Amyloidosis is a systemic disease characterized by impaired protein metabolism and is accompanied by extracellular deposition of a complex protein-polysaccharide complex in organs and tissues.

Traditionally, there are several forms of this disease:

- 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 involves several organs. Primary amyloidosis occurs in an autosomal dominant hereditary manner. Often the causes of the disease remain unclear (idiopathic amyloidosis).

Secondary amyloidosis appears against the background of pulmonary tuberculosis and extracellular forms of tuberculosis, 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 violations of the swallowing reflex (dysphagia) when swallowing dry and dense food. X-ray shows a decrease in the tone of the tissues of the esophagus.

Amyloidosis of the intestine is the most common. 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, a syndrome of insufficiency of absorption and a violation of parietal digestion develop.

As an independent disease, tumor-like amyloidosis of the intestine occurs, which is difficult to diagnose because of the tumor. In most cases, this pathology is detected only during surgical intervention. Typical symptoms of a tumor are pain and intestinal 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. AT this case the patient feels heaviness in the epigastric region after eating, as well as digestive disorders: heartburn, belching, nausea, etc.

The radiograph 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.

Hepatic amyloidosis is common. His characteristic symptoms are hardening of the liver and enlargement of the spleen. Liver enlargement is observed at a late stage of the disease. On palpation, the edge of the liver is smooth, soreness is not observed or is expressed slightly.

Sometimes the patient feels pain in the right hypochondrium. In addition, digestive disorders 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 occurs as a result of 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 content of bilirubin, 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. Amyloidosis of the intestine may be accompanied by intestinal bleeding, amyloid ulcers, violation of the integrity and narrowing of the intestine, 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 gastric ulcers, 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 disability of patients. A lethal outcome is possible as a result of renal or heart failure, as well as with general exhaustion of the body. Particularly severe prognosis for amyloidosis of infectious etiology.

With timely and proper treatment of amyloidosis at an early stage, its reverse development is possible. The treatment of secondary amyloidoses is primarily reduced to the treatment of the underlying disease, against which they arose. As a rule, after the treatment 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 intravenous and subcutaneous multivitamins, as well as plasma transfusion. In case of severe edema, diuretic drugs are recommended to remove excess fluid from the body. In intestinal amyloidosis, astringents are prescribed: basic bismuth nitrate, adsorbents.

Liver extracts and hydrolysates are used in liver amyloidosis. In this case, it is also recommended to eat raw liver. In primary liver amyloidosis, anticholinergic drugs are indicated: delagil, plaquenil.

Surgical intervention is necessary for isolated tumor-like amyloidosis of the gastrointestinal tract. Prevention of amyloidosis consists in timely diagnosis, proper 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 is very common 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 submucosal 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 glandular lesions without atrophy, atrophic (pronounced striasis), and gastritis with restructuring of the gastric mucosa.

According to the place 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 on the background of taking rough, indigestible, too cold or too hot food. As a result, irritation of the gastric mucosa occurs. Alcohol and smoking can also cause gastritis.

In addition, acute gastritis can develop against the background of food poisoning or food allergies. An irritant 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 overstrain 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, followed by pathological changes.

The most common is simple gastritis. Corrosive gastritis develops when concentrated ethyl alcohol, salts of heavy metals, 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 ulcers, 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 malnutrition, vitamin deficiency, frequent consumption of spicy, hot and cold foods, poor chewing of food, alcohol and tobacco abuse, as well as long-term use of drugs that cause irritation of the gastric mucosa.

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 disorders of the stomach, which leads to inflammatory and degenerative changes, violations of the regeneration process in the epithelium of the surface of the layers of the gastric mucosa, which can atrophy or completely rebuild.

To prevent gastritis, it is necessary to visit the dentist regularly and treat caries, since chronic infection in the oral cavity contributes to diseases of the gastrointestinal tract.

Manifestations of acute gastritis, as a rule, are expressed. 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, and 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 appears 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. Full recovery of the gastric mucosa occurs within 10-15 days.

At the beginning of the disease, there is an increase in secretion, after which the reverse process occurs: acidity decreases. Gastroscopy reveals redness of the mucous membrane, mucus secretion. In severe cases, hemorrhages and erosion may occur. In this case, the transition of the disease to a chronic form is possible.

Corrosive gastritis gives severe pain behind the sternum, burning sensation and pain in the mouth, pharynx, esophagus and stomach. This form of the disease is usually accompanied by repeated painful vomiting. Traces of a chemical burn are observed on the mucous membrane of the mouth, pharynx and larynx: swelling, redness, ulcers. Acetic acid usually leaves 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 of the voice is observed. Perhaps the development of vascular collapse and the addition of a secondary infection.

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) shortly after the irritant 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. Among the complications of corrosive gastritis are motor insufficiency of the stomach, peritonitis, dysphagia, microgastria, acute mediastinitis.

During the first 2-3 days, the risk of death remains, which may occur as a result of shock or acute peritonitis. With phlegmonous gastritis of the stomach, an abscess of its wall occurs. 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 inflammation of the peritoneum, fever, confusion, circulatory failure.

On palpation, there is bloating and pain in the epigastric region. As a result of pathological changes, the patient progresses exhaustion. 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 unfavorable. The most common complications are subdiaphragmatic abscess, liver abscess, purulent mediastinitis, thrombophlebitis of large abdominal vessels, pleurisy.

Gastritis with reduced secretory function of the stomach is characterized by a decrease in the acidity of gastric juice and atrophic changes in the mucous membrane. The elderly are most susceptible to this disease. Typical symptoms of the disease are belching with air, heaviness in the epigastric region, an unpleasant aftertaste in the mouth, nausea in the morning, and indigestion. The disease proceeds slowly, with alternating periods of exacerbation and remission.

A 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 a targeted biopsy of the gastric mucosa.

With a long course of the disease, a significant decrease in the patient's body weight, symptoms of polyhypovitaminosis, insufficiency of the endocrine glands, the development of cholecystitis, intestinal dysbacteriosis, normochromic or iron deficiency anemia are observed.

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 lesions of the gastric glands without atrophy. As a rule, this disease occurs at an early age as a result of alcohol abuse.

Gastritis with preserved and increased secretory function of the stomach is characterized by aching pain and heaviness in the epigastric region, which occurs 2-3 hours after ingestion of spicy or spicy food. Patients complain of constant heartburn, belching and nausea.

At the same time, symptoms of nervous breakdown and vegetovascular dystonia are often observed: sleep disturbance, 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 pyloric peristalsis, fluid in the stomach and uneven relief of the mucous membrane. Gastroscopy shows swelling and redness of the gastric mucosa.

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 of the stomach.

Symptoms of rigid gastritis are pain of moderate intensity in the epigastric region, increased secretion of gastric juice, dyspepsia. The radiograph shows a tubular narrowing of the pylorus. In 50% of cases, there is a significant probability of the transition of the disease to oncology.

With erosive gastritis, erosions form on the gastric mucosa. The 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. A complication of the disease can be gastric bleeding. Often, bleeding is due to increased permeability of the vessels of the stomach or injuries to its mucous membrane.

The healing process of erosion depends on individual features the patient's body, but, as a rule, it takes at least two months. Hypertrophic gastritis most often occurs in men over 40 years of age. 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.

The radiograph shows enlargement and swelling of the folds of the gastric mucosa. Gastroboboscopy 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 exhaustion of the body.

Polypous gastritis is characterized by atrophy of the gastric mucosa, accompanied by its disregenerative hyperplasia and achlorhydria. The symptomatology of the disease is in many ways similar to the clinical picture of gastritis with secretory insufficiency. Polypous 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 indicated.

In the event that the disease arose as a result of alkali poisoning, washing with a weak solution of acetic acid or citric acid is indicated, in case of acid poisoning - 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 when the patient's condition is serious. Medicines are prescribed depending on the etiology of the disease. So, with gastritis of an allergic nature, antihistamines are indicated, with an infectious nature - antibacterial, as well as absorbent substances: activated carbon, kaolin, etc.

If the patient's body is dehydrated, appoint up to 1 liter of isotonic sodium solution subcutaneously and 5% glucose solution. The development of acute heart failure is an indication for the use of caffeine, cordiamine, mezaton, norepinephrine. In case of 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, anestezin is indicated at 0.3 g 2-4 times a day.

With corrosive gastritis, the patient is washed with a large amount of water through a probe 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 washing through a tube is contraindicated if there is destruction of the esophagus or collapse. Since in the first days of treatment the patient is contraindicated in eating, he is given saline, 5% glucose solution subcutaneously and isotonic sodium chloride solution intravenously.

In addition, vitamins, plasma and protein hydrolysers are administered subcutaneously or intravenously. In case of secondary infection, antibiotics are prescribed. Gastric perforation and laryngeal edema are indications for surgical intervention. 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 mandatory. Broad-spectrum antibiotics are administered intravenously or subcutaneously to the patient. 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 needed to relieve pain. In chronic gastritis with a reduced secretory function of the stomach, ganglion blocking drugs that have an antispasmodic effect are used for this purpose. Preparations of this group have practically no effect on secretion (gangleron, kvateron).

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 astringents and enveloping agents is effective. During remission, if an exacerbation is suspected, replacement therapy is carried out 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 preserved or increased secretory function of the stomach, antispasmodic, anticholinergic and ganglion blocking drugs (atropine, arpenal, spasmolitin, platyfillin, benzohexonium) are used in combination with antacids (almagel, vikalin). In addition, drugs are used that 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 reduced secretory function of the stomach, since all these diseases are characterized by the presence of secretory insufficiency.

In acute gastritis, the patient is shown therapeutic nutrition. 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 normal 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. In the following days, the same diet is shown as with ordinary gastritis.

The basis of the treatment of gastritis is proper nutrition. All therapy is carried out on the basis of 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 nutrition of the patient depends on the nature of the secretory disorders. Thus, in chronic gastritis with reduced secretory function, diet No. 2 is prescribed; in gastritis with preserved or increased secretory function of the stomach, diet No. 1a is indicated during an exacerbation of the disease.

During periods of remission of the disease, the patient is shown a full-fledged diet with a limited content of salt, carbohydrates and ecstatic substances. In particular, this applies to patients with increased acidity of gastric juice.

With gastritis, eating spicy dishes, marinades 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 conduct an examination of the gastrointestinal tract and, in case 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's disease, yellow fever, secondary infectious, arising from paratyphoid fever, relapsing fever, lobar pneumonia, and toxic (drug-induced hepatitis) resulting from exposure to drug liver tissue.

Viral hepatitis is divided into epidemic (hepatitis A) and serum (hepatitis B). In addition, acute hepatitis of alcoholic origin is distinguished.

Chronic hepatitis is divided into 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, and septic bacterial infection.

The most common viral hepatitis is caused by virus A, which is contained in the patient's blood and urine at the end of the incubation period, in the acute preicteric and early icteric periods, and by virus B, contained in the blood (patient's serum).

The development of toxic acute hepatitis is associated with exposure to drugs, industrial poisons, mushroom poisons, radiation exposure, and severe body burns. Currently, there are 1000 drugs that can provoke acute hepatitis in the course of treatment, including isonicotinic acid derivatives, sodium salt, para-aminosalicylic acid (PAS), MAO inhibitors - hydrazine derivatives, male fern extract.

The greatest danger of developing hepatitis occurs with prolonged use of Voltaren, indomethacin, cordarone, chloramphenicol, mercazolil and other drugs.

Alcoholic acute hepatitis is caused by large amounts of alcohol or prolonged abuse alcoholic drinks. 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.

Often, chronic gastritis develops in people with chronic diseases of the abdominal organs: gastritis, pancreatitis, enterocolitis, peptic ulcer and gallstone diseases, etc. In case of a disease caused by industrial, drug and household intoxications, the most common causes are lead compounds, trinitrotoluene, chloroform, atofan, chlorpromazine, benzene, isoniazid.

Of the narcotic substances, barbiturates, narcolan, halothane, hexenal, and halothane can provoke hepatitis. In chronic hepatitis caused by exposure to toxic substances or an allergic reaction, liver parenchyma is damaged and enzyme metabolism is impaired.

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 blockage by a stone or cicatricial compression of the common bile duct, as well as as a result of cancer of the pancreatic head with prolonged subhepatic cholestasis and accompanying inflammation of the bile ducts and passages, as well as with primary toxic or toxic-allergic lesions of cholangiol .

Holistic hepatitis can be caused by: medications: phenothiazine derivatives, methyltestosterone and some of its derivatives.

In the pathogenesis of the disease, the direct impact of etiological factors (viruses, toxins, etc.) on the liver parenchyma is of particular importance, which leads to dystrophy and necrobiosis of hepatocytes. chronic course and further development pathological processes of inflammation and dystrophy due to specific immunological disorders.

In the case of a mild course of acute hepatitis, symptoms may be absent or manifest slightly. This makes it difficult to diagnose the disease, which can only be carried out as a result of a special examination. A change in the color of the patient's skin, characteristic of hepatitis, is noticeable only in daylight. First of all, staining of the outer membranes of the eyes (sclera) and the mucous membrane of the soft palate is observed.

The severe course of the disease, on the contrary, is characterized by pronounced symptoms. Distinctly viscous 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 in size, and with liver dystrophy, its decrease is observed.

Blood tests show hyperbilirubinemia, increased activity some serum enzymes. There are disturbances in the production of fibrinogen, prothrombin, coagulation factors VII and V by the liver, 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 necrosis of the parenchyma, severe hemorrhagic syndrome and jaundice, severe pain in the liver. As a result of pathological changes, hepatic coma may occur.

In cholestatic hepatitis, symptoms of liver damage appear 1-2 weeks after taking the drug that caused the allergic effect. A characteristic symptom of the disease is pruritus, which usually precedes jaundice. At the same time, the patient's liver remains normal, and the body temperature is slightly elevated.

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, there are manifestations of pancreatitis. In such patients, symptoms of chronic alcoholism are observed: hand tremor, decreased sensitivity in the lower extremities, severe weakness, and neuropsychiatric disorders.

Alcohol provokes dystrophy of liver cells, causing violations of 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 can occur in 1-2 months.

Chronic hepatitis can only be diagnosed if the disease lasts more than 6 months.

Chronic hepatitis of infectious etiology (for example, Botkin's disease) is characterized by a symptom of jaundice (visible 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. Characteristic signs are liver enlargement, dull pain and a feeling of heaviness in the right hypochondrium, skin itching (in particular, with drug-induced 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, 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 albumins, and 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, a slight increase in the liver, weakness. Almost all patients have an increase in serum protein. With a diet and a complete rejection of alcohol, a complete recovery of the patient is possible.

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, fatigue, rapid decline in working capacity, lack of appetite, pain in the liver, a slight increase in body temperature.

In severe cases 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 usually also enlarged. In 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 the 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, however, 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, a fatal outcome may occur.

In the treatment of acute viral hepatitis (Botkin's disease) and other hepatitis of infectious etiology, the patient must be hospitalized in a special department for infectious patients in a timely manner. During the peak 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 an isotonic sodium chloride solution subcutaneously or in the form of drip enemas.

To restore the functioning of the liver, agents are used to improve the metabolism of liver cells: B vitamins, glucuronic acid preparations, cocarboxylase, lipoic acid.

In severe viral hepatitis, characterized by a protracted course and severe intoxication of the body, glucocorticosteroid hormones are indicated. Preparations of this group are also used for cholestatic hepatitis, edematous-ascitic syndrome, as well as for suspected liver dystrophy.

The patient is prescribed 20-40 mg of prednisolone per day. The duration of treatment with the drug varies from 3-4 weeks to several months. With persistent hepatitis and the transition of acute hepatitis to the chronic form of the disease, the use of prednisolone is extended to 1.5 years. In this case, the daily rate of the drug is reduced to 10-20 ml. An indication for reducing the dose of the drug is an improvement in the patient's condition and a decrease in the content of bilirubin in the blood serum to 0.02-0.03 g per 1 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 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 sera. With hepatitis of toxic etiology, patients are hospitalized in the poisoning department and gastric lavage is carried out in order to remove the irritant that provoked the development of the disease from the body.

In addition, the use of drugs that relieve the effects of intoxication and improve the function of liver cells is shown. Also, the patient is prescribed bed rest, a strict diet that provides for a limited intake of fats, the introduction of B and C vitamins, lipoic and folic acid. In addition, drugs are prescribed that 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 unitiol 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 hepatitis of an infectious nature. In severe hepatocellular insufficiency, the patient must be shown glucocorticoids.

With alcoholic hepatitis, the patient is contraindicated in taking alcoholic beverages. At the same time, a sparing diet with a sufficient content of vitamins and proteins is prescribed. 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 suspected dystrophy or cirrhosis of the liver, Essentiale is used in the amount of 2 capsules 3 times a day. As for chronic hepatitis, even in the remission stage, it is necessary to follow a diet.

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 exchange of liver cells, additional vitamin therapy is carried out. At the same time, vitamins C, B1, B2, B6, B12 are administered to the patient. In addition, cocarboxylase, ascorbic, nicotinic and folic acid. 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 decrease in dose, or 20-50 mg per week of retabolil intramuscularly.

At the stage of exacerbation, patients require hospitalization, bed rest and a strict diet rich in proteins and vitamins. In cholestatic hepatitis, small doses of immunosuppressants and corticosteroid hormones are prescribed as an anti-inflammatory and immunosuppressive agent. The drug prednisolone is prescribed in an amount of 20-40 mg per day for 2-3 months, then gradually reduce the dose 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. With regard to therapy with hydrolysates and liver extracts, it must be carried out with great care, since these drugs, administered in the acute stage, can activate the process and enhance the further development of the disease.

With persistent and active chronic hepatitis, cholagogues, liver extracts, and anabolic hormones should not be taken. In addition, any physiotherapy procedures are strictly contraindicated.

With timely and rational treatment with 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 unable to work.

With viral hepatitis, the patient is shown diet No. 5 with a restriction of fats, 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. Increase the amount of carbohydrates in the patient's diet. Signs of the development of a precomatose state are an indication for a decrease in protein.

Patients with persistent and aggressive chronic hepatitis should avoid fried foods, refractory animal fats, spicy and spicy foods. It is recommended to consume dairy products at least 100-150 g per day, as well as mild cheeses. Useful lean boiled fish. The patient is calculated daily diet, which should contain 100-120 g of protein, 70-80 g of fat, 400-500 g of carbohydrates and a total of 3000-3500 kcal.

In 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 early diagnosis is of great importance.

Healthy people need to follow strict hygiene rules. To prevent infection with serum hepatitis during the passage of 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 dangerous compounds.

Do not eat unfamiliar or old mushrooms, as well as any medications without consulting a doctor.

Prevention of chronic hepatitis should be aimed at eliminating the factors provoking exacerbation, taking into account the etiology of the disease.

Hepatosis

Hepatosis is a liver disease in which dystrophy of the parenchyma, the functional epithelial tissue of the liver, is observed. This disease in most cases is caused by excessive consumption of high-calorie foods and alcoholic beverages, which leads to pathological processes in the liver epithelium.

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 with severe poisoning with arsenic, phosphorus, and 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 protein and vitamin deficiency, obesity and malnutrition, anemia, enteritis, pancreatitis, and some infectious lung 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 disruption in the process of fat oxidation.

Since the process of formation of lipoproteins, phospholipids and lecithin is sharply slowed down, the process of removing fat from the liver becomes more difficult. In acute or chronic cholestatic hepatosis, bile pigment accumulates in hepatocytes, followed by dystrophy, manifested in a lack of proteins.

A characteristic sign of holistic hepatosis is a violation of the 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 analogues, 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, becomes soft. In a later stage, the liver is not palpable, and percussion reveals a decrease in its size.

The size of the spleen, as a rule, remain 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 these disorders are accompanied by renal failure. In the case of secondary hemorrhagic events and in hepatic coma, a fatal 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. In this case, the symptoms of the disease are practically not observed. 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, stool disorders are possible.

A characteristic feature is a moderate enlargement of the liver with a smooth surface, moderate density, rounded or sharp edge, as well as pain on palpation. In severe and prolonged course of the chronic form of hepatosis, a significant decrease in the patient's body weight, bloating, and pruritus are observed. In some cases, there is an increased content of cholesterol, total protein and beta-lipoproteins in the blood serum.

Recovery of the patient is possible only with the complete exclusion of contact with irritating factors and full 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 elevated bilirubin content).

Quite often at patients with a hepatosis the feverish condition 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 measures aimed at removing toxins from the body that caused the development of the disease.

The patient is given gastric lavage, siphon enemas, saline laxatives. In the presence of intoxication phenomena and suspected hypokalemia, the patient is shown hemodez, a 5% glucose solution in combination with B vitamins and vitamin C, as well as panangin intravenously.

With the manifestation of hemorrhagic syndrome, rutin and a 1% solution of vikasol 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 best effect gives the use of lipotropic drugs. The patient is prescribed 3-5 g of a 20% solution of choline chloride orally, if the drug is in a 200 ml vial, 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, vitamin B12 are used. Of the extracts and hydrolysers of the liver, Essentiale is used.

Assign 5 ml per day of sirepar, ripazon or progepar 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 an increased content of proteins and a limited content of fats, 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.

hiatal hernia

A hernia is a disease characterized by a protrusion internal organs through the modified 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 abdominal organ: the abdominal segment of the esophagus, the cardial 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 (fundal and antral);

- congenital short esophagus, in which there is a thoracic location of the stomach.

The formation of hernias 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 aperture of the diaphragm, as well as their degenerative changes;

- shortening of the esophagus as a result of cicatricial inflammation, tumors, etc.;

- decreased muscle tone;

- the disappearance of adipose tissue under the diaphragm;

- stretching of the esophageal opening of the diaphragm, etc.

These 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 hypertonic 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 any symptoms at all. The most characteristic manifestation of a hiatal hernia is pain behind the sternum or in the abdominal cavity that occurs during meals or when changing body position.

In addition, the patient may experience dysphagia (difficulty swallowing), belching, hiccups, and 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, regurgitation, etc. Paraesophageal hernias are prone to strangulation. In this case, the patient feels sharp pains, he has signs of intestinal obstruction and collapse.

The most common complications of hiatal hernia are esophageal-gastric bleeding, peptic esophagitis, cicatricial changes in the esophagus with its subsequent shortening, arrhythmia, angina pectoris, aspiration, etc.

The diagnosis of the disease is made on the basis of X-ray examination. A 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, according to 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 promote bloating. Alcoholic beverages and smoking are also prohibited.

The patient is advised to sleep in a reclining position. In addition, antispastic and alkalizing therapy is recommended. For oral administration, local anesthetic and sedative drugs are indicated. With anemia, the patient needs iron preparations and hemostimulin. Enveloping 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, surgical intervention is indicated, during which the stomach is returned to the abdominal cavity and a plate of the esophageal opening of the diaphragm is inserted. It must be remembered that even after a successful operation, relapses of the disease are possible.

Esophageal diverticula

Diverticula of the esophagus is a disease characterized by a protrusion of its wall. With this disease, there is a disorder of the swallowing act, namely regurgitation and belching.

Diverticula are divided into congenital (pulsion), acquired (traction) and mixed. Most diverticula are acquired. The reason for the development of pharyngeal-esophageal diverticula is a congenital or acquired inferiority of the connective tissue structures and the muscular apparatus of the pharyngeal-esophageal junction.

The factor in the occurrence of diverticulum in this case is esophageal dyskinesia, accompanied by a sharp increase in pressure during swallowing. In addition, pharyngeal-esophageal diverticula can occur as a result of 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, and chronic mediastinitis.

Subsequently, congenital factors are attached, for example, incomplete fusion of the esophageal-bronchial fistula, which is characteristic of the embryonic period and subsequently forms the esophageal-bronchial cord.

The occurrence of epiphrenal diverticula is usually associated with reflux esophagitis caused by hiatal hernia, shortening of the esophagus, or insufficiency of the cardia (the part of the esophagus located in front of its entrance to the stomach).

Clinical manifestations of the disease depend on the location of the diverticulum. At the initial stage of development of the diverticulum of the upper esophagus (pharyngeal-esophageal) there is an increased secretion of mucus, a burning sensation and coughing. Then, the sensation of a foreign body, nausea, impaired swallowing, and regurgitation of food join the listed symptoms.

As a result, the so-called blockade phenomenon develops, characterized by reddening of the face, a feeling of lack of air, dizziness and fainting. After vomiting, the listed 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, adhesive processes, and oncology in the diverticulum develop.

Diverticula of the lower esophagus are also characterized by minor symptoms. In some cases, there is a swallowing disorder, pain behind the lower part of the sternum, cough, regurgitation, nausea, vomiting, anorexia, reflex dyspnea, palpitations, bronchospasm.

The disease is characterized by a slow course, but 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 a contrast X-ray examination of the esophagus. The presence of pharyngeal-esophageal diverticula can sometimes be established by external examination and palpation (a characteristic protrusion is observed on the neck).

In the treatment of diverticula of the esophagus, the prevention of delay in the diverticulum of food masses is of great importance, so 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.

When rapid development disease or suspicion of dangerous complications, the patient should be hospitalized for surgical treatment.

Intestinal dysbacteriosis

Intestinal dysbacteriosis is a disease characterized by a change in the composition and quantitative ratio of microflora, the representatives of which prevent the penetration into the intestine and the rapid reproduction of pathogenic and opportunistic microorganisms in it.

In clinical practice, there are syndromes of large intestine and small intestine 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 absolutely 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 which type of microorganisms is predominant, dysbacterioses are divided into medicinal (post-antibiotic), fungal, staphylococcal, proteus, and also caused by the paracoli group, Pseudomonas aeruginosa or association of microbes.

According to the classification of A.F. Bilibin, three forms of dysbacteriosis are distinguished:

- compensated, characterized by the absence of a pathological process in response to a violation of the microflora;

- 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 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 proximal small intestine. Another reason for the pathological process is a change in environmental conditions, which becomes favorable for 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 reproduction 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 normal microflora(bifidobacteria, lactic acid and Escherichia coli, etc.) and the appearance of pathological and conditionally pathological microorganisms (staphylococci, fungi of the genus Candida, Proteus, Pseudomonas aeruginosa, etc.).

These changes lead to inflammatory processes of varying severity, and a sharp decrease in immunity and 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 metabolism, as a result of which their deficiency develops in the patient's body.

There are many reasons for the development of dysbacteriosis. In most cases, these are diseases such as hypochlorhydria and achlorhydria of the stomach, in particular, accompanied by impaired evacuation of its contents, afferent loop syndrome that appears after gastric resection, jejunal and doudenal diverticula, chronic pancreatitis, intestinal obstruction.

Treatment with antibiotics and sulfanilamide preparations, in which a significant part of beneficial microorganisms sensitive to the drug dies and pathogenic or opportunistic microflora resistant to its effects multiply. The impact of such adverse factors as protein starvation, climate change, vitamin deficiency, alcohol abuse, also leads to the development of dysbacteriosis.

After antibiotic therapy, in most cases, candidiasis develops, characterized by the disappearance of substances that have a fungistatic effect, resulting in favorable conditions for the development of Candida albicans fungi. Candidiasis can affect individual organs, mucous membranes, or proceed in a generalized manner.

After treating a patient with large doses of antibiotics, aspergillosis develops, the causative agent of which is the fungus Aspergillus fumigatus. Staphylococcal dysbacteriosis is caused by acute intestinal diseases. In addition, staphylococcal dysbacteriosis may be accompanied by chronic diseases of the digestive system or other diseases characterized by a decrease in the protective functions of the body.

In this case, the allergic or toxic effects of antibiotics directly on the intestinal mucosa, as well as a lack of vitamins, act as a provoking factor.

Proteus dysbacteriosis, as a rule, develops in patients with chronic bowel 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 undergone such intestinal infections, as dysentery, salmonellosis, and also as a concomitant disease in chronic ulcerative colitis, chronic enterocolitis and after antibiotic treatment.

Characteristic manifestations of dysbacteriosis are loss of appetite, an unpleasant aftertaste in the mouth, digestive disorders, weakness, weight loss, anemia. In severe forms, an increase in body temperature up to 37-38 ° is possible.

With a long course, hypovitaminosis occurs, especially group B. Symptoms of intestinal candidiasis are loose stools mixed with blood, bleeding and focal necrosis. In severe cases, perforations and peritonitis may occur. The pathological process can cover all parts of the intestine, stomach and oral cavity. As a complication, candidiasis sepsis can develop, which often leads to death.

Aspergillosis is characterized by an acute onset and a severe course. The patient has diarrhea and hemorrhagic-necrotic changes in the intestine.

The prognosis of the disease can be both favorable and unfavorable. Important for the diagnosis of candidiasis, aspergillosis and other mycoses that occur while taking antibiotics is the development of acute enteritis or enterocolitis during treatment with drugs of this group.

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 dysbacteriosis occurs as enterocolitis and is characterized by such symptoms as abdominal pain, nausea, vomiting, weakness, fever, and electrolyte disturbances in the blood. If these symptoms are accompanied by dehydration and a violation of cardiac activity, an infectious-allergic shock with a fatal outcome may develop.

The symptoms of intestinal dysbacteriosis caused by the paracoli group resemble the clinical picture of chronic recurrent enterocolitis. In general, the disease proceeds benignly. In the acute stage, abdominal pain and diarrhea appear. During the period of remission, the patient begins constipation.

Proteus dysbacteriosis is characterized by local intestinal damage, 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 during antibiotic treatment.

With dysbacteriosis 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 place of which ulcers and erosion then appear. If Pseudomonas aeruginosa is a consequence of food poisoning, 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 onset. Death occurs as a result of cardiovascular failure or paralysis. Pseudomonas aeruginosa due to antibiotic treatment occurs in a milder form and, as a rule, has a favorable prognosis. Enterocolitis in mixed Pseudomonas aeruginosa-phylococcal-proteus infection is characterized by a severe course and is often complicated by the formation of metastatic foci in parenchymal organs, as well as the development of sepsis.

The following methods are used to establish an accurate diagnosis:

- bacteriological examination of feces;

- aspiration of the contents of the jejunum;

– breath test with carbon;

- a test to determine the level of 5% hydroxyindoleacetic acid in the 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 a cancerous tumor, in which the same symptoms are observed as in dysbacteriosis (abdominal pain, stool disorders, bloating, weight loss, anemia).

It must be remembered that dysbacteriosis and irritable bowel syndrome have similar clinical manifestations and often appear in combination.

When the first signs of enteritis and enterocolitis appear, antibiotics must be canceled, fasting should be prescribed to the patient 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 and parenteral protein nutrition are indicated. In addition, corticosteroid drugs are prescribed, and, if necessary, electrolytes.

With drug dysbacteriosis, 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 a laboratory test reveals the causative agent of the disease, targeted antibiotic therapy is carried out. However, antibacterial drugs should be prescribed with great care and for the shortest possible time.

With fungal dysbacteriosis, drugs that have a fungicidal effect (nystatin, levorin, mycostatin) are indicated. In the event that the use of these 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, when they cause dysbacteriosis, furadinin, furazolidone 0.1 g 3-4 times a day are prescribed for a course of 7-10 days.

With proteus dysbacteriosis, 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, the course of treatment is repeated. In addition, mexaform, intestopan, as well as the combined preparation Bactrim, which includes trimethoprim and sulfamethoxazole, are recommended. 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 dysbacteriosis caused by the association of microbes with a predominance of staphylococcus is treated with antibiotics to which this drug is sensitive: oxacillin, methicillin, lincomycin, cephaloridine, cephaloglycine, carbomycin, etc. In severe cases, the patient is prescribed repeated courses of treatment with several antibacterial drugs. During 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.). with dysbacteriosis with a predominance of Pseudomonas aeruginosa, in addition to antibiotics, antipseudomonal serum and antipseudomonal gamma globulin are indicated.

With dysbacteriosis caused by the association of microbes, combined treatment is carried out, that is, drugs are used that are directed against all identified microbes. In this case, antibiotics are combined with antifungal drugs.

For all types of dysbacteriosis, biological preparations (colibacterin, bifidumbacterin, bifikol) are indicated, 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 dysbacteriosis consists in the inadmissibility of the unreasonable and uncontrolled use of any antibacterial drugs, as well as the need to take bacterial drugs during antibiotic treatment. For debilitated patients, general strengthening therapy and a balanced diet are recommended.

Biliary dyskinesia

Biliary dyskinesia is a disease characterized by functional disorders of the motility of the gallbladder and ducts.

Biliary dyskinesia can be primary, caused by a disorder in the 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), hypertonic and hyperkinetic forms of biliary dyskinesia.

Primary dyskinesias occur as a result of general necrosis, diencephalic crisis, after suffering Botkin's disease and other infectious diseases, with intoxication, general allergies, alimentary insufficiency, endocrine-hormonal disorders.

Secondary dyskinesias, as a rule, are associated with anomalies 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 shoulder blade, shoulder, collarbone. Acute pains can be short-term, and aching, as a rule, last from several hours to several days. Severe pain attacks often give rise to an erroneous diagnosis of gallstone disease.

The most characteristic sign 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, increased heart rate, numbness of the extremities, urinary retention.

Most patients have general neurotic disorders, hypo- or hyperthyroidism and other endocrine disorders. In patients with biliary dyskinesia, there are changes in the blood. In some cases, there is an increase in body temperature, but in general, for this disease, an increase in temperature is atypical.

During the period of exacerbation of the pain syndrome, there is tension in the abdomen in the area of ​​the gallbladder. 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 region.

To establish the form of dyskinesia of the gallbladder and ducts, the method of chromatic and continuous fractional probing is used. Cholicistography reveals an intense shadow of the gallbladder, as well as its delayed or shortened emptying, in some cases - omission 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 bile excretion and eliminating autonomic dystonia. nervous system.

Secondary dyskinesias appear against the background of anomalies in the development of the biliary tract, cholecystitis, cholangitis, cholelithiasis or adhesive process, accompanied by a violation of the biliary tract.

Esophageal dyskinesia

Esophageal dyskinesia 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 dysregulation of esophageal motility. Secondary dyskinesia of the esophagus is often a complication of diseases such as esophagitis, peptic ulcer and cholelithiasis. Esophageal dyskinesia very often accompanies diseases that are characterized by the development of a general convulsive syndrome. In this regard, if esophageal dyskinesia is suspected, the patient needs to consult 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 retrosternal pain that occurs when swallowing. For some, they resemble coronary pain. Dysphagia is intermittent and sometimes paradoxical in nature: it appears when taking liquids, but is absent when swallowing dense food. The diagnosis is made on the basis of x-ray examination of the esophagus.

Spastic contractions of the esophagus are recorded graphically during esophagotonokymography. The patient is shown sedative, antispasmodic 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 there are violations of intestinal motility. 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 disease that occurs as a result of acute or chronic traumatic situations. In addition, acute intestinal infections and a low-slag diet can provoke the development of the disease.

With intestinal dyskinesia, there is a violation of the cholinergic and adrenergic 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 increase, and with diarrhea, on the contrary, they weaken.

Secondary dyskinesia 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, monoamide oxidases, opiates, diuretics, antibiotics, psychotropic drugs.

In primary intestinal dyskinesia, there is a combination of neurological and intestinal disorders. The clinical picture is characterized by abdominal pain, bloating, stool disorders. Quite often, the patient cannot determine the location of the pain. Pain can be aching, pulling, strong or weak. Disorders of the stool are noted in 90% of cases. As a rule, this is diarrhea, alternating with constipation.

In addition to intestinal disorders, patients may complain of pain in the heart, joints, and back. Examination revealed no organic changes. An objective study of the clinical picture of the disease, as a rule, practically does not provide information, so the diagnosis is made by exclusion.

First, such intestinal pathologies as polyps, tumors, diverticula, developmental anomalies are excluded, then a distinction is made between dyskinesia and non-ulcerative colitis, and only after that the primary dyskinesia is differentiated from the secondary one and the causes of the secondary disease are clarified.

First, the usual studies are carried out, recommended for the detection of pathologies of the colon: scatological examination of feces for occult blood and dysbacteriosis, irrigoscopy and endoscopy, as well as colon biopsy.

The coprogram shows the presence of dysbacteriosis, in particular, with constipation. Endoscopic examination determines the signs of impaired intestinal motility in the absence of organic changes. Unlike 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 a consultation with a psychotherapist, who determines how to treat the psychopathological syndrome, which is the main cause of dyskinesia. To eliminate it, the patient is prescribed psychotropic drugs.

First in small doses, then gradually increasing.

If the patient is anxious, in connection with which vegetative disorders occur, he is shown tranquilizers: seduxen, sonapax, elenium, phenazepam. With depression, a positive result is achieved by 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 life of the patient.

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. Polyps, villous tumors, lipomas, leiomyomas, fibromas, hemangiomas, lymphangiomas, and carcinoids can form in the large (colon) intestine.

The most common tumors of the stomach are fibroids and polyps, and among the tumors of the colon - single and multiple adenomatous and glandular-villous polyps. Benign tumors can be of epithelial, connective tissue, muscular or nervous origin.

Benign tumors, as a rule, are located in the submucosal, muscular or subserous layer of the stomach. In most patients, the tumor is detected during surgery, the reason for which is the suspicion of oncology or gastric lesions of unknown etiology, or at autopsy.

Polyps of the stomach are formed from the integumentary pit epithelium of its mucosa. They can be adenomatous and inflammatory-hyperplastic. The polyp tissue consists of glands of various sizes and shapes, separated from each other by connective tissue layers and lined with prismatic cells. Often, a mucoid secret accumulates in the lumen of the glands, resulting in the formation of cysts.

As a rule, polyps are located in the pyloroanthral compartment, less often in the body or cardia.

Polyps may be single or multiple. The most common are spherical and oval polyps. Like all benign tumors, polyps are clearly demarcated from the surrounding mucosa.

The surface of the polyps is usually smooth or granular and is pink, orange, or bright red in color.

In some cases, the diameter of the polyp can reach several centimeters. Polyposis is considered a precancerous condition. The larger the size of 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 that protrude into the intestinal lumen and have the structure of an adenoma. Adenomatous polyps with a long thin stalk 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 may be single or grouped. Their etiology has not yet been fully elucidated, however, there is an assumption about their viral nature. special shape widespread multiple lesions is called diffuse polyposis of the colon. Often it is combined with polyposis of the entire gastrointestinal tract (total polyposis).

Clinical manifestations in benign tumors of the stomach 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 section of the stomach in most cases becomes the cause of its obstruction.

Bending of the tumor into the pyloric canal or duodenum leads to the development of acute obstruction. Quite often tumors ulcerate, provoking bleedings.

Myomas, leiomyomas, fibromyomas and rhabdomyomas in most cases are localized in the subserous or muscular layer. Large tumors on palpation are defined as motionless formations of a spherical or oval shape with a dense elastic consistency.

The diagnosis of the disease is made on the basis of X-ray and gastroscopic examination. The radiograph reveals filling defects that have smooth contours (unlike a malignant tumor), most often preserved mucosa. They are mobile on palpation. 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 wall of the stomach with a wide base. The mucosa covering the tumor is smooth, its structure and color are not changed. The base of the tumor and the surrounding mucosa are not soldered together. They are connected by short radial folds.

Polyposis of the stomach in most cases occurs without severe symptoms. The manifestation of clinical signs, as a rule, is due to the presence of concomitant diseases, in some cases - complications of polyps. Polyposis may be complicated by bleeding or malignancy. This disease is often accompanied by iron deficiency anemia.

The main methods for diagnosing polyposis of the stomach are x-ray and gastroscopic studies. The degeneration of a tumor into a malignant one can be confirmed only after histological and cytological studies of biopsies.

The characteristic symptoms of intestinal polyposis are mucous or bloody discharge from the rectum, constipation, and abdominal pain. It should be borne in mind that often polyposis is asymptomatic and is detected only during irrigoscopy, colonoscopy or sigmoidoscopy. Polyps may not grow for a long time and not bother 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, an increase in digestive disorders, leading to depletion of the body. In most patients, polyps become malignant over time, while the oncological tumor is characterized by rapid growth.

Benign tumors of the stomach are removed by surgery. Complete cure is achieved after resection of the stomach. With polyposis of the stomach, the same treatment is shown as with chronic gastritis with low acidity of gastric juice.

Patients with polyposis should be examined at least 1-2 times a year 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, it is shown surgery. The main goal of treating adenomatous and villous intestinal polyps is to prevent their development into a malignant tumor.

Polyps are removed by electrocoagulation through an endoscope. After surgery, the patient is put on a dispensary record, since this disease quite often gives relapses.

In diffuse polyposis, all or almost all of the large intestine is surgically removed. With a 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 as ulcer-like, pancreatic-like and mixed forms. Primary duodenitis, as a rule, is caused by the influence of harmful exogenous factors - such as malnutrition 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 ankislotomidoz. Much less often, it is combined with diseases of the kidneys, cardiovascular system, and allergies.

Quite often, the development of duodenitis is associated with impaired motility of the duodenum. In addition, the causes of the disease may 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, decreased appetite, headaches, weakness, and general malaise. On examination, the tongue is dry and furred. In some cases, short-term jaundice is observed. In the right part of the abdominal cavity, a cylindrical seal, or infiltrate, is palpated.

Characteristic signs of duodenitis are a sharp decrease in weight, hypovitaminosis, pain on palpation in the right side of the abdominal cavity.

With an ulcer-like form of chronic duodenitis, the patient complains of pain in the epigastric region, which can occur when feeling hungry, eating, at night. Characteristic features 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, retrosternal pain, swallowing disorders, and various autonomic disorders are observed.

With cholecysto- and pancreatic-like forms of chronic duodenitis, symptoms of dysfunction of the gallbladder and pancreas join 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.

There are no signs of inflammation, however, cholecystitis and pancreatitis often develop gradually against the background of functional disorders of the gallbladder and pancreas. 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. With aspiration duodenobiopsy, the presence or absence of edema, cell infiltration, and changes in the villi are detected.

Duodenitis is dangerous because it is quite 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 (slow progress of the contents through the lumen of the duodenum), antiperistalsis, stenosis. Bleeding in this disease is also plentiful, as in peptic ulcer.

Treatment of duodenitis is similar to the treatment of acute gastritis. In the case of a pronounced inflammatory process (phlegmonous duodenitis), the patient is shown broad-spectrum antibiotics. 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 rarely leads to death. As a prophylaxis of duodenitis, it is recommended to observe a diet, exclude the use of alcohol, treat helminthic-protozoal invasions in a timely manner.

Cholelithiasis

Gallstone disease is a disease 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, pigmented, consisting of calcium salts and bilirubin, mixed, consisting of cholesterol, bilirubin and calcium salts. The most common are cholesterol stones.

Gallstone disease can develop as a result of a violation of the metabolism of cholesterol and some 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 the state of an unstable colloidal solution.

Cholesterol is kept in a dissolved state due to the action of fatty acids. In the case of a decrease in their content, cholesterol crystallizes and precipitates. Violation of the formation of fatty acids occurs as a result of the development of functional insufficiency of liver cells.

As a result of infectious inflammation of the gallbladder and biliary tract, chemical composition bile, causing cholesterol, bilirubin and calcium to precipitate to form 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 bedsores and perforation of the gallbladder wall. Gallstone disease develops as a result of excessive consumption of fatty foods, metabolic disorders, atherosclerosis, infection of the biliary tract, liver damage after Botkin's disease.

Bile stasis can be triggered by biliary dyskinesia, adhesions and scars in the gallbladder and bile ducts, and increased intra-abdominal pressure. The latter can be caused by pregnancy, constipation, obesity, lack of physical activity.

The most common symptoms of cholelithiasis 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 contrary, 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 neuropsychic overstrain. Such attacks begin suddenly, most often at night. First, pain of a stabbing or cutting nature is felt in the right hypochondrium with irradiation to the right shoulder blade, 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 may be accompanied by fever, as well as nausea and vomiting. The listed signs disappear immediately after the elimination of the pain syndrome.

The duration of attacks 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 on 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 region 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 may be minor and determined only by palpation of the abdomen.

The clinical manifestations of cholelithiasis tend to 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.

Especially dangerous blockage of the cystic duct, 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 thickens. As a result of a violation of the outflow of bile in the gallbladder and biliary tract, inflammatory processes develop.

Stones are detected using ultrasound examination (ultrasound) of the abdominal cavity, cholongiography, 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. Patients with biliary colic syndrome are hospitalized. In this case, painkillers are prescribed, including narcotic drugs, as well as antibacterial and sulfanilamide drugs. Cold is applied to the abdomen to relieve swelling.

As a prevention of cholelithiasis or its exacerbations, a special diet, therapeutic exercises, and elimination of constipation are recommended. In addition, the drug olimetin is indicated, 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 treatment does not give a positive result, surgical intervention is recommended to remove the gallbladder. Indications for the appointment of the operation are perforation of the gallbladder with the development of developed or limited bile 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 a non-functioning gallbladder.

FACTORS DAMAGED TO THE DIGESTIVE ORGANS

Physical nature:

Rough, poorly chewed or unchewed food;

Foreign bodies - buttons, coins, pieces of metal, etc.;

Excessively cold or hot food; - ionizing radiation.

Chemical nature:

Alcohol; - tobacco combustion products that enter the gastrointestinal tract with saliva;

Medications such as aspirin, antibiotics. cytostatics;

Toxic substances that penetrate the digestive organs with food are salts of heavy metals, fungal toxins, etc.

biological nature:

Microorganisms and their toxins; -helminths;

Excess or lack of vitamins, such as vitamin C, group B, PP.

Causes of diseases of the digestive system

Each disease of the digestive system has its own specific causes, but among them are those that are characteristic of most diseases of the digestive system. All these reasons can be divided into external and internal.

The main ones are, of course, external reasons. These, first of all, include food, liquids, drugs: Unbalanced diet (lack or excess of proteins, fats, carbohydrates) irregular meals (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 often the only cause of such digestive disorders as constipation, diarrhea, increased gas formation and other digestive disorders. From liquids in the first place diseases of the digestive system can cause alcohol and its surrogates, carbonated and other drinks containing preservatives and dyes.

And, of course, drugs. 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 diseases and bowel is rare, but it, together with insufficient oral hygiene, causes diseases of the oral cavity (gingivitis, stomatitis, periodontal disease, lip cancer). More external causes of diseases of the stomach and intestines include frequent stress, negative emotions, worries for any reason.

For internal causes diseases of the digestive system are genetic - this is a predisposition (that is, the presence of a disease of the digestive system in previous generations), intrauterine development disorders (mutations in the genetic apparatus), autoimmune (when the body for one reason or another begins to attack its organs).

Types of digestive disorders:

Disruption of the receptor apparatus:

Hypergeusia (Disorder of taste, manifested by an increase in taste sensations);

Hypogeusia (reduced taste sensitivity).

ageusia (inability to distinguish the taste of substances, due to diseases of the mucous membrane of the tongue and palate).

parageusia (Perversion of taste sensitivity, the appearance of taste sensations in the absence of a corresponding stimulus. It is observed when the central part of the taste analyzer in the cerebral cortex (opercular region and hippocampus) or the pathways of taste sensitivity is damaged).

dysgeusia (taste disorder characterized by the loss or perversion of the perception of certain taste stimuli).

Violations of the formation and secretion of saliva: hyposalivation (decreased secretion of saliva) and hypersalivation (increased secretion of saliva)

Pathology of the esophagus: heartburn (burning sensation, mainly in the lower esophagus, due to the throwing of acidic gastric contents into the esophagus), belching (exit of gases formed in the stomach through the mouth, sometimes accompanied by particles of stomach contents entering the mouth), regurgitation (ejection of food from the esophagus and stomach).

Pathology of the stomach: Secretory function disorders, Motor function disorders (see question 52)

Intestinal pathology : disorders of the digestive function, absorption function, motor function and barrier-protective.

53. pathology of protein metabolism. Metabolic disorders underlie all functional and organic damage to organs and tissues leading to the onset of the disease. At the same time, metabolic pathology can aggravate the course of the underlying disease, acting as a complicating factor. One of the most common reasons common disorders of protein metabolism is a quantitative or qualitative protein deficiency of primary (exogenous) origin. It may be due to:

1. violation of the breakdown and absorption of proteins in the digestive tract;

2. slowing down the supply of amino acids to organs and tissues;

3. violation of protein biosynthesis;

4. violation of the intermediate exchange of amino acids;

5. change in the rate of protein breakdown;

6. pathology of the formation of end products of protein metabolism.

Protein digestion and absorption disorders. In the digestive tract, proteins are broken down under the influence of proteolytic enzymes. At the same time, on the one hand, protein substances and other nitrogenous compounds lose their specific features.

Main causes insufficient breakdown of proteins - a quantitative decrease in the secretion of hydrochloric acid and enzymes, a decrease in the activity of proteolytic enzymes (pepsin, trypsin, chymotrypsin) and the associated insufficient formation of amino acids, a decrease in the time of their exposure (acceleration of peristalsis).

In addition to the general manifestations of amino acid metabolism disorders, there may be specific disorders associated with the absence of a particular amino acid. Thus, a lack of lysine (especially in a developing organism) retards growth and general development, lowers the content of hemoglobin and red blood cells in the blood. With a lack of tryptophan in the body, hypochromic anemia occurs. Deficiency of arginine leads to impaired spermatogenesis, and histidine - to the development of eczema, stunting, inhibition of hemoglobin synthesis.

In addition, insufficient digestion of protein in the upper gastrointestinal tract is accompanied by an increase in the transfer of products of its incomplete cleavage to the large intestine and an increase in the process of bacterial breakdown of amino acids. This leads to an increase in the formation of toxic aromatic compounds (indole, skatole, phenol, cresol) and the development of a general intoxication of the body with these decay products.

Slowing down the supply of amino acids to organs and tissues. Since a number of amino acids are the starting material for the formation of biogenic amines, their retention in the blood creates conditions for the accumulation of corresponding proteinogenic amines in tissues and blood and the manifestation of their pathogenic effect on various organs and systems. An increased content of tyrosine in the blood contributes to the accumulation of tyramine, which is involved in the pathogenesis of malignant hypertension. A prolonged increase in the amount of histidine leads to an increase in the concentration of histamine, which contributes to impaired blood circulation and capillary permeability. In addition, an increase in the content of amino acids in the blood is manifested by an increase in their excretion in the urine and the formation of a special form of metabolic disorders - aminoaciduria. Aminoaciduria can be general, associated with an increase in the concentration of several amino acids in the blood, or selective - with an increase in the blood content of any one amino acid.

Violation of protein synthesis. The synthesis of protein structures in the body is the central link in protein metabolism. Even small violations of the specificity of protein biosynthesis can lead to profound pathological changes in the body.

The absence of at least one (out of 20) essential amino acid in cells stops protein synthesis as a whole.

Violation of the rate of synthesis protein may be due to a dysfunction of the corresponding genetic structures on which this synthesis takes place (DNA transcription, translation).

Damage to the genetic apparatus can be both hereditary and acquired, arising under the influence of various mutagenic factors (ionizing radiation, ultraviolet rays, etc.). Some antibiotics can cause a violation of protein synthesis. So, "mistakes" in reading the genetic code can occur under the influence of streptomycin, neomycin and a number of other antibiotics. Tetracyclines inhibit the addition of new amino acids to the growing polypeptide chain. Mitomycin inhibits protein synthesis due to DNA alkylation (the formation of strong covalent bonds between its chains), preventing the splitting of DNA strands.

Allocate qualitative and quantitative violations of protein biosynthesis. The importance of qualitative changes in protein biosynthesis in the pathogenesis of various diseases can be judged by the example of some types of anemia with the appearance of pathological hemoglobins. Replacing only one amino acid residue (glutamine) in the hemoglobin molecule with valine leads to a serious illness - sickle cell anemia.

Of particular interest are quantitative changes in the biosynthesis of proteins in organs and blood, leading to a shift in the ratios of individual fractions of proteins in the blood serum - dysproteinemia. There are two forms of dysproteinemia: hyperproteinemia (an increase in the content of all or certain types of proteins) and hypoproteinemia (a decrease in the content of all or certain proteins). So, a number of diseases of the liver (cirrhosis, hepatitis), kidneys (nephritis, nephrosis) are accompanied by a pronounced decrease in the content of albumins. A number of infectious diseases, accompanied by extensive inflammatory processes, lead to an increase in the content of gamma globulins. The development of dysproteinemia is accompanied, as a rule, by serious shifts in the homeostasis of the body (violation of oncotic pressure, water metabolism). A significant decrease in the synthesis of proteins, especially albumin and gamma globulins, leads to a sharp decrease in the body's resistance to infection, a decrease in immunological resistance. The significance of hypoproteinemia in the form of hypoalbuminemia is also determined by the fact that albumin forms more or less stable complexes with various substances, ensuring their transport between various organs and transport through cell membranes with the participation of specific receptors. It is known that iron and copper salts (extremely toxic to the body) are hardly soluble at blood serum pH and their transport is possible only in the form of complexes with specific serum proteins (transferrin and ceruloplasmin), which prevents intoxication with these salts. About half of the calcium is retained in the blood in a form bound to serum albumin. At the same time, a certain dynamic balance is established in the blood between the bound form of calcium and its ionized compounds. In all diseases accompanied by a decrease in the content of albumin (kidney disease), the ability to regulate the concentration of ionized calcium in the blood is also weakened. In addition, albumins are carriers of some components of carbohydrate metabolism (glucoproteins) and the main carriers of free (non-esterified) fatty acids and a number of hormones.

With damage to the liver and kidneys, a number of acute and chronic inflammatory processes (rheumatism, infectious myocardium, pneumonia), special proteins with altered properties or unusual norm begin to be synthesized in the body. A classic example of diseases caused by the presence of abnormal proteins are diseases associated with the presence of abnormal hemoglobin (hemoglobinosis). Blood clotting disorders occur when pathological fibrinogens appear. Unusual blood proteins include cryoglobulins that can precipitate at temperatures below 37°C, leading to thrombus formation. Their appearance is accompanied by nephrosis, cirrhosis of the liver and other diseases.

Pathology of interstitial protein metabolism (violation amino acid exchange).

The transamination reaction, as the main source of the formation of new amino acids, occupies a central place in the interstitial metabolism of proteins. Violation of transamination can occur as a result of deficiency in the body of vitamin B-6. This is due to the fact that the phosphorylated form of vitamin B-6 - phosphopyrodoxal is an active group of transaminases - specific enzymes for transamination between amino and keto acids. Pregnancy, prolonged use of sulfonamides inhibit the synthesis of vitamin B6 and can serve as the basis for a violation of amino acid metabolism. Finally, the reason for the decrease in the activity of transamination may be the inhibition of the activity of transaminases due to a violation of the synthesis of these enzymes (during protein starvation), or a violation of the regulation of their activity by a number of hormones.

The processes of transamination of amino acids are closely related to the processes of oxidative deamination, during which the enzymatic elimination of ammonia from amino acids takes place. Deamination determines both the formation of end products of protein metabolism and the entry of amino acids into energy metabolism. Weakening of deamination may occur due to a violation of oxidative processes in tissues (hypoxia, hypovitaminosis C, PP, B2). However, the most severe violation of deamination occurs with a decrease in the activity of aminooxidases, either due to a weakening of their synthesis (diffuse liver damage, protein deficiency), or as a result of a relative insufficiency of their activity (an increase in the content of free amino acids in the blood). The consequence of a violation of the oxidative deamination of amino acids will be a weakening of urea formation, an increase in the concentration of amino acids and an increase in their excretion in the urine - aminoaciduria.

Intermediate exchange of a number of amino acids takes place not only in the form of transamination and oxidative deamination, but also through their decarboxylation (loss of CO2 from the carboxyl group) with the formation of the corresponding amines, called "biogenic amines". So, when histidine is decarboxylated, histamine is formed, tyrosine - tyramine, 5-hydroxytryptophan - serotin, etc. All these amines are biologically active and have a pronounced pharmacological effect on the vessels.

Change in the rate of protein breakdown. A significant increase in the rate of breakdown of tissue and blood proteins is observed with an increase in body temperature, extensive inflammatory processes, severe injuries, hypoxia, malignant tumors, etc., which is associated either with the action of bacterial toxins (in case of infection), or with a significant increase in the activity of proteolytic blood enzymes (with hypoxia), or the toxic effect of tissue decay products (with injuries). In most cases, the acceleration of protein breakdown is accompanied by the development of a negative nitrogen balance in the body due to the predominance of protein breakdown processes over their biosynthesis.

Pathology of the final stage of protein metabolism. The main end products of protein metabolism are ammonia and urea. The pathology of the final stage of protein metabolism can be manifested by a violation of the formation of end products, or a violation of their excretion.

The main mechanism of ammonia binding is the process of urea formation in the citrulline-arginine-nornithine cycle. Violations of the formation of urea can occur as a result of a decrease in the activity of the enzyme systems involved in this process (hepatitis, cirrhosis of the liver), general protein deficiency. If urea formation is impaired, ammonia accumulates in the blood and tissues and the concentration of free amino acids increases, which is accompanied by the development of hyperazotemia. In severe forms of hepatitis and cirrhosis of the liver, when its urea-forming function is sharply impaired, severe ammonia intoxication develops (impaired functions of the central nervous system).

In other organs and tissues (muscles, nervous tissue), ammonia binds in the amidation reaction with the addition of free dicarboxylic amino acids to the carboxyl group. The main substrate is glutamic acid.

Another end product of protein metabolism, formed during the oxidation of creatine (muscle nitrogen) is creatinine. With starvation, avitaminosis E, febrile infectious diseases, thyrotoxicosis and a number of other diseases, creatinuria indicates a violation of creatine metabolism.

If the excretory function of the kidneys (nephritis) is impaired, urea and other nitrogenous products are retained in the blood. Residual nitrogen increases - hyperazotemia develops. The extreme degree of violation of the excretion of nitrogenous metabolites is uremia.

With simultaneous damage to the liver and kidneys, there is a violation of the formation and excretion of end products of protein metabolism.

In pediatric practice, hereditary aminoacidopathy is of particular importance, the list of which today includes about 60 different nosological forms. By type of inheritance, almost all of them are autosomal recessive. The pathogenesis is due to the insufficiency of one or another enzyme that catabolizes and anabolizes amino acids. A common biochemical sign of aminoacidopathy is tissue acidosis and aminoaciduria. The most common hereditary metabolic defects are four enzymopathies that are related to each other by a common pathway of amino acid metabolism: phenylketonuria, tyrosinemia, albinism, alkaptonuria.

54. pathology of carbohydrate metabolism make up the obligatory and most part of human food (about 500 g / day). Carbohydrates are the most easily mobilized and utilized material. They are deposited in the form of glycogen, fat. During carbohydrate metabolism, NADP H2 is formed. Carbohydrates play a special role in the energy of the central nervous system, since glucose is the only source of energy for the brain.

A carbohydrate metabolism disorder may be due to a violation of their digestion and absorption in the digestive tract. Exogenous carbohydrates enter the body in the form of poly-, di- and monosaccharides. Their cleavage mainly occurs in the duodenum and small intestine, the juices of which contain active amylolytic enzymes (amylase, maltase, sucrase, lactase, invertase, etc.). Carbohydrates are broken down into monosaccharides and absorbed. If the production of amylolytic enzymes is insufficient, then the di - and polysaccharides that come with food are not broken down to monosaccharides and are not absorbed. Glucose absorption suffers when its phosphorylation in the intestinal wall is impaired. The basis of this violation is the insufficiency of the hexokinase enzyme, which develops during severe inflammatory processes in the intestine, in case of poisoning with monoiodoacetate, phloridzin. Unphosphorylated glucose does not pass through the intestinal wall and is not absorbed. Carbohydrate starvation may develop.

Violation of the synthesis and breakdown of glycogen. A pathological increase in the breakdown of glycogen occurs with a strong excitation of the central nervous system, with an increase in the activity of hormones that stimulate glycogenolysis (STG, adrenaline, glucagon, thyroxine). An increase in glycogen breakdown with a simultaneous increase in glucose consumption by muscles occurs during heavy muscle exercise. Glycogen synthesis can change towards a decrease or a pathological increase.

Decreased glycogen synthesis occurs with severe damage to liver cells (hepatitis, poisoning with liver poisons), when their glycogen-forming function is impaired. Glycogen synthesis decreases during hypoxia, since under conditions of hypoxia, the formation of ATP, which is necessary for the synthesis of glycogen, decreases.

hyperglycemia- an increase in blood sugar levels above normal. May develop under physiological conditions; at the same time, it has an adaptive value, since it ensures the delivery of energy material to the tissues. Depending on the etiological factor, the following types of hyperglycemia are distinguished.

Alimentary hyperglycemia, which develops after taking a large amount of easily digestible carbohydrates (sugar, sweets, flour products, etc.).

Neurogenic (emotional) hyperglycemia - with emotional arousal, stress, pain, ether anesthesia.

Hormonal hyperglycemia accompany violations of the functions of the endocrine glands, the hormones of which are involved in the regulation of carbohydrate metabolism.

Hyperglycemia in insulin deficiency is the most pronounced and persistent. It can be pancreatic (absolute) and extrapancreatic (relative).

pancreatic insulin deficiency develops when the insular apparatus of the pancreas is destroyed or damaged. A common cause is local hypoxia of the islets of Langerhans in atherosclerosis, vasospasm. At the same time, the formation of disulfide bonds in insulin is disrupted and insulin loses its activity - it does not have a hypoglycemic effect.

Destruction of the pancreas by tumors, damage to it by an infectious process (tuberculosis, syphilis) can lead to insulin deficiency. The formation of insulin can be impaired in pancreatitis - acute inflammatory and degenerative processes in the pancreas.

The insular apparatus is overstressed and can be depleted with excessive and frequent consumption of easily digestible carbohydrates (sugar, sweets), overeating, which leads to alimentary hyperglycemia.

A number of drugs (thiazide groups, corticosteroids, etc.) can cause impaired glucose tolerance, and in persons predisposed to diabetes, be a triggering factor in the development of this disease.

extrapancreatic insulin deficiency. It can be caused by excessive binding of insulin to blood carrying proteins. Protein-bound insulin is active only against adipose tissue. It provides the transition of glucose into fat, inhibits lipolysis. In this case, the so-called obese diabetes develops.

In diabetes, all types of metabolism are disturbed.

Disorders of carbohydrate metabolism determine the characteristic symptom of diabetes - persistent pronounced hyperglycemia. It is determined by the following features of carbohydrate metabolism in diabetes mellitus: a decrease in the passage of glucose through cell membranes and its assimilation by tissues; slowing down the synthesis of glycogen and accelerating its breakdown; increased gluconeogenesis - the formation of glucose from lactate, pyruvate, amino acids and other products of non-carbohydrate metabolism; inhibition of the conversion of glucose into fat.

The significance of hyperglycemia in the pathogenesis of diabetes mellitus is twofold. It plays a certain adaptive role, since it inhibits the breakdown of glycogen and partly increases its synthesis. Glucose penetrates tissues more easily, and they do not experience a sharp lack of carbohydrates. Hyperglycemia also has negative implications. With it, the entry of glucose into the cells of insulin-independent tissues (the lens, liver cells, beta cells of the islets of Langerhans, nervous tissue, erythrocytes, and the aortic wall) sharply increases. Excess glucose is not phosphorylated, but converted into sorbitol and fructose. These are osmotically active substances that disrupt the metabolism in these tissues and cause damage to them. With hyperglycemia, the concentration of gluco- and mucoproteins increases, which easily fall out in the connective tissue, contributing to the formation of hyaline.

With hyperglycemia exceeding 8 mol / l, glucose begins to pass into the final urine - glucosuria develops. This is a manifestation of decompensation of carbohydrate metabolism.

In diabetes mellitus, the processes of phosphorylation and dephosphorylation of glucose in the tubules cannot cope with the excess glucose in the primary urine. In addition, hexokinase activity is reduced in diabetes, so the renal threshold for glucose is lower than normal. Glucosuria develops. In severe forms of diabetes, the sugar content in the urine can reach 8-10%. This increases the osmotic pressure of the urine, and therefore a lot of water passes into the final urine. During the day, 5-10 liters or more of urine (polyuria) is excreted with a high relative density due to sugar. As a result of polyuria, dehydration of the body develops, and as a result of it, increased thirst (polydipsia).

With a very high level of sugar in the blood (30-50 mol / l and above), the osmotic pressure of the blood increases sharply. The result is dehydration. Hyperosmolar coma may develop. The condition of the patients is extremely grave. Consciousness is absent. Signs of tissue dehydration are pronounced (eyeballs are soft on palpation). With very high hyperglycemia, the level of ketone bodies is close to normal. As a result of dehydration, damage to the kidneys occurs, their function is impaired, up to the development of renal failure.

55. Pathological changes in fat metabolism can occur at its various stages: in violation of the processes of digestion and absorption of fats; in violation of the transport of fat and its transition into tissues; in violation of the oxidation of fats in tissues; in violation of intermediate fat metabolism; in violation of the metabolism of fat in adipose tissue (excessive or insufficient formation and deposition of it).

Violation of the process of digestion and absorption of fats is observed:

1. with a lack of pancreatic lipase,

2. with a deficiency of bile acids (inflammation of the gallbladder, blockage of the bile duct, liver disease). Violated fat emulsification, activation of pancreatic lipase and the formation of the outer shell of mixed micelles, in which higher fatty acids and monoglycerides are transferred from the site of fat hydrolysis to the absorption surface of the intestinal epithelium;

3. with increased peristalsis of the small intestine and lesions of the epithelium of the small intestine with infectious and toxic agents

4. with an excess of calcium and magnesium ions in food, when water-insoluble salts of bile acids - soaps are formed;

5. with avitaminosis A and B, lack of choline, as well as in violation of the phosphorylation process (fat absorption is inhibited).

As a consequence of impaired absorption of fat, steatorrhea develops (feces contain a lot of higher fatty acids and undigested fat). Along with fat, calcium is also lost.

Fatty infiltration and fatty degeneration.

If the fat entering the cells is not broken down, not oxidized, not removed from it, this indicates fatty infiltration. If it is combined with a violation of the protoplasmic structure and its protein component, then they speak of fatty degeneration. A common cause of fatty infiltration and fatty degeneration is the suppression of the activity of oxidative and hydrolytic enzymes of fat metabolism (in case of poisoning with arsenic, chloroform, vitamin deficiency, etc.).

Fatty infiltration develops with:

1) alimentary and transport hyperlipemia;

2) violation of the formation of phospholipids;

3) excess cholesterol.

Violation of intermediate fat metabolism leads to ketosis, which manifests itself in an increase in the level of ketone bodies in the blood (ketonemia) and their excretion in increased amounts in the urine (ketonuria).

Causes of ketosis:

1) deficiency of carbohydrates in the body;

2) stress, in which, due to the activation of the sympathetic system, the carbohydrate reserves of the body are depleted;

3) when the liver is damaged by toxicoinfectious factors, its ability to synthesize and store glycogen is impaired, there is an increase in the flow of NEFA into the liver and the development of ketosis;

4) deficiency of vitamin E, which slows down the oxidation of higher fatty acids;

5) suppression of the oxidation of ketone bodies in the Krebs cycle;

6) violation of the resynthesis of ketone bodies into higher fatty acids with a lack of hydrogen sources.

Pronounced ketosis leads to intoxication of the body (CNS), electrolyte balance is disturbed due to loss of sodium in the urine (sodium forms salts with acetoacetic and β-hydroxybutyric acids), acidosis develops; a decrease in the sodium content in the blood can cause secondary aldosteronism. All this characterizes a diabetic coma.

Violation of the metabolism of fats in adipose tissue. Obesity - This is the tendency of the organism to excessive increase in body weight under the influence of certain conditions. At the same time, body weight increases due to abnormal accumulation of fat in the depot.

According to the etiology, obesity is of three types: alimentary, hormonal, cerebral. The role of heredity in the pathogenesis of obesity is essential. Obesity develops as a result of the following three main pathogenetic factors:

1) increased intake of food (carbohydrates, fats) with energy consumption of fat that does not correspond to this intake;

2) insufficient use (mobilization) of depot fat as an energy source;

3) excess formation of fat from carbohydrates.

Consequences of obesity:

1) impaired glucose tolerance,

2) hyperlipemia due to TG and cholesterol, more often pre-β-lipoproteinemia,

3) hyperinsulinemia,

4) an increase in the excretion of glucocorticoids in the urine, in contrast to patients with Cushing's syndrome, the ratio of excretion of glucocorticoids and creatinine remains normal in obese patients,

5) after exercise, during sleep, after the introduction of arginine, there are smaller fluctuations in the concentration of growth hormone in plasma,

6) decreased insulin sensitivity of enlarged adipocytes and muscles,

7) an increase in the content of NEFA in the blood - an increased consumption of their muscles,

8) hypertrophied lipocytes are more responsive to norepinephrine and other lipolytic substances.

Patients with obesity often develop cardiovascular diseases, hypertension, cholelithiasis (bile in obesity is lithogenic, i.e. contains few detergents that dissolve cholesterol esters). Obese people do not tolerate anesthesia and surgical interventions. As a postoperative complication, thromboembolism often occurs. One of the major complications of obesity is diabetes. With obesity, the likelihood of cirrhosis of the liver is increased, women who are obese are more likely to develop endometrial cancer, because. their adipose tissue has a greater ability to metabolize androstenedione to estrone. With obesity, shortness of breath is observed, because. massive subcutaneous fat deposits limit the movement of the chest, the accumulation of fat in the abdominal cavity prevents the diaphragm from lowering. The need for oxygen is increased, but gas exchange is difficult, relative pulmonary insufficiency increases, and frequent shallow breathing develops.

Excessive feeding of a child during the first year of life contributes to the development of hyperplastic (multicellular) obesity (an abnormal increase in the number of fat cells). This obesity has a poor prognosis for weight loss. It is constantly combined with hypertrophy and is observed in high obesity. Obesity that develops in older childhood is hypertrophic (an increase in the volume of fat cells). It is usually the result of overeating.

With normal (according to energy expenditure) function of the food center, the cause of obesity may be insufficient use of fat from fat depots as an energy source. This can occur with a decrease in the tone of the sympathetic and an increase in the tone of the parasympathetic nervous system, with an inhibitory effect of the cerebral cortex on the centers of the sympathetic department of the diencephalic region. Interstitial neuritis is found in the nerve branches of adipose tissue.

Since the processes of mobilization of fat from the depot are under the control of hormonal and humoral factors, a violation of the production of these factors leads to a restriction in the use of fat. This is observed with insufficiency of the thyroid gland and pituitary gland.

Increased secretion of glucocorticoids causes hyperglycemia by enhancing gluconeogenesis. An increase in the concentration of glucose in the blood reduces the release of fat from the depot and increases the absorption of NEFA and HM by adipose tissue.

The main action of insulin:

● on carbohydrate metabolism - activates glycogen synthetase (promotes glycogen synthesis), activates hexokinase, inhibits gluconeogenesis, promotes glucose transport through the cell membrane;

● on fat metabolism - inhibits lipolysis in fat depots, activates the transition of carbohydrates into fat, inhibits the formation of ketone bodies, stimulates the breakdown of ketone bodies in the liver;

● for protein metabolism - enhances the transport of amino acids into the cell, provides energy for protein synthesis, inhibits the oxidation of amino acids, inhibits protein breakdown;

● on water-salt metabolism - enhances the absorption of potassium by the liver and muscles, provides sodium reabsorption in the tubules of the kidneys, promotes water retention in the body.

Obesity ( lat. adipositas - literally: "obesity" and lat. obesitas - literally: fullness, obesity, fattening) - the deposition of fat, an increase in body weight due to adipose tissue. Adipose tissue can be deposited both in places of physiological deposits, and in the area of ​​​​the mammary glands, hips, and abdomen.

Obesity divided into degrees(according to the amount of adipose tissue) and into types(depending on the reasons that led to its development). Obesity leads to an increased risk of diabetes, hypertension and other diseases associated with being overweight. The causes of excess weight also affect the distribution of adipose tissue, the characteristics of adipose tissue (softness, firmness, percentage of fluid content), as well as the presence or absence of skin changes (stretching, enlarged pores, the so-called "cellulite").

Obesity can develop as a result of:

Disbalance between food intake and energy expended, i.e. increased food intake and reduced energy expenditure;

Obesity of a non-endocrine pathology appears due to disorders in the systems of the pancreas, liver, small and large intestines;

genetic disorders.

Predisposing Factors for Obesity

Sedentary lifestyle

Genetic factors, in particular:

Increased activity of lipogenesis enzymes

Decreased activity of lipolysis enzymes

Increased intake of easily digestible carbohydrates:

drinking sweet drinks

a diet rich in sugars

Certain diseases, in particular endocrine diseases (hypogonadism, hypothyroidism, insulinoma)

Eating disorders (for example, binge eating disorder), in Russian literature called eating disorders, a psychological disorder leading to an eating disorder

Tendency to stress

sleep deprivation

Psychotropic drugs

In the process of evolution, the human body has adapted to accumulate a supply of nutrients in conditions of an abundance of food in order to use this reserve in conditions of a forced absence or restriction of food - a kind of evolutionary advantage that made it possible to survive. In ancient times, fullness was considered a sign of well-being, prosperity, fertility and health.

There are differences in the distribution of excess body fat and in the presence or absence of symptoms of damage to the nervous or endocrine system.

Most common alimentary obesity , usually in individuals with a hereditary predisposition to be overweight. It develops in cases where the caloric content of food exceeds the energy expenditure of the body, and is observed, as a rule, in several members of the same family. This type of obesity is more common among middle-aged and elderly women who lead a sedentary lifestyle. When collecting an anamnesis with a detailed clarification of the daily diet, it is usually established that patients systematically overeat. For alimentary obesity is characterized by a gradual increase in body weight. Subcutaneous adipose tissue is distributed evenly, sometimes accumulates to a greater extent in the abdomen and thighs. There are no signs of damage to the endocrine glands.

hypothalamic obesity observed in diseases of the central nervous system with damage to the hypothalamus (with tumors, as a result of injuries, infections). This type of obesity is characterized by the rapid development of obesity. The deposition of fat is noted mainly on the abdomen (in the form of an apron), buttocks, thighs. Often there are trophic changes in the skin: dryness, white or pink stretch marks (stretch marks). Based on clinical symptoms (eg, headache, sleep disturbances) and neurologic findings, the patient can usually be diagnosed with brain pathology. As a manifestation of hypothalamic disorders, along with obesity, various signs of autonomic dysfunction are observed - increased blood pressure, impaired sweating, etc.

endocrine obesity develops in patients with certain endocrine diseases (for example, hypothyroidism, Itsenko-Cushing's disease), the symptoms of which predominate in the clinical picture. On examination, along with obesity, which is usually characterized by uneven deposition of fat on the body, other signs of hormonal disorders (for example, masculinization or feminization, gynecomastia, hirsutism) are revealed, and striae are found on the skin.

A peculiar type of obesity is the so-called painful lipomatosis (Derkum's disease), which is characterized by the presence of fatty nodes, painful on palpation.

Prevention of obesity is to eliminate hypodynamia and rational nutrition. In children, compliance with the rules of feeding and regular monitoring of the physical development of the child by systematically measuring height and body weight (especially with a constitutional predisposition to obesity) are necessary. Early detection and treatment of diseases accompanied by hypothalamic and endocrine obesity is important.

Diseases of the digestive system are usually directly related to what and how a person eats. The regularity of food intake, the balance of nutrients in the diet, the very nature of the meal and much more - all this can become both a prevention of diseases of the digestive system and the cause of their occurrence.

The most popular diseases

Diseases of the digestive system are a frequent companion modern man, which, due to the overly dynamic rhythm of life, does not always take the time to pay attention to its nutrition. Therefore, the following negative habits appear that ultimately lead a person to the gastroenterologist's office: eating "on the go", excess junk food, irregular meals, overeating, alcohol. All this can provoke the following diseases of the digestive system:

1. Gastritis. Inflammation of the gastric mucosa. The most common consequence of malnutrition, occurring in both adults and children. It manifests itself in the form of local (nausea, heartburn, heaviness after eating) and general (weakness, drowsiness after eating, irritability, intestinal disorders) symptoms.
2. Peptic ulcer of the stomach and duodenum. Aggressive exposure to spicy, fatty foods, smoked meats, salted foods, as well as alcohol and a number of medications can lead to a mucosal defect. Where and how pain manifests itself depends on localization: pain after eating is typical for a stomach ulcer, pain on an empty stomach is for a duodenal ulcer.
3. Dyspepsia of the stomach or violation of the motor function of the stomach. Appears in those who do not give themselves time to chew food thoroughly, and also eat too large portions and include in their diet a large number of fatty proteins. It makes itself felt with heartburn, frequent belching, nausea, the appearance of flatulence and pain in the abdomen.

These diseases are most closely associated with malnutrition, but other diseases of the gastrointestinal tract can also be triggered by this factor.

Getting rid of bad habits

Diseases of the digestive system not only bring negative and painful sensations, but are also quite dangerous for their complications. Therefore, for many, the diagnosis itself and the recommendations of the doctor are a reason to refuse bad habits. The main thing that plays a role here is willpower and prioritization. If you have firmly decided for yourself that your health is much more important, then do not delay and start moving on to proper nutrition. In this case, the treatment of the disease will be much more effective.

Diseases of the digestive tract are distinguished by the variety of their clinical and morphological features. They include independent primary diseases, which are studied by the science called gastroenterology, as well as other, secondary ones, which are a manifestation of a number of diseases of an infectious and non-infectious nature, of an acquired or hereditary origin. These diseases can be based on various general pathological processes, such as alteration, inflammation, hyper- and dysplastic processes, autoimmune disorders, and, finally, tumors.

INFLAMMATORY DISEASES OF THE STOMACH

Inflammatory processes in the stomach, denoted gastritis(from Greek. gaster- stomach), as well as in other organs, can be downstream acute and chronic. The pathogenesis of chronic gastritis is complex. Until recently, it was believed that in one of the forms of chronic gastritis - type A, autoimmune reactions are observed, and in the second form (non-immune gastritis type B), inflammation occurs as a result of prolonged exposure to various non-specific stimuli, such as exogenous (for example, hot drinks or acute spices), or endogenous (eg, bile reflux). Type B chronic gastritis has now been proven to be a response to a bacterial infection. This group excludes gastritis, which develops as a result of bile reflux.

ACUTE GASTRITIS

Acute gastritis most often develops after exposure to various factors:

1. chemical substances(alcohol, junk food);

2. some medicinal substances(non-steroidal anti-inflammatory substances containing aspirin).

3. consumption of spicy, cold or hot foods.

4. Helicobacter pylori.

5. other infections(salmonella, staphylococcus, etc.).

6. toxic products of endogenous origin(with uremia).

According to the area of ​​\u200b\u200bdamage, they distinguish:

ü acute diffuse gastritis;

ü acute focal gastritis (fundal, antral, pyloroanthral and pyloroduodenal).

Depending on the severity of the lesion, changes in the mucosa range from vasodilation and edema lamina propria to erosion and hemorrhage. Erosion is a section of the mucous membrane with a partial violation of the epithelium, while in the ulcer there is a violation of the muscular layer of the mucous membrane. Erosions in acute gastritis are usually multiple, so bleeding from them can be very dangerous. However, there is usually a rapid (within 24-48 hours) healing by regeneration. With frequent recurrences of acute gastritis, chronic gastritis may develop.

CHRONIC GASTRITIS

Currently, the following forms of chronic gastritis are distinguished:

q autoimmune chronic gastritis;

q Helicobacter-associated chronic gastritis;

q chemical reflux gastritis;

q other forms of gastritis.

Table 1

Types of chronic gastritis

Etiology	Pathogenetic mechanism	Histological changes	Associated clinical changes
autoimmune	Antibodies against parietal cells and receptors for external factor Castle. Sensitized T-lymphocytes.	Atrophy of the glands in the body of the stomach. Intestinal metaplasia.	pernicious anemia.
bacterial infection (H. pylori)	Cytotoxins. mucolytic enzymes. Synthesis of ammonium ions by bacterial urease. Tissue damage in an immune response.	Active chronic inflammation. Multifocal atrophy, more in the antrum. Intestinal metaplasia.	Peptic ulcers. Stomach cancer.
Chemical damage Non-steroidal anti-inflammatory drugs. Reflux of bile Alcohol.	Direct damage. Damage to the mucous layer. Degranulation of mast cells.	Hyperplasia of the pit epithelium. Edema. Vasodilation. A small number of inflammatory cells.	Peptic ulcers. Stomach cancer.

Other forms of gastritis

Separately, the following types of chronic gastritis are distinguished:

v lymphocytic;

v eosinophilic;

v granulomatous.

At lymphocytic gastritis the main histological manifestation is the presence of numerous mature lymphocytes in the superficial layers of the epithelium. This form is sometimes found in patients with specific erosions along the enlarged mucosal folds. Etiology and relationship with Helicobacter-associated gastritis has not been established.

Eosinophilic gastritis characterized by mucosal edema and the presence of numerous eosinophils in the inflammatory infiltrate. It is assumed that eosinophilic gastritis is an allergic response to a food antigen to which the patient is sensitized.

Granulomatous gastritis - This is a rare form of gastritis, in which epithelioid cell granulomas are formed. These granulomas can be a manifestation of Crohn's disease or sarcoidosis, but in rare cases it can be cryptogenic.

Peptic ulcer of the stomach and duodenum

Peptic ulceration - these are violations of the integrity of the epithelial cover and underlying tissues of the digestive tract as a result of damage to them by acid and pepsin. According to the clinical course, ulcers are divided into acute and chronic.

Acute ulcers

Reasons for development:

• Severe course of acute gastritis.
• Severe stress (major trauma, surgical interventions).
• Pronounced increase in acidity.
• Poisoning.
• Sepsis.
• Multiple organ failure.

Morphology. Multiple, often combined with chronic ulcers. The diameter does not exceed 1 cm, but giant ulcers are also found. Macroscopically oval, rounded, the bottom of which is covered with grayish-yellow necrotic masses, when rejected, their defect has a gray-red color with arosated blood vessels. The edges of the ulcer are soft. After healing of an acute ulcer, a flat, stellate, re-epithelialized scar remains.

chronic ulcers

The cause of the development of chronic ulcers can be:

1. Infection Helicobacter pylori.
2. Chemical exposures, including steroid drugs and non-steroidal anti-inflammatory drugs.
3. Chronic distress syndrome.

Chronic peptic ulcers most often form at the junction of different types of mucous membranes. So, for example, in the stomach, ulcers are observed at the point of transition of the body to the antrum, in the duodenum - in the proximal area on the border with the pylorus, in the esophagus - in the stratified epithelium in front of the esophageal-gastric junction, postoperative ulcers are localized in the stoma (in the anastomosis ). I.e, ulcers appear where acid and pepsin come into contact with unprotected mucosa.

Pathogenesis. It is not acidity that plays the main role in the development of ulcers, but the ratio of aggression factors and mucosal defense factors. It is believed that in the genesis of duodenal ulcer leading role an increase in factors of aggression plays, and in the development of gastric ulcer, a decrease in defense factors comes first. With a decrease in the latter, it is possible to develop ulcers even with low acidity.

Gastric ulcer. Ulceration occurs as a result of either violation and destruction of the mucous barrier, or violation of the integrity of the epithelium. As a result of bile reflux, the mucous barrier is easily destroyed by its components. Acid and bile together destroy the surface epithelium, increasing the permeability and vulnerability of the mucous membrane. This leads to congestion and swelling in lamina propria, which is observed with reflux gastritis.

The epithelial barrier may also be disrupted by the use of NSAIDs, as they disrupt the synthesis of prostaglandins, which normally protect the epithelium. Also, infection plays a significant role in the destruction of the epithelium. Helicobacter pylori, in which both cytotoxins and ammonium ions and an inflammatory reaction have a destructive effect.

Ulcer of the 12 duodenal ulcer. Factors that damage the anti-acid defense in the stomach usually do not affect the duodenum: Helicobacter pylori does not populate the duodenal mucosa, the mucosa is resistant to the action of bile and alkaline ions of pancreatic juice, drugs are significantly diluted and absorbed before entering the intestine. However Helicobacter pylori affects ulcer formation, tk. infection promotes gastric hypersecretion, which leads to the development of gastric metaplasia in the duodenum, and then colonization of the metaplastic epithelium occurs Helicobacter pylori, which leads to the development of chronic inflammation, which also provokes ulceration.

Morphological changes.

Macroscopically chronic ulcers are usually round or oval in shape. Their sizes, as a rule, do not exceed 2 cm in diameter, however, cases are described when ulcers reached 10 cm in diameter or more. The depth of the ulcer is different, sometimes it reaches the serous membrane. The edges of the ulcer are clear, dense and rise above the normal surface, the pyloric edge of the ulcer is flat (terraced), and the cardial edge is undermined.

During the period of exacerbation microscopically four zones are distinguished in the bottom of the ulcer:

1. exudations
2. fibrinoid necrosis
3. granulation tissue
4. Fibrous tissue (fibrinoid changes and significant narrowing are often observed in the vessels blood vessels as a result of intimal proliferation and sclerosis).

During the period of remission, scar tissue is found at the edges of the ulcer. The mucosa is thickened at the edges, hyperplastic.

Complications.

Ulcerative-destructive:

1. 1. perforation the walls of the stomach or duodenum 12, while the contents of the digestive tract are poured into the abdominal cavity, which leads to the development of peritonitis.
2. penetration - there is a perforation of the ulcer in the closer lying organs, for example, the pancreas or liver.
3. bleeding , which can be lethal.

Inflammatory:

1. 1. gastritis, perigastritis.
2. 2. duodenitis, periduodenitis.

Ulcerative scars:

1. 1. stenosis.
2. 2. deformations .

Malignancy of stomach ulcers (duodenal ulcers are very rarely malignant).

Combined complications.

APPENDICITIS

Appendicitis - primary inflammation of the appendix of the caecum with a peculiar clinical syndrome. Therefore, not every inflammation of the appendix in clinical and anatomical terms should be considered as appendicitis (for example, when the inflammatory process spreads from adjacent organs, when it is affected by tuberculosis, etc.)

There are two clinical and anatomical forms of appendicitis: acute and chronic.

Acute appendicitis is the most common cause of emergency operations in surgery. It is found in all age groups but most common in adolescents.

The most common causes of acute appendicitis are obstruction of the lumen of the appendix coprolite or enlarged submucosa as a result of lymphoid hyperplasia, as well as with an inflection of the appendix. In this case, in the distal segment, there is an increased reproduction of microorganisms, such as Escherichia coli, Streptococcus faecalis and anaerobic bacteria. These bacteria then invade the mucosa and other linings of the appendix, causing acute inflammation.

pathological changes. It is customary to distinguish the following main morphological forms of acute appendicitis:

1) simple;

2) superficial;

3) destructive (which in turn is divided into phlegmonous, apostematous, phlegmonous-ulcerative, gangrenous).

All these forms, in essence, are a morphological reflection of the phases of an acute inflammatory process in the appendix, which ultimately ends in necrosis. The duration of this process is 2-4 days.

For acute simple appendicitis characterized by the presence of stasis in the capillaries and venules, edema, hemorrhage, marginal standing of leukocytes, leukodiapedesis, most often in the distal appendix. Outwardly, the appendix looks normal, however, the diagnosis is confirmed by histological examination.

Acute superficial appendicitis characterized by the presence in the distal focus of exudative purulent inflammation in the mucous membrane, referred to as primary effect. Changes characteristic of simple or superficial appendicitis may be reversible. However, as a rule, they progress, and develops destructive appendicitis.

By the end of the first day, the leukocyte infiltrate (neutrophils predominate) extends to the entire thickness of the process wall. (phlegmonous appendicitis). Macroscopically, the inflamed appendix looks edematous and red, its surface is often covered with fibrinous-purulent exudate. Sometimes, against this background, small multiple abscesses are detected, in which case such appendicitis is designated as apostematic. Acute inflammation of the mucous membrane leads to the formation of ulcers and inflammation of the muscle layer - this phlegmonous-ulcerative appendicitis. Purulent-destructive changes are completed with the development gangrenous appendicitis. The process in this form is thickened, its wall is gray-dirty in color, structureless with a fetid odor, pus is released from the lumen. Microscopically, there are extensive foci of necrosis with colonies of microbes, hemorrhages, blood clots in the vessels. The mucous membrane is desquamated almost throughout.

Complications.

"appendicular infiltrate"

peritonitis

distant abscesses (eg, in the rectovesical and subdiaphragmatic spaces)

thrombophlebitis of the portal vein with the formation of multiple pylephlebitic liver abscesses.

Chronic appendicitis characterized by the presence of sclerotic and atrophic processes, against which signs of inflammatory and destructive changes can be detected. There are adhesions with surrounding tissues. With cicatricial obliteration of the proximal section, serous fluid can accumulate in the lumen of the appendix and a cyst is formed - edema of the process. If the contents of the cyst are represented by mucus, such a complication is designated as mucocele. With the rupture of such a cyst and the contents entering the abdominal cavity, implantation of cells on the peritoneum and the development of formations resembling a tumor are possible - pseudomyxoma peritoneum.

NONSPECIFIC ULCERATIVE COLITIS

UC is a nonspecific inflammatory disease of the colon that usually develops in the rectum and then spreads proximally.

Etiology. It is assumed that there is a clear genetic predisposition to ulcerative colitis; this genetic defect can affect both the immune response and the structure of the intestinal mucosa. So in ulcerative colitis, the HLA-DR2 genes and some cytokines play an important role. There is an increase in the synthesis of IgG 2 compared with IgG 1 . An increase in the permeability of the mucous membrane and a change in the composition of mucus glycoproteins are found.

Now there is evidence that UC develops as a result of autoimmune processes, and mucosal damage occurs through inadequate activation of T-cells and mediated damage by cytokines, proteases and oxygen radicals synthesized by macrophages and neutrophils.

In the normal state, the mucosal immune system is tolerant to external antigens located in the intestinal lumen; this tolerance is maintained by the interaction of the intestinal epithelium and T-suppressors. A change in the state of epithelial cells, leading to an acquired increase in the synthesis of MHC class II molecules (HLA-DR), activates T-helpers, which leads to the development of cascade immune and biochemical reactions under the influence of cytokines. The most likely antigen or triggering factor is the microorganisms that colonize the gut. The start of this process can be significantly affected by stress, inflammation of the intestinal mucosa, and smoking.

Regardless of the cause, it has been proven that mucosal damage in UC occurs as a result of the accumulation of polymorphonuclear leukocytes in the mucosa, which secrete proteases, nitric oxide and free radicals.

Morphology. In NUC, a consistent and continuous type of lesion is observed. Usually, the initial lesion occurs in the rectum, where the maximum severity of changes is observed, and then spreads to the sigmoid and colon (Fig. 1).

Rice. 1. Pathological changes in nonspecific ulcerative colitis

The ulcers are irregularly rimmed and may coalesce, and they spread horizontally to areas that are still intact, forming large islands of lesions. Usually ulcers are superficial, they capture the mucous and submucosal membranes, however, in severe cases, all layers of the intestine can be damaged, up to perforation. In the intact mucosa, pronounced hyperemia is found, bleeding often occurs from ulcers.

Microscopically mucosal infiltration by cells of acute and chronic inflammation is determined. Polymorphonuclear leukocytes are found in the interstitium, however, in some crypts they form aggregates (crypt abscesses). Widespread degenerative changes develop both in superficial epitheliocytes and in crypts, and the synthesis of mucins sharply decreases. In the acute period, complete destruction of the crypts can be observed. Then their regeneration begins, the newly formed crypts are characterized by a significant expansion and often have connections with neighboring crypts. So, a biopsy of the rectum reveals atrophy and a significant expansion of the crypts, in which signs of metaplasia of the epithelium are sometimes found. UC is a precancerous disease, therefore epithelial dysplasia is found in some areas.

table 2

Complications of ulcerative colitis

Complication