, including hereditary predisposition and emotional overload in combination with permanent alimentary inaccuracies (irregular eating, abuse of spicy foods, dry food, etc.). The main reasons are considered to be a disorder of the nervous and hormonal mechanisms of the stomach and duodenum, an imbalance between the factors of aggression (hydrochloric acid, pepsins, pancreatic enzymes, bile acids) and protective factors (mucus, bicarbonates, cell regeneration, synthesis of PG). Ulceration is associated with prolonged hyperchloride hydria and peptic proteolysis caused by vagotonia, hypergastrinemia and hyperplasia of the main glands of the stomach, as well as with gastroduodenal dysmotility and prolonged acidification of the anthrobulbar zone.
An important role in the development of peptic ulcer disease is played by 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 played by the central nervous system, which has a double 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 disrupting the balance between protective and aggressive factors, contributing to the formation of an ulcer.
CLASSIFICATION
The classification of gastric ulcer and duodenal ulcer is given in table. 16-3.
Table 16-3.Classification of peptic ulcer disease 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 have night pains. A clear "Moynigam" rhythm of pain is noted: hunger-pain-food intake-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 roller, with a bottom covered with fibrin overlays of gray-yellow or white color.
In the stomach, ulcers are located mainly in the pyloroantral 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 deformity of the bulb.
II stage (beginning of epithelialization of the ulcer)
Most children persist with late epigastric pain, but they occur mainly during the day, and after eating, persistent relief comes. The pains become more dull, aching. The abdomen is easily accessible by superficial palpation, but with deep palpation, muscle protection is preserved. Dyspeptic manifestations are less pronounced.
At endoscopic examination, the hyperemia of the mucous membrane is less pronounced, the edema around the ulcer defect is reduced and the inflammatory shaft disappears. The bottom of the defect begins to clear of fibrin, the folds converge to the ulcer, which reflects the healing process.
III stage (ulcer healing)
Pain in this stage persists only on an empty stomach; at night, their equivalent can be a feeling of hunger. The abdomen becomes accessible to deep palpation, the pain 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, which have various shapes - linear, circular, stellate. Possible deformation of the wall of the stomach or duodenum. Signs of an inflammatory process in the mucous membrane of the stomach and duodenum, as well as motor-evacuation disorders, remain.
IV stage (remission)
The general condition is satisfactory. 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 disease are recorded in 8-9% of children. In boys, complications occur 2 times more often than in girls.
In the structure of complications, bleeding dominates, and with a duodenal ulcer, they develop much more often than with a stomach ulcer.
Ulcer perforation in children often occurs with stomach ulcers. This complication is accompanied by acute "dagger" pain in the epigastric region, often a state of shock develops.
Characterized by the disappearance of hepatic dullness with abdominal percussion due to the ingress of air into the abdominal cavity.
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 onset pain radiating to the back and repeated vomiting. The diagnosis is clarified using FEGDS.
DIAGNOSTICS
The diagnosis of peptic ulcer disease, in addition to the above clinical endoscopic justification, is confirmed by the following methods:
Fractional probing of the stomach with determination of gastric acidity, 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 contrasting with a barium mixture. Direct signs of an ulcer are a symptom of a niche and a typical deformation of the duodenal bulb, indirect ones are pyloric spasm, dyskinesia of the duodenal bulb, gastric hypersecretion, etc.
Revealing Helicobacter pylori.
Repeated determination of occult blood in feces (Gregersen reaction).
TREATMENT
Treatment of patients with gastric ulcer and duodenal ulcer should be complex, it is carried out in stages, taking into account the clinical and endoscopic phase of the disease.
Stage I - exacerbation phase. Inpatient treatment.
Stage II - the phase of subsidence of manifestations, the beginning of clinical remission. Dispensary observation and seasonal prophylaxis.
Stage III - the phase of complete clinical and endoscopic remission. Sanatorium treatment.
Stage I
Conservative treatment of peptic ulcer disease begins immediately after the diagnosis. In many patients, ulcers heal 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 (in remission). Meals should be fractional (5-6 times a day).
Reducing the damaging effect of hydrochloric acid and pepsins.
Non-absorbable antacids: algeldrat + magnesium hydroxide, aluminum phosphate, simaldrat, 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 disorders of digestion and absorption - polyenzyme drugs (pancreatin).
II stage
The treatment is carried out by the local pediatrician. He examines the child once every 2 months and carries out 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 at drinking balneological resorts (Zheleznovodsk, Essentuki).
PREVENTION
Exacerbations of peptic ulcer disease are usually seasonal, therefore, secondary prophylaxis requires regular examination by a pediatrician and the appointment of preventive therapy (antacids), if necessary, a diet, limiting school load (1-2 fasting days per week in the form of home education). Providing a favorable psychoemotional 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 observation of the patient by a pediatric gastroenterologist, adherence to the rules of seasonal prevention of exacerbations, hospitalization in a specialized department during exacerbation significantly improve the prognosis of the disease.
DISEASES OF THE SMALL AND LARGE INTESTINAL
Chronic non-infectious diseases of the small and large intestine develop quite often, especially in preschool children. They represent a serious medical and social problem due to their high prevalence, difficulties in diagnosis and the severity of the consequences that disrupt the growth and development of the child. Bowel 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 are often simultaneously involved in the pathological process (enterocolitis). 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 either primary or secondary.
Great importance is attached to alimentary factors: dry food, overeating, excess carbohydrates and fats in food with a lack of protein, vitamins and microelements, early transfer to artificial feeding, etc.
In recent years, etiological factors such as exposure to poisons, salts of heavy metals (lead, phosphorus, cadmium, etc.), drugs (salicylates, glucocorticoids, NSAIDs, immunosuppressants, cytostatics, some anti-
biotics, especially with prolonged use), ionizing radiation (for example, during X-ray therapy).
The onset of diseases of the small intestine is facilitated by congenital and acquired enzymopathies, intestinal malformations, impaired immunity (both local and general), food allergies, surgical interventions on the intestines, diseases of other digestive organs (primarily of 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 lack of immune and compensatory-adaptive reactions. The enzymatic activity of the intestinal glands is disrupted, the passage of the chyme is accelerated or slowed down, conditions are created for the proliferation of microbial flora, the digestion and absorption of basic nutrients are disrupted.
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 concomitant pathology. There are two main clinical syndromes - local and general.
Local intestinal (enteral) syndrome is caused by a violation of parietal (membrane) and cavity digestion. They observe flatulence, rumbling, abdominal pain, and diarrhea. The bowel movements are usually copious, with bits of undigested food and mucus. Alternating diarrhea and constipation are possible. 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 "pseudo-ascites" is possible. Intestinal symptoms are more likely to occur with the intake of milk, raw vegetables and fruits, and confectionery.
General intestinal (enteral) syndrome is associated with water-electrolyte imbalance, disorders of absorption of macro- and micronutrients and involvement of other organs in the pathological process (malabsorption syndrome). Characterized by: 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 fragility of bones, seizures. The severity of the general and local enteric syndromes determines the severity of the disease.
Diagnostics is based on data from anamnesis, clinical manifestations, results of laboratory and instrumental examination methods. Differentiated carbohydrate loads with mono- and disaccharides, a test with d-xylose are carried out. Endoscopy with targeted biopsy and subsequent histological examination of the biopsy is also informative. The coprogram reveals creatorrhea, steatorrhea, amilorrhea.
Differential diagnosis is carried out with the most frequently developing hereditary and acquired diseases occurring with malabsorption syndrome - acute enteritis, intestinal cystic fibrosis, gastrointestinal food allergy, celiac disease, disaccharidase deficiency, etc.
Treatment
See the Chronic enterocolitis section.
Chronic enterocolitis
Chronic enterocolitis is a polyetiological inflammatory dystrophic disease in which the small and large intestines are simultaneously affected.
Etiology
The disease occurs most often after suffering from acute intestinal infections (salmonellosis, dysentery, escherichiosis, typhoid fever, viral diarrhea), helminthiasis, diseases caused by protozoa, errors in the dietary regime (prolonged irregular, insufficient or excessive nutrition), food allergic reactions. The development of the disease is facilitated by congenital and acquired enzymopathies, defects in immunity, diseases of the stomach, liver, bile ducts and pancreas, anomalies in the development of the intestines, dysbiosis, vitamin deficiency, neurogenic, hormonal disorders, radiation exposure, irrational use of drugs, in particular antibiotics, etc. ...
Pathogenesis
The pathogenesis is not fully understood. It is believed, for example, that infectious agents can cause disruption of the integrity of the cells of the tissues of the digestive tract, contributing to their destruction or morphological metaplasia. As a result, Ar, genetically alien to the body, are formed, causing the development of autoimmune reactions. The accumulation of clones of cytotoxic lymphocytes and the production of AT, directed against the Ag structures of the autologous tissues of the digestive tract, take place. They attach importance to the deficiency of secretory IgA, which prevents the invasion of bacteria and allergens. A change in the normal intestinal microflora contributes to the formation of chronic enterocolitis, secondarily increasing the permeability of the intestinal mucosa for microbial allergens. On the other hand, dysbiosis 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: the 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 may vary. 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, worse before defecation, when running, jumping, driving, etc. Dull pulling pains are more characteristic of the defeat of the small intestine, intense - the large intestine. Equivalents of pain: loose stools after eating or, especially in young children, refusal to eat, taste selectivity.
Another most important symptom of chronic enterocolitis is stool disorder in the form of alternating diarrhea (with a predominant lesion of the small intestine) and constipation (with lesions of the large intestine). Frequent urge to defecate prevails (5-7 times a day) with small portions of feces of different consistency (liquid with an admixture of undigested food, with mucus; gray, shiny, foamy, foul-smelling - with a predominance of putrefactive processes). Often there is a "sheep" or ribbon-like feces. 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 stool.
Permanent symptoms of chronic enterocolitis in children also include bloating and a feeling of bloating in the abdomen, rumbling and transfusions in the intestines, increased passing of gas, etc. Sometimes the clinical picture of the disease is dominated by the psychovegetative syndrome: weakness, rapid fatigue, poor sleep, irritability, and headache develop. Complaints about intestinal dysfunction fade into the background. With a prolonged course of the disease, there is a delay in the growth of body weight, less often - growth, anemia, signs of hypovitaminosis, metabolic disorders (protein, mineral).
Diagnostics and differential diagnostics
Chronic enterocolitis is diagnosed on the basis of anamnestic data, clinical presentation (long-term intestinal dysfunction, accompanied by the development of dystrophy), laboratory examination results (anemia, hypo- and dysproteinemia, hypoalbuminemia, decreased concentration of cholesterol, total lipids, β-lipoproteins, calcium, potassium, sodium in blood serum, detection in feces of mucus, leukocytes, steatorrhea, creatorrhea, amilorrhea), the results of instrumental research methods (sigmoidoscopy, colonofibroscopy, X-ray and morphological studies).
Chronic enterocolitis should be differentiated from lingering dysentery (see the chapter “Acute intestinal infections”), congenital enzymopathies [cystic fibrosis, celiac disease, disaccharidase deficiency, exudative enteropathy syndrome (see section “Congenital enzymopathies and other exudative”) and enteropathies.
Treatment
Treatment for chronic enteritis and chronic enterocolitis is aimed at restoring disturbed intestinal functions and preventing exacerbations of the disease. The basis of the ongoing therapeutic measures is nutritional therapy (appoint table No. 4 according to Pevzner). Also prescribed multivitamins, enzyme preparations (pancreatin), pre- and probiotics [bifidobacteria bifidum + activated carbon ("Probifor"), "Linex", lactobacilli acidophilus + kefir fungi ("Acipol"), "Khilak-forte" (enterosorbents) dioctahedral smectite), prokinetics (trimebutin, loperamide, mebeverine, etc.). According to strict indications, antibacterial drugs are prescribed: "Intetrix", nitrofurans, nalidixic acid, metronidazole, etc. They use herbal medicine, symptomatic agents, physiotherapy, exercise therapy. Sanatorium treatment is indicated no earlier than 3-6 months after an 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 unified 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 the act of defecation) and dyspeptic disorders (flatulence , rumbling, diarrhea, constipation or their alternation, feeling of incomplete emptying of the intestines, 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 attributed to neuropsychic factors. It has been established that with irritable bowel syndrome, the evacuation function of both the small and large intestines is impaired. Changes in the motor function of the intestine may be associated with the fact that in these patients the sensitivity of the receptors of the intestinal wall to stretching is increased, as a result of which pain and dyspeptic disorders occur in them with a lower threshold of excitability than in healthy people. A certain role in the formation of irritable bowel syndrome in children is played by dietary habits, in particular, insufficient intake of vegetable fiber. Significant importance is also attached to the loss of the conditioned reflex to the act of defecation and the asynergy of the muscular structures of the pelvic diaphragm, leading to disturbances in the evacuation function of the intestine.
Irritable bowel syndrome can develop secondarily in other diseases of the digestive system: gastritis, duodenitis, gastric ulcer and duodenal ulcer, pancreatitis, etc. A certain role can be played by the transferred AEI, gynecological diseases in girls, and pathology of the urinary system.
Clinical picture
Depending on the clinical manifestations, there are 3 variants of irritable bowel syndrome: 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 residues, usually 4 times a day, more often in the morning, after breakfast, especially with emotional stress. Sometimes there is an imperative urge 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 accompanied by prolonged straining, a feeling of incomplete emptying of the intestines, a change in the shape and nature of the stool (hard, dry, such as sheep's, etc.). In some children, prolonged constipation is replaced by diarrhea, followed by a recurrence of constipation.
In patients with the third variant of irritable bowel syndrome, cramping or dull, pressing, bursting pains in the abdomen, combined with swelling, prevail. Pain occurs or intensifies after eating, during stress, before defecation, and disappears after passing gas.
In addition to local manifestations, patients have frequent headaches, a feeling of a lump in the throat when swallowing, vasomotor reactions, nausea, heartburn, belching, heaviness in the epigastric region, etc. The hallmark 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.
Diagnostics and differential diagnostics
The 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), syndrome of impaired intestinal absorption (lactase deficiency, celiac disease, etc.), gastrointestinal allergy, acute and chronic constipation, etc.
Treatment
Treatment of patients with irritable bowel syndrome is based on the normalization of the regimen and nature of the diet, 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. Cisapride, loperamide, pinaverium bromide, mebeverine, etc. are the drugs of choice.
In irritable bowel syndrome with diarrhea, dioctahedral smectite, which has pronounced adsorption and cytoprotective properties, has a positive effect. They also use pre- and probiotics to restore normal microflora [Enterol, bifidobacteria bifidum, bifidobacteria bifidum + activated carbon (“Probifor”), lactobacilli acidophilus + kefir fungi (“Acipol”), “Khilak-forte”, “Linex” etc.], antibacterial agents ("Intetrix", nifuroxazide, furazolidone, metronidazole, etc.), herbal preparations [lingonberry leaves + St. John's wort grass + a series of tripartite grass + rosehip fruit ("Brusniver"), calendula flowers + chamomile flowers + licorice roots + series of grass + sage leaves + eucalyptus leaf ("Elekasol")], reducing bloating, rumbling in the stomach, the amount of mucus in the stool.
In case of irritable bowel syndrome, proceeding 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 supervision of the patient by a pediatrician and a neuropsychiatrist.
Forecast
The prognosis is favorable.
Congenital enzymopathies and exudative enteropathy
The most common congenital gastrointestinal enzymopathies are celiac disease and disaccharidase deficiency.
PATHOGENESIS AND CLINICAL PICTURE Celiac disease
Gluten enteropathy is a congenital disease caused by a deficiency 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 copious foamy stools. Then anorexia, vomiting, symptoms of dehydration, a picture of false ascites join. Severe dystrophy develops.
An X-ray examination of the intestines with the addition of flour to a barium suspension reveals a sharp hypersecretion, accelerated peristalsis, a change in the intestinal tone 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 breastfeeding, sucrose intolerance - from the moment sugar (sweet water, supplementary food) is introduced into the baby's diet. Characterized by flatulence, watery stools with a sour odor, the gradual development of persistent hypotrophy. The stool, as a rule, quickly normalizes after the abolition of the corresponding disaccharide.
Exudative enteropathy syndrome
It is characterized by the loss of a large amount of blood plasma proteins through the intestinal wall. As a result, children develop persistent hypoproteinemia and a tendency to edema. 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 during morphological examination. Secondary syndrome of exudative enteropathy is observed in celiac disease, cystic fibrosis, Crohn's disease, ulcerative colitis, liver cirrhosis and a number of other diseases.
DIAGNOSTICS
Diagnostics is based on a set of clinical and laboratory data, the results of endoscopic and morphological studies. In diagnostics, stress tests are used (for example, a 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 DIAGNOSTICS
When carrying out differential diagnostics, it is important to take into account the patient's age at 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
The organization of individual therapeutic nutrition is of decisive importance, in particular, the appointment of elimination diets, depending on the period of the illness, 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 limited milk. In case of disaccharidase deficiency, it is necessary to exclude the use of sugar, starch or fresh milk (with lactose intolerance). With exudative enteropathy, a protein-rich diet with limited fat is prescribed (medium-chain triglycerides are used). According to indications in severe cases, parenteral nutrition is prescribed. Shown are enzyme preparations, probiotics, vitamins, symptomatic therapy.
FORECAST
The prognosis with strict adherence to 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, medicinal herbs, probiotics, and also
neral water (in case of a tendency to diarrhea, Essentuki 4 is prescribed, warmed up to 40-50? C); therapeutic exercises and abdominal massage; protecting the child from intercurrent diseases and injuries; the exception of swimming in open water.
With chronic enteritis and chronic enterocolitis in the period of stable remission, physical education and preventive vaccinations are allowed.
The supervision 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 an exacerbation. The sanatorium complex includes: a gentle 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 intestinal lesions 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 diagnosed in children of all age groups. The peak incidence occurs at 13-20 years. Among the cases, the ratio of boys and girls is 1: 1.1.
Etiology and pathogenesis
The etiology and pathogenesis of the disease are unknown. The role of infection (mycobacteria, viruses), toxins, food, and some drugs, which are considered as the starting point for the development of acute inflammation, are discussed. Great importance is attached to immunological, dysbiotic, genetic factors. A relationship has been established between the HLA histocompatibility system and Crohn's disease, in which the DR1 and DRw5 loci are often identified.
Clinical picture
The clinical picture of the disease is very diverse. The onset of the disease, as a rule, is gradual, for many years 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 lesion in the small intestine: the higher it is, the more frequent the stool, and, accordingly, the more severe the disease. Lesion of the small intestine is accompanied by malabsorption syndrome. Blood impurities periodically appear in the stool.
Abdominal pain is a mandatory symptom for all children. The intensity of pain varies from minor (at the onset 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, vomiting. In the later stages, the pain is very intense, accompanied by bloating.
General symptoms of the disease: general weakness, weight loss, fever. With significant damage to the small intestine, the absorption and metabolism of proteins, carbohydrates, fats, vitamin B 12, folic acid, electrolytes, iron, magnesium, zinc, etc. are impaired. Hypoproteinemia is clinically manifested by edema. Growth and sexual development retardation is 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, bowel perforation, and peritonitis. Possible intestinal obstruction, acute toxic dilatation of the colon.
A general blood test reveals anemia (decreased erythrocytes, Hb, hematocrit), reticulocytosis, leukocytosis, increased 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 length of the inflammatory process. Endoscopically, 3 phases of the disease are distinguished: infiltration, ulcers, cracks, scarring.
In the phase of infiltration (the process is localized in the submucosa), the mucous membrane looks like a "quilt" with a matte surface, the vascular pattern is not visible. Subsequently, erosions of the aft type appear with individual superficial ulcerations and fibrinous overlays.
In the phase of ulcers-cracks, individual or multiple deep longitudinal ulcerative defects are revealed, affecting the muscular layer of the intestinal wall. The intersection of cracks gives the mucosa a "cobblestone" appearance. 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.
Typical X-ray 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 with preservation of haustration along the lower one. At the stage of ulcers-cracks - a kind of "cobblestone pavement".
Diagnostics and differential diagnostics
The diagnosis is made 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 protracted 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 diseases *
* According to Kanshina O.A., 1999.
Treatment
The regime in the period of exacerbation is bed, then - sparing. Health food - a table? 4 according to Pevzner. The nature of the diet largely depends on the location and extent of the intestinal lesion, the phase 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 lesions, 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 (for example, loperamide), 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, electrolytes are performed. According to indications, surgical treatment is performed - removal of the affected parts of the intestine, excision of fistulas, anastomosis to restore patency.
Prophylaxis
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. Achievement of long-term clinical remission is possible.
Nonspecific ulcerative colitis
Ulcerative colitis is a chronic inflammatory dystrophic disease of the colon with a recurrent or continuous course, local and systemic complications.
Ulcerative colitis is widespread mainly among the population of industrially developed countries (widespread
number among adults - 40-117: 100,000). In children, it develops relatively rarely, accounting for 8-15% of the incidence of adults. In the past 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 sex distribution is 1: 1, with boys being more likely to get sick at an early age, and girls in adolescence.
Etiology and pathogenesis
Despite many years of study, the etiology of the disease remains unclear. Among the various theories of the development of ulcerative colitis, the most widespread are infectious, psychogenic and immunological. The search for any single cause of the ulcerative process in the colon is still unsuccessful. As etiological factors, viruses, bacteria, toxins, and 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, unfavorable environmental factors, psychological stress, iatrogenic drug effects. In ulcerative colitis, a cascade of self-sustaining pathological processes occurs: first, nonspecific, then autoimmune, damaging target organs.
Classification
The modern classification of ulcerative colitis takes into account the length of the process, the severity of clinical symptoms, the presence of relapses, 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 flow with stools, and abdominal pain. In almost half of cases, the disease begins gradually. With mild colitis, single streaks of blood in the stool are noticeable, with severe colitis, a significant admixture of it. Sometimes the stool takes on the appearance of a fetid, liquid, bloody mass. Most patients develop diarrhea, stool frequency varies from 4-8 to 16-20 times or more per day. In addition to blood, loose stools contain a large amount of mucus and pus. Bloody diarrhea is accompanied and sometimes preceded by abdominal pain - more often during meals or before a bowel movement. Cramping pains, localized in the lower abdomen, in the left iliac region or around the navel. Occasionally, a dysentery-like onset of the disease develops. An increase in body temperature (usually not higher than 38 ° C), decreased appetite, general weakness, weight loss, anemia, and delayed puberty are very characteristic of severe ulcerative colitis.
Complicationsulcerative colitis are systemic and local.
Systemic complications are manifold: arthritis and arthralgias, 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 are rare in children. These include: profuse intestinal bleeding, bowel perforation, acute toxic dilatation or stricture of the colon, damage to the anorectal region (cracks, fistulas, abscesses, hemorrhoids, weakness of the sphincter with fecal and gas incontinence); colon cancer.
Laboratory and instrumental research
The blood test reveals leukocytosis with neutrophilia and a shift in the leukocyte formula to the left, a decrease in the content of erythrocytes, Hb, serum iron, total protein, dysproteinemia with a decrease in the concentration of albumin and an increase in γ-globulins; possible violations of the electrolyte composition of the blood. According to the severity and phase of the disease, ESR and the concentration of C-reactive protein increase.
Endoscopic research methods play a decisive role in the diagnosis of ulcerative colitis. During colonoscopy in the initial period of the disease, the mucous membrane is hyperemic, edematous, easily vulnerable. In the future, a picture of typical
th 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 colon is disrupted. With a prolonged course of the disease, folding disappears, the lumen of the intestine becomes tubular, its walls are rigid, anatomical bends are smoothed out. Hyperemia and edema of the mucous membrane increase, its granularity appears. The vascular pattern is not determined, contact bleeding is expressed, erosions, ulcers, microabscesses, pseudopolyps are found.
Radiographically, a violation of the gaustral pattern of the intestine is revealed: asymmetry, deformation, or its complete disappearance. The intestinal lumen looks like a hose, with thickened walls, shortened sections, and smoothed anatomical bends.
Diagnostics and differential diagnostics
The diagnosis is made on the basis of clinical and laboratory data, the results of sigmoidoscopy, sigmoidoscopy and colonoscopy, irrigography, as well as histological examination of 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
The greatest importance in the treatment of ulcerative colitis in children is given to diet. Prescribing a dairy-free table? 4 according to Pevzner, enriched with protein from 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 are determined individually. In severe ulcerative colitis, glucocorticoids are additionally prescribed. According to strict indications, immunosuppressants (azathioprine) are used. They also carry out symptomatic therapy and local treatment (microclysters).
An alternative to conservative treatment is operative - subtotal bowel resection with the imposition of ileorectal anastomosis.
Prophylaxis
Prevention is aimed primarily at preventing relapse. After discharge from the hospital, all patients should be recommended
recommend courses of supportive and anti-relapse treatment, including basic drug therapy, diet and protective and restorative regimen. Patients with nonspecific ulcerative colitis are subject to mandatory dispensary observation. Prophylactic vaccination is carried out only according to epidemiological indications, weakened by vaccine preparations. Children are exempted from exams, physical activity (physical education, 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. Shows regular monitoring of changes in the mucous membrane of the colon due to the possibility of its dysplasia.
DISEASES OF THE CHILIAR EXTRACTIVE SYSTEM
Etiology and pathogenesis
The formation of the pathology of the biliary system in children is facilitated by qualitative and quantitative disturbances in the diet: an increase in the intervals between meals, early introduction of fatty and spicy foods into the diet, overeating, an excess of sweets, a sedentary lifestyle. Disorders of the psychoemotional sphere, previous perinatal encephalopathy, SVD, stressful situations predispose to the development of 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 inflammatory processes in the gallbladder and bile ducts, prevail E. coli and a variety of 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 gallbladder motility, 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 dyskinesias, an important role is played by the functional state of the stomach and duodenum. Dysfunction of the sphincters, duodenostasis, edema and spasm of the large duodenal nipple lead to hypertension in the biliary system and impaired bile secretion. There are various mechanisms that lead to a violation of the passage of bile. Two possible variants of such mechanisms are shown in Fig. 16-2.
CLINICAL PICTURE AND DIAGNOSTICS
There are hypotonic (hypokinetic) and hypertensive (hyperkinetic) types of dyskinesias. A mixed form is also possible.
Hypotonic dyskinesia
The main signs of hypotonic dyskinesia are: a decrease in the muscle tone of the gallbladder, its weak contraction, 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 rapid fatigue. Sometimes it is possible to palpate a large atonic gallbladder. Ultrasound reveals an enlarged, sometimes elongated gallbladder with normal or delayed emptying. When receiving an irritant (egg yolk), the transverse size of the gallbladder usually decreases by less than 40% (normally 50%). With fractional duodenal intubation, an increase in the volume of portion B is detected at normal or high
Rice. 16-2.Mechanisms of bile passage disturbance.
the rate of outflow of cystic 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 dyskinesia
The main signs of hypertensive dyskinesia: a decrease in the size of the gallbladder, acceleration of its emptying. Clinically, this option is characterized by short-term, but more intense attacks 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%. With fractional duodenal intubation, a decrease in the volume of portion B is detected with an increase in the outflow rate of bile.
TREATMENT
Treatment can be carried out both in a hospital and at home. When prescribing treatment, the type of dyskinesia should be considered.
Medical nutrition:
Table? 5 full of proteins, fats and carbohydrates;
Fasting days, for example, fruit-sugar and kefir-curd (for the purpose of detoxification);
Fruit and vegetable juices, vegetable oil, eggs (to naturally enhance the outflow of bile).
Choleretic drugs. Choleretic therapy must 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 pancreas and the mucous membrane of the small intestine ("Cholenzym"), hydroxymethylnicotinamide, osalmide, cyclovalon, rosehip fruit extract ( "Holosas"); plants (mint, nettle, chamomile, St. John's wort, etc.).
Cholekinetics (promoting the secretion of bile) - increasing the tone of the gallbladder (for example, preparations of common barberry, sorbitol, xylitol, egg yolk), reducing the tone of the bile ducts (for example, papaverine, platifillin, belladonna extract).
To eliminate cholestasis, Tubage is recommended according to G.S. Demyanov with mineral water or sorbitol. In the morning, the patient is given a glass of mineral water to drink on an empty stomach (warm, without gas), 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 option for tyubage: after taking a glass of mineral water, the patient takes 15 deep breaths with the participation of the diaphragm (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 desquamation of the epithelium, influence
They affect the neuromuscular apparatus and sphincters of the gallbladder and biliary tract.
The 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 lower corner of the right scapula, the right supraclavicular region or the right half of the neck. More often, pain occurs after eating fatty, spicy or spicy foods, as well as emotional experiences.
Dyspeptic syndrome is manifested by nausea and vomiting, sometimes constipation.
The main manifestations of intoxication syndrome are febrile fever, chills, weakness, sweating, etc.
On palpation of the abdomen, the tension of the anterior abdominal wall, positive symptoms of Kera, Murphy, Ortner and de Mussi-Georgievsky (phrenicus symptom) are determined. Enlargement of the liver is possible. Less commonly, jaundice is possible due to obstruction of the common bile duct (due to edema or calculi).
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.Acute catarrhal cholecystitis is usually treated conservatively in a hospital or at home.
Bed rest (duration depends on the patient's condition).
Is the diet a table? 5. Fasting 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 good. However, in approximately 1/3 of patients, acute cholecystitis is transformed 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 is largely associated with the state of the biliary system, duodenum and stomach. Disruption of the sphincter apparatus, duodenostasis, edema and spasm of the large duodenal nipple lead to hypertension in the biliary system, impaired bile passage and hypomotor dyskinesia of the gallbladder. As well as in the development of acute cholecystitis, a certain role is played by an infectious process (usually bacterial), which promotes the formation of cholesterol crystals.
Pathogenesis.Allergic factors are of certain importance in the formation of chronic cholecystitis. Bacterial toxins, chemical and drug influences aggravate dyskinetic disorders. The role of intestinal dysbiosis is noted. In a simplified way, the pathogenesis of chronic cholecystitis is shown in Fig. 16-3.
The clinical picture. The disease is manifested by recurrent paroxysmal pain in the epigastric region, right hypochondrium and around the navel, often radiating to the right scapula. 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 disorder
Rice. 16-3.Pathogenesis of chronic cholecystitis.
functions of other internal organs. So, the insufficiency or complete cessation (acholia) of the flow of bile into the intestine leads to impaired 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, there are signs of chronic intoxication: weakness, low-grade 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 coated, sometimes swollen, with imprints of teeth along the edges. On palpation of the abdomen, tenderness is determined in the right hypochondrium and epigastric region.
Diagnostics.During the period of exacerbation in the peripheral blood, moderate leukocytosis with neutrophilia, an increase in ESR, an increase in the concentration of bilirubin, and the activity of alkaline phosphatase (due to cholestasis) are possible. The diagnosis is made 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 can acquire a spherical shape.
Differential diagnostics. Acute and chronic cholecystitis is differentiated from other diseases of the gastroduodenal zone - chronic gastroduodenitis, biliary dyskinesia, hepatitis, chronic pancreatitis, etc.
Treatmentchronic cholecystitis in the period of exacerbation is based on the same principles as the treatment of acute cholecystitis: bed rest, diet? 5 and? 5а with a ratio of proteins, fats and carbohydrates 1: 1: 4, plenty of fruits and vegetables, fractional meals. Table? 5 for 2 years is recommended during remission. After the second year of follow-up, the diet can be extended. With a severe exacerbation of chronic cholecystitis, detoxification therapy is indicated - the introduction of intravenous glucose, saline solutions. Otherwise, drug therapy is the same as for acute cholecystitis.
Prevention.With the threat of the development of 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 congestion, 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 has been 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 with 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, precipitation of cholesterol, calcium, bilirubin occurs, especially in the parietal layer of bile, followed by the formation of stones. In young children, pigment stones (yellow in color, 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.
The clinical picture. There are two options for the clinical picture of calculous cholecystitis in children. More often, the disease proceeds without typical bouts of abdominal pain, only aching pains, heaviness in the upper abdomen, bitterness in the mouth and belching are noted. Less often, a typical course with repeated bouts of acute pain in the right hypochondrium (biliary colic) is observed. Pain can be repeated many times at regular intervals. Colic is often accompanied by nausea, vomiting, and cold sweats. Passage of a stone can cause temporary blockage 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 are stopped.
Diagnostics.The diagnosis is made on the basis of clinical data and special research methods: ultrasound and radiological (cholecystography). With an ultrasound of the gallbladder and bile ducts, dense formations are found in them. With cholecystography, multiple or single defects in the filling of the gallbladder are recorded.
Treatment.Both medicinal 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. Cholecystectomy - removal of the gallbladder - should be considered a radical method. Currently, the endoscopic method is widespread - laparoscopic cholecystectomy.
DISEASES OF THE PANCREAS
Of all the diseases of the pancreas, pancreatitis is the most commonly diagnosed in children. 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, hemorrhagic lesions, acute fatty necrosis and purulent inflammation.
Etiology
The main etiological factors of acute pancreatitis are as follows.
Acute viral diseases (eg mumps, viral hepatitis).
Bacterial infections (eg, dysentery, sepsis).
Traumatic damage to 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 the effect of 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 pancreatic necrosis 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 distinguished.
Clinical picture
Symptoms of the disease largely depend on its clinical form and the age of the child (Table 16-6).
Table 16-6.Clinical presentation and treatment of acute pancreatitis *
* From: A.A. Baranov et al. Pediatric gastroenterology. M., 2002.
Diagnostics
The diagnosis is made on the basis of the clinical picture and data from laboratory and instrumental studies.
In the general analysis of blood, leukocytosis is revealed with a shift of the leukocyte formula to the left, an increase in hematocrit.
In 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 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.
An ultrasound scan reveals an increase in the size of the pancreas, its induration and swelling.
Differential diagnosis
The differential diagnosis of acute pancreatitis is carried out with gastric ulcer and duodenal ulcer, 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, a decrease in the exocrine and endocrine function of the organ.
Etiology
In most children, chronic pancreatitis is secondary in nature and is associated with diseases of other digestive organs (gastroduodenitis, pathology of the biliary system). As a primary disease, chronic pancreatitis develops in children in only 14% of cases, most often due to fermentopathy or acute abdominal trauma. The toxic effect of drugs cannot be ruled out.
Pathogenesis
The mechanism of development of the disease can be due to two factors: the obstruction of the outflow of pancreatic enzymes and the reasons 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 prolonged 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 Monotonic |
Severity of current (form) | Easy Moderate Heavy |
Disease period | Aggravation Subside exacerbation Remission |
The 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, pancreatolithiasis, diabetes mellitus, pleurisy, etc. |
|
Accompanying illnesses | Peptic ulcer, gastroduodenitis, cholecystitis, hepatitis, enterocolitis, colitis, ulcerative colitis |
* From: A.A. Baranov et al. Pediatric gastroenterology. M., 2002.
The main clinical manifestation of chronic pancreatitis is pain syndrome. 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 activity or an infectious disease. The duration of the pain is different - from 1-2 hours to several days. The pain often radiates to the back, right or left side of the chest; in a sitting position, it weakens, especially when the trunk is tilted forward. The knee-elbow position is most typical for a patient with chronic pancreatitis (with it, the pancreas is, as it were, in a "suspended" state).
Of the pathological symptoms in the period of exacerbation of the disease, symptoms of Mayo-Robson, Kacha, de Mussi Georgievsky, Grotte are often found. In most children, a dense and painful head of the pancreas can be palpated.
Chronic pancreatitis is characterized by dyspeptic disorders: decreased appetite, nausea, vomiting at altitude
pain attack, belching, heartburn. More than a third of patients have constipation, followed by diarrhea with an exacerbation of the disease.
Common symptoms of chronic pancreatitis: weight loss, asthenovegetative disorders (fatigue, emotional instability, irritability).
The severity of clinical symptoms is associated with the severity of the disease. The process is aggravated by concomitant organic changes in the duodenum (duodenostasis, diverticula) and the biliary system (chronic cholecystitis, cholelithiasis).
Diagnostics
The diagnosis is based on clinical, laboratory and instrumental data.
When examining the content of pancreosimin and secretin, pathological types of pancreatic secretion are found.
Provocative tests with glucose, neostigmine methyl sulfate, pancreosimin 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 mainstay of treatment for chronic pancreatitis is a diet that reduces pancreatic and gastric secretion. The patient's diet should have a sufficient amount of protein while limiting fats (55-70 g) and carbohydrates (250-300 g). For relief of pain syndrome, drotaverine, papaverine, bencyclan are prescribed.
The negative effect of hydrochloric acid 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 impaired motility of the duodenum and dyskinesia of the biliary tract, metoclopramide and domperidone are prescribed.
In the period of exacerbation of chronic pancreatitis, the first 3-4 days recommend hunger, allow unsweetened tea, alkaline mineral waters, rosehip decoction. Inhibitors of proteolytic enzymes (for example, aprotinin) serve as pathogenetic therapy. The drugs are injected 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 the 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, antibiotics of a wide spectrum of action 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, Yessentuki, Borjomi, etc.
CHRONIC HEPATITIS
Chronic hepatitis is a diffuse inflammatory process in the liver, proceeding without improvement for at least 6 months.
The classification of chronic hepatitis, adopted at the International Congress of Gastroenterology (Los Angeles, 1994), is presented in table. 16-8.
Table 16-8.Classification of chronic hepatitis
The prevalence of chronic hepatitis has not been precisely established due to the large number of erased and asymptomatic forms and the lack of population 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
the clinical and morphological picture of diffuse liver inflammation lasting more than 6 months and the 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 primary chronic disease or arising after an erased or subclinical form of an acute infection. The transition of acute hepatitis B into chronic is noted in 2-10% of cases, mainly with mild or latent forms of the disease. The vast majority of patients with chronic hepatitis have no history of acute hepatitis.
It is assumed that the cause of the development of chronic hepatitis B may be a deficiency of the immune response due to genetic reasons 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 the carriage of HB s Ag are often recorded in diseases associated with dysfunction of the immune system: immunodeficiency states, chronic diseases kidney, chronic lymphocytic leukemia, etc.
Chronic hepatitis B has several phases: initial (immune tolerance); immune response (replicative), proceeding with pronounced clinical and laboratory activity; integrative, carrier HB s Ag. The process usually remains active for 1-4 years and is replaced by the phase of integration of the 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 seem to cause cytolysis. Damage to hepatocytes is associated with immune responses arising in response to viral (HB s Ag, HB ^ g) and hepatic Ag circulating in the blood. In the replication phase of the virus, all three Ar of the hepatitis B virus are expressed, the immune aggression is more pronounced, which causes massive necrosis of the liver parenchyma and mutation of the virus. As a result of the mutation of the virus, the composition of serum Ags changes; therefore, the replication of the virus and the destruction of hepatocytes occur for a long time.
Replication of the virus is also possible outside the liver - in bone marrow cells, mononuclear cells, thyroid and salivary glands, which, apparently, explains the extrahepatic manifestations of the disease.
Clinical picture
The clinical picture of chronic hepatitis B is associated with the phase of viral replication and 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 in patients, subicterus or mild icterus of the sclera is revealed.
Hemorrhagic syndrome, which correlates with the severity of the process, is recorded in approximately 50% of patients; it is expressed in abundant nosebleeds, petechial rash on the face and neck, hemorrhages on the skin of the extremities.
Vascular manifestations (the so-called extrahepatic signs) occur in 70% of patients. These include telangiectasias (“spider veins”) on the face, neck, and shoulders, and erythema palmar — symmetrical erythema of the palms (“hepatic 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 failure and concomitant damage biliary tract, pancreas, gastroduodenal zone.
Hepatomegaly is the main and sometimes the only clinical symptom of chronic hepatitis B. The sizes of both lobes of the liver are enlarged both percussion and palpation. Sometimes the liver protrudes 6-8 cm from under the edge of the costal arch, has a dense 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, the size of the liver decreases, palpation becomes less painful, pain in the liver area worries the child less.
A pronounced enlargement of the spleen is found with high activity of hepatitis.
Endocrine disorders are possible - menstrual irregularities in girls, striae on the hips, acne, hirsutism, etc.
Extrahepatic systemic manifestations include nervous tics, erythematous spots on the skin, urticaria, erythema nodosum, and transient arthralgias.
In the general analysis of blood in the active period and in severe chronic hepatitis B, anemia, leukopenia, thrombocytopenia, lymphopenia and an increase in ESR are revealed. In the blood serum, there is 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. Using ELISA, RIF, DNA hybridization and PCR, hepatitis B virus replication markers (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 routes of transmission are similar to those for 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 consequence, the replication of the virus and its persistence in the body are associated with the activity and progression of hepatitis.
The clinical picture. The clinical manifestations of chronic hepatitis C are usually mild or absent. Patients are worried about fatigue, weakness, dyspeptic disorders. On examination, hepatomegaly, telangiectasia, palmar erythema are found. The course of the disease is wave-like and long-lasting. A biochemical blood test reveals an increase in the activity of alanine aminotransferase (ALT). The diagnosis is based on the detection of specific markers of chronic hepatitis C - virus RNA and antibodies to it (in the absence of markers of hepatitis B virus).
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 the 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 superinfection or coinfection in patients with acute or chronic hepatitis B. Hepatitis D virus has a cytopathogenic effect on hepatocytes, maintains activity and promotes the progression of the process in the liver.
The clinical picture. Clinically, symptoms of liver failure are detected (severe weakness, drowsiness during the day, insomnia at night, bleeding, dystrophy). Most patients have jaundice and pruritus, extrahepatic systemic manifestations, enlargement and thickening of the liver. Chronic hepatitis D is characterized by a severe course. In the blood, markers of chronic hepatitis D are detected - the DNA of the virus and AT to its Ag. Replication of the hepatitis B virus is suppressed as cirrhosis of the liver rapidly develops.
DIAGNOSTICS
Diagnosis of chronic viral hepatitis is based on anamnestic, clinical (intoxication, hemorrhagic syndrome, enlargement and thickening of the liver, extrahepatic signs), biochemical (increased ALT, thymol test, dysproteinemia, hyperbilirubinemia, etc.), immunological (signs of immune inflammation, specific markers ) and morphological data.
DIFFERENTIAL DIAGNOSTICS
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 regimen and diet, the appointment of vitamins.
The regimen of patients with chronic hepatitis should be as gentle as possible, in the active period of the disease - half-bed. Limit physical and emotional stress.
When prescribing a diet, the individual tastes and habits of the patient, the tolerance of certain 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 fruits. Meals should be fractional (4-5 times a day).
To normalize metabolic processes and vitamin balance, vitamin C (up to 1000 mg / day) and multivitamin preparations are prescribed.
Symptomatic therapy includes the appointment of courses of mineral waters, choleretic and antispasmodic agents, enzyme preparations and probiotics for the treatment of concomitant dysfunctions of the biliary system and the gastrointestinal tract.
In case of severe intoxication, drip intravenous administration of povidone + sodium chloride + potassium chloride + calcium chloride + magnesium chloride + sodium bicarbonate ("Gemodeza"), 5% glucose solution for 2-3 days is necessary.
In the active phase of the disease (the phase of viral replication), therapy is carried out with interferon preparations (interferon alpha-2b - subcutaneously 3 times a week for 6 months at a dose of 3 million IU / m2 of body surface; interferon alpha-2a is also used; interferon alpha-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, it is possible to combine interferon alfa with antiviral drugs (for example, ribavirin). Chronic hepatitis B is also treated with lamivudine.
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 period of dispensary observation, it is recommended, in addition to examination to determine the size of the liver, to conduct a biochemical study of blood serum (total bilirubin, transaminase activity, sediment samples, specific markers, etc.). Shown are 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 likelihood of a complete recovery is negligible. As the process progresses, liver cirrhosis and hepatocellular carcinoma develop.
Autoimmune hepatitis
Autoimmune hepatitis is a progressive hepatocellular inflammation of unknown etiology, characterized by the presence of periportal hepatitis, hypergammaglobulinemia, hepatic-associated serum autoantibodies and a 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 primarily mediated impairment of the immune response. Viruses (Epstein Barr, measles, hepatitis A and C) and some drugs (for example, interferon) are indicated as possible starting (triggering) factors contributing to the onset of the disease.
In the presence of an appropriate genetic predisposition, under the influence of trigger factors or without them, a violation of immune regulation 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 the HLA DR4 allele, which is more common in Japan and other countries of Southeast Asia). As a result, uncontrolled synthesis of IgG ATs by B-cells occurs, destroying the membranes of normal hepatocytes. In total, DR3 and / or DR4 alleles are detected in 80-85% of patients with autoimmune hepatitis. Currently, autoimmune hepatitis I, II and III types are isolated.
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). In the blood serum, antinuclear (antinuclear antibodies, ANA) and / or anti-smooth muscle (smooth muscle antibody, SMA) AT in a titer of more than 1:80 in adults and more than 1:20 in children. Perinuclear neutrophilic cytoplasmic antibodies (pANCA) are also found in 65-93% of patients with this type of hepatitis.
Autoimmune type II hepatitis 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 Ar microsomes of the liver
and kidney type I (liver kidney microsomes, LKM-1). In type II autoimmune hepatitis, 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.
Autoimmune type III 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%), antimitochondrial antibodies (22%), rheumatoid factor (22%), and anti-hepatic membrane antibodies (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 autonomic disorders, pain in the right hypochondrium, minor jaundice. The latter often appears in the later stages of the disease, is inconstant and intensifies during exacerbations. The appearance of telangiectasias (on the face, neck, arms) 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, and boys may develop gynecomastia. Development of acute recurrent migratory polyarthritis with involvement of large joints without their deformities is possible. 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 IgG concentration, a decrease in the concentration of total protein, and a sharp increase in ESR. Leukopenia and thrombocytopenia are detected in patients with hypersplenism and portal hypertension syndrome. Autoantibodies against liver cells are detected in the blood serum.
Diagnostics and differential diagnostics
Distinguish between "definite" 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 at 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 AT titers (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, damage to the bile ducts, copper deposition in 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 symptoms present 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, pronounced hypergammaglobulinemia, a selective increase in the serum IgG content, 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 signs 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, a 1 -antitrypsin deficiency, Wilson-Konovalov's disease.
Treatment
The mainstay of treatment is immunosuppressive therapy. Prescribe prednisone, azathioprine, or a combination of both. Combined therapy is recommended to reduce the likelihood of adverse reactions from the use of glucocorticoids: in this case, prednisolone is prescribed in 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 ruled out, since it is possible for the patient to violate the regimen of taking drugs or insufficient dosage. The goal of treatment is to achieve complete remission. By remission, we mean the absence of biochemical signs of inflammation [the activity of aspartate aminotransferase (AST) is not more than 2 times higher than the norm] and histological data indicating the activity of the process.
Therapy with prednisolone or a combination of prednisolone with azathioprine can achieve 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 liver cirrhosis 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 amounts to 89 and 90%, respectively. Prednisolone is prescribed at a dose of 2 mg / kg (maximum dose 60 mg / day), followed by a decrease by 5-10 mg every 2 weeks under weekly monitoring of biochemical parameters. When the content of transaminases is normalized, the dose of prednisolone is reduced to the lowest possible maintenance dose (usually 5 mg / day). If during the first 6-8 weeks of therapy there is no normalization of liver function tests, azathioprine is additionally prescribed at an initial dose of 0.5 mg / kg. In the absence of signs of toxic effects, the dose of the drug is increased to 2 mg / day. Although a decrease in transaminase activity by 80% of the initial one occurs during 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 the dose of prednisolone is temporarily increased. 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, in most cases, it is not possible to completely cancel immunosuppressive therapy. In case of repeated recurrence of autoimmune hepatitis after the withdrawal of immunosuppressive drugs, prescribe
life-long 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. In case of ineffectiveness of glucocorticoid therapy, cyclosporine, cyclophosphamide are used.
Primary resistance to treatment is observed in 5-14% of patients with a confirmed diagnosis of autoimmune hepatitis. This small group of patients can be clearly distinguished within 14 days after the start of treatment: their liver function tests do not improve, and their subjective well-being remains the same or even worsens. The mortality rate among patients in this group is high. They are subject to mandatory consultation in liver transplantation centers, as well as those patients who, during or after treatment, develop a relapse resistant to therapy. Medical treatment of such patients usually turns out to be ineffective, the continuation of taking glucocorticoids in high doses only leads to the loss of precious time.
Prophylaxis
Primary prevention has not been developed. 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 enhancement of immunosuppressive therapy. Important points: adherence to the daily regimen, limiting physical and emotional stress, diet, withdrawal from vaccination, minimum intake of medicines. Periodic courses of hepatoprotectors and maintenance therapy with glucocorticoids are shown.
Forecast
The disease without treatment progresses continuously and does not have spontaneous remissions. Improvements in well-being are short-term; biochemical parameters do not normalize. As a result of autoimmune hepatitis, liver cirrhosis of the macronodular or micronodular type is formed. The prognosis is poor in children with primary treatment resistance. If immunosuppressive therapy is ineffective, liver transplantation is indicated. After liver transplantation, the 5-year survival rate in patients with autoimmune hepatitis is more than 90%.
Amyloidosis is a systemic disease characterized by impaired protein metabolism and accompanied by extracellular deposition of a complex protein-polysaccharide complex in organs and tissues.
Traditionally, several forms of this disease are distinguished:
- primary amyloidosis (congenital fermentopathy);
- secondary amyloidosis (occurs with a long course of chronic diseases, accompanied by tissue breakdown and absorption of decay products or pathological immunological disorders);
- senile amyloidosis.
This disease is difficult to classify, since in most cases the lesion covers several organs. Primary amyloidosis occurs in a hereditary autosomal dominant manner. Often, the causes of the onset of the disease remain unclear (idiopathic amyloidosis).
Secondary amyloidosis appears against the background of pulmonary tuberculosis and extracellular forms of tuberculosis, with bronchiectasis, chronic pleural empyema, chronic osteomyelitis, serum sickness, ulcerative colitis, various tumors and some other diseases.
Amyloidosis of the esophagus is manifested by belching and impaired swallowing reflex (dysphagia) when dry and dense food is swallowed. The X-ray shows a decrease in the tone of the esophageal tissues.
The most common is intestinal amyloidosis. A typical manifestation of this form of the disease is a feeling of heaviness in the stomach. In addition, stool disorders are observed: diarrhea or constipation. A blood test shows anemia, leukocytosis, an increase in the erythrocyte sedimentation rate. As a result, malabsorption syndrome and impaired parietal digestion develop.
As an independent disease, intestinal tumor amyloidosis proceeds, which is difficult to diagnose due to a tumor. In most cases, this pathology is detected only during surgery. Typical symptoms of a tumor are pain and bowel obstruction.
X-ray examination reveals thickening of the folds, smoothness of the relief of the mucous membrane, elevation of the intestinal loops. Amyloidosis of the stomach develops against the background of amyloidosis of the intestine or other organs. In this case, the patient feels heaviness in the epigastric region after eating, as well as digestive disorders: heartburn, belching, nausea, etc.
The X-ray shows the smoothness of the relief of the mucous membrane, a noticeable weakening of peristalsis and the removal of food from the stomach.
Pancreatic amyloidosis occurs quite rarely and is characterized by manifestations of chronic pancreatitis: dull pain in the left hypochondrium, indigestion, pancreatogenic diarrhea, steatorrhea. As a result of the disease, exocrine pancreatic insufficiency develops.
Liver amyloidosis is common. Its characteristic symptoms are a hardening of the liver and an enlarged spleen. An enlarged liver is observed at a late stage of the disease. On palpation, the edge of the liver is even, pain is not noted or is expressed slightly.
Sometimes the patient feels pain in the right hypochondrium. In addition, indigestion and jaundice may occur. The severe course of the disease is characterized by hemorrhagic syndrome. In this case, there is an increase in pressure in the portal vein, which arises as a result of the difficulty in the outflow of blood from it (portal hypertension), and the accumulation of fluid in the abdominal cavity (ascites). Changes in blood serum are observed: an increase in the bilirubin content, an increased activity of alkaline phosphatase, hyperglobulinemia, aminotransferase, etc.
Amyloidosis of the esophagus gives severe complications in the form of esophageal bleeding and amyloid ulcers of the esophagus. Intestinal amyloidosis may be accompanied by intestinal bleeding, amyloid ulcers, impaired intestinal integrity and narrowing, hypovitaminosis. Against the background of a significant violation of the absorption processes, the patient may develop hypoproteinemia.
Amyloidosis of the stomach in most cases is complicated by gastric bleeding, amyloid stomach ulcers, and perforation of ulcers. Severe forms of pancreatic amyloidosis give secondary development of diabetes mellitus. Liver amyloidosis is complicated by liver failure.
The disease is characterized by rapid development, which leads to the disability of patients. Death is possible as a result of renal or heart failure, as well as with general depletion of the body. Especially difficult prognosis for amyloidosis of infectious etiology.
With timely and correct treatment of amyloidosis at an early stage, its reverse development is possible. Treatment of secondary amyloidosis is primarily reduced to the treatment of the underlying disease, against the background of which they arose. As a rule, after the cure of the disease that served as a factor in the development of amyloidosis, the symptoms of amyloidosis itself disappear.
In the treatment of amyloidosis, immunosuppressants and corticosteroids are mainly used. In addition, the patient is shown multivitamins intravenously and subcutaneously, as well as plasma transfusion. In the case of severe edema, diuretic drugs are recommended to remove excess fluid from the body. With intestinal amyloidosis, astringent preparations are prescribed: basic bismuth nitrate, adsorbents.
Hepatic extracts and hydrolysates are used for liver amyloidosis. In this case, eating raw liver is also recommended. With primary amyloidosis of the liver, anticholinergic drugs are indicated: delagil, plaquenil.
Surgical intervention is necessary for isolated tumor amyloidosis of the gastrointestinal tract. Prevention of amyloidosis consists in timely diagnosis, correct treatment and prevention of a number of chronic diseases, including those of an infectious nature.
Gastritis
Gastritis is a disease characterized by inflammation of the stomach lining. Gastritis occurs very often and is acute, chronic, erosive (hemorrhagic), hypertrophic (Menetre's disease) and polyposis. In some classifications, the last two types are classified as special forms of chronic gastritis.
Acute gastritis, depending on the prevalence of the disease, is simple (catarrhal) and corrosive. In the first case, inflammation covers only the gastric mucosa, in the second, the submucous layer is also affected, resulting in erosion, hemorrhage, and necrosis. In addition, phlegmonous gastritis is isolated, which is characterized by inflammation of the stomach wall with diffuse or limited spread of pus.
There are also superficial (moderate) gastritis, gastritis with lesions of the glands without atrophy, atrophic (pronounced nastritis), as well as gastritis with restructuring of the gastric mucosa.
At the site of localization, common gastritis, antral (rigid) and isolated chronic gastritis of the fundus of the stomach are distinguished. In addition, the classification takes into account whether gastritis is the main (primary) or concomitant (secondary) disease.
According to the degree of secretory deviations, gastritis is divided into gastritis with reduced secretion (acidity) and gastritis with preserved or increased secretion.
Acute gastritis is usually caused by bacterial, chemical, mechanical, or thermal causes. It can develop against the background of eating rough, indigestible, too cold or too hot food. As a result, irritation of the stomach lining occurs. Alcohol and smoking can also cause gastritis.
In addition, acute gastritis can develop against the background of food poisoning or food allergies. An irritating effect on the gastric mucosa can be exerted by drugs such as salicylates, sulfonamides, antibiotics, steroid hormones, bromides, butadione, etc.
Acute gastritis quite often develops against the background of acute and chronic infectious diseases (pneumonia, measles, scarlet fever, influenza, etc.). Metabolic disorders, strong breakdown of proteins, neuropsychic stress can also cause acute gastritis.
As a result of the development of the disease, dystrophy and necrobiotic damage to the surface epithelium and glandular apparatus of the gastric mucosa are observed with subsequent pathological changes.
The most common is simple gastritis. Corrosive gastritis develops when concentrated ethyl alcohol, heavy metal salts, mercury compounds, strong acids and alkalis, lysol enter the stomach. Phlegmonous gastritis is extremely rare. The causative agents of this form of the disease are streptococci, sometimes in combination with Escherichia coli.
Phlegmonous gastritis can also be caused by staphylococci, pneumococci, proteus. Against the background of the disease, complications develop in the form of an ulcer, stomach cancer.
Chronic gastritis develops in the presence of gastroenterological pathologies and is characterized by inflammation, accompanied by a violation of the secretory. Motor and some other functions. Quite often, chronic gastritis develops against the background of appendicitis, chronic cholecystitis, colitis. The causes of chronic gastritis are unhealthy diet, vitamin deficiency, frequent consumption of spicy, hot and cold foods, poor chewing, alcohol and tobacco abuse, and prolonged use of drugs that irritate the stomach lining.
The development of chronic gastritis is often due to internal factors. For example, diseases in which the gastric mucosa secretes uric acid, urea, indole, skatole, etc. Diseases that cause metabolic disorders, diseases of the gallbladder, pancreas and thyroid glands can also cause chronic gastritis.
Prolonged exposure to irritating factors causes functional, secretory and motor disturbances in the functioning of the stomach, which leads to inflammatory and dystrophic changes, disturbances in the regeneration process in the epithelium of the surface of the layers of the gastric mucosa, which can atrophy or completely rebuild.
For the prevention of gastritis, it is necessary to regularly visit the dentist and treat caries, since a chronic infection in the oral cavity contributes to diseases of the gastrointestinal tract.
The manifestations of acute gastritis are usually pronounced. The inflammatory process begins 2-4 hours after the irritant enters the gastric mucosa, and after 8-12 hours the first symptoms may appear.
Acute gastritis is characterized by a feeling of heaviness and cutting pains in the epigastric region, partial or complete loss of appetite, nausea, vomiting, indigestion, increased heart rate, a slight increase in body temperature.
The skin and mucous membranes of the patient turn pale. Dryness appears in the mouth, and a grayish-white coating on the tongue. Palpation reveals pain in the stomach. A blood test shows leukocytosis and an increase in the erythrocyte sedimentation rate. The duration of acute gastritis is 2-6 days. Complete restoration of the gastric mucosa occurs within 10-15 days.
At the beginning of the disease, an increase in secretion is noted, after which the opposite process occurs: the acidity decreases. Gastroscopy reveals redness of the mucous membrane, mucus secretion. In severe cases, hemorrhage and erosion may occur. In this case, the transition of the disease to a chronic form is possible.
Corrosive gastritis gives severe chest pain, burning sensation and pain in the mouth, pharynx, esophagus and stomach. This form of the disease is usually accompanied by repeated painful vomiting. On the mucous membrane of the mouth, throat and larynx, traces of a chemical burn are observed: swelling, redness, ulcers. Acetic acid will usually leave superficial whitish-gray spots.
On palpation, the patient complains of discomfort in the abdomen and epigastric region; in severe cases, symptoms of peritoneal irritation are noted. With damage to the larynx, hoarseness is observed. The development of vascular collapse and the addition of a secondary infection are possible.
Corrosive gastritis is characterized by cirrhosis of the gastric mucosa with the formation of erosions and ulcers. Against this background, there is often a violation of the integrity of the stomach wall (perforation) soon after the stimulus enters the mucous membrane. With a favorable outcome, the gastric mucosa is regenerated, with an unfavorable outcome, cicatricial changes occur in the esophagus and stomach. Complications of corrosive gastritis include gastric motor failure, peritonitis, dysphagia, microgastria, acute mediastinitis.
During the first 2-3 days, there is a risk of death, which can occur as a result of shock or acute peritonitis. With phlegmonous gastritis of the stomach, an abscess occurs in its wall. This disease is very difficult to distinguish from acute peritonitis and perforated ulcers.
As a rule, the final diagnosis is made only after surgery. The disease is accompanied by severe pain in the epigastric region, nausea, vomiting. In addition, there are signs of peritoneal inflammation, fever, confusion, and circulatory failure.
On palpation, there is bloating and pain in the epigastric region. As a result of pathological changes in the patient, exhaustion progresses. A blood test shows neutrophilic leukocytosis with toxic granularity, an increase in the erythrocyte sedimentation rate, and a change in protein fractions. In the later stages of the disease, the clinical picture of the disease corresponds to the picture of peritonitis.
Against the background of the disease, the development of peritonitis, perigastritis is possible. In most cases, the prognosis of the disease is poor. The most common complications are subphrenic abscess, liver abscess, purulent mediastinitis, thrombophlebitis of large vessels of the abdominal cavity, pleurisy.
Gastritis with reduced gastric secretory function is characterized by a decrease in gastric acidity and atrophic changes in the mucous membrane. Elderly people are most susceptible to this disease. Typical symptoms of the disease are belching with air, heaviness in the epigastric region, an unpleasant taste in the mouth, nausea in the morning, and indigestion. The disease proceeds slowly, with alternating periods of exacerbation and remission.
The study of gastric juice using histamine or pentagastrin reveals a sharp decrease in the production of hydrochloric acid. For a more accurate diagnosis, gastroscopy is performed with targeted biopsy of the gastric mucosa.
With a long course of the disease, there is a significant decrease in the patient's body weight, symptoms of polyhypovitaminosis, insufficiency of the endocrine glands, the development of cholecystitis, intestinal dysbiosis, normochromic or iron deficiency anemia.
Another type of chronic gastritis is gastritis with preserved and increased secretory function of the stomach. Quite often, there is a superficial form or gastritis with damage to the gastric glands without atrophy. Typically, this disease occurs at an early age as a result of alcohol abuse.
For gastritis with a preserved and increased secretory function of the stomach, aching pain and heaviness in the epigastric region is characteristic, which occurs 2-3 hours after ingestion of spicy or spicy food. Patients complain of constant heartburn, belching and nausea.
In this case, the manifestation of symptoms of a nervous disorder and vascular dystonia is often observed: sleep disturbance, increased irritability, fatigue, arterial hypotension, sweating, etc. The prognosis of the disease is usually favorable, and the patient's condition is satisfactory.
In the diagnosis of the disease, fluoroscopic examination is of particular importance, which shows increased peristalsis of the pylorus, fluid in the stomach and uneven relief of the mucous membrane. Gastroscopy shows swelling and redness of the stomach lining.
Rigid gastritis is degenerative-dystrophic in nature and is accompanied by sclerosis of the stomach wall with inflammation, scarring and subsequent deformation and narrowing of the antrum.
Symptoms of rigid gastritis are pain of moderate intensity in the epigastric region, increased secretion of gastric juice, dyspeptic symptoms. X-ray shows tubular constriction of the pylorus. In 50% of cases, there is a significant likelihood of the transition of the disease to oncology.
With erosive gastritis, erosion forms on the gastric mucosa. An exacerbation of the disease occurs in the autumn-spring period as a result of a violation of the diet, emotional overstrain, etc. The disease can occur against the background of any acidity.
With erosive gastritis, the patient experiences severe pain, most often occurring immediately after eating. Gastric bleeding can be a complication of the disease. Often, bleeding is explained by increased permeability of the vessels of the stomach or trauma to its mucous membrane.
The erosion healing process depends on the individual characteristics of the patient's body, but, as a rule, it takes at least two months. Hypertrophic gastritis most often occurs in men over 40. This form of gastritis is characterized by multiple formation of cysts and adenomas, which leads to thickening of the folds of the gastric mucosa. In addition, against the background of the disease, there is a multiple loss of protein with gastric juice, in severe cases hypoproteinemia develops.
The disease proceeds with periods of exacerbation, which may be associated with various adverse factors. The clinical picture is atypical for gastritis, with the exception of low acidity of gastric juice. The disease is characterized by vomiting and epigastralgia.
X-ray shows enlargement and swelling of the folds of the gastric mucosa. Gastroboscopy with targeted biopsy shows hypertrophy with an increase in mucus-forming cells and a decrease in digestive cells. The most common complications are bleeding, swelling, and general wasting of the body.
Polypoid gastritis is characterized by atrophy of the gastric mucosa, accompanied by its dysregenerative hyperplasia and achlorhydria. The symptomatology of the disease is in many ways similar to the clinical picture of gastritis with secretory insufficiency. Polypoid gastritis can be combined with rigid gastritis and turn into oncology.
In the treatment of acute gastritis, it is necessary to cleanse the stomach and intestines of food debris and other irritants in it. This must be done within 30 minutes of poisoning. For this, washing with alkaline water, 0.5% sodium bicarbonate solution or isotonic sodium chloride solution is shown.
In the event that the disease has arisen as a result of alkali poisoning, washing with a weak solution of acetic acid or citric acid is indicated, in case of acid poisoning - with warm water with the addition of magnesium oxide, egg yolk or milk. In some cases, laxatives are required if dehydration is not observed.
During the first 2 days, the patient should refrain from eating and observe bed rest. Hospitalization is necessary only if the patient is in serious condition. Medicines are prescribed depending on the etiology of the disease. So, with gastritis of an allergic nature, antihistamines are shown, with an infectious nature - antibacterial, as well as absorbing substances: activated carbon, kaolin, etc.
If the patient's body is dehydrated, up to 1 liter of isotonic sodium solution is prescribed subcutaneously and 5% glucose solution. The development of acute heart failure is an indication for the use of caffeine, cordiamine, mezaton, norepinephrine. For severe pain, the patient is injected with 0.5-1 ml of a 0.1% solution of anthropin subcutaneously or 1 ml of a 0.2% solution of platifillin hydrotartrate subcutaneously.
It is also possible to use antispasmodics, for example, 1 ml of a 2% solution of papaverine hydrochloride subcutaneously. With severe nausea, anesthesin is indicated, 0.3 g 2-4 times a day.
With corrosive gastritis, the patient is lavaged with a large amount of water through a tube lubricated with vegetable oil. Before this, the use of narcotic analgesics (promedol, morphine hydrochloride, fentanyl with droperidol) is recommended. This is especially necessary if the patient is in severe pain.
In addition, anti-shock drugs are prescribed. It should be borne in mind that lavage through a probe is contraindicated if destruction of the esophagus or collapse is observed. Since food intake is contraindicated in the first days of treatment, the patient is injected with physiological saline, 5% glucose solution subcutaneously and isotonic sodium chloride solution intravenously.
In addition, vitamins, plasma and protein hydrolyzers are administered subcutaneously or intravenously. In the case of a secondary infection, antibiotics are prescribed. Gastric perforation and laryngeal edema are indications for surgery. To prevent narrowing of the esophagus, bougienage is performed after 2 weeks.
In the event that the latter did not give a positive result, surgical intervention is required. With cicatricial changes, it is necessary to create an artificial esophagus. With phlegmonous gastritis, hospitalization is required. The patient is injected intravenously or subcutaneously with broad-spectrum antibiotics. Against the background of the use of antibiotics, drainage is performed.
Treatment of chronic gastritis is individual in each case. In addition, it is necessary to take into account the form of the disease. During periods of exacerbation, bed rest is required. Measures are required to relieve pain. In chronic gastritis with reduced gastric secretory function, ganglion-blocking drugs are used for this purpose, which have an antispasmodic effect. The drugs of this group have practically no effect on secretion (gangleron, quateron).
In addition, drugs are prescribed that, along with antispasmodic and anti-inflammatory effects, cause an increase in secretion and enhance the motor function of the stomach.
Vitamins C, B6, and PP are also shown to normalize the secretory function of the stomach. In addition, the use of astringent and coating agents is effective. During the period of remission, if an exacerbation is suspected, substitution therapy is performed using hydrochloric acid preparations (natural gastric juice, acipepsol, betacid, pepsalin) and enzymes (pancreatin, pepsin, pepsidol, pepsicon, pepsigen, abomin, panzinorm).
In the treatment of chronic gastritis with a preserved or increased secretory function of the stomach, antispasmodic, anticholinergic and ganglion-blocking drugs (atropine, arpenal, spasmolitin, plati-phillin, benzohexonium) are used in combination with antacids (almagel, vikalin). In addition, drugs are used to improve regenerative functions (licorice preparations, pentoxin, methyluracil, etc.).
Treatment of rigid polyposis gastritis and Menetre's disease is carried out according to the same scheme as the treatment of gastritis with a reduced gastric secretory function, since all these diseases are characterized by the presence of secretory insufficiency.
In acute gastritis, the patient is shown nutritional therapy. Within 2 days the patient is given strong warm tea in small portions and Borjomi. On the 2-3rd day, the so-called slimy diet is shown: low-fat broth, soup with butter. During the entire period of treatment, the patient needs vitamin therapy: 300 ml of vitamin C and 100 ml of vitamin PP.
With a positive effect of treatment, after 1 week, the patient is transferred to a regular diet. With corrosive gastritis, it is necessary to stop eating and drinking. After that, it is recommended to consume 200 g of vegetable oil per day, beaten egg whites, butter. On the following days, the same diet is shown as for normal gastritis.
The mainstay of gastritis treatment is proper nutrition. All therapy is based on diet therapy. In the first days of the disease, diet No. 1 is prescribed. The patient takes food in small quantities 5-6 times a day. At the stage of completion of the exacerbation, the patient's nutrition depends on the nature of the secretory disorders. So, for chronic gastritis with a reduced secretory function, diet No. 2 is prescribed, for gastritis with a preserved or increased secretory function of the stomach during an exacerbation of the disease, diet No. 1a is indicated.
During periods of remission of the disease, the patient is shown full nutrition with a limited content of table salt, carbohydrates and ecstatic substances. In particular, this applies to patients with high acidity of gastric juice.
With gastritis, eating spicy foods, pickles and seasonings is contraindicated. A patient with gastritis should also refuse to take alcoholic beverages.
Prevention of gastritis is based on a rational and nutritious diet. In addition, it is necessary to regularly examine the gastrointestinal tract and, in the event of a disease, take timely measures.
Hepatitis
Hepatitis is a disease accompanied by an inflammatory process in the liver, which, as a rule, occurs in combination with a change in the intermediate liver tissue.
Depending on the course, hepatitis can be acute or chronic. According to the prevalence of the disease, focal and diffuse hepatitis are distinguished. Acute hepatitis is divided into primary infectious, which include viral hepatitis (Botkin's disease), Vasiliev-Weil disease, yellow fever, secondary infectious diseases arising from paratyphoid fever, relapsing fever, lobar pneumonia, and toxic (medicinal hepatitis) arising from exposure to liver tissue of drugs.
Viral hepatitis is divided into epidemic (hepatitis A) and serum (hepatitis B). In addition, acute alcoholic hepatitis is isolated.
Chronic hepatitis is classified as persistent chronic hepatitis, active chronic hepatitis (lupoid), and cholestatic chronic hepatitis.
Hepatitis can be caused by various causes. Acute hepatitis can be triggered by pathogens of intestinal infections, enteroviruses, viruses, infectious mononucleosis viruses, as well as a septic bacterial infection.
The most common viral hepatitis caused by the A virus, which is found in the blood and urine of the patient at the end of the incubation period, in the acute preicteric and early icteric periods, and the B virus contained in the blood (patient serum).
The development of toxic acute hepatitis is associated with the effects of drugs, industrial poisons, mushroom poisons, radiation exposure, severe burns of the body. Currently, there are 1000 drugs capable of provoking acute hepatitis in the course of treatment, including isonicotinic acid derivatives, sodium salt, paraaminosalicylic acid (PAS), MAO inhibitors - hydrazine derivatives, male fern extract.
The greatest danger of developing hepatitis arises with prolonged use of voltaren, indomethacin, cordarone, chloramphenicol, mercazolil and other drugs.
Alcoholic acute hepatitis is caused by the intake of large amounts of alcohol or with prolonged abuse of alcoholic beverages. The disease, as a rule, develops against the background of fatty hepotasis, liver cirrhosis, chronic hepatitis, but it can also occur with a healthy liver.
It should be noted that infections, intoxication, allergies and alcohol abuse play a leading role in the etiology of chronic hepatitis. In most cases, chronic hepatitis is preceded by viral hepatitis (Botkin's disease). In addition, the causes of the disease can be brucellosis, tuberculosis, septic endocarditis, visceral leishmaniasis, chronic malaria.
Chronic gastritis often develops in people with chronic diseases of the abdominal organs: gastritis, pancreatitis, enterocolitis, peptic ulcer and cholelithiasis, etc. chlorpromazine, benzene, isoniazid.
From narcotic substances, barbiturates, narcolan, halothane, hexenal, fluorothane can provoke hepatitis. In chronic hepatitis caused by exposure to toxic substances or an allergic reaction, damage to the liver parenchyma and impaired enzyme metabolism occur.
Chronic alcoholism, to a greater extent than other factors, contributes to the development of hepatitis, since it leads to endogenous protein-endocrine insufficiency. Cholestatic gastritis occurs as a result of stone blockage or cicatricial compression of the common bile duct, as well as as a result of cancer of the pancreatic head with a prolonged course of subhepatic cholestasis and the accompanying inflammation of the bile ducts and ducts, as well as with primary toxic or toxic-allergic lesion of cholangiol ...
The following drugs can cause holistatic hepatitis: phenothiazine derivatives, methyltestosterone and some of its derivatives.
In the pathogenesis of the disease, the direct effect of etiological factors (viruses, toxins, etc.) on the liver parenchyma is of particular importance, which leads to dystrophy and necrobiosis of hepatocytes. The chronic course and further development of pathological processes of inflammation and dystrophy is due to specific immunological disorders.
In the case of a mild course of acute hepatitis, symptoms may be absent or insignificant. This makes it difficult to diagnose the disease, which can only be carried out as a result of a special examination. The change in the color of the patient's skin, characteristic of hepatitis, is noticeable only in daylight. First of all, there is a staining of the outer membranes of the eyes (sclera) and the mucous membrane of the soft palate.
The severe course of the disease, on the contrary, is characterized by pronounced symptoms. Distinctly prickly membranes, the patient suffers from epistaxis. In addition, minor hemorrhages on the skin and mucous membranes may appear.
The disease also affects the central nervous system: the patient is in a depressed mental state, he is irritable, complains of sleep disturbance and fatigue. The liver and spleen, as a rule, are enlarged, and with liver dystrophy, its decrease is observed.
A blood test shows hyperbilirubinemia, an increased activity of certain serum enzymes. Disruptions in the production of fibrinogen, prothrombin, coagulation factors VII and V by the liver occur, which leads to the development of hemorrhagic syndrome.
Acute hepatitis of toxic etiology is characterized by moderate transient jaundice. In severe cases, there are multiple parenchymal necrosis, severe hemorrhagic syndrome and jaundice, severe pain in the liver. As a result of pathological changes, a hepatic coma may occur.
With cholestatic hepatitis, symptoms of liver damage appear 1-2 weeks after taking the drug that caused the allergic effect. Pruritus is a characteristic feature of the disease, which usually precedes jaundice. In this case, the patient's liver remains normal, and the body temperature is slightly increased.
With alcoholic hepatitis, pronounced jaundice is observed, which manifests itself within 1-2 days after taking a large dose of alcohol. The patient's body temperature rises, he feels pain of varying intensity in the right hypochondrium or upper abdomen. In addition, nausea and vomiting may occur.
In this case, the liver greatly increases in size, and the spleen remains normal. With hepatitis of this nature, fluid accumulates in the abdominal cavity. In addition, manifestations of pancreatitis are noted. Such patients have symptoms of chronic alcoholism: hand tremors, decreased sensitivity in the lower extremities, severe weakness, neuropsychiatric disorders.
Alcohol provokes degeneration of liver cells, causing disturbances in intracellular structures, which subsequently leads to their complete destruction. In this case, the disease turns into cirrhosis of the liver. In the case of a favorable course of the disease, recovery may occur in 1-2 months.
Chronic hepatitis can only be diagnosed if the illness lasts more than 6 months.
Chronic hepatitis of infectious etiology (for example, Botkin's disease) is characterized by a symptom of jaundice (noticeable staining of the sclera and mucous membranes). In chronic hepatitis of toxic etiology, jaundice is usually absent.
In most cases, this form of hepatitis manifests itself in violations of the chemical composition of the blood. Typical signs are an enlarged liver, dull pain and a feeling of heaviness in the right hypochondrium, itchy skin (in particular, with medicinal hepatitis) and a slight increase in body temperature. The spleen is slightly enlarged or remains normal.
In addition, chronic hepatitis is characterized by general malaise, rapid fatigue, sweating, decreased appetite, nausea and vomiting, and stool disorders.
A blood test reveals an increase in the erythrocyte sedimentation rate, a decrease in the concentration of albumin, an increase in globulins. In most cases, an increased content of bilirubin is found in the blood serum of patients.
Chronic persistent hepatitis is characterized by mild symptoms. Possible pain in the right hypochondrium, slight enlargement of the liver, weakness. An increase in serum protein is observed in almost all patients. If the diet is followed and alcohol is completely avoided, the patient may recover completely.
Chronic active hepatitis develops against the background of viral hepatitis and is characterized by pronounced inflammatory-necrotic changes. In most cases, this disease occurs in women under 30 years of age. Patients complain of weakness, rapid fatigue, rapid decline in working capacity, lack of appetite, pain in the liver, a slight increase in body temperature.
With a severe course of the disease, hemorrhagic syndrome develops, so-called spider veins appear on the patient's chest and shoulders. The liver increases in size, on palpation it is dense and painful. The spleen is also usually enlarged. In the case of damage to other organs, syndromes atypical for the disease are observed: fever, joint pain, inflammatory processes in the affected organs, hormonal disorders.
On the part of the blood, there is a significant increase in the erythrocyte sedimentation rate. Changes in urine are noticeable only in the later stages of the disease.
With timely and correct treatment of acute hepatitis, regardless of the depth and stage of the process, the patient recovers completely, but in some cases, acute hepatitis becomes chronic. As a result of acute liver dystrophy, occurring with a clinical picture of hepatic or hepatic-renal failure, death can occur.
In the treatment of acute viral hepatitis (Botkin's disease) and other hepatitis of infectious etiology, the patient must be promptly hospitalized in a special department for infectious patients. During the height of the disease, the patient is shown bed rest and diet No. 5. The time of treatment in the hospital depends on the severity and course of the disease. As a rule, it is 2-4 weeks, however, in some cases, the treatment and the recovery period of the patient's body take several months.
In severe cases of the disease, accompanied by vomiting and loss of appetite, the patient is given an infusion of up to 500 ml of a 10-40% solution of glucose or fructose intravenously. In addition, a 5% glucose solution is used in combination with isotonic sodium chloride solution subcutaneously or in the form of drip enemas.
To restore liver function, agents are used to improve the metabolism of hepatic cells: B vitamins, glucoronic acid preparations, cocarboxylase, lipoic acid.
In severe viral hepatitis, characterized by a protracted course and severe intoxication of the body, gluco-corticosteroid hormones are indicated. Drugs of this group are also used for cholestatic hepatitis, edematous-ascites syndrome, as well as for suspected liver dystrophy.
The patient is prescribed 20-40 mg of prednisolone per day. The duration of drug treatment varies from 3-4 weeks to several months. With persistent hepatitis and the transition of acute hepatitis into a chronic form of the disease, the use of prednisolone is extended to 1.5 years. In this case, the daily dose of the drug is reduced to 10-20 ml. An indication for reducing the dose of the drug is to improve the patient's condition and reduce the serum bilirubin content to 0.02-0.03 g per liter.
In case of symptoms of hepatic coma, up to 500-1000 mg of cortisone and hydrocortisone are prescribed subcutaneously or intravenously. With the development of a coma, the patient needs plasmaphoresis. In the absence of a positive result, the procedure is repeated daily until the patient's condition improves.
For all infectious forms of hepatitis, with the exception of Botkin's disease, broad-spectrum antibiotics are prescribed, as well as special therapeutic serums. With hepatitis of toxic etiology, patients are hospitalized in the poisoning department and the stomach is washed in order to remove the irritant from the body that provoked the development of the disease.
In addition, the use of drugs is shown that removes the effects of intoxication and improves the functions of liver cells. Also, the patient is prescribed bed rest, a strict diet that provides for a limited intake of fats, the introduction of vitamins B and C, lipoic and folic acid. In addition, drugs are prescribed to neutralize the effect of the toxin.
In case of poisoning with compounds of mercury, lead and arsenic, 5-10 ml of a 30% solution of sodium thiosulfate is prescribed intravenously, in case of poisoning with heavy metals, a 5% solution of unithiol is administered intramuscularly.
With hepatitis of drug etiology, it is necessary to cancel the drug that provoked the development of the disease. In general, treatment does not differ from treatment for acute infectious hepatitis. In severe hepatocellular insufficiency, glucocorticoids are compulsorily shown to the patient.
With alcoholic hepatitis, the patient is contraindicated in taking alcoholic beverages. At the same time, a sparing diet is prescribed with a sufficient content of vitamins and proteins. The use of fruit juices is recommended. The patient is injected intramuscularly with vitamin B19 in combination with folic acid, lipocaine, carsil, methionine.
In case of suspicion of liver dystrophy or cirrhosis, Essentiale is used in the amount of 2 capsules 3 times a day. As for chronic hepatitis, it is necessary to follow a diet even in the stage of remission.
In chronic gastritis of medicinal, toxic, allergic and alcoholic etiology, it is necessary to stop the patient's contact with the irritant. To improve the metabolism of liver cells, additional vitamin therapy is performed. In this case, the patient is injected with vitamins C, B1, B2, B6, B12. In addition, cocarboxylase, ascorbic, nicotinic and folic acid are used. Lipoic acid and lipoic acid amide are prescribed 1 tablet (0.025 g) 2-4 times a day for 1-2 months.
To improve anabolic processes, steroid hormones are prescribed: 15-20 mg per day of methandrostenolone orally with a gradual dose reduction or 20-50 mg of retabolil per week intramuscularly.
At the stage of exacerbation, patients require hospitalization, bed rest and a strict diet rich in proteins and vitamins. In cholestatic hepatitis, immunosuppressants are prescribed in small doses as an anti-inflammatory and immunosuppressive agent, as well as corticosteroid hormones. The drug prednisolone is prescribed in an amount of 20-40 mg per day for 2-3 months, then the dose is gradually reduced to 10-15 mg per day.
At the same time, the patient takes 0.25 g per day of the drug delagil. In case of exacerbation of hepatitis with cholecystitis, choleretic agents are prescribed. As for therapy with liver hydrolysates and extracts, it must be carried out with great care, since these drugs, administered in the acute stage, can activate the process and intensify the further development of the disease.
With persistent and active chronic hepatitis, cholagogues, hepatic extracts, and anabolic hormones should not be taken. In addition, any physiotherapy procedures are strictly contraindicated.
With timely and rational treatment with adherence to a diet and abstinence from alcohol, viral hepatitis is completely cured while maintaining the patient's ability to work. During the period of exacerbation of the disease, patients are disabled.
With viral hepatitis, the patient is shown diet No. 5 with limited fat, since the affected liver cannot cope with the latter. First of all, this is necessary with repeated vomiting and the general serious condition of the patient. In the patient's diet, the amount of carbohydrates is increased. Signs of the development of a precomatose state are an indication for a decrease in protein.
Patients with persistent and aggressive chronic hepatitis need to give up fried foods, refractory animal fats, spicy and spicy foods. It is recommended to consume at least 100-150 g of dairy products per day, as well as mild varieties of cheese. Lean boiled fish is useful. The patient is calculated a daily diet, which should contain 100-120 g of proteins, 70-80 g of fat, 400-500 g of carbohydrates and a total of 3000-3500 kcal.
For chronic persistent gastritis, four meals a day are recommended. At the same time, smoked, dried, canned foods, pastry products, fried foods, mushrooms, chocolate, and alcohol should be excluded from the diet. The consumption of animal fats should be limited.
Since acute hepatitis can occur for a number of reasons, the prevention of this disease involves a whole range of measures. Acute viral hepatitis in most cases takes on the character of an epidemic, so the first thing to do is to isolate the patient. In the prevention of hepatitis, its diagnosis at an early stage is of great importance.
Healthy people need to follow strict hygiene rules. To prevent infection with serum hepatitis while undergoing certain medical procedures, it is necessary to use disposable syringes and sterilized instruments. As for the prevention of hepatitis of toxic etiology, it consists in sanitary and technical supervision at enterprises, aimed at eliminating the possibility of poisoning with hazardous compounds.
You should not eat unfamiliar or old mushrooms, as well as any medications without consulting your doctor.
Prevention of chronic hepatitis should be aimed at eliminating the factors that provoke exacerbation, taking into account the etiology of the disease.
Hepatosis
Hepatosis is a disease of the liver in which there is a degeneration of the parenchyma, the functional epithelial tissue of the liver. This disease in most cases is caused by excessive consumption of high-calorie foods and alcoholic beverages, which leads to pathological processes in the epithelium of the liver.
Hepatosis can be acute or chronic. Some classifications also distinguish fatty and cholestatic hepatosis. Acute hepatosis is usually caused by viral hepatitis and sepsis. The disease can develop against the background of toxic liver damage, which occurs in severe poisoning with arsenic, phosphorus, alcohol. In addition, the disease can be triggered by drugs such as tetracycline, fern extract. There are frequent cases of liver dystrophy as a result of severe mushroom poisoning.
Chronic fatty hepatosis is usually caused by alcohol abuse. The development of the disease is also possible against the background of a deficiency of protein and vitamins, obesity and malnutrition, anemia, enteritis, pancreatitis, and some infectious pulmonary diseases.
Toxic forms of chronic hepatosis are associated with prolonged intoxication with toxic substances. In the development of the disease, a violation of lipid metabolism is of great importance. As a result of overloading the liver with dietary fats and carbohydrates, the fat content increases significantly, the amount of glycogen decreases, which leads to a violation of the fat oxidation process.
Since the process of formation of lipoproteins, phospholipids and lycetin sharply slows down, the process of removing fat from the liver becomes difficult. In acute or chronic cholestatic hepatosis, there is an accumulation of bile pigment in hepatocytes, followed by dystrophy, manifested in a lack of proteins.
A characteristic sign of holistatic hepatosis is a violation of the process of flow of bile into the stomach (cholestasis). The most common cause of this disorder is the toxic effects of certain substances, in particular drugs (antibiotics, testosterone analogs, chlorpromazine).
Acute fatty hepatosis is characterized by signs of general intoxication of the body. The disease is characterized by an acute course. The patient develops jaundice, shortness of breath, a feeling of heaviness in the epigastric region. At the initial stage of the development of the disease, the liver increases in size and becomes soft. In a later stage, the liver is not palpable, and when percussion, a decrease in its size is revealed.
The size of the spleen, as a rule, remains normal. In severe cases of the disease, there is a decrease in the concentration of potassium in the blood serum, an increase in the erythrocyte sedimentation rate. Often, renal failure is added to the listed disorders. In the case of secondary hemorrhagic events and with hepatic coma, a lethal outcome is likely
Pathological changes in the liver and its functional disorders are very difficult to determine even on the basis of biochemical analyzes.
The disease can become chronic. At the same time, there are practically no symptoms of the disease. Chronic hepatosis, as a rule, cannot be diagnosed due to the clinical picture of concomitant diseases: disorders of the digestive system, diabetes mellitus, toxic and toxic-allergic lesions.
With the rapid development of the disease, manifestations of jaundice, aching pain in the right hypochondrium, a feeling of heaviness in the epigastric region, general weakness, decreased ability to work, headache, nausea, vomiting, and stool disorders are possible.
A characteristic sign is a moderate enlargement of the liver with a smooth surface, moderate density, rounded or sharp edges, as well as painful sensations on palpation. With a severe and prolonged course of the chronic form of hepatosis, there is a significant decrease in the patient's body weight, bloating, and itching. In some cases, there is an increased content of cholesterol, total protein and beta-lipoproteins in the blood serum.
The patient's recovery is possible only with the complete exclusion of contact with irritating factors and full-fledged timely treatment. Often, chronic hepatosis turns into chronic hepatitis or cirrhosis of the liver. The most characteristic signs of cholestatic hepatosis are severe jaundice, pruritus, and dark urine (due to increased bilirubin content).
Often in patients with hepatosis, a febrile state is observed.
With prolonged fatty hepatosis, hospitalization of the patient is necessary. In acute hepatosis of infectious etiology, the patient must be hospitalized in a special department. At the same time, special attention is paid to the treatment of the underlying disease and the prevention of renal failure. It is also necessary to carry out activities aimed at removing toxins from the body that caused the development of the disease.
The patient is given gastric lavage, siphon enemas, and saline laxatives are given. In the presence of symptoms of intoxication and suspicion of hypokalemia, the patient is shown hemodez, 5% glucose solution in combination with B vitamins and vimamin C, as well as panangin intravenously.
With the manifestation of hemorrhagic syndrome, rutin and a 1% solution of vicasol are used, 1-3 ml 3-4 times a day. In addition, the patient is given a transfusion of fresh frozen plasma (1.5-2 liters or more). To remove toxic substances from the blood, the patient is given plasmaphoresis.
In the treatment of chronic hepatosis, the use of lipotropic drugs gives the best effect. The patient is prescribed 3-5 g of a 20% solution of choline chloride inside, if the drug is in a 200 ml bottle, and intravenously in 100 ml of isotonic sodium chloride solution, if the drug is in 10 ml ampoules. The course of treatment is 14-20 injections. In addition, folic and lipoic acids, lipocaine, and vitamin B12 are used. Essentiale is used from liver extracts and hydrolyzers.
Assign 5 ml per day of sirepar, ripazon or prohepar intramuscularly. The patient receives injections daily for 20-40 days. The patient's diet should be complete and rich in vitamins. In chronic hepatosis, diet No. 5 is prescribed. The diet should have a high protein content and a limited fat content, in particular, of animal origin.
Products containing lipotropic factors are recommended: yeast, cottage cheese, boiled cod, oatmeal and buckwheat, etc. prevention of hepatosis is to prevent the possibility of domestic and industrial poisoning with hepatotropic poisons. Timely treatment of viral hepatitis is also of great importance.
Patients with a chronic form of hepatosis should be registered at the dispensary and at least 1-2 times a year undergo a course of treatment with lipotropic drugs and take measures to prevent exacerbations.
Hernia of the esophageal opening of the diaphragm
A hernia is a disease characterized by protrusion of internal organs through the altered wall of the cavity in which they are located.
A hernia of the alimentary opening of the diaphragm is characterized by a displacement through this opening into the posterior mediastinum of any organ of the abdominal cavity: the abdominal segment of the esophagus, the cardiac part of the stomach, intestinal loops, spleen, etc.
There are the following forms of this disease:
- fixed and non-fixed axial or sliding (cardiac, cardiofundal, subtotal-gastric and total-gastric);
- fixed and non-fixed paraesophageal (fundic and antral);
- congenital short esophagus, in which there is a thoracic position of the stomach.
Hernia formation in most cases is due to the following factors:
- a sharp increase in intra-abdominal pressure caused by excessive physical exertion;
- congenital underdevelopment of connective tissue structures that strengthen the esophagus in the opening of the diaphragm, as well as their dystrophic changes;
- shortening of the esophagus as a result of cicatricial-inflammatory process, tumors, etc .;
- a decrease in muscle tone;
- the disappearance of adipose tissue under the diaphragm;
- stretching the esophageal opening of the diaphragm, etc.
The listed factors contribute to the development of axial hernias, that is, the exit into the chest cavity of the abdominal segment of the esophagus. In clinical practice, there are three types of hernias: with normal, non-functioning and hypertensive gastroesophageal sphincter, as well as four clinical forms - asymptomatic, dyspeptic, algic and cardialgic.
The clinical picture of the disease is always pronounced, often the disease proceeds without symptoms at all. The most typical manifestation of a hiatal hernia is pain behind the sternum or in the abdominal cavity, which occurs during eating or when changing the position of the body.
In addition, the patient may experience dysphagia (difficulty swallowing), belching, hiccups, vomiting. As a result of the displacement of the mediastinal organs, the patient may experience shortness of breath, tachycardia, reflex angina pectoris. A blood test usually reveals anemia. This disease is characterized by a chronic course, accompanied by relapses.
Axial hernias are characterized by angina pectoris syndrome, regurgitation, etc. Paraesophageal hernias are prone to infringement. In this case, the patient feels sharp pains, he has signs of intestinal obstruction and collapse.
The most common complications of a hiatal hernia are esophageal-gastric bleeding, peptic esophagitis, cicatricial changes in the esophagus followed by its shortening, arrhythmia, angina pectoris, aspiration, etc.
The diagnosis of the disease is made on the basis of X-ray examination. Physical examination reveals displacement of the mediastinal organs, in particular the heart, as well as peristalsis and tympanitis (severe swelling). A blood test shows anemia and an increase in ESR.
In the treatment of this disease, frequent fractional meals are prescribed in accordance with the expanded diet No. 1. During the period of treatment, the patient is contraindicated in spicy, sour and salty foods, as well as foods that contribute to intestinal bloating. Drinking alcoholic beverages and smoking are also prohibited.
The patient is advised to sleep in a reclining position. In addition, anti-spastic and alkalizing therapy is recommended. For oral administration, local anesthetic and sedative drugs are indicated. In case of anemia, the patient needs iron preparations and hemostimulin. Coating and astringent agents are also used. If necessary, antibiotics and antihistamines are introduced into the course of therapy.
In the event that conservative treatment does not give a positive result, surgery is indicated, during which the stomach is returned to the abdominal cavity and the plate of the esophageal opening of the diaphragm is carried out. It should be remembered that even after a successful operation, relapses of the disease are possible.
Diverticula of the esophagus
Diverticula of the esophagus is a disease characterized by protrusion of its wall. With this disease, there is a disorder of the swallowing act, namely regurgitation and belching.
Diverticula are subdivided into congenital (pulsatile), acquired (traction), and mixed. Most diverticulums are acquired. The cause of the development of pharyngeal-esophageal diverticulum is congenital or acquired inferiority of the connective tissue structures and the muscular apparatus of the region of the pharyngeal-esophageal junction.
A factor in the occurrence of a diverticulum in this case is esophageal dyskinesia, accompanied by a sharp increase in pressure during swallowing food. In addition, pharyngeal-esophageal diverticula can result from mechanical damage to the pharynx or esophagus.
Epibronchial diverticula are most often acquired and are formed as a result of mediastinal lymphadenitis of tuberculous or banal etiology, pleurisy, chronic mediasthenitis.
Subsequently, congenital factors join, for example, incomplete overgrowth of the esophageal-bronchial fistula, which is characteristic of the embryonic period and subsequently forms the esophageal-bronchial cord.
Epiphrenal diverticulum is usually associated with reflux esophagitis caused by hiatal hernia, esophageal shortening, or cardiac insufficiency (the part of the esophagus located in front of its entrance to the stomach).
The clinical manifestations of the disease depend on the location of the diverticulum. At the initial stage of development of diverticulums of the upper part of the esophagus (pharyngeal-esophageal), there is an increased secretion of mucus, a burning sensation and cough. Then, the listed symptoms are joined by a foreign body sensation, nausea, impaired swallowing, regurgitation of food.
As a result, the so-called blockade phenomenon develops, characterized by facial flushing, a feeling of lack of air, dizziness and fainting. After vomiting, these symptoms usually disappear.
Diverticula of the middle part of the esophagus in most cases do not give specific symptoms. Sometimes there is a violation of swallowing, chest pain and bleeding from hyperemic or eroded mucous membranes.
Quite often, with an even course of the disease, complications such as mediastinal abscesses, bleeding, esophageal-bronchial fistulas, adhesions, and oncology in the diverticulum develop.
Diverticula in the lower esophagus are also mildly symptomatic. In some cases, swallowing disorder, pain behind the lower sternum, cough, regurgitation, nausea, vomiting, impaired appetite, reflex shortness of breath, palpitations, bronchospasm are observed.
The disease is characterized by a slow course, but it can be complicated by bleeding, bronchitis, aspiration pneumonia, lung abscess and the development of oncology.
The diagnosis of the disease is made on the basis of contrast x-ray examination of the esophagus. The presence of pharyngeal-esophageal diverticulums can sometimes be established by external examination and palpation (a characteristic protrusion is observed on the neck).
In the treatment of esophageal diverticula, prevention of delay in the diverticulum of food masses is of great importance, therefore, the patient is shown a sparing diet. Drink slowly in small sips. If a contrast suspension is found in the diverticulum, it is necessary to drink water.
This position is determined by X-ray examination. Often there is a need to treat the disease that caused the diverticulum.
In case of rapid development of the disease or suspicion of dangerous complications, the patient should be hospitalized for surgical treatment.
Intestinal dysbiosis
Dysbacteriosis of the intestine is a disease characterized by a change in the composition and quantitative ratio of microflora, whose representatives prevent the penetration into the intestine and the rapid reproduction of pathogenic and opportunistic microorganisms in it.
In clinical practice, there are syndromes of colonic and small bowel dysbacteriosis syndrome. Both syndromes can provoke an exacerbation of colitis. Dysbacteriosis can be an independent or concomitant disease in various diseases of the large intestine.
The gastrointestinal tract of newborns is completely sterile. A few hours after birth, the process of its settlement with strains of streptococci, Escherichia coli, etc. begins. After 24 hours, anaerobic lactobacilli and enterococci are found in the intestine, and from the 10th day - bacteroids. Normal intestinal microflora is established by the 1st month of life.
Depending on what type of microorganisms is predominant, dysbacteriosis is divided into medicinal (post-antibiotic), fungal, staphylococcal, proteus, and also caused by the paracoli group, Pseudomonas aeruginosa or the association of microbes.
According to A.F.Bilibin's classification, there are three forms of dysbiosis:
- compensated, characterized by the absence of a pathological process in response to microflora disturbance;
- subcompensated, characterized by the concomitant development of local inflammatory processes;
- decompensated, characterized by the formation of metastatic foci of inflammation in various parenchymal organs with intoxication, and in some cases with the development of sepsis.
For the self-regulation of the intestinal microflora, the normal functioning of the stomach and other digestive organs is of great importance. For example, a change in the bacterial flora can be caused by a decrease in the acidity of gastric juice or a weakening of the enzyme systems of other organs of the digestive system.
As a result of these disorders, various microorganisms begin to colonize the stomach and the proximal small intestine. Another reason for the pathological process is a change in environmental conditions, which becomes favorable for the life and reproduction of harmful microorganisms.
Dysbacteriosis leads to dysfunction of bile acids, which normally dissolve fats and are themselves absorbed in the ileum. Because of this, the solubility of fats and their absorption by the body are significantly reduced. As a result of the increased multiplication of bacteria, the absorption of carbohydrates is disturbed, the secretion of water and electrolytes into the intestinal lumen increases.
These processes stimulate the motility of the small intestine and the growth of bacterial flora in it, similar to the microflora of the large intestine. Dysbacteriosis is characterized by the disappearance of some representatives of normal microflora (bifidobacteria, lactic acid and Escherichia coli, etc.) and the appearance of pathological and conditionally pathological microorganisms (staphylococcus, fungi of the genus Candida, Proteus, Pseudomonas aeruginosa, etc.).
The listed changes lead to inflammatory processes of varying severity, and a sharp decrease in immunity and a weakening of the body can lead to the development of a generalized form of endogenous infection, up to sepsis. Microbes that multiply in the small intestine use nutrients and vitamins for their own exchange, as a result of which their deficiency develops in the patient's body.
There are many reasons for the development of dysbiosis. In most cases, these are diseases such as hypochlorhydria and achlorhydria of the stomach, in particular, accompanied by a violation of the evacuation of its contents, the adductor loop syndrome that appears after resection of the stomach, jejunal and preodenal diverticula, chronic pancreatitis, intestinal obstruction.
Treatment with antibiotics and sulfa drugs, in which a significant part of beneficial microorganisms sensitive to the drug perishes and pathogenic or opportunistic microflora that is resistant to its effects multiply. The impact of such unfavorable factors as protein starvation, climate change, vitamin deficiency, alcohol abuse, also leads to the development of dysbiosis.
After antibiotic therapy, in most cases, candidiasis develops, characterized by the disappearance of substances that have a fungistatic effect, as a result of which favorable conditions are created for the development of Candida albicans fungi. Candidamycosis can affect individual organs, mucous membranes, or proceed in a generalized manner.
After treating the patient with large doses of antibiotics, aspergillosis develops, the causative agent of which is the fungus Aspergillus fumigatus. Staphylococcal dysbiosis is caused by acute intestinal diseases. In addition, staphylococcal dysbiosis can accompany chronic diseases of the digestive system or other diseases characterized by a decrease in the protective functions of the body.
In this case, the provoking factor is the allergic or toxic effect of antibiotics directly on the intestinal mucosa, as well as a lack of vitamins.
Proteus dysbiosis, as a rule, develops in patients with chronic intestinal diseases: ulcerative colitis, chronic enterocolitis, as well as after surgery in the abdominal organs.
Dysbacteriosis, the causative agent of which is Pseudomonas aeruginosa, occurs with a decrease in the protective properties of the body in patients who have had intestinal infections such as dysentery, salmonellosis, as well as a concomitant disease in chronic ulcerative colitis, chronic enterocolitis and after antibiotic treatment.
The characteristic manifestations of dysbiosis are decreased appetite, unpleasant taste in the mouth, indigestion, weakness, weight loss, anemia. In severe forms, the body temperature may rise to 37-38 °.
With a prolonged course, hypovitaminosis occurs, especially of group B. Symptoms of intestinal candidiasis are loose stools with an admixture of blood, bleeding and focal necrosis. In severe cases, perforation and peritonitis are possible. The pathological process can cover all parts of the intestine, stomach and oral cavity. As a complication, candidiasis sepsis can develop, which is often fatal.
Aspergillosis is characterized by an acute onset and severe course. The patient has diarrhea and hemorrhagic-necrotic changes in the intestines.
The prognosis of the disease can be either favorable or unfavorable. Of great importance for the diagnosis of candidiasis, aspergillosis and other mycoses that occur while taking antibiotics, it develops against the background of treatment with drugs of this group of acute enteritis or enterocolitis.
In such cases, microscopic examination of scrapings from the mucous membrane for the presence of fungi is necessary. The diagnosis is made on the basis of a positive test result.
Staphylococcal dysbiosis occurs as an enterocolitis and is characterized by symptoms such as abdominal pain, nausea, vomiting, weakness, fever, and electrolyte disturbances in the blood. In the event that dehydration and a violation of cardiac activity join these symptoms, an infectious-allergic shock with a fatal outcome may develop.
Symptoms of intestinal dysbiosis caused by the paracoli group resemble the clinical picture of chronic recurrent enterocolitis. In general, the disease is benign. In the acute stage, abdominal pain and diarrhea appear. During the period of remission, the patient begins to experience constipation.
Proteus dysbiosis is characterized by a local lesion of the intestine, which is accompanied by symptoms of enterocolitis. Quite often, the disease is complicated by the development of proteus sepsis. The diagnosis is confirmed by the deterioration of the patient's condition against the background of antibiotic treatment.
With dysbiosis caused by Pseudomonas aeruginosa, the process can be catarrhal or fibrinous-purulent. The latter is characterized by the formation of foci of necrosis and hemorrhages, in the place of which ulcers and erosion then appear. If Pseudomonas aeruginosa is a consequence of foodborne toxicoinfection, the disease is characterized by an acute course with severe intoxication, severe abdominal pain, nausea, vomiting, and stool disorders.
As a rule, the disease ends in death in the first 10 days from the beginning. Death occurs as a result of cardiovascular failure or paralysis. Pseudomonas aeruginosa dysbiosis caused by antibiotic treatment is milder and usually has a favorable prognosis. Enterocolitis with mixed Pseudomonas aeruginosa-phylococcal-proteus infection is characterized by a severe course and is often complicated by the formation of metastatic foci in the parenchymal organs, as well as the development of sepsis.
To establish an accurate diagnosis, the following methods are used:
- bacteriological examination of feces;
- aspiration of the contents of the jejunum;
- breath test with carbon;
- test to determine the level of 5% hydroxyindoleacetic acid in urine;
- glucose hydrogen breath test.
In addition, an endoscopic and X-ray examination of the colon is carried out in order to exclude the presence of polyps, polyposis or cancer, in which the same symptoms are observed as in dysbiosis (abdominal pain, stool disorders, bloating, weight loss, anemia).
It must be remembered that dysbiosis and irritable bowel syndrome have similar clinical manifestations and quite often appear in combination.
When the first signs of enteritis and enterocolitis appear, it is necessary to cancel antibiotics, prescribe the patient fasting for 1-2 days in order to provide the intestines with complete rest and stop the inflammatory process.
To normalize the electrolyte composition of the blood, intravenous fluid administration and parenteral protein nutrition are indicated. In addition, corticosteroids are prescribed and electrolytes if necessary.
With drug dysbiosis, regardless of which pathogen is the cause of its occurrence, hypovitaminosis develops, in particular, there is a violation of the synthesis and absorption of B vitamins and vitamin K.
Therefore, the patient must be prescribed vitamins.
In the event that laboratory research identifies the causative agent of the disease, targeted antibiotic therapy is carried out. However, antibacterial drugs should be administered with great care and for the shortest possible time.
With fungal dysbiosis, drugs are shown that have a fungicidal effect (nystatin, levorin, mycostatin). In the event that the use of the listed drugs did not give a positive result, the patient is prescribed amphotericin B, the dose of which is set individually at the rate of 250 U / kg. The duration of the course of treatment depends on the severity, duration and characteristics of the course of the disease.
E. coli and Proteus are highly resistant to most antibacterial drugs, so their use does not always give a positive result. These microorganisms are sensitive to drugs of the nitrofuran group, therefore, with the dysbacteriosis caused by them, furadinin, furazolidone are prescribed 0.1 g 3-4 times a day for a course of 7-10 days.
With protean dysbiosis, a positive result is obtained by the use of nalidixic acid preparations, which are taken orally 0.5 g 3-4 times a day for 7-10 days. If necessary, repeat the course of treatment. In addition, Mexaform, Intestopan are recommended, as well as the combined preparation Bactrim, which includes trimethoprim and sulfamethoxazole. The drug Bactrim has an effect on both gram-positive and gram-negative microflora.
Bactrim is prescribed 1 tablet 3 times a day or 2 tablets 2 times a day after meals. The course of treatment is 8-10 days.
Intestinal dysbiosis caused by the association of microbes with a predominance of staphylococcus is treated with antibiotics to which this drug is sensitive: oxacillin, methicillin, lincomycin, cephaloridin, cephaloglycin, carbomycin, etc. In severe cases, the patient is prescribed repeated courses of treatment with several antibacterial drugs. With antibiotic therapy, the patient is prescribed B vitamins, as well as drugs that have a desensitizing and antifungal effect.
In addition, agents that increase the body's resistance are recommended (anti-staphylococcal gamma globulin, staphylococcal toxoid, etc.). in case of dysbiosis with a predominance of Pseudomonas aeruginosa, in addition to antibiotics, antipseudomonal serum and antipseudomonas aeruginosa gamma globulin are indicated.
With dysbiosis caused by the association of microbes, combined treatment is carried out, that is, drugs are used against all identified microbes. In this case, antibiotics are combined with antifungal drugs.
For all types of dysbiosis, biological preparations (colibacterin, bifidumbacterin, bificol) are shown, which are taken 1 ampoule 2-3 times a day 30-40 minutes before meals. The course of treatment with biological preparations is 1.5 months. If necessary, a second course of treatment is prescribed.
Prevention of dysbiosis consists in the inadmissibility of unreasonable and uncontrolled use of any antibacterial drugs, as well as in the need to take bacterial drugs during antibiotic treatment. Weakened patients are recommended to carry out restorative therapy and a balanced diet.
Biliary dyskinesia
Biliary dyskinesia is a disease characterized by functional disorders of the motility of the gallbladder and ducts.
Dyskinesia of the biliary tract can be primary, caused by a disorder of neurohumoral regulation of bile secretion, and secondary, which accompanies chronic diseases of the biliary tract.
In clinical practice, it is customary to distinguish between hypotonic and hypokinetic (atonic), hypertensive and hyperkinetic forms of biliary dyskinesia.
Primary dyskinesias result from general necrosis, diencephalic crisis, after Botkin's illness and other infectious diseases, with intoxication, general allergies of nutritional deficiency, endocrine-hormonal disorders.
Secondary dyskinesias, as a rule, join abnormalities in the development of the biliary tract, and are also often complications of chronic cholecystitis and cholelithiasis.
The patient complains of aching or cramping pains in the right hypochondrium, radiating to the right scapula, shoulder, collarbone. Acute pains can be short-lived, and aching, as a rule, lasts from several hours to several days. Severe pain attacks often give rise to an erroneous diagnosis of gallstone disease.
The most characteristic symptom of dyskinesia is the occurrence of pain during neuropsychic overstrain. An attack of biliary colic may be accompanied by a feeling of cardiac arrest or, on the contrary, an increased heartbeat, numbness of the extremities, and urinary retention.
Most patients have general neurotic disorders, hypo- or hyperthyroidism and other endocrine disorders. In patients with biliary dyskinesia, changes in the blood are noted. In some cases, an increase in body temperature is observed, however, in general, an increase in temperature is not typical for this disease.
During the period of exacerbation of the pain syndrome, there is a tension in the abdomen in the gallbladder region. Symptoms of intoxication do not appear. On palpation, not during an attack, the patient complains of slight pain in the epigastric region and in the gallbladder.
To establish the form of dyskinesia of the gallbladder and ducts, the method of chromatic and continuous fractional probing is used. Holicystography reveals an intense shadow of the gallbladder, as well as its delayed or shortened emptying, in some cases - a prolapse or increase in the size of the gallbladder without any organic changes.
Treatment of biliary dyskinesia depends on the form of the disease and the cause of its occurrence. However, treatment in any case should be aimed at improving the neurohumoral regulation of biliary excretion and eliminating dystonia of the autonomic nervous system.
Secondary dyskinesias appear against the background of abnormalities in the development of the biliary tract, cholecystitis, cholangitis, gallstone disease or adhesions, accompanied by impaired patency of the biliary tract.
Dyskinesia of the esophagus
Dyskinesia of the esophagus is a disease characterized by a violation of the conduction capacity of this organ. As a result of dyskinesia, there is a violation of the peristalsis of the esophagus.
There are several forms of esophageal dyskinesia: primary, secondary, reflex and symptomatic. Primary esophageal dyskinesia develops as a result of cortical disturbances in the regulation of esophageal peristalsis. Secondary dyskinesia of the esophagus is often a complication of diseases such as esophagitis, peptic ulcer and gallstone disease. Dyskinesia of the esophagus very often accompanies diseases that are characterized by the development of a general convulsive syndrome. In this regard, if there is a suspicion of esophageal dyskinesia, the patient needs a consultation with the attending physician.
The esophagus is a narrow, long tube that connects the pharynx to the stomach. The esophagus consists of several sections: cervical, thoracic and abdominal.
Esophagospasm is manifested by a disorder of the act of swallowing (dysphagia), as well as chest pain that occurs when swallowing. For some, they resemble coronary pains. Dysphagia is fickle and sometimes paradoxical: it appears when you ingest liquid, but is absent when swallowing solid food. The diagnosis is made on the basis of an x-ray examination of the esophagus.
Spastic contractions of the esophagus are recorded graphically during esophagotonokymography. The patient is shown sedatives, spasmodic and choleretic drugs. With repeated esophagospasm, intensive treatment of the underlying disease is carried out.
Intestinal dyskinesia
Intestinal dyskinesia is a psychosomatic disease in which intestinal motility disorders occur. With dyskinesia, the motor function of the intestine is disturbed without its organic changes.
Intestinal dyskinesias are divided into primary and secondary. Primary dyskinesia affects the colon and is a psychosomatic illness that occurs as a result of acute or chronic traumatic situations. In addition, the development of the disease can be provoked by acute intestinal infections and a low-slag diet.
With intestinal dyskinesia, there is a violation of the cholinergic and edrenergic regulation of the colon, as well as certain changes in the levels of gastrointestinal hormones, as a result of which the motor function of the colon is impaired. With constipation, bowel contractions intensify, and with diarrhea, on the contrary, they are weakened.
Secondary dyskinesias can occur for a number of reasons, including diseases of the digestive system, endocrine system. In addition, drugs affect the motility of the colon: anesthetics, muscle relaxants, anticonvulsants, anticholinergics, inhibitors, monoamidoxidases, opiates, diuretics, antibiotics, psychotropic drugs.
With primary intestinal dyskinesia, a combination of neurological and intestinal disorders is observed. The clinical picture is characterized by abdominal pain, bloating, and stool disturbance. Quite often, the patient cannot determine the location of the pain. The pain can be aching, pulling, strong or weak. Stool disorders occur in 90% of cases. As a rule, it is diarrhea, alternating with constipation.
In addition to intestinal disorders, patients may complain of pain in the heart, joints, back. On examination, no organic changes are found. An objective study of the clinical picture of the disease, as a rule, practically does not provide information, therefore the diagnosis is made by the method of exclusion.
First, intestinal pathologies such as polyps, tumors, diverticula, developmental anomalies are excluded, then a distinction is made between dyskinesia and non-ulcer colitis, and only after that primary dyskinesia is differentiated from secondary and the causes of the secondary disease are clarified.
First, the usual examinations are carried out, recommended for the detection of colon pathologies: scatological examination of feces for occult blood and dysbiosis, irrigoscopy and endoscopy, as well as colon biopsy.
The coprogram shows the presence of dysbiosis, in particular, with constipation. Endoscopic examination determines signs of intestinal motility disorders in the absence of organic changes. In contrast to non-ulcerative colitis, the histological picture of the intestine with dyskinesia remains within the normal range.
In most cases, it is especially difficult to distinguish between primary and secondary dyskinesia. As for the diagnosis of the causes of secondary dyskinesia, it is based primarily on the data of the anamnesis and general clinical examination of the patient.
Patients with intestinal dyskinesia are first of all referred for consultation to a psychotherapist, who determines how to treat psychopathological syndrome, which is the main cause of dyskinesia. To eliminate it, the patient is prescribed psychotropic drugs.
At first in small doses, then gradually increasing.
If the patient is anxious, in connection with which vegetative disorders arise, tranquilizers are shown to him: seduxen, sonapax, elenium, phenazepam. In depression, a positive result is achieved with the use of tricyclic antidepressants. The course of treatment with psychotropic drugs should not be too long. Symptomatic treatment of intestinal disorders (constipation and diarrhea) is also carried out.
Benign tumors of the digestive system
Benign tumors are diseases characterized by a favorable prognosis: they grow slowly and do not metastasize. It should be noted that the benign nature of such tumors is relative, since under the influence of certain conditions they can cause serious complications that endanger the patient's life.
Benign tumors can occur in all organs of the digestive system, but the esophagus, small intestine, gallbladder, liver and pancreas are extremely rare. The stomach and colon are most susceptible to this disease.
Benign tumors of the stomach include myoma, fibroma, hemangioma, neurinoma, homedectoma, carcinoid, and polyps. The colon (colon) can form polyps, villous tumors, lipomas, leiomyomas, fibromas, hemangiomas, lymphangiomas, and carcinoids.
The most common gastric tumors are fibroids and polyps, and among the colon tumors are single and multiple adenomatous and glandular villous polyps. Benign tumors can be of epithelial, connective tissue, muscle, or nerve origin.
Benign tumors are usually located in the submucosa, muscle or sub-serous layer of the stomach. In most patients, a tumor is detected during an operation, the reason for which is a suspicion of oncology or a lesion of the stomach of unknown etiology, or during autopsy.
Polyps of the stomach are formed from the integumentary fossa epithelium of its mucosa. They can be adenomatous and inflammatory-hyperplastic. Polyp tissue consists of glands of various sizes and shapes, separated from each other by connective tissue layers and lined with prismatic cells. Often, mucoid secretions accumulate in the lumen of the glands, resulting in the formation of cysts.
As a rule, polyps are located in the pyloroantral compartment, less often in the body or cardia.
Polyps can be single or multiple. The most common are spherical and oval polyps. Like all benign tumors, polyps are clearly demarcated from the surrounding mucous membrane.
The surface of the polyps is usually smooth or granular, and the color is pink, orange, or bright red.
In some cases, the diameter of a polyp can reach several centimeters. Polyposis is considered a precancerous condition. The larger the polyp, the wider and softer its base, the more likely it is to degenerate into a cancerous tumor.
Intestinal polyposis is characterized by formations in this organ, which protrude into the intestinal lumen and have the structure of an adenoma. Adenomatous polyps with a long, thin stem can move along the intestinal lumen. In the anal canal, as a rule, fibrous polyps are formed, which is associated with the presence of inflammatory processes in the mucous membrane of the overlying sections of the colon.
Adenomatous and villous polyps are mucosal hyperplasia and can be single or group. Their etiology is still not fully understood, but there is an assumption about their viral nature. A special form of common multiple lesions is called diffuse colon polyposis. Often it is combined with polyposis of the entire gastrointestinal tract (total polyposis).
Clinical manifestations in benign stomach tumors occur only after reaching a large size.
The patient complains of a feeling of heaviness and pain in the epigastric region. A tumor located in the outlet of the stomach in most cases becomes the cause of its obstruction.
Tumor bending into the pyloric canal or duodenum leads to the development of acute obstruction. Often, tumors ulcerate, causing bleeding.
Fibroids, leiomyomas, fibroids and rhabdomyomas are in most cases localized in the subserous or muscular layer. Large tumors on palpation are defined as immobile formations of a spherical or oval shape with a densely elastic consistency.
The diagnosis of the disease is made on the basis of X-ray and gastroscopic examination. X-ray reveals filling defects that have smooth contours (as opposed to a malignant tumor), most often preserved mucous membranes. On palpation, they are mobile. Distinguishing a benign tumor from oncology is quite simple with the help of gastroscopy.
Benign tumors in most cases are solitary, have a spherical shape and are associated with the stomach wall with a wide base. The mucous membrane covering the tumor is smooth, its structure and color are not changed. The base of the tumor and the surrounding mucosa are not welded together. They are connected by short radial folds.
Polyposis of the stomach in most cases proceeds without pronounced symptoms. The manifestation of clinical signs, as a rule, is due to the presence of concomitant diseases, in some cases - complications of polyps. Polyposis can be complicated by bleeding or malignancy. This disease is often accompanied by iron deficiency anemia.
The main methods for diagnosing gastric polyposis are X-ray and gastroscopic examinations. The degeneration of a tumor into a malignant one can be confirmed only after histological and cytological studies of biopsies.
Typical symptoms of intestinal polyposis are mucous or mucous-bloody discharge from the rectum, constipation, and abdominal pain. It should be borne in mind that often polyposis is asymptomatic and is detected only with irrigoscopy, colonoscopy or sigmoid copy. Polyps may not grow for a long time and not disturb the patient. However, such a clinical picture of the disease is especially dangerous, since oncological degeneration of pathological neoplasms is possible.
Diffuse polyposis is characterized by early development of anemia, increased frequency of digestive disorders, leading to exhaustion of the body. In most patients, polyps become malignant over time, and the oncological tumor is characterized by rapid growth.
Benign stomach tumors are removed by surgery. Complete cure is achieved after gastric resection. With polyposis of the stomach, the same treatment is shown as for chronic gastritis with low acidity of gastric juice.
Patients with polyposis should be examined at least 1-2 times a year in order to prevent the development of malignant tumors. If necessary, patients are prescribed electrocoagulation of polyps using a gastroscope.
With multiple polyposis, as well as if the polyp has a wide base and its diameter exceeds 2 cm, surgical treatment is indicated. The main goal of the treatment of adenomatous and villous intestinal polyps is to prevent them from growing into a malignant tumor.
Polyps are removed by electrocautery through an endoscope. After surgery, the patient is put on a dispensary record, since the disease often gives relapses.
In diffuse polyposis, all or almost all of the colon is surgically removed. With timely surgical intervention, the prognosis of the disease is favorable.
Duodenitis
Duodenitis is a disease characterized by inflammation of the duodenal mucosa and occurs mainly in men. There are two forms of duodenitis, acute and chronic.
Chronic duodenitis can manifest itself in ulcerative, pancreatic and mixed forms. Primary duodenitis is usually caused by exposure to harmful exogenous factors, such as unhealthy diet and alcohol abuse. Secondary duodenitis is associated with the presence of chronic gastritis, peptic ulcer, diseases of the liver, gallbladder, intestines, pancreas, as well as giardiasis and ankylotomidosis. Much less often it is combined with diseases of the kidneys, cardiovascular system, allergies.
Quite often, the development of duodenitis is associated with impaired motility of the duodenum. In addition, the causes of the disease can be giardiasis and malnutrition, which makes it difficult to diagnose the disease.
The main manifestations of the acute form of the disease are severe pain, a feeling of heaviness in the epigastric region, loss of appetite, headaches, weakness, and general malaise. On examination, the tongue is dry and coated. In some cases, short-term jaundice is observed. On the right side of the abdominal cavity, a cylindrical seal, or infiltration, is felt.
The characteristic signs of duodenitis are a sharp weight loss, hypovitaminosis, pain on palpation in the right side of the abdominal cavity.
With an ulcerative form of chronic duodenitis, the patient complains of pain in the epigastric region, which can occur when hunger, eating, at night. The characteristic signs of this form of duodenitis are also heartburn, belching, increased acidity of gastric juice, constipation.
Chronic duodenitis is characterized by alternating periods of lack of appetite with periods of severe hunger. In addition to pain in the epigastric region, chest pains, impaired swallowing, various autonomic disorders are observed.
In holicysto- and pancreatic forms of chronic duodenitis, symptoms of dysfunction of the gallbladder and pancreas are added to the signs indicating damage to the duodenum. In this case, the patient complains of pain in the right or left hypochondrium, a moderate and short-term increase in the activity of pancreatic enzymes in the blood and urine.
At the same time, there are no signs of inflammation, however, gradually, against the background of functional disorders of the gallbladder and pancreas, cholecystitis and pancreatitis often develop. To establish the diagnosis, the patient is prescribed duodenofibroscopy, X-ray examination and aspiration duodenobiopsy.
Duodenofibroscopy shows signs of inflammation and edema, as well as cicatricial changes and deformation in the duodenal bulb or its descending part. X-ray examination reveals changes in the relief of the intestinal mucosa. Aspiration duodenobiopsy reveals the presence or absence of edema, cell infiltration, and changes in the villi.
Duodenitis is dangerous because it is often complicated by periduodenitis or bleeding. Periduodenitis, as a rule, is asymptomatic, so its presence can only be established by X-ray examination for the presence of duodenostasis (delayed movement of contents through the lumen of the duodenum), antiperistalsis, stenosis. Bleeding in this disease is also profuse, as in peptic ulcer disease.
Treatment of duodenitis is similar to that of acute gastritis. In the case of a pronounced inflammatory process (phlegmonous duodenitis), the patient is shown antibiotics of a wide spectrum of action. Treatment of chronic duodenitis is similar to therapy for duodenal ulcer.
In the absence of complications, the prognosis of the disease is favorable. Even massive bleeding is rarely fatal. As a prophylaxis of duodenitis, it is recommended to follow the diet, exclude alcohol consumption, and timely treat helminthic-protozoal invasions.
Cholelithiasis
Gallstone disease is a condition in which stones form in the liver, gallbladder, or bile ducts. The formation of stones is due to stagnation of bile or a violation of natural metabolic processes. This disease is most susceptible to women aged 35-60 years.
There are three main types of gallstones: cholesterol, consisting of cholesterol crystals, pigment, consisting of calcium and bilirubin salts, mixed, consisting of cholesterol, bilirubin and calcium salts. The most common are cholesterol stones.
Gallstone disease can develop as a result of impaired metabolism of cholesterol and certain salts, stagnation of bile in the bladder and infection of the biliary tract. The main factor contributing to the development of this disease is a change in the ratio of cholesterol, bilirubin and calcium contained in bile in a state of unstable colloidal solution.
Cholesterol is kept in solution by the action of fatty acids. In the case of a decrease in their content, cholesterol crystallizes and precipitates. Disruption of the formation of fatty acids occurs as a result of the development of functional insufficiency of liver cells.
As a result of an infectious inflammation of the gallbladder and bile ducts, the chemical composition of bile is disrupted, as a result of which cholesterol, bilirubin and calcium precipitate with the formation of stones. As a result of the formation of stones, inflammation of the gallbladder develops. In the absence of inflammation, the wall of the gallbladder gradually atrophies and sclerotizes.
The pressure of the stone leads to the development of pressure ulcers and perforation of the gallbladder wall. Gallstone disease develops as a result of excessive consumption of fatty foods, metabolic disorders, atherosclerosis, biliary tract infection, liver damage after Botkin's disease.
Stagnation of bile can be triggered by biliary dyskinesia, adhesions and scars in the gallbladder and bile ducts, increased intra-abdominal pressure. The latter can be caused by pregnancy, constipation, obesity, lack of physical activity.
The most common symptoms of gallstone disease are biliary colic (pain in the right hypochondrium) and dyspeptic disorders. It should be noted that the occurrence of biliary colic is due not so much to the number and size of stones as to their location.
For example, there may be no pain if the stones are located at the bottom of the gallbladder. Moving stones to the neck of the gallbladder or cystic duct, on the other hand, gives severe pain resulting from spasm of the gallbladder or ducts.
An attack of biliary colic, as a rule, begins after ingestion of fatty foods, hypothermia, physical or neuropsychiatric stress. Such attacks begin suddenly, most often at night. At first, pain of a stabbing or cutting nature is felt in the right hypochondrium with irradiation to the right scapula, neck, jaw, then it is localized in the gallbladder and epigastric region.
The pain syndrome is so severe that many patients develop pain shock. Often, pain leads to the development of an attack of angina pectoris. If the pain caused by prolonged spasm or blockage of the bile duct is prolonged, the patient develops mechanical jaundice.
Attacks can be accompanied by fever, nausea and vomiting. The listed signs disappear immediately after the elimination of the pain syndrome.
The duration of bouts of biliary colic can vary from a few minutes to several hours, and in severe cases, up to several days. After the disappearance of pain, the patient's condition quickly returns to normal.
When examining patients in the upper eyelid and ears, xanthomatous plaques (cholesterol deposits) are found. In addition, patients have bloating, tension and soreness of the abdominal wall, in particular, in the area of the right hypochondrium.
Quite often, an exacerbation of gallstone disease is manifested exclusively by dyspeptic syndrome, which is characterized by a feeling of heaviness in the epigastric region, belching and vomiting. Pain in the right hypochondrium can be insignificant and is determined only by palpation of the abdomen.
The clinical manifestations of gallstone disease, as a rule, change as complications develop (acute cholecystitis or cholangitis), as well as as a result of blockage of the bile duct caused by the movement of stones.
Blockage of the cystic duct is especially dangerous because it leads to dropsy of the gallbladder, which is accompanied by acute pain. Dropsy of the gallbladder is manifested by a feeling of heaviness in the right hypochondrium. In the event that an infection joins the dropsy, the body temperature rises and the general condition of the patient worsens. A blood test shows leukocytosis and an increase in ESR.
In case of complete blockage of the bile duct, jaundice develops, the liver enlarges and hardens. As a result of a violation of the outflow of bile in the gallbladder and biliary tract, inflammatory processes develop.
Stones are detected by ultrasound examination (ultrasound) of the abdominal cavity, holongiography, cholecystography. It should be borne in mind that the latter research method is contraindicated in the presence of jaundice.
Treatment in most cases is aimed at stopping the inflammatory process, improving the motor function of the gallbladder and the outflow of bile from it. Hospitalization is indicated for patients with biliary colic syndrome. In this case, pain relievers are prescribed, including narcotic drugs, as well as antibacterial and sulfa drugs. Cold is applied to the abdomen to relieve swelling.
As a prophylaxis of gallstone disease or its exacerbations, a special diet, therapeutic exercises, and elimination of constipation are recommended. In addition, the drug olimetin is shown, 2 capsules 3-4 times a day. The outflow of bile and the discharge of cholesterol crystals are facilitated by low-mineralized alkaline waters.
In the event that the treatment does not give a positive result, surgical intervention is recommended in order to remove the gallbladder. The indications for the appointment of surgery are perforation of the gallbladder with the development of developed or limited biliary peritonitis, obstructive jaundice, dropsy of the gallbladder, biliary fistulas. The operation is also indicated in the presence of multiple stones, repeated attacks of biliary colic, as well as in the case of a non-functioning gallbladder.
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 influenced by various environmental factors - the nature of nutrition, working and living conditions.
In addition to structural changes in the organs of the digestive system, functional disorders can also occur. The internal organs of digestion include the esophagus, stomach, intestines, liver, pancreas. The biliary tract is 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 goes into a chronic form, surgical intervention may be required.
Diseases of the digestive system
Diseases of the digestive tract are distinguished by the variety of their clinical and morphological signs.
They include independent primary diseases, which are studied by a science called gastroenterology, as well as others, secondary, which are a manifestation of a number of diseases of an infectious and non-infectious nature, 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 disorders of the digestive system are:
Exogenous, endogenous, as well as genetic factors can provoke diseases of the digestive system.
Exogenous
These primary causes of the disease include:
- dry food intake,
- eating very hot foods,
- abuse of various spices and herbs,
- excessive alcohol consumption,
- smoking,
- eating poor quality food,
- lack of diet,
- a hasty meal
- defects of the human chewing apparatus,
- uncontrolled intake of medications,
- unfavorable ecological situation.
Diseases caused by exogenous factors include gastritis and enteritis, colitis, stomach 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, 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 of the esophagus and the stomach), diagnosed abnormal development of the pancreas (for example, cystic fibrosis of the pancreas itself), as well as congenital hypoplasia of the pancreas ...
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 chair changes;
- belching;
- vomit;
- flatulence;
- violation of appetite;
- fast fatiguability;
- weight loss;
- abdominal pain in various locations;
- insomnia.
The rest of the 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 carefully examine 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 urine analysis,
- analysis of feces.
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 using 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 biopsy:
- colonoscopy,
- esophagogastroduodenoscopy,
- sigmoidoscopy,
- laparoscopy.
For the purpose of examining the stomach, the use of functional tests is practiced, which allows obtaining detailed information about the acid secretion of the stomach, its motor function, as well as the state of the pancreas and small intestine.
Treatment of diseases of the digestive system
The method of treatment is determined after the diagnosis is made. With infectious and inflammatory pathologies, antibiotic therapy is required. The following drugs are used: "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 the articles on the treatment of certain diseases). A specially selected diet is essential in the treatment of diseases of the digestive system and is the key to successful treatment.
If usual enteral nutrition is impossible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter the blood immediately, I bypass 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, aminofusine), fats (lipofundin), carbohydrates (glucose solutions). Also, electrolytes and vitamins are 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 to maintain a healthy lifestyle.
This includes giving up bad habits (smoking, alcohol and others), regular physical education, exclusion of physical inactivity (leading an active lifestyle), compliance with 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 annual ultrasound examination of the abdominal organs and esophagogastroduodenoscopy.
And in no case should the disease be started, 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 bitterness appears 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 disturbance in the work of the biliary tract. You need an in-person consultation with a doctor for examination.
Question:Hello! I'm 52 years old. Somewhere in 2000, I was examined by a doctor, diagnosed with gastritis and 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 tormented by heartburn, there are pains in the stomach and liver. I take various medications for heartburn, and during the year, after each meal, I feel a heaviness in my stomach and after a while I constantly fall asleep and again frequent heartburn. I almost constantly save myself only with antacids. Please tell me why after a meal I start to fall asleep and is not the frequent use of Rennie and Almagel A harmful?
Answer: First of all, you need to decide on the stones in the gallbladder. If you have them, all your problems will only get worse. An examination by a gastroenterologist is required.
