Gastrointestinal diseases(gastrointestinal tract) are currently the most common pathologies in the world. And no matter what symptoms they manifest, what form they take (mild or severe), almost every person (95% of the population) suffers from these diseases.
Among other things, gastrointestinal diseases are the causes of other pathologies: immune, endocrine, nervous, cardiovascular and other systems.

The processes that occur in our body are a consequence of the digestion process and it becomes clear that the normal functionality of the gastrointestinal tract is the beginning of the principles on which human health and his condition depend.

Gastrointestinal diseases: classification

The classification of pathologies in this group is elementary. Gastrointestinal diseases are distinguished:

1. By localization of the disease process.
- stomach diseases;
- diseases of the esophagus;
- vomiting of the large and small intestines;
- diseases of the biliary tract and liver.

2. For reasons of occurrence:
- infectious;
- non-infectious.

3. According to the intensity of the pathological process:
- acute form;
- moderate form.

Gastrointestinal diseases: causes

In order of importance, we list the causes of gastrointestinal diseases in this order:

1. Poor nutrition.
This is the main cause of all pathologies of our gastrointestinal tract, and this reason has the following aspects: insufficient or excessive food consumption; improper diet; improper diet; deficiency of nutrients in food; a huge amount of preservatives and various artificial substances in food; small amount of plant fiber in food...

Diseases of the gastrointestinal tract, as a rule, are a consequence of a violation of its beneficial microflora, which leads to the predominance of pathogenic and opportunistic microorganisms, which, in turn, cause various diseases of the gastrointestinal tract, and then the immune, endocrine, nervous, cardiovascular and others body systems.

Transfer factor is an immunomodulator, which is based on molecules of the same name - components of our immune system. Once in the body, this drug:
- restores immunity and normal metabolic processes in the body;
- enhances the therapeutic effect of the drugs used, helping to normalize the microflora of the gastrointestinal tract;
- neutralizes possible side effects from the therapy used (no matter what).

It remains to be said that the listed drugs for the treatment of gastrointestinal diseases have no contraindications, do not cause any side effects, are not addictive and overdose is impossible, these are 100% natural drugs that we recommend using not only in the complex treatment of gastrointestinal pathologies, but and for their prevention.

Prevention of gastrointestinal diseases

1. Eat right.
This point in the prevention of gastrointestinal diseases includes adherence to the diet and regimen. Eat more often, but eat in small quantities. Eat 5-6 times a day, but don't overeat.
Limit your consumption of fried, smoked, fatty and salty foods. Increase your fiber intake (vegetables, fruits, cereals, bran bread).

2. Control your weight.
Calculate your body mass index and stick to it, fight obesity, lose excess weight, but do it correctly (!!!).

3. Minimize your alcohol consumption.
And if you have a gastrointestinal disease, give it up (and urgently).

4. Quit smoking.

5. Avoid stressful situations.
Review your life and understand one thing: there is nothing more valuable for you and your loved ones than your health in this life, and no problems are worth your nervous costs.

6. Lead an active lifestyle.
Gastrointestinal diseases are caused by low physical activity of a person (including). And to prevent these diseases, do exercises in the morning, jogging in the evenings, and if you have a “sedentary” job, try to do warm-up exercises for 5-10 minutes after an hour or two.

7. Take probiotic and prebiotic supplements on a regular basis.
Our gastrointestinal tract needs a constant supply of beneficial microorganisms.

The human body is very dependent on the supply of essential substances from the external environment with food. The work of organs and systems has a good reserve, is capable of providing increased load for a long time, but is interrupted if the energy balance is not maintained. And calories are formed only as a result of complex biochemical processes.

Humans obtain “reagents” for synthesis from food products. The best medicines cannot replace the natural process of nutrition through the stomach and deliver the substances necessary for life.

Diseases of the gastrointestinal tract are one of the first areas of therapy in ancient medical manuscripts, along with help for injuries. How to treat individual symptoms was taught even under Hippocrates and Avicenna.

Terms and classifications

The term “gastrointestinal tract” is very old, taken from anatomy. It implies and justifies its name - the stomach and intestines. More precisely, let's say - from the place of attachment of the esophagus to the anus. This means that only the pathology of these organs should be considered diseases of the gastrointestinal tract.

Modern knowledge about the digestive system has accumulated many facts about the inextricable connections between the work of the stomach, the causes of intestinal pathology and the functioning of other organs - the liver, gallbladder and ducts, and pancreas. Today's medical professionals more often use the term “diseases of the digestive system”; the old name refers to its expanded concept.

The International Statistical Classification has identified a separate class of diseases and calls it “Diseases of the digestive organs.” However, let us explain the features of statistical accounting. Gastrointestinal diseases in this group exclude the pathology that we are accustomed to attributing to digestive problems:

The list of diseases would be incomplete without congenital anomalies and defects (for example, achalasia of the esophagus)

Therefore, when territories report a stable state of gastrointestinal morbidity, they separately take into account the growth of viral hepatitis, outbreaks of intestinal infections, the danger of cancerous degeneration and identified new cases of neoplasms.

According to statistics published by the Ministry of Health, the number of gastrointestinal diseases has been trending downward in recent years. It firmly holds 4th–6th place in the total number after diseases of the respiratory system, genitourinary system, and skin (excluding injuries).

However, targeted studies and visits to medical institutions allow us to conclude that:

• up to 60% of the adult population suffer from digestive system disorders, and in large cities and metropolitan areas - up to 95%;
• among visits to therapists, gastrointestinal problems account for 37%;
• Men under 50 years of age suffer from peptic ulcers 3 times more often than women:
• ulcerative changes in the duodenum exceed those in the stomach by 8–10 times;
• the population remains insufficiently informed about the possibilities of early detection and timely diagnosis of malignant neoplasms of the stomach and intestines.

Data from attending physicians indicate that 4.5–5% of people in the Russian Federation die annually from diseases of the digestive system. In the structure of cancer mortality, colorectal cancer ranks second, and stomach cancer ranks third.

Doctors of various specialties treat diseases of the gastrointestinal tract: therapists, pediatricians, gastroenterologists, infectious disease specialists, oncologists, surgeons.

What happens in the human digestive tract

The main functions of the digestive system are:

• motor-mechanical - allows you to crush, mix and move the food bolus along parts of the tract, remove toxins from the body;
• secretory - responsible for the chemical processing of food particles with the connection of various enzymes found in the juices of interested organs;
• suction - ensures the selection and assimilation of only the substances and liquids needed by the body from the contents.

In recent years, another importance of the digestive organs has been proven - participation in the synthesis of certain hormones and elements of the immune system. Diseases of the stomach and intestines are caused by a malfunction of one or more areas.

Of particular importance is the sufficient functioning of the duodenum, liver, and pancreas. According to their anatomical structure, these organs are very closely related to the gastrointestinal tract. Disruption of their work leads to dysfunction of the entire gastrointestinal tract.

The most important causes of gastrointestinal disorders

An important cause of diseases of the digestive system is poor nutrition. Main mistakes:

• long breaks in food intake - disrupt the reflex mechanism for the production of digestive juices, allowing significant concentrations of enzymes to accumulate in the stomach and intestines without food intake, which causes dangerous damage to one’s own mucous membrane;
• the predominance of fatty meat foods, fried and smoked dishes, hot seasonings and sauces - contributes to the failure of the formation and flow of bile into the intestines, congestion in the bladder and increases the risk of stone formation;
• excessive consumption of alcoholic beverages - has a direct toxic effect on liver cells, the mucous membrane of the stomach and intestines, leads to increased consumption of enzymes, atrophic processes, contributes to atherosclerotic damage to blood vessels and impaired nutrition of the walls;
• consuming foods of contrasting temperatures is an excessive irritant to the stomach; the habit of very hot drinks plays a role in the occurrence of gastritis.

Passion for vegetarianism damages the supply of essential amino acids obtained only from animal proteins, and therefore the construction of the cell membranes of the digestive organs themselves

Toxic substances with a damaging effect on the gastrointestinal tract include:

• industrial contact with pesticides, alkalis, salts of heavy metals, concentrated acids, household and suicidal poisoning;
• medications of the antibiotic class, some antifungals, cytostatics, hormonal drugs;
• nicotine and drugs.

After treating the gastrointestinal tract with antibacterial agents, it is necessary to use additional agents that restore beneficial microflora. Infectious diseases affecting the gastrointestinal tract are caused by: different strains of Escherichia coli, staphylo- and streptococci, enterococci, Klebsiella, Proteus, salmonella, shigella, hepatitis viruses, herpes, helminths (ascariasis), amoebas, echinococci, lamblia.

High infection of the population with Helicobacter is considered one of the factors in the spread of chronic inflammation of the stomach (gastritis).

The penetration of infection through the stomach and intestines, the creation of a comfortable environment for living and reproduction, is accompanied by damage to the entire body, a toxic effect on the brain, and cells of the hematopoietic system. As a rule, it is possible to cure such diseases only with specific agents that can specifically destroy the infectious agent.

Abdominal injuries and wounds disrupt the blood supply to internal organs, stomach, and intestines. Ischemia is accompanied by vascular thrombosis, necrotic manifestations with rupture of sections of the intestine. The negative effects of ecology and ionizing radiation are among the first to disrupt the functioning of the secreting cells of the glandular epithelium. During treatment with chemotherapy and irradiation of tumors of various locations, the liver, intestines and stomach suffer.

Heredity among members of the same family is expressed in a predisposition to gene mutations when encountering risk factors, which is expressed in structural anomalies, functional underdevelopment, and high sensitivity to other causes.

Ecological troubles in nature affect the stomach and intestines through low quality drinking water, increased intake of pesticides and nitrates from vegetables, and antibiotics, hormones, and harmful preservatives from meat products.

An irresistible stress load on a person can lead to digestive disorders. The spread of pathology of the endocrine organs due to diabetes mellitus, diseases of the thyroid gland and parathyroid glands disrupts the regulation of the secretion of juices and enzymes.

Great importance is attached to violations of hygienic skills, sanitary illiteracy of children and adults, non-compliance with the rules of culinary processing and storage of food

What gastrointestinal diseases do people encounter most often?

Of the diseases caused by pathology of the stomach and intestines, the following pathologies should be noted as the most common diseases of inflammatory origin.

Gastritis

inflammation proceeds from a more favorable superficial one, to the formation of erosions and atrophy of the inner membrane, very different with high and low acidity, and dyspepsia is sure to occur.

Impaired motor function of the muscular layer of the stomach and sphincters

When the upper cardiac sphincter is weakened, the formation of gastroesophageal reflux disease with reverse reflux of acidic contents and damage to the esophagus is possible. If the contractility of the pyloric part changes, then pylorospasm or reflux of bile from the duodenum appears. This is how biliary reflux gastritis is formed.

Duodenitis

Duodenums, usually a complement and continuation of gastritis, somewhat change the nature of the symptoms. The pain becomes “late”, 1.5–2 hours after eating, and there is an admixture of bile in the vomit.

Gastroenteritis

The general name for diseases of the stomach and intestines, most often caused by infectious genesis, poisoning with low-quality products. They occur acutely with high fever, nausea and vomiting, pain of various localizations, and diarrhea. Children experience a dangerous symptom - dehydration.

Enterocolitis

Infectious and non-infectious lesions of the intestinal mucosa, possible manifestations of dysentery, typhoid fever, cholera. Patients are bothered by spastic pain in the left or right half of the abdomen, false urge to go to the toilet (tenesmus), and fever. The whole body suffers from intoxication.

Appendicitis

Local inflammation of the appendix has its own symptoms, but always requires differential diagnosis due to the anatomical features of the location.

Haemorrhoids

A disease of the rectal veins that affects the majority of the adult population. In origin, a tendency to constipation, sedentary work, and difficult childbirth in women are important. It manifests itself as severe pain in the anus, itching of the skin, and bleeding during bowel movements. Lack of treatment leads to the transfer of inflammation from dilated veins to nearby tissues, pinching of venous nodes, formation of cracks in the rectal mucosa, and cancer.

Dysbacteriosis

It is not considered an independent disease, but due to the nature of digestive disorders, the condition requires correction, additional therapy and special examination of stool for intestinal flora. It can be caused either by inflammation or by medications.

A decrease in the proportion of beneficial bifidobacteria and lactobacilli contributes to disruption of food digestion and activates opportunistic bacteria. Prolonged diarrhea is especially difficult for young children.

Peptic ulcer of the stomach and duodenum

Persistent painful symptoms, seasonality and damage to the mucous membrane up to the muscular layer, signs of bleeding are found in the stool. Severe complications are possible in the form of perforation of the ulcer into the abdominal cavity or neighboring organs. They manifest themselves as dagger pains and the patient’s state of shock.

Neoplasms of different localization

This includes polypous growths and cancer. Tumors form under the influence and against the background of various gastroenterological diseases. It is known that colorectal cancer is transformed from colon polyps, stomach cancer from atrophic gastritis.

If the tumor grows inward, then manifestations are detected by a mechanical obstruction to the movement of feces (constipation). With external growth (exophytic), symptoms are not detected for a long time or have general intestinal manifestations (vague pain, unstable stool).

Quite rare gastrointestinal diseases include:

• Crohn's disease is a severe lesion of the entire digestive “tube” from the oral cavity to the rectum, in half of the cases - the ileum and rectum, and is classified as a hereditary autoimmune pathology in origin. The exact reason is unknown. Granulomatous growths grow throughout the entire thickness of the intestinal wall. The clinical manifestations are characterized by diarrhea, abdominal pain, and prolonged fever. It occurs as inflammation, spasm or perforation with the formation of fistula tracts.
• Whipple's disease- affects mainly men, is considered an infectious disease (the causative bacterium has been isolated), but researchers emphasize the role of an excessive perverted reaction of the immune system. It manifests itself as prolonged diarrhea, fever and general symptoms (joint pain, damage to the skin, heart, eyes, hearing, neurological signs).

In a hiatal hernia, a protrusion into the chest cavity forms the esophagus and the upper edge of the stomach

The role of esophageal pathology

On the one hand, the esophagus is considered in the gastrointestinal tract simply as a connecting tube from the mouth to the stomach, so the condition of the muscle base for “pushing” food matters. But on the other hand, the connection with the stomach causes changes in the mucous membrane in the lower sections and leads to local disease. The most frequently identified pathologies are those described below.

Esophagitis - inflammation with painful swallowing of liquid and solid food, a burning sensation in the epigastric region, heartburn, belching. The culprit is reflux of acid from the stomach. In severe cases, the disease is called gastroesophageal reflux.

Hiatal hernia - pathology caused by a violation of the localization of the esophagus, displacement of the lower border, protrusion of the diaphragm from the esophageal opening. The disease can be inherited or formed as a result of long-term inflammatory processes in the esophagus and stomach. The main manifestation is reflux of food into the esophagus with heartburn, belching, pain, bloody vomiting, and difficulty swallowing. Treatment is surgical only.

Barrett's esophagus is the leading cause of esophageal ademocarcinoma. It is detected by fibrogastroscopy after examining a biopsy specimen. A sign such as prolonged heartburn is the reason for mandatory examination. Typical detection is the growth of squamous epithelial tissue in place of the esophagus.

If detected, the affected areas are removed using a laser beam. It is still possible to prevent cancerous transformation.

Ulcerative non-infectious colitis of autoimmune etiology is attracting increasing attention due to its spread among children and adults

Serious secondary disorders of the gastrointestinal tract are caused by:

• viral and non-infectious hepatitis;
• cirrhosis with liver and kidney failure;
• diseases of the pancreas from functional disorders to pancreatitis and cancer;
• cholecystitis and cholelithiasis.

Symptoms of gastrointestinal diseases

Therapy of digestive diseases requires taking into account the pathogenetic mechanisms of the occurrence of disorders. It is most correct to treat the gastrointestinal tract according to clinical syndromes.

Dyspepsia

Dyspepsia syndrome includes subjective symptoms. It is customary to distinguish between the gastric and intestinal types. Most stomach diseases are characterized by:

• pain in the epigastric region of varying intensity, but always associated in time with food intake;
• feeling of fullness in the stomach;
• heartburn;
• nausea and vomiting;
• belching;
• loss of appetite.

The combination of these symptoms depends on the nature of the disease, the stage of the process and the degree of functional impairment

So, according to the set of symptoms, dyspepsia is divided:

• for reflux - manifested by a burning sensation behind the sternum, belching, heartburn, difficulty swallowing;
• ulcer-like - the patient experiences intermittent “hungry” pain, worsening may occur at night (late pain);
• dyskinetic - patients complain of heaviness in the epigastrium, a feeling of fullness in the stomach, nausea, loss of appetite, vomiting;
• systemic - characterized by bloating, rumbling in the intestines, stool disorders, possible painful spasms.

Dyspepsia of the human intestinal tract is accompanied by: flatulence, transfusion and rumbling in the intestines, spastic or bursting pain in the abdomen without constant localization, unstable stool. Symptoms occur when the function of the stomach and intestines is impaired. Observed in hypoacid gastritis, enterocolitis, tumors, adhesions, chronic pancreatitis, cholecystitis, hepatitis.

Signs of intestinal dyspepsia are constant, not related to feeding, more intense in the afternoon, and usually subside by night. They intensify when consuming dairy products and vegetables high in fiber (cabbage, beets). Patients attribute improvement in their condition to defecation and release of gases.

Hyperacid syndrome

Symptoms of gastrointestinal disease with increased acidity of gastric juice appear with gastritis, duodenitis, peptic ulcers, and are typical for heavy smokers. An increased concentration of hydrochloric acid is associated with increased secretion, insufficient neutralization, and delayed evacuation of stomach contents into the duodenum.

Hyperacidity of the stomach is distinguished by the following symptoms:

• heartburn on an empty stomach, after eating, at night;
• belching sour;
• increased appetite;
• vomiting of sour contents;
• pain in the epigastrium and right hypochondrium, “hungry”, late at night;
• tendency to constipation due to spasm of the pylorus and slower evacuation of food masses.

Hypoacid syndrome

Occurs when the acidity of gastric juice decreases. It is observed with stomach ulcers, atrophic gastritis, cancer, gastrointestinal infections, chronic cholecystitis, anemia, and general exhaustion. Signs of hypoacidity:

• poor appetite (in severe cases, weight loss);
• intolerance to certain foods;
• nausea;
• flatulence;
• “hungry” pain in the stomach;
• diarrhea (the pyloric opening is constantly gaping, so the intestinal mucosa is irritated by undigested food).

The nature of the pain is different (spastic or bursting)

Enteral and colitic insufficiency syndrome

Manifested by intestinal and general symptoms. Intestinal symptoms include: pain around the navel 3-4 hours after eating, dyspepsia and dysbacteriosis. The stool is loose, foamy, foul-smelling several times a day, or constipation with atony in old age.

Common symptoms include:

• weight loss due to increased appetite;
• fatigue, insomnia, irritability;
• skin manifestations (dryness, peeling, brittle nails, hair loss);
• iron deficiency conditions, anemia;
• hypovitaminosis with bleeding gums, stomatitis, blurred vision, petechial rash (lack of vitamins C, B2, PP, K).

General principles of treatment of gastrointestinal diseases

Treatment of the stomach and intestines cannot be done without following a single regimen, which necessarily includes diet, exercise therapy and physiotherapy outside the acute stage, if the symptoms and examination results do not raise concerns about cancerous degeneration.

Basic menu requirements:

• Regardless of the nature of the pathology of the stomach or intestines, meals should be taken in small portions 5–6 times a day;
• all irritants to the mucous membrane are excluded (alcohol, carbonated water, strong tea and coffee, fried and fatty foods, canned food, smoked foods and pickles);
• the selection of a diet is carried out taking into account the type of gastric secretion of a particular patient; in an anacid state, stimulating dishes are allowed, in a hyperacid state they are prohibited;
• in the first week of exacerbation, crushed, pureed food, liquid porridge with water are recommended;
• expansion of the diet depends on the results of treatment of the stomach and intestines, and the patient’s well-being;
• the possibility of consuming dairy products is decided individually;
• It is necessary to prepare food in stewed, boiled and steamed form.

Dyskinesia and functional disorders of the stomach and intestines can be effectively relieved by physical therapy

Drug treatment

Upon receipt of a conclusion about the presence of Helicobacter in the stomach, a course of eradication with antibiotics and bismuth preparations is recommended. Its effectiveness is monitored by repeated studies.
To support the secretory function of the stomach, drugs such as Pepsin, gastric juice, and Plantaglucid are used.

With increased acidity, gastric secretion blockers (proton pump inhibitors) and enveloping agents (Almagel, Denol, Hefal) are needed. To relieve pain, antispasmodics (No-Shpa, Platyfillin) are prescribed. Cerucal helps with hypotonic damage to the stomach and intestines, relieves nausea, vomiting, and activates peristalsis.

To stimulate healing for stomach ulcers, Riboxin, Gastrofarm, Solcoseryl, and anabolic hormones are used. In case of chronic damage to the intestines and stomach with symptoms of vitamin deficiency and anemia, injections of vitamins and iron supplements are prescribed.

Moderate signs of bleeding indicate the involvement of a small-diameter vessel in the process; general anti-inflammatory therapy helps in eliminating it. In case of bloody vomiting and black stools with symptoms of blood loss and signs of obstruction, surgery with resection of the damaged part of the stomach or intestine is necessary.

Cancerous changes are treated with courses of chemotherapy and radiation. The extent of surgical intervention depends on the stage. Physiotherapeutic procedures can improve the regeneration of the epithelium of the stomach and intestines, relieve hypertension, and normalize motility.

For this we use:

• electrophoresis with the introduction of the necessary drug from the active electrode;
• diadynamic currents;
• phonophoresis.

Spa treatment with water and mud applications from natural sources helps to achieve long-term remission.

Phytotherapy

Treatment with herbal remedies should be used after the acute symptoms of inflammation of the intestines and stomach have been eliminated. Decoctions of chamomile, yarrow, calendula, oak bark, and plantain have anti-inflammatory properties.

The enveloping effect on the stomach of oatmeal jelly and flaxseed decoction is beneficial

Diseases of the stomach and intestines are treated by specialists from clinics. Oncologists consider it necessary, for the purpose of early diagnosis of cancer, to conduct ultrasound examination and esophagogastroduodenoscopy for all persons over 40 years of age, even if there are no symptoms.

And if there are complaints about bowel function, try to examine the patient using colorectoscopy. This study is still less accessible and is carried out in specialized hospitals or private clinics. But a timely diagnosis is worth the cost.

A correctly and carefully collected anamnesis is important for making the correct diagnosis of a perforated ulcer of the stomach and duodenum.

Ulcer history is an important sign of a perforated ulcer. In some patients it may be absent, and perforation occurs in them in a state of apparent complete health. Making a diagnosis of a “silent” ulcer is difficult, since it is made solely on the basis of objective data.

According to a number of authors, perforation of “silent” ulcers occurred from 5% to 12.7%. However, when collecting anamnesis, it is necessary to attach importance to identifying even minor pain in the epigastric region in the past; it must be taken into account that peptic ulcer of the stomach and duodenum sometimes gives mild pain in the epigastric region for a long time, appearing periodically. Establishing a history of pain in the epigastric region and other dyspeptic disorders with an appropriate clinical picture can have important diagnostic value.

Differential diagnosis of diseases of the abdominal organs is easier to carry out in the initial stage of the disease. Subsequently, when peritonitis develops, its source is often difficult to establish.

Differential diagnosis for perforated ulcers of the stomach and duodenum must be carried out with the following diseases: acute appendicitis, acute cholecystitis, acute pancreatitis, acute intestinal obstruction, thromboembolism of mesenteric vessels, renal colic, gastralgic form of myocardial infarction, basal pleuropneumonia and pleurisy, food intoxication, acute gastritis and acute enterocolitis, tabetic crisis.

The most acceptable classification is G. Mondor, which more fully reflects all sources of diagnostic errors in perforated gastric and duodenal ulcers.

G. Mondor divided the sources of diagnostic errors into 4 groups: 1) errors due to insufficient examination of the patient or incorrect analysis of existing symptoms; 2) clinical perforation syndrome in the absence of perforation; 3) errors due to “false calm” in the stage of “imaginary well-being”; 4) clinical perforation syndrome in diseases of organs located outside the abdominal cavity.

Diagnostic errors can be made with the so-called atypical form of perforated gastroduodenal ulcers - covered perforation.

The clinical picture of a covered perforated ulcer at the onset of the disease does not differ from that with open perforation (sudden acute pain in the epigastric region, “board-shaped” anterior abdominal wall, a history of peptic ulcer disease, etc.). After 20-30 minutes or several hours from the onset of the attack, all acute symptoms are interrupted, the perforation is covered, and the process is limited, and a noticeable improvement in the patient’s general condition begins. Of all the symptoms, only limited local tension in the muscles of the anterior abdominal wall in a small area corresponding to the location of the perforated ulcer is more persistent.

Work pages

NOVOSIBIRSK STATE MEDICAL ACADEMY

Department of Faculty Therapy for the Faculty of Pediatrics.

DISCHARGE EPICRISIS.

Ds - Peptic ulcer of the pyloric part of the stomach, unassociated, single, medium size, typical, highly secretory, recurrent. Condition after suturing the ulcer.

City Clinical Hospital No. 1 dept. Gastroenterology.

Completed by: student IV candidate of pedagogical faculty.

Novosibirsk 2005.

Epicrisis

Patient 40 years old Entered the clinic on 02/15/05. with complaints of nausea, mainly morning vomiting. Pain in the epigastrium and left hypochondrium, appearing after 30 minutes. after meal; having an aching, cutting nature, spreading upward into the mediastinum, radiating to the right arm. Daily nausea, weakness, dizziness. Pain when bending and turning the body to the painful (left) side. From the medical history it was established that the first diagnosis of duodenal ulcer was made in 1986. According to the patient, he was treated independently, taking vitamins and antacids irregularly. He noted an exacerbation in the spring-autumn period. In 1988, after minor physical activity, I felt sharp cutting pains in the mesogastric region of the abdominal cavity. The general condition gradually worsened, he called an ambulance and was taken to ICD-25. He was operated on as an emergency due to a perforated ulcer complicated by peritonitis. Due to significant blood loss (about 2 liters) he was transferred to surgical intensive care. To date, no monitoring has been carried out. His life history includes chronic alcoholism, smoking, according to the patient, for 5 years before the first manifestation of the disease (in 1986), he still smokes. An appendectomy was previously performed. Chronical bronchitis.

Family history - the daughter has signs of incipient gastritis.

The reason for this visit to the doctor was the deterioration of the general condition, pain in the epigastrium, appearing after 30 minutes. after meal; having an aching, cutting character. I went to the clinic and was sent for hospitalization to City Clinical Hospital No. 1.

An objective examination revealed: slight yellowness of the skin and visible mucous membranes. Severe hypotrophy of the subcutaneous fat layer. Spider veins on the subclavian region of the chest wall. The abdomen is soft on palpation, moderately painful in the epigastrium. The percussion sound over the entire surface of the lungs has a tympanic tint.

Currently, there is still pain on palpation in the epigastric region; daily nausea, vomiting, general weakness, malaise. AD-155/90mmHg Increased basal secretion. Yellowness of the skin, sclera and visible mucous membranes.

Additional research methods:

Diseases of the digestive system. Stomach diseases

Main symptoms of stomach diseases

Appetite. Appetite is a feeling associated with the body's need to eat food. When the body's tissues do not receive enough nutrients, a feeling of hunger occurs. However, appetite largely depends on the secretory function of the stomach. I.P. Pavlov wrote that appetite is gastric juice.

The feeling of appetite arises from the stimulation of the “food center,” during which the active secretion of gastric juice occurs, which I. P. Pavlov called “appetizing” juice. With reflex separation of gastric juice, appetite usually increases, and when the secretory function of the stomach is suppressed, appetite decreases or disappears completely (anorexia).

When a person sees food or smells it, his reflex (conditioned reflex) begins to intensely secrete gastric juice and a feeling of hunger appears.

Well-prepared and tasty food, its smell and appearance reflexively cause increased secretion of gastric juice and increased appetite. Sometimes the patient refuses food not because he has a poor appetite, but because every meal causes him severe pain in the stomach. If food is retained in the stomach or gastric secretion is impaired, appetite weakens or disappears. Strong emotions, especially negative ones (fear, melancholy, anger), inhibit the food center, and appetite disappears.

In case of infectious diseases with elevated body temperature and various serious diseases (cancer, malignant anemia, etc.), appetite may decrease or disappear completely. This also largely depends on the reflex decrease in the secretory function of the stomach, although there may not be morphological changes in the wall of the stomach.

From the above it follows that appetite largely depends on the secretory function of the stomach, but its disturbances are observed in many diseases not related to stomach disease.

Thirst. The feeling of thirst, as well as the feeling of appetite, is a physiological phenomenon. It appears with the so-called dehydration of body tissues, i.e. in cases where they do not contain enough water. Thirst occurs if a person has not drunk for a long time or has lost a lot of fluid (vomiting, diarrhea, significant sweating, blood loss). Sometimes thirst appears due to certain diseases of the digestive system, for example, with significant narrowing of the esophagus or stomach, when water does not pass into the stomach and the body tissues become dehydrated.

Thirst can also be a pathological symptom. With the development of edema (cardiac, renal, etc.), diabetes mellitus and diabetes insipidus, a strong, sometimes unquenchable thirst appears. With edema, the feeling of thirst is explained by a lack of water in the tissues due to its accumulation in the subcutaneous fat, and in diabetes, thirst is caused by polyuria.

Although thirst is not a symptom of gastric diseases, when asking a patient about appetite, they also ask about the presence of thirst.

Pain. One of the main symptoms of stomach diseases is pain.

If pain in the stomach is associated in time with food intake, with its quantity or quality, this usually indicates their gastric origin. The pain can be minor, nagging, dull or sharp, cutting, paroxysmal. Pain occurs due to overfilling and distension of the stomach, with inflammation of its mucous membrane. When the inflammatory process moves to the peritoneum, peritoneal pain appears (see “Intestinal Diseases,” p. 252). Severe, paroxysmal (colicky) pain occurs as a result of stretching of smooth muscles or its spastic contractions. Sharp pain that occurs 1-2 hours after eating is characteristic of gastric ulcer; often they give it to the back. “Hungry pains”, pain at night, are characteristic of duodenal ulcers.

Dyspepsia. Dyspepsia is a functional disorder of gastrointestinal digestion. For example, after a significant overeating, a person developed a feeling of heaviness in the stomach and then vomited.

Dyspeptic symptoms include belching, heartburn, nausea, vomiting, constipation and diarrhea, unless they are the result of any organic disease of the gastrointestinal tract.

Belching. Belching is the release of gas from the stomach through the mouth. Frequent belching usually indicates a stomach problem. Belching sour indicates an increase in acidity, belching rotten indicates rotting processes in the stomach.

Heartburn. Heartburn is a burning sensation in the epigastric region that occurs as a result of acidic contents refluxing into the esophagus from the stomach, irritating the mucous membrane of the esophagus. Since heartburn also occurs with low acidity, it must be assumed that in these cases it occurs due to increased sensitivity of the mucous membrane of the esophagus.

Vomit. Vomiting occurs due to irritation of the vomiting center located in the medulla oblongata.

Polyuria is increased urine output.

Esophageal vomiting has already been mentioned. Vomiting can be of central nervous, cerebral, or neuroreflex origin.

The so-called cerebral vomiting occurs due to direct irritation of the vomiting center by any poisons (toxins) circulating in the patient’s blood. Thus, in infectious diseases, for example scarlet fever, vomiting is caused by irritation of the vomiting center by toxins secreted by microbes; The cause of vomiting in uremia is irritation of the vomiting center by toxic substances accumulated in the blood, products of protein metabolism. Cerebral vomiting occurs with toxicosis of pregnant women, with carbon monoxide poisoning, with headaches of various origins (for example, migraines) and organic diseases of the central nervous system (concussion, brain tumor). It usually occurs without a preliminary feeling of nausea and there is no feeling of relief after vomiting.

Nervous reflex vomiting is often a protective-adaptive reaction of the body to various irritations of the gastric mucosa caused by swallowed foreign bodies, toxic substances, and poor-quality food. Thanks to the vomiting reaction, the body is freed from harmful and sometimes life-threatening substances. Nervous reflex vomiting can be induced by tickling the back of the throat.

Nervous reflex vomiting occurs with severe irritation of internal organs. More often it is observed in various diseases of the stomach (peptic ulcer, cancer, gastritis). Gastric vomiting is always preceded by nausea, and after vomiting the patient experiences more or less relief. Esophageal vomiting, like gastric vomiting, is a neuroreflex. Reflex vomiting can also occur in diseases of other organs: intestinal diseases (appendicitis, intestinal obstruction, helminthic infestations1), inflammation of the peritoneum, hepatic and renal colic.

The nurse should know that the presence of vomiting is a symptom that occurs not only in diseases of the stomach, but also in many other diseases. Caregivers should monitor how often the patient vomits, when (after eating, with a headache, etc.) and what he vomits.

The nurse is obliged to examine the vomit and store it until the doctor arrives, since sometimes it is possible to make a diagnosis by the type of vomit: whether it consists of the remnants of food just eaten or only mucus and gastric juice; what impurities are present, for example blood, bile, etc. You need to pay attention to the color of the vomit: with fresh gastric bleeding, the vomit is red; stagnant blood in the stomach gives them a brown color; Sometimes, when a cancerous tumor disintegrates, the vomit turns the color of coffee grounds.

With strong vomiting, bile from the duodenum enters the stomach, and then the vomit becomes yellow-green in color. In addition to color, you need to pay attention to the smell of gastric contents. Vomit may smell sour if the stomach is acidic, or rotten if there is rotting in the stomach. In case of alcohol poisoning, the vomit smells of alcohol, wine, in case of poisoning with vinegar essence - vinegar, in case of poisoning with ammonia - ammonia, etc.; with inflammation of the kidneys, uremia - with urine, with intestinal obstruction, intestinal contents with the smell of feces are found in them.

In some cases, vomit may need to be sent to a laboratory for testing. All utensils intended for collecting vomit must be absolutely clean, since foreign impurities can distort the results of laboratory analysis, which in turn can mislead the doctor. If the patient suddenly vomits on his clothes, on the bed or on the floor, then in some cases, especially if any poisoning is suspected, you should use a spatula, spoon, some kind of spatula or rag to collect the vomit in a jar and show it to the doctor. The procedure for sending vomit to the laboratory is the same as for sputum and other secretions of the patient.

Stomach bleeding. Gastric bleeding is a serious complication of any disease. Most often it is observed with a stomach ulcer, cancer (due to the disintegration of a cancerous tumor), with venous congestion in the walls of the stomach and esophagus, caused, for example, by cirrhosis of the liver, with increased bleeding. Significant bleeding is usually accompanied by vomiting (hematemesis) or tarry stools (see Peptic Ulcers, page 245); minor bleeding may occur unnoticed, since the blood flows from the stomach to the intestines, where it is digested. In such cases, blood in the stool is detected by chemical testing (see “Fecal Occult Blood Tests,” page 400).

Methods for examining the stomach

Survey. For diseases of the stomach, interviewing the patient and his anamnesis are of great importance.

Most stomach diseases are chronic, develop gradually, and begin with minor symptoms. It is necessary to ask the patient in detail about how he eats.

Then you should take an interest in the patient’s complaints and ask him about the above symptoms. Moreover, the appearance of each symptom must be associated with food intake, as well as with the onset and development of the disease.

It is extremely important to find out the diet: how often the patient eats, at a certain time, whether he has lunch regularly or eats dry food, whether he is in a hurry while eating, whether he chews food well, whether his teeth are healthy, whether he smokes, whether he drinks alcoholic beverages.

Interviewing a patient suffering from a stomach disease is of great importance not only for making a diagnosis, but also for eliminating the cause of the disease, and for prescribing treatment, an appropriate diet and diet.

Inspection and feeling (palpation). When examining the abdomen, a protrusion of the epigastric region is sometimes noted due to excessive filling of the stomach or a significant tumor present in it. The main physical method of examining the stomach is palpation. By palpating the stomach area, you can identify a tumor, as well as pain points in the area of ​​the pylorus or other parts of the stomach. Sometimes by palpation it is possible to determine the lower border of the stomach and distinguish it from the surrounding intestines and other organs. (For deep sliding palpation according to Obraztsov, see “Methods for examining the intestines,” p. 257).

Percussion and auscultation of the stomach do not have much diagnostic value, since the stomach and intestines usually produce the same tympanic sound. Sometimes, when filling the stomach with food, percussion can be used to separate it from the intestines.

Study of the secretory function of the stomach. In diseases of the stomach, its secretory function sometimes changes: secretion increases, i.e., there is increased acidity (hyperaciditas), normal (normaciditas), decreased (hypaciditas), lack of acidity (anaciditas) or a complete absence of gastric juice (achylia).

To determine the degree of acidity of gastric juice, it is examined. To judge the increase or decrease in gastric secretion, the patient is given a strictly defined amount of food, since the quantity and quality of gastric juice changes depending on the quantity and quality of it. This standard food given to the patient on an empty stomach is called a trial breakfast. The nurse gives the patient a trial breakfast at a precisely defined time.

Sometimes, before giving the patient a test breakfast, a gastric tube is inserted into his stomach to make sure there are no remnants of food taken the previous day.

On an empty stomach, a healthy person’s stomach is empty, and therefore either nothing can be removed through the tube, or only a small amount of liquid content is extracted. Normally, the amount of gastric juice obtained on an empty stomach should not exceed 30-50 ml. Under various pathological conditions, the stomach on an empty stomach may contain quite a significant amount of food debris. It can stagnate with significant expansion of the stomach and a decrease in its motor function, as well as with narrowing of the pylorus (scars from ulcers, cancer); sometimes the stomach contains remnants of food taken several days ago.

Many trial breakfasts have been proposed, which are given to patients on an empty stomach to study gastric juice.

A single extraction of gastric contents after a test breakfast is performed with a thick probe.

To extract gastric juice, a thin probe is most often used, which can be left in the stomach for a long time - 2-3 hours or longer. The advantage of this method is the ability to extract gastric contents at certain intervals and thereby determine the different phases of digestion. In these cases, only liquid breakfasts can be trial.

Determining the amount of gastric juice and the degree of its acidity is of great diagnostic and, therefore, therapeutic importance. With the same gastric diseases, in some cases there may be increased, and in others - decreased acidity, and the prescription of the appropriate diet and treatment depends on the state of acidity.

It must be borne in mind that an increase and decrease in acidity, as well as complete achylia, can be functional and can be observed in nervous people whose gastric mucosa is completely healthy.

Study of the motor function of the stomach. The motor function of the stomach may be increased or decreased compared to normal.

With excitability of the nervous system, an increase in the motor function of the stomach is sometimes observed, resulting in faster emptying. A similar phenomenon is often observed with low acidity and especially with achylia.

An increase in motor function is also observed with stenosis (narrowing) of the pylorus. The stomach forcefully pushes the contents through the narrowed opening. In such cases, the stomach muscle hypertrophies.

Decreased motor function occurs due to weakness of the muscular lining of the stomach. This phenomenon is observed in emaciated anemic people, as well as with an enlarged and prolapsed stomach. Food is retained in the stomach, and in severe cases, remnants of food taken by the patient several days ago can be found in it.

Gastric motor function is best determined by x-ray examination.

X-ray examination of the stomach. X-ray examination of the stomach (as well as the esophagus and intestines) is of great diagnostic importance. Since the stomach and intestines transmit x-rays, in order to see the shape of the stomach, it must be filled with a mass that would block the rays (contrast mass).

Such a substance is barium salts. Barium sulfate powder is mixed with water and given to the patient to drink during candling.

A contrast mass fills the stomach, which makes it possible to determine its shape and peristalsis.

When sending a patient for an X-ray examination, it is necessary to ensure that the stomach and intestines are empty. The night before, as well as in the morning on the day of the study, the patient needs to have an enema. In the morning before the test, he should neither drink nor eat, nor take any medications orally.

Using X-ray examination, the shape and size of the stomach is determined. The lower border of the stomach can be used to determine its prolapse. Normally, the lower border of the stomach should not be below the navel or, more precisely, not below the line connecting the anterior iliac spines (linea biiliaca). X-raying can reveal the rate of gastric emptying and the nature of its peristalsis. On the walls of the stomach (as well as intestines) you can see various pathological changes - thickening of the mucous membrane, ulcers, cancerous tumors, cicatricial narrowings.

Finally, by palpating the stomach during fluoroscopy, it can be determined whether the pain points are located in the stomach area or outside it.

Acute gastritis

Acute gastritis, or acute catarrh of the stomach, is an acute inflammation of the mucous membrane.

Causes of the disease. The most common cause of acute inflammation of the gastric mucosa is food poisoning caused by poor quality food, rotting products and bacteria, as well as strong alcoholic drinks. Often inflammation occurs as a result of irritation of the stomach wall by food products when eating excessive amounts of food, especially coarse, indigestible, too fatty (fried pork, goose, fried pies, etc.), too cold, etc. All kinds of poisons - acids, alkalis, mercury preparations , long-term use of certain medications (Adonis, digitalis, sodium salicylate, iodine preparations, etc.), as well as increased sensitivity of the body to certain foods (eggs, crayfish, strawberries, etc.) can also cause acute gastritis.

In acute gastric catarrh, the mucous membrane swells, turns red and becomes covered with a layer of mucus.

With significant damage to the stomach, for example, with burns, in addition to the mucous membrane, the muscular layer and even the serosa of the stomach are often involved in the process.

Symptoms and course of the disease. The main signs of acute gastritis are pain in the epigastric region, often cramping, and vomiting, which continues until the stomach is empty of food. If the mucous membrane is severely irritated, then gagging, often very painful, continues even with an empty stomach. In such cases, only mucus is released, sometimes colored with bile. If there is significant damage to the mucous membrane and even the muscle layer, blood is mixed with the mucus. The epigastric region is often swollen and sharply painful on palpation. There is no appetite, the tongue is coated; Dyspeptic symptoms are often observed - belching, heartburn, nausea.

In acute gastritis, especially caused by the consumption of poor-quality products and infection, phenomena of general intoxication are observed: the patient becomes weaker, he has a headache, dizziness, sometimes the body temperature rises, and in severe cases there is a sharp decline in cardiovascular activity (collapse): the patient is pale, limbs he is cold, his pulse is rapid, his filling is weak, his blood pressure drops.

After the cause of the disease has been eliminated, acute symptoms subside within a few days and health is gradually restored. In some cases, especially when stomach irritation (rough food, alcohol, etc.) continues, acute gastritis can become chronic. In various acute poisonings, the patient may die from general intoxication of the body.

Treatment and care. First of all, the substances that caused the disease should be removed from the stomach: poisons, poor-quality foods, alcohol, coarse irritating foods taken in large quantities.

To extract gastric contents, the most rational means is to insert a gastric tube. If you suspect that gastritis is caused by poor-quality foods, poisons, alcohol, you cannot limit yourself to extracting gastric contents, but you should lavage the stomach, since food debris and various poisons that cause poisoning are retained in the folds of its mucous membrane.

If a gastric tube is not at hand, vomiting can be induced reflexively by tickling the root of the tongue and pharynx.

In the absence of a tube, instead of gastric lavage, the patient is given large quantities of warm water with soda or warm milk, after which, reflexively (tickling the throat), they induce vomiting. Large amounts of liquid introduced into the stomach and then excreted through vomiting, to a certain extent, replace gastric lavage.

In earlier times, various emetics were used to induce vomiting. Now this method has been abandoned - preference is given to gastric lavage.

The nurse should pay attention to the nature of the vomit, regardless of whether the patient vomited independently or the vomiting was artificially induced.

After gastric lavage, the patient is often given a laxative (castor oil, Glauber's salt, magnesium sulfate) in order to quickly remove from the intestines those poisons that managed to get into it from the stomach.

In case of weakness, elevated body temperature or severe pain in the epigastric region, the patient should be put to bed, a warming compress or heating pad should be placed on the epigastric region, and if the extremities are cold, heating pads should be applied to the arms and legs.

For severe pain, atropine, promedol, omnopon or morphine are injected under the skin.

For burns of the stomach with strong alkalis and acids, the same measures are used as for burns of the esophagus. The patient is given to swallow pieces of ice, drink sips of cold (ice) water, cream, and swallow ice cream in small portions. In these cases, instead of a heating pad, an ice pack is placed on the stomach area, since when a burn occurs, the mucous membrane usually bleeds.

If the body becomes dehydrated due to persistent vomiting, a subcutaneous infusion of saline or glucose solution is given.

In the absence of diarrhea, these infusions can be performed through the rectum using drip enemas.

In case of acute gastritis, it is necessary to provide rest to the inflamed mucous membrane. Therefore, the patient is recommended not to eat anything for the first 1-2 days of illness.

Drinks (tea, milk, coffee with milk or boiled water) are given warm or hot in small portions. To stop the painful urge to vomit, they are sometimes given pieces of ice to swallow, but only if the stomach is completely free of food debris and toxic substances. Sometimes drinking hot water is better at reducing gastric peristalsis.

In case of persistent vomiting, a hypertonic solution of table salt is administered intravenously, since with vomiting a person loses a lot of sodium chloride, the stomach is washed, and a solution of novocaine and chlorpromazine is given orally; the latter can also be used in the form of subcutaneous injections.

Anesthesin and belladonna, which is usually used with alkalis - soda or magnesia, have a good analgesic effect.

After the acute symptoms have passed, give non-irritating liquid and semi-liquid food: broth, mucous decoctions, jelly, jelly, well-cooked milk porridge with butter or sugar.

For acute gastritis, a mechanically and chemically gentle diet is prescribed. First they give you table No. 1a, then table No. 16 and finally table No. 1.

Prevention. It is necessary to eliminate the causes of the disease - eat only benign foods, and also monitor the intake of medications that can cause stomach irritation.

Chronic gastritis

Causes of the disease. If the cause of acute gastritis is not eliminated, it can become chronic. More often, chronic gastritis develops gradually due to constant irritation of the gastric mucosa.

A monotonous diet, poor chewing of food, rare meals, irregular meals at large intervals, eating hastily, dry food, eating too much or coarse food, rich in plant fiber, lead to the development of gastritis. Excessively hot and cold food and drink, spicy seasonings, and frequent alcohol consumption also gradually lead to catarrhal symptoms.

When smoking, nicotine, partially entering the stomach, causes an increase in the secretion and acidity of gastric juice, which irritates the mucous membrane directly, and when absorbed into the blood, it affects the autonomic nervous system, which also leads to the development of gastritis. Chronic gastritis can also be caused by pathogenic microbes. Constant ingestion of purulent sputum containing a large number of bacteria due to lung abscess, bronchiectasis and other diseases can contribute to the development of chronic gastritis. Sometimes chronic gastritis occurs as a complication or as a concomitant phenomenon in various diseases: ulcers and stomach cancer, cholecystitis, tuberculosis, cardiac decompensation (as a result of venous stagnation in the gastric mucosa), inflammation of the kidneys (excretion of urea and other metabolic products from the gastric mucosa).

Poor nutrition and lack of vitamins, in particular C, complex B, etc. lead to disruption of regenerative processes in the wall of the stomach, which contributes to atrophy of its mucous membrane.

Pathological anatomy. Due to constant irritation, the gastric mucosa hypertrophies, and therefore such chronic gastritis is called hypertrophic. With increased secretion of hydrochloric acid in the stomach there will be more than normal; This type of gastritis is also called (acid) hyper-acid. Gastritis with reduced secretion of hydrochloric acid is called hypoacid. Gastritis can also occur with normal acidity - normacid gastritis.

With chronic gastritis, epithelial cells gradually atrophy, being replaced by connective tissue, and the production of gastric juice decreases or completely stops, i.e. gastric achylia occurs. Such gastritis, with a sharp decrease or complete absence of gastric juice, in particular hydrochloric acid, is called atrophic, or achilic.

Chronic gastritis with high acidity is a favorable soil for the development of peptic ulcers, and with low acidity or achylitis - for stomach cancer,

Symptoms and course of the disease. Heaviness or pain in the epigastric region, loss of appetite, belching, heartburn, and sometimes nausea with vomiting. Usually all these phenomena are observed or intensified in connection with food intake, especially if the patient does not comply with dietary requirements. With acid gastritis, sour belching and vomiting are often observed, and the vomit has a sour smell.

Belching can also be sour if the secretion of hydrochloric acid is below normal, and increased acidity occurs due to fermentation in the stomach, during which organic acids are formed in it: acetic, lactic and butyric. Achilles gastritis often causes diarrhea (gastrogenic diarrhea).

In chronic gastritis, rotten belching is sometimes observed due to the rotting process occurring in the stomach. In this case, the tongue is covered with a thick yellow-gray coating.

When palpating the abdomen, diffuse pain is noted in the epigastric region. When examining gastric juice, increased or decreased acidity or even a complete absence of hydrochloric acid and enzymes is determined. The disease can last for years with periodic improvements and deteriorations, depending on the patient’s lifestyle and appropriate treatment measures.

Treatment and care. Patients with chronic gastritis are usually not treated in hospitals - they are able to work. Their treatment consists mainly of following the correct regimen and an appropriate diet.

First of all, it is necessary to eliminate the causes that led to the development of gastritis. If the patient eats hastily. food is poorly digested, chews it insufficiently, or eats at indeterminate times, he must change his diet and follow the diet recommended by his doctor.

If a patient has bad teeth, they must be treated, and if they are missing, dentures must be inserted.

In cases where gastritis is caused by alcohol, treatment is possible only if the patient refuses to drink alcohol.

If nicotine was one of the etiological factors of gastritis, then it is necessary to stop smoking. But the main method of treatment should be a properly organized diet. The diet should generally be mechanically and chemically gentle. Do not use food that is too hot or too cold.

To properly treat gastritis, you need to know how much hydrochloric acid is contained in the patient’s stomach - more or less than normal, or is it completely absent - and whether there are other acids in it - acetic, lactic, butyric, which do not normally exist. The diet is prescribed in accordance with the results of a chemical study of gastric juice. With gastritis, you need to eat often, but in small portions and chew food well, which is especially necessary if the acidity of the gastric juice is low. Food should not burden the stomach, so you should avoid foods that are too “heavy” (for example, freshly baked bread, cakes, fatty meats and fried fish). At the same time, food must be nutritious, contain a sufficient amount of calories and vitamins, and should not irritate the inflamed mucous membrane.

With acid gastritis, you should not eat anything “spicy” (spices, hot sauces and gravies, pickles, marinades), since spicy dishes, irritating the mucous membrane, increase the secretion of gastric juice. Alcohol is harmful in all forms.

If you have high acidity, you should not eat anything sour - sour black bread, sauerkraut, sour milk, sour fruits, and you should not overuse meat, as it increases acidity. The patient's diet should include milk, cream, mucous pureed soups (mashed cereals and vegetables), butter, stale white bread, eggs, steamed cutlets, boiled lean meat and fish, pureed cereals and vegetables, mashed potatoes, non-acidic fruits. Food should be lightly salted.

For atrophic and hypoacid gastritis, the same diet is generally prescribed. Food products must be served chopped or pureed. But some seasonings and spices are allowed here, which, by irritating the mucous membrane, can increase the acidity of gastric juice.

Food can be salted to taste, you can eat meat soups (broths), which stimulate the secretion of the gastric mucosa, and sour mashed fruits and jelly. Consequently, with acid gastritis, the table should be mechanically and chemically gentle (table No. 1), and with atrophic catarrh, it should be predominantly mechanically gentle (table No. 2).

For chronic gastritis, mineral waters are also prescribed. If acidity increases, Borzhom, Smirnovskaya or Batalinskaya water is prescribed, and if acidity decreases, Essentuki No. 17 or No. 4, Izhevsk water, containing sodium chloride, which increases the secretion of gastric juice.

Mineral water is usually given half an hour before meals, half a glass per meal; You should drink it slowly, in sips.

It is preferable to be treated with mineral waters at those resorts where these springs are available, since bottled water loses some of its healing properties. Spa treatment also has the advantage that, while on it, the patient follows a certain regime, uses a dietary table, and appropriate rest.

Physiotherapeutic procedures also have a beneficial effect: warming compresses, heating pads, poultices, paraffin, diathermy, pine baths.

Among the medications for high acidity, atropine (belladonna), magnesia, soda (substances that reduce the acidity of gastric juice), vikalin, almagel are prescribed.

Complex tablets - vikalin, containing mainly bismuth and magnesium salts, as well as soda, have a good effect.

When acidity is reduced or completely absent, natural gastric juice, a solution of hydrochloric acid, sometimes with pepsin (to enhance the digestive function of the stomach), as well as tablets containing pepsin and hydrochloric acid - acidinpepsin, are prescribed.

In some cases, periodic gastric lavages are done, especially when it is dilated, when there is stagnation of food residues (for example, when there is narrowing of the pylorus, in the presence of a large amount of mucus, frequent vomiting and especially during putrefactive processes in it); if the acidity is high, the stomach is washed with a 2% solution of bicarbonate of soda, and if the acidity is low, with a physiological solution of table salt, but these solutions should be taken in larger quantities than indicated in the recipes.

Food for chronic gastritis should be rich in vitamins. It is especially necessary to prescribe ascorbic and nicotinic acids, vitamins B6, Bi2 for hypoacid and achilic gastritis, since ascorbic, nicotinic acids and vitamin B6 increase the secretory function of the stomach, and with achilic gastritis the content of vitamin Bl2 in the body decreases

Prevention. Prevention of chronic gastritis consists of treating acute gastritis and other diseases predisposing to their development. A proper daily diet is necessary. Food must be complete and contain sufficient amounts of vitamins. Too spicy (irritating) and rough foods should be avoided, and alcohol should not be abused. You need to take care of your teeth, treat them in a timely manner, and if they are missing, use dentures.

Peptic ulcer of the stomach and duodenum

Etiology and pathogenesis of peptic ulcer. According to the teachings of I.P. Pavlov, dysfunction of the cerebral cortex is of primary importance in the occurrence of peptic ulcer disease. Prolonged mental experiences of a negative nature, constant overstrain of the psyche (higher nervous activity). overwork, mental trauma, concussion and concussion play a large role in the occurrence of peptic ulcer disease.

Overexcitation of higher nerve centers (cerebral cortex), fatigue and exhaustion of cortical cells weakens the inhibitory activity of the cerebral hemispheres, and foci of excitation arise in the subcortical and vegetative centers, freed from the inhibitory influence of the cerebral cortex. This, in turn, causes increased excitability of the autonomic nervous system, resulting in spasms of blood vessels and smooth muscles of various parts of the stomach or duodenum. These spasms lead to local anemia (ischemia) of the stomach wall, which in turn reduces its resistance to the effects of gastric juice, which could digest the stomach wall if the healthy mucous membrane did not have the ability to resist its digestive action. When the function of the autonomic nervous system is disrupted, trophism, (nutrition) of cells and tissues is disrupted. When the nutrition of the stomach wall is weakened, the protective properties of the mucous membrane decrease, and the acidic contents of the stomach begin to digest, “corrode” the mucous membrane, resulting in the formation of an ulcer.

Hence it is clear that increased acidity of gastric contents and especially chronic hyperacid gastritis contribute to the occurrence of peptic ulcers.

All kinds of mechanical and chemical irritants of the gastric mucosa are of great importance in the formation of ulcers, as discussed in the chapter on gastritis: irregular diet, rough food rich in spices, too hot or too cold food, alcohol, etc.

Sometimes stomach ulcers occur in weakened, anemic people.

Smoking is of particular importance, since nicotine is a vascular poison that causes spasm of blood vessels.

Hereditary predisposition to this disease also plays some role in the occurrence of ulcers. Peptic ulcer disease in members of the same family can be explained by the same nutritional pattern and unstable nervous system.

Blockage or narrowing of the blood vessels of the stomach due to embolism, thrombosis or sclerosis also predisposes to the development of ulcers.

Pathological anatomy. An ulcer forms in various parts of the stomach, but more often it occurs at the exit of the stomach (pylorus) or in the duodenum; however, it can be of different sizes. The ulcer has a round or oval shape and can penetrate to the muscular and even serous membrane.

As it deepens, its diameter decreases, and it takes on the appearance of a cone, with its base facing the cavity of the stomach. There is usually one ulcer, but there may be two or more ulcers.

With ulcerative damage to the mucous membrane and especially the muscular membrane, the blood vessels feeding these membranes are also destroyed, resulting in gastric bleeding. Sometimes the bleeding is minor, but when the wall of a large blood vessel, especially an artery, is destroyed, it can be profuse and even fatal. In some cases, the ulcer also destroys the serous membrane; then a perforation of the stomach wall occurs, gastric contents penetrate into the abdominal cavity, which leads to peritonitis. Under favorable conditions, the ulcer heals, connective tissue grows in place of the destroyed mucous membrane and scars form.

If the scars are located near the outlet of the stomach, the pyloric part of it narrows.

Symptoms and course of the disease. The first sign of a gastric ulcer is severe pain in the epigastric region, often radiating to the back, and this pain appears or intensifies after eating food, especially coarse, sour, salty and difficult to digest (fatty fried meat, rich pies, etc.). Sometimes the pain is so sharp that the patient is afraid to eat, fearing its occurrence.

With a duodenal ulcer, “late” pain is noted, occurring 3-4 hours or more after eating. This disease is characterized by pain at night and “hungry” pain on an empty stomach, caused by the action of free hydrochloric acid on the ulcer. To reduce them, the patient must eat something.

The second characteristic symptom of a stomach ulcer is vomiting.

Vomiting often occurs at the height of digestion, when the patient feels the most severe pain. After vomiting, the patient usually feels relief due to the reduction and sometimes cessation of pain due to the release of the stomach from acidic contents. Therefore, with severe pain, patients sometimes artificially induce vomiting.

Bloody vomiting often occurs due to the destruction of blood vessels by the ulcer. Bloody vomiting is so characteristic of a peptic ulcer that its appearance is often enough to make a correct diagnosis.

With minor gastric bleeding, there may be no vomiting - the blood enters the intestines, and in these cases it can only be detected by examining the stool. If a significant amount of blood enters the intestines, the stool becomes dark, tarry in color.

With a duodenal ulcer, vomiting usually does not occur. In these cases, even significant bleeding must be judged by the appearance of the stool (tarry stool) or by chemical examination of the stool for the presence of blood in it.

Prolonged or heavy bleeding leads to general weakness, anemia, weight loss; with significant bleeding (bloody vomiting), collapse phenomena may occur: thread-like pulse or its complete disappearance, sharp paleness of the skin, coldness of the extremities.

In addition to vomiting, other dyspeptic symptoms are observed with peptic ulcers: belching, heartburn and nausea. Belching is usually sour, since in most cases there is increased acidity of gastric juice. Sometimes patients, especially with high acidity, experience severe heartburn. Nausea usually precedes vomiting, but can occur independently without subsequent vomiting.

In most cases, appetite remains the same, and sometimes even increases. The tongue is usually coated with a whitish coating.

When palpating the abdomen in the epigastric (epigastric) region, patients feel sharp pain at the location of the ulcer. “Protecting” the affected body, the abdominal muscles in this place tense up - a symptom of muscular protection.

A gastric ulcer is characterized by a painful point in the midline under the xiphoid process, and a duodenal ulcer is above the navel, to the right of the midline.

It is sometimes possible to accurately determine the presence of a stomach and duodenal ulcer only by x-ray examination, which gives a characteristic niche for an ulcer (a contrast mass fills the depression in the gastric mucosa formed by the ulcer).

The course of peptic ulcer disease is very diverse. The disease can occur chronically, for years, without causing much concern to the patient. In some cases, the ulcer completely heals and scars, but often even after a few years it reappears. More often there is a known periodicity - “seasonality” - during the course of the disease. Exacerbations usually occur at certain times of the year, most often in late autumn or early spring. Their immediate cause is, as a rule, nervous fatigue, strong emotions, and eating disorders. Sometimes peptic ulcer disease occurs as chronic gastritis, with “minor” signs of peptic ulcer disease. Patients note heaviness in the epigastric region after eating, belching, and heartburn. In some cases, asymptomatic, so-called hidden, “silent” ulcers are observed, and then peptic ulcer disease may first manifest itself as severe complications: gastric bleeding or perforation (perforation of the ulcer).

A scarring ulcer of the stomach, located near its exit into the duodenum (pyloric part), causes a narrowing of the pylorus. Persistent cicatricial narrowing leads to food retention in the stomach, which causes a number of painful symptoms. The peristalsis of the stomach reflexively increases, the muscles of which hypertrophy in order to push the contents of the stomach into the duodenum.

Due to the constant presence of food in the stomach, appetite decreases, and profuse vomiting is often observed; in the vomit they find the remains of yesterday's food and even food eaten several days ago. With significant and complete closure of the pylorus, vomiting occurs daily and even several times a day.

Retention of food and especially fluid leads to exhaustion and dehydration of the body. Dilatation of the stomach gradually develops. If surgical intervention is not undertaken in a timely manner, the patient may die from complete exhaustion.

Another serious complication of an ulcer is its perforation (perforation), when the ulcerative process destroys all layers of the stomach wall and the contents of the stomach penetrate into the abdominal cavity, causing acute purulent peritonitis.

With severe bleeding and perforation of the ulcer, the disease can be fatal.

Severe complications include the observed degeneration of an ulcer into a cancerous tumor.

Treatment and care. The main methods of treating patients with peptic ulcer disease are rest, both physical (bed rest) and mental, and diet. It is necessary to create a calm environment for such patients so that they do not become nervous, excited, etc.

It is necessary to achieve sufficient normal sleep in patients.

If the patient is too excitable and does not sleep well, then drugs that calm the nervous system and sleeping pills are prescribed, since sleep is absolutely necessary for the patient.

Intravenous infusions of sodium bromide and novocaine have a good calming effect on the nervous system.

For peptic ulcers, the table should be mechanically and chemically gentle, rich in vitamin C (vitamin juices). The diet begins with table No. 1a, and then moves to table No. 16 and after 2 weeks - to general table No. 1 (see “Basics of therapeutic nutrition,” p. 366).

Food should be rich in vitamins, especially vitamins C and B complex.

For acute pain, place a heating pad on the stomach area. Warming compresses have a good effect. If there is a suspicion that the ulcer is bleeding, then a heating pad and other thermal procedures are contraindicated.

Of the medications, the best painkillers are atropine and its drug belladonna, which act as a depressant on the vagus nerve, as a result of which smooth muscle spasms relax and the secretion of gastric juice decreases. Initially, it is recommended to administer atropine subcutaneously. To reduce the acidity of gastric juice, belladonna is prescribed together with alkalis.

Among other painkillers, anesthesin, papaverine, and platiphylline have a good effect. Often, for peptic ulcers, vikalin is prescribed, which contains bismuth, magnesium, soda and some other substances, almagel. Ganglioblockers have a good effect. They inhibit the conduction of nervous stimulation in the autonomic ganglia, which are in a state of increased tone. These include benzohexonium, pyrylene, ganglerone.

In case of gastric bleeding, the patient is given complete rest and ice is placed on the epigastric region.

Hemostatic agents are injected intravenously: calcium chloride, sodium chloride, intramuscular Vika-sol. If there is significant bleeding, a blood transfusion is performed.

For the first 1-2 days, it is better not to give the patient anything to drink or eat. In order not to dehydrate the body, subcutaneous infusions or drip enemas are made from saline solution, or even better from glucose solution. Glucose is also administered intravenously.

If bleeding continues and to avoid its intensification, you should not introduce a lot of fluid into the body. To relieve thirst, the patient is allowed to rinse his mouth with water, which he must spit out.

In case of prolonged bleeding or after it has stopped, first give food only cold and in small portions: cream in teaspoons, egg white and pieces of unsalted butter. Then they gradually move on to the usual anti-ulcer table, starting with table No. 1a.

The patient should lie in bed until the acute symptoms finally pass. In the absence of bleeding, the course of inpatient treatment lasts on average 20-21 days. If there are complications, treatment may take longer. As a rule, the patient is discharged from the hospital after a repeat X-ray examination shows a healed ulcer.

Physiotherapeutic procedures work well: pine baths, diathermy on the epigastric region, etc.

During remission and during the chronic course of the disease, treatment and care are approximately the same as for chronic gastritis with high acidity. The basis of treatment is an appropriate diet. The patient must follow a certain regimen. He is strictly prohibited from smoking, since nicotine has a stimulating effect on the central and autonomic nervous system, which leads to spastic contractions of the blood vessels and smooth muscles of the stomach. Alcoholic drinks should also be prohibited. It is necessary to periodically examine the gastric juice and repeat fluoroscopy of the stomach. Only if the ulcer has completely healed and all clinical phenomena are absent for a year, the patient can switch to the general regimen. For patients with chronic ulcers, resort treatment in Zheleznovodsk or Borjomi is recommended.

Surgical treatment of stomach ulcers is resorted to in cases where long-term therapeutic treatment does not have the desired effect. The operation is performed if constant severe pain exhausts the patient, repeated bleeding and cicatricial narrowing of the pylorus are observed, preventing food from leaving the stomach. If the ulcer is perforated, surgery must be performed immediately.

To prevent relapses, patients with peptic ulcer disease should be registered with a dispensary at the district clinic. They undergo periodic X-ray and laboratory tests.

Prevention. First of all, you need to strengthen the nervous system, smoking, drinking alcohol and other stimulating drinks should be prohibited. Regular, nutritious nutrition and restorative treatment are required: proper daily routine, healthy rest, exercise.

Since chronic gastritis predisposes to the development of peptic ulcers, the patient should be systematically and persistently treated without starting them.

Stomach cancer

Of all organs, cancer most often affects the stomach. In women, stomach cancer ranks second in frequency of lesions, and uterine cancer is in first place.

Gastric cancer is most often observed in the pylorus and on the lesser curvature of the stomach, then in the inlet of the stomach, i.e. in places that are most susceptible to irritation from food.

Chronic gastritis, especially with low acidity or in the absence of acidity (achilia), old ulcerative process, gastric polyps predispose to the development of a cancerous tumor in the pathologically altered wall of the stomach.

Symptoms and course of the disease. The disease begins gradually, imperceptibly. The patient's appetite decreases, he loses weight, and pallor appears. Dyspeptic symptoms - belching, heartburn, nausea - often begin after these general phenomena. Pain in the epigastric region is usually considered a later symptom. Subsequently, appetite disappears, an aversion to food appears, especially meat, severe weight loss and exhaustion develop with symptoms of severe anemia - cancer cachexia.

With a significant tumor, especially if it prevents food from leaving the stomach, vomiting occurs, which can occur daily or even several times a day. If the cancerous tumor disintegrates, the vomit takes on the appearance of coffee grounds due to the admixture of decomposed blood.

In advanced cases, a hard, lumpy tumor can be felt in the epigastric region, which can metastasize to other organs, most often to the liver.

In order to make a diagnosis in time, it is necessary to examine the gastric juice and perform an X-ray examination of the stomach at the very initial, barely noticeable symptoms, especially in people over 40 years of age (from 40 to 60 years of age, cancer most often appears). Usually, patients with stomach cancer have achylia, sometimes low and rarely high acidity.

Often in the initial stages of the disease, the presence of a cancerous tumor is determined by x-ray examination. Stomach cancer usually lasts 1-2 years, and sometimes longer; the patient dies from general weakness and exhaustion of the body if appropriate treatment is not carried out in a timely manner.

Treatment and care. The main means in the fight against cancer is the earliest possible removal of the tumor by surgery. Late surgery rarely achieves its goal, since it is difficult to remove the entire tumor without leaving a residue, and sometimes even with its complete removal, metastases remain in other organs.

Therefore, it is important to know the early signs of cancer in order to promptly refer the patient for additional studies (primarily x-ray) and perform surgical intervention in a timely manner.

Caring for a patient with stomach cancer is basically the same as for a patient with esophageal cancer, especially since in case of stomach cancer, food is also delayed, and sometimes does not pass at all. If the tumor grows in the area of ​​the pylorus, it narrows so much that food passes into the duodenum with great difficulty; in some cases, complete closure of the pylorus occurs.

If the patient’s condition allows for surgical intervention, but removal of the tumor is no longer possible, then a gastroenterostomy is performed - the stomach is connected to the small intestine, sewing it into the healthy wall of the stomach. In this case, food from the stomach enters directly into the small intestines, bypassing the duodenum.

Prevention. It is necessary to carefully treat chronic stomach diseases that predispose to the development of cancer, primarily chronic gastritis and peptic ulcers. These patients need periodic X-ray examinations of the stomach to determine the appearance of a cancerous tumor at the very beginning of its development. Patients with atrophic catarrh of the stomach, with a lack of acidity (achylia), deserve special attention, since it is they who most often develop stomach cancer.

Topic: Questioning and general examination of patients with organ diseases

gastrointestinal tract. Inspection, percussion and auscultation of the abdomen.

3. Test questions on the topic of the lesson.

1. Complaints of patients with diseases of the esophagus, stomach and intestines.

2. Features of collecting anamnesis of disease and life in patients with gastrointestinal pathology.

3. General examination and examination of the oral cavity in patients with diseases of the digestive system.

4. Topographic areas of the abdomen.

5. Examination of the abdomen. Distinctive signs of abdominal enlargement with ascites, obesity and flatulence.

6. Percussion of the abdomen: the nature of the percussion sound, percussion of the abdomen according to Mendel’s method.

7. Method of percussion palpation (succussion) of the stomach according to the method of V.P. Obraztsova. Diagnostic value.

8. Diagnostic value of the auscultatory afriction method.

9. Determination of free and encysted fluid in the abdominal cavity.

10. Auscultation of the abdomen. Diagnostic value of listening to peristaltic sounds and friction sounds of the peritoneal layers.

determination of the presence of free and encysted fluid in the abdominal cavity.

6. Listening to intestinal sounds and friction sounds of the peritoneum.

1. Complaints of patients with diseases of the esophagus, stomach and intestines.

Patients with gastrointestinal pathology can present a variety of complaints, which are conventionally divided into local, general and additional general pathological.

I. Local complaints - indicate damage to the esophagus, stomach and intestines.

1. 
   Dysphagia.
2. 
   Dyspepsia:

a) gastric – heaviness and pain in the epigastric region, heartburn, belching, nausea, vomiting;

b) intestinal – abdominal pain, splashing and rumbling, bloating, intestinal vomiting.

3. Defecation disorders - diarrhea, constipation, painful bowel movements, false urges.

4. Bloody vomiting and bloody stools.

II. General complaints are extra-esophageal, extra-gastric, extra-intestinal, but observed in the pathology of these organs.

1. Loss of appetite.

2. Changes in taste.

3. Weight loss (loss of body weight).

III. Additional general pathological complaints.

1. Increased fatigue, decreased performance, muscle weakness.

2. Neurotic disorders – sleep disturbance, irritability, etc.

Dysphagia (dysphagia) is a violation of the act of swallowing and the passage of food through the esophagus

The cause of dysphagia is a narrowing of the esophagus, which can be organic (stenosis) or functional (spasm).

Causes of organic narrowing of the esophagus:

– tumor of the esophagus;

– a scar that appears at the site of a former ulcer;

– syphilitic gumma;

– thermal or chemical burn of the mucous membrane of the esophagus with acids and alkalis;

– pressure on the wall of the esophagus from a bolus of food stuck in the diverticulum;

– pressure on the esophagus from a tumor or enlarged mediastinal lymph nodes;

– aortic aneurysm;

– pronounced paricardial effusion.

2. Causes of functional narrowing of the esophagus is a spasm of the muscles of the esophagus, which occurs reflexively under the influence of irritations emanating from other organs (pathology of the mediastinum, gallstones, worms), with disorders of the autonomic innervation of the muscular wall of the esophagus, with tetanus, with neuroses.

With organic stenosis, dysphagia gradually and continuously increases; with functional spasm of the esophagus, it often alternates with normal swallowing, but can become permanent. With a slight narrowing of the esophagus, difficulty in swallowing only solid food is observed, and difficulties gradually arise when taking mushy and, later, liquid food. In cases of functional spasm of the esophagus, solid food is easier to swallow than liquid food, since the heavier bolus is able to overcome the spasm.

Dysphagia can be painful (with esophagitis, burns of the esophageal mucosa) and is manifested by an unpleasant feeling of rawness or pain behind the sternum immediately after swallowing food. Pain arising in the esophagus often radiates to the interscapular region.

Gastric dyspepsia (dyspepsia) - a violation of the digestive processes, occurs due to insufficient or excessive secretion of hydrochloric acid and pepsin or due to excessively rapid evacuation of food from the stomach.

Gastric dyspepsia has the following clinical manifestations .

1. Burping- sudden, sometimes loud, involuntary release of stomach contents into the oral cavity.

A distinction is made between belching with air (eructatio) - empty belching and belching with food (regurgitatio). The mechanism of belching is reduced to contraction of the muscles of the stomach when the cardiac opening is open.

Belching of air occurs with increased habitual swallowing of air (aerophagia, which occurs due to neurosis) or with increased formation of gases in the stomach due to fermentation or rotting food. If, as a result of fermentation, carbon dioxide is released in the stomach, then the belching is odorless, but if organic acids (butyric, lactic) are formed, the belching takes on the smell of rancid oil. When protein breakdown in the stomach occurs under the influence of bacteria, when reduced gastric secretion is combined with impaired gastric emptying (chronic gastritis, stomach cancer), belching has the smell of rotten eggs (admixture of hydrogen sulfide). Belching sour may indicate increased acidity of gastric juice. Belching with duodeno-gastric reflux has a bitter taste.

2. Heartburn (pirosis) - a feeling of heat or burning along the esophagus, in the retrosternal or epigastric region, caused by the entry of gastric contents into the esophagus.

In most cases, heartburn is felt when the acidity of the gastric juice is high, but it can occur when its level is normal.

The mechanism of heartburn is the same as belching, but the regurgitated liquid does not reach the oral cavity. Characteristic of reflux esophagitis.

3. Nausea (nausea) - painful pressure in the epigastric region and at the same time an unpleasant sensation in the oral cavity, accompanied by pallor of the skin, dizziness, salivation, coldness of the extremities, decreased blood pressure and sometimes fainting.

Nausea can be a preliminary phase of vomiting or an independent phenomenon. Nausea is based on stimulation of the vomiting center and increased tone of the vagus nerve. Nausea and the gag reflex have similar causes.

4. Vomiting (vomitus) is a complex reflex act caused by the excitation of the vomiting center, during which an involuntary push-like ejection of the stomach contents occurs through the mouth (less often through the nasal passages). Vomiting is a protective reaction of the digestive system, namely the stomach, to the entry or formation of toxic and other damaging substances in it.

The following pathogenetic variants of vomiting are distinguished:

1. 
   Central (nervous, cerebral) vomiting - occurs with increased intracranial pressure, spasm of cerebral vessels, hysteria.
2. 
   Hematogenous-toxic vomiting - observed with uremia, liver failure and other intoxications.
3. 
   Peripheral (visceral) vomiting – esophageal, gastric, intestinal

In addition, the source of the gag reflex can be the “vomiting zones” of the pharynx, peritoneum, coronary and mesenteric vessels, bile ducts, etc. Vomiting occurs when they are irritated.

The diagnostic evaluation of vomiting should consider:

a) time of onset of vomiting;

b) the amount of vomit;

c) chemical reaction of vomit;

d) impurities in gastric contents.

Each type of vomiting has its own clinical features:

Central vomiting– occurs suddenly, without previous nausea and other dyspeptic symptoms, and has no connection with food intake. The vomit is scanty and odorless. Vomiting does not bring relief to the patient; there are no signs of gastrointestinal disease.

Gastric vomiting occurs most often: with inflammation of the gastric mucosa; when irritating chemicals, medications, or spoiled foods enter the stomach; due to spasm of the pylorus (pylorospasm); due to organic pyloric stenosis (pyloric stenosis).

Vomiting that occurs in the morning on an empty stomach - vomitus matutinus - with a large amount of mucus is characteristic of alcoholic gastritis and hyperacidosis. When the esophagus narrows, vomiting occurs a few minutes after eating. Vomiting occurs just as quickly after eating with an ulcer of the cardial part of the stomach and with acute gastritis. Vomiting after 2-3 hours, at the height of digestion, is characteristic of ulcers and cancer of the body of the stomach. With an ulcer of the pylorus or duodenum, vomiting occurs 4-6 hours after eating. Vomiting of food eaten the day before or even 1-2 days before is typical for pyloric stenosis (“congestive vomiting”), in this case the volume of vomit is large. Gastric vomiting brings relief to the patient.

The smell of vomit is often sour, but it can be putrefactive (rotting processes in the stomach, disintegration of a stomach tumor), ammonia (in case of kidney failure), alcohol (in case of acute alcohol poisoning).

Of the impurities in vomit, mucus (for chronic gastritis), bile (for impaired contractility of the pylorus, for narrowing of the duodenum), pus (phlegmonous gastritis, breakthrough of pus from an abscess of the chest or abdominal cavity into the stomach) and blood ( bloody vomiting).

Esophageal vomiting(late symptom, signs of significant dilation of the esophagus) differs from gastric in the following features:

• 
  occurs without preliminary nausea;
• 
  occurs immediately after eating;
• 
  the vomit is not voluminous, consists of undigested food, does not have a sour taste or smell (with large diverticula of the esophagus, the vomit may consist of long-ingested food and have a putrid odor).

5 . Epigastric pain (dolor)

It is necessary to distinguish from pain in the proper sense of the word the feeling of heaviness, pressure and bloating in the epigastric region that occurs in connection with food.

Mechanisms of occurrence of stomach pain:

• 
  spasm of smooth muscles (usually pylorospasm) - spastic pain, colic;
• 
  stretching of the stomach wall by its contents – distension pain;
• 
  irritation of intramural nerve elements as a result of the transfer of an inflammatory process to them, pressure from a scar or tumor - ganglion pain;
• 
  tension of nerve fibers when the stomach is displaced (gastroptosis).

If you have pain in the epigastrium, you should clarify:

• 
  precise localization of pain;
• 
  the nature of the pain, its frequency, seasonality;
• 
  connection of pain with food intake, its quantity and quality;
• 
  does pain decrease after vomiting, eating, alkalis, applying heat and antispasmodics;
• 
  connection of pain with physical stress.

In diseases of the stomach itself, pain occurs in the epigastric region. The uncomplicated course of stomach diseases is characterized by moderate pain; very severe pain is characteristic of such complications of peptic ulcer disease as perforation and penetration of the ulcer. If the pain is caused by spastic contraction of the stomach muscles, then it is periodic. Pain with gastroptosis, with irritation of the nerve elements of the gastric wall, and with perivisceritis is constant. Seasonality of pain (the appearance of periodic pain in spring and autumn) is typical for peptic ulcer disease, especially when the ulcer is localized in the peripyloric zone and duodenum.

The connection between pain and food intake to a certain extent indicates the location of the pathological process. With pathology of the esophagus, pain occurs while eating. Increased pain immediately after eating or during the first hour after eating (early pain) occurs when the stomach is damaged. Late pain (occurs 2-3 hours after eating), hunger pain and night pain are characteristic of diseases of the duodenum (duodenitis, peptic ulcer). Gastric pain decreases after vomiting, taking alkali (soda) and liquid food that helps dilute gastric juice.

If a connection between pain and food is established, you should find out whether the quality and quantity of food affects them. If pain occurs after eating spicy juice food, one can think about the role of hypersecretion in the occurrence of pain. If pain occurs after eating a large amount of food, regardless of its nature, this indicates that the cause of the pain is gastric distension or perigastritis.

The connection of pain with physical activity and changes in body position is characteristic of gastroptosis and perivisceritis.

Pain emanating from the stomach is characterized by irradiation into the back, into the shoulder blades, the lower part of the interscapular space, and into the left hypochondrium.

Intestinal dyspepsia – disruption of the process of digesting food in the intestines as a result of enzymatic deficiency of the small intestine, pancreas, liver or accelerated movement of food through the intestines. Dysbacteriosis plays a certain role in the development of intestinal dyspepsia.

Intestinal dyspepsia has the following clinical manifestations:

1. Intestinal pain.

Mechanisms of development of intestinal pain:

• 
  spastic contraction of intestinal muscles - intestinal pain;
• 
  stretching of the intestinal wall by its contents - gas, liquid (distension pain);
• 
  mesenteric pain (mesenteric lymphadenitis);
• 
  transition of the inflammatory process, pressure of scars or tumors on intramural nerve endings - ganglion pain;
• 
  ischemic pain (a consequence of intestinal vascular pathology).

General signs that distinguish intestinal pain from stomach pain:

• 
  lack of strict dependence on meal times;
• 
  connection of pain with the act of defecation (pain can occur before, during, and, less often, after bowel movement);
• 
  reduction of pain after bowel movements or passing gas.

Distension pain differs from spastic pain in two main ways:

1) lack of periodicity - they are long-lasting and gradually dull with the prolonged existence of swelling, their nature is monotonous, aching;

2) the ability to localize them quite accurately.

Spastic pain most often occurs when:

• 
  inflammatory process in the intestines;
• 
  acute and chronic poisoning (arsenic, lead);
• 
  taking large amounts of rough, difficult-to-digest food;
• 
  helminthiasis;
• 
  diseases of the central nervous system (spinal cord tuberculosis);
• 
  vegetoneurosis.

Spasmodic pain has the character of colic. The following symptoms are characteristic of colicky pain:

• 
  they are paroxysmal, in the form of repeated attacks, contractions, begin and end suddenly;
• 
  quickly change their localization, but more often arise paraumbilically;
• 
  often accompanied by flatulence, rumbling in the stomach and decrease after the passage of gas.

Appendiceal colic is of great diagnostic value. The pain is initially localized around the navel and in the epigastrium, and then descends to the right iliac region and increases here.

A special type of colic is tenesmus - rectal colic. This is an extremely painful and frequent urge to defecate, usually ineffective (“false urge”), accompanied by a sensation of convulsive contraction in the rectum and anal sphincter. Tenesmus is observed during inflammatory processes and ulcerations in the area of ​​the sigmoid and rectum; typical for dysentery.

Pain in the left half of the abdomen that occurs immediately before defecation often indicates inflammatory processes in the descending colon and sigmoid colon. Pain that occurs during defecation and is felt in the anus is caused by pathological processes in the rectum (hemorrhoids, proctitis, anal fissure, etc.).

In diseases of the duodenum, pain is localized in the pancreato-duodenal zone of the abdomen. With diseases of the small intestine, pain is felt in the middle of the abdomen in the navel area and below. In diseases of the colon transversum, pain is localized in a horizontal strip passing above the navel.

With pathology of the sigmoid and cecum, pain is felt in the left and right iliac region, respectively.

It should be remembered that pain caused by perivisceritis and intestinal adhesions can radiate to areas significantly distant from the place of their origin - to the lower back, chest, lower extremities.

2. Flatulence (flatulentio)

This is bloating, which occurs due to excessive formation of gases in the digestive tract, impaired absorption and discharge.

The most common causes of flatulence:

• 
  enzymatic insufficiency of the stomach, intestines, pancreas;
• 
  dysbacteriosis;
• 
  aerophagia;
• 
  violation of gas absorption by the intestinal wall during inflammation.

Patients complain of heaviness, distension and increased volume of the abdomen; there may be intestinal colic, shortness of breath and heart pain associated with displacement of the diaphragm.

3. Rumbling (borborygmi) - noises and splashing in the stomach arising from the collision of gases and liquids while simultaneously passing through a bottleneck in the intestines. It is observed in spastic conditions of the intestines, often accompanied by colic, and may precede diarrhea.

4. Intestinal vomiting – characteristic of low-lying intestinal obstruction. It is caused by antiperistaltic bowel movement. Vomit does not contain real feces, but only stagnant food masses, putrefactively decomposed, with dirty brown particles of fecal appearance and smell. A real one can also be observed fecal vomiting, which indicates the presence of a fistula between the stomach and the transverse colon. Fecal vomiting is repeated and persistent, accompanied by retention of stool and gases.

Defecation disorders

1. Diarrhea (diarrhoea) - This is frequent bowel movements with the release of liquid feces containing an abnormal amount of digestive juices, mucus, and products of fermentation or putrefaction.

Diarrhea is usually associated with accelerated intestinal motility, the rapid passage of its contents; decreased absorption of water and electrolytes; increased transudation of secretions into the intestinal cavity and increased mucus formation.

The following types of diarrhea are distinguished depending on the causative factors:

1. 
   intestinal;
2. 
   gastrogenic;
3. 
   pancreatogenic;
4. 
   hepatogenic;
5. 
   endocrine;
6. 
   metabolic;
7. 
   for systemic diseases;
8. 
   nutritional;
9. 
   neurogenic;

10) medicinal.

Diarrhea is characteristic of fermentative, putrefactive and fatty (“soapy”) dyspepsia.

Intestinal diarrhea, depending on the localization of the pathological process that caused it, can be enteral and colitic.

Enteral diarrhea are characterized by more rare (4-6 times a day) and less painful bowel movements. They are characterized by polyfecality, indicating insufficient intestinal absorption (malabsorption), and if undigested food remains are found in the feces, it indicates a violation of intestinal digestion (maldigestion).

Colitic diarrhea characterized by more frequent bowel movements (10 or more times a day); stools are scanty, sometimes bloody, and there is often “rectal spitting.” Tenesmus is characteristic of colitic diarrhea.

2. Constipation (obstipatio) – rare (less than 3 times a week) bowel movements with the passage of a small amount of feces of excessively dense consistency. No stool for 3 days.

Depending on the cause, constipation can be:

1. 
   nutritional;
2. 
   neurogenic (dyskinetic);
3. 
   reflex;
4. 
   hypodynamic;
5. 
   inflammatory;
6. 
   proctogenic;
7. 
   mechanical;
8. 
   due to abnormalities in the development of the colon;
9. 
   toxic;

10) medications;

11) endocrine;

12) due to disturbances in water-electrolyte metabolism.

Depending on the nature of the disorder of intestinal motor function, constipation can be atonic or spastic.

The main mechanism for the development of constipation is the slow movement of intestinal contents (due to mechanical obstruction along the intestinal tract, impaired motor function of the intestine, insufficient amount of intestinal contents) and its prolonged stay in the intestine, which contributes to increased absorption of liquid parts of feces and greater compaction.

Bloody vomiting (haemotemesis).

Bloody vomiting most often occurs with gastroduodenal erosions and ulcers, bleeding from dilated veins of the esophagus and stomach with portal hypertension, and malignant tumors of the stomach.

Vomiting (regurgitation - ruminatio) with a mouthful of dark, unchanged blood with clots allows one to suspect bleeding from varicose veins of the esophagus or cardia of the stomach with portal hypertension. With minor esophageal bleeding, blood can accumulate in the stomach, causing vomit to look like coffee grounds.

With massive gastric bleeding, vomiting with vomit the color of coffee grounds is characteristic, and with less intense bleeding, bloody vomiting may be absent, since all the blood flows from the stomach into the intestines and is excreted in the form of black tarry stool.

Bloody stool.

It is an important sign of gastrointestinal bleeding. Depending on the location of the source of bleeding, the stool may have a different color - from red to black tarry. It is observed in peptic ulcers, polyps and intestinal cancer, ulcerative colitis, dysentery, etc.

Black, tarry stools (melaena) indicate prolonged residence of significant amounts of blood in the upper parts of the digestive tube. Dark cherry-colored feces occur with moderate bleeding from the distal parts of the small intestine or the right half of the large intestine. “Raspberry jelly” type stool with a large amount of mucus is characteristic of bleeding from parts of the colon. Scarlet blood on the surface of formed stool is a sign of bleeding from the lower intestines, most often found with hemorrhoids and anal fissures.

Loss of appetite, change in taste.

Appetite is an important factor regulating food intake, affecting salivation, gastric secretion and its motor function.

Changes in appetite can be of central origin or peripheral, i.e. reflex, mainly from the digestive tract. The following types of appetite disorders are distinguished in patients with pathologies of the digestive system.

1. 
   Decreased appetite up to its complete loss (anorexia) is observed with decreased gastric secretion, acute gastritis, and stomach cancer. Abstinence from eating due to fear of pain (cibophobia) should be distinguished from loss of appetite.
2. 
   Increased appetite (polyphagia), sometimes expressed to a sharp degree (bulimia), is characteristic of conditions with increased gastric secretion and mental illness.
3. 
   Perversion of appetite (the desire to eat inedible substances) – occurs in people suffering from achlorhydria and in pregnant women; with stomach cancer, patients experience an aversion to meat foods, and with acholia - to fatty foods.
4. 
   Changes in taste (unpleasant taste in the mouth, dullness of taste) often depend on pathological processes in the oral cavity (carious teeth, chronic inflammation of the tonsils). A coated tongue can also cause a bad taste in the mouth.

Weight loss (exhaustion).

Characteristic of gastrointestinal diseases with a chronic course. Particularly pronounced weight loss up to cachexia occurs in patients with esophageal strictures, stenosis of the gastric outlet, tumors of the digestive organs, and prolonged diarrhea.

2. Features of collecting anamnesis of disease and life in patients with gastrointestinal pathology.

Collecting an anamnesis of illness and life in patients with pathologies of the digestive organs - see the methodological manual ""Scheme of the educational history of the disease in the clinic of propaedeutics of internal diseases."
3. General examination and examination of the oral cavity in patients with diseases of the digestive system.

A general examination of a patient with gastrointestinal diseases is carried out according to the generally accepted scheme.

In severe chronic diseases, accompanied by impaired intake and utilization of food, weight loss is observed, sometimes an extreme degree of exhaustion - cachexia.

In cases of perforation of an ulcer, intestinal obstruction, diffuse peritonitis, a specific appearance of the face is observed - “facies abdominalis seu Hyppocratica”.

When examining the skin from the mucous membranes, color changes can be detected: pallor with malignant tumors of the esophagus, stomach and intestines, after gastroduodenal bleeding and with anemia; When malignant tumors of the stomach or intestines metastasize to the liver or lymph nodes at the porta hepatis, jaundice may occur. Dryness of the skin or loss of elasticity, decreased muscle tone, thinning of subcutaneous fat, trophic disorders such as cracked lips, hair loss, and brittle nails may be detected.

When examining the lymphatic system in patients in the late stages of stomach and intestinal cancer, enlarged lymph nodes can be detected (in case of stomach cancer, an enlarged lymph node is detected in the left supraclavicular fossa - Virchow's gland).

A local detailed examination begins with the tongue and oral cavity. Lack of teeth and the presence of carious teeth lead to poor chewing of food, as well as to the entry of pathogenic microflora into the stomach. Chronic inflammation of the tonsils and mucous membrane of the pharynx is a constant source of infection in the body. Loosening of the gums and bleeding from them are signs of hypovitaminosis.

In acute and chronic diseases of the stomach and intestines, inflammatory and dystrophic changes in the mucous membrane of the tongue occur, which manifests itself in the form of plaque of various colors. A wet and clean tongue is characteristic of an uncomplicated peptic ulcer; covered with a gray-white coating - occurs in acute gastritis; dry, with a dirty gray coating – in case of “disasters” in the abdominal cavity (peritonitis); atrophic tongue with smoothing of the papillae (“lacquered tongue”) - with atrophic gastritis and hypovitaminosis group B.

4. Topographic areas of the abdomen.

When examining the abdomen, for convenience of description and topographical orientation in the location of the abdominal organs, the anterior wall and, accordingly, the abdominal cavity are divided into certain areas by conventional lines. Using two horizontal lines (the first connects the tenth ribs, the second connects the upper iliac spines), the anterior abdominal wall is divided into three regions, located one below the other: epigastric, mesogastric and hypogastric. Using two parallel vertical lines drawn along the outer edges of the rectus abdominis muscles, the epigastric region is divided into two subcostal regions (right and left) and the epigastric region (in the middle); mesogastric - on the two lateral iliac regions (flanks) and on the umbilical region; hypogastric - into two lateral groin areas and suprapubic.
5. Examination of the abdomen. Distinctive signs of abdominal enlargement with ascites, obesity and flatulence.

When examining the abdomen, you can identify a number of symptoms related not only to gastrointestinal diseases, but also to pathologies of the liver, as well as the cardiovascular system.

Examination of the abdomen should begin with the patient lying on his back. At the beginning of the examination, the shape of the abdomen and its size are determined. In a healthy person, the shape of the abdomen varies depending on the constitution: with asthenic body types, the stomach is somewhat retracted, with hypersthenic body types, it is somewhat protruded. A retracted, navicular abdomen indicates general exhaustion or spastic contractions of the muscles of the abdominal wall and intestines. Excessive protrusion, up to a significant and sharp increase, is most often caused by three main reasons: obesity, bloating (flatulence), accumulation of free fluid in the abdominal cavity due to exudation (peritonitis) or transudation (ascites).

Less common is asymmetrical enlargement of the abdomen, which occurs as a result of a significant enlargement of any abdominal organ (liver, spleen). The cause of an enlarged abdomen may be the presence of a cyst in the abdominal cavity containing a significant amount of fluid.

Obesity and ascites can be differentiated by certain examination details. With ascites, the skin of the abdomen is thin, shiny, without folds, the navel protrudes above the surface of the abdomen (umbilical hernia). In obesity, the skin has folds, characteristic stretch marks of the skin (striae) of a reddish color are revealed, the navel is usually retracted. You can more accurately determine the cause of abdominal enlargement using percussion.

With gastro- and enteroptosis, the abdomen acquires a peculiar shape, which is better revealed in the patient’s vertical position: the upper part of the abdomen looks sunken, and the lower part protrudes.

In order to more accurately judge the size of the abdomen and its dynamics, especially in patients with ascites, it is recommended to measure the abdominal circumference. The measurement is made using a soft measuring tape, which is placed without tension around the abdomen at the level of the navel.

In some cases, when examining the abdomen, peristalsis of the stomach and intestines can be detected. Physiological peristalsis is visible only with a sharp thinning of the abdominal wall or divergence of the rectus muscles. If there is an obstacle to the movement of food in the stomach or intestines, increased peristalsis occurs above the obstacle, often accompanied by loud rumbling. Such peristalsis can be seen through the abdominal wall. It is caused by light tapping on the abdominal wall. Less commonly, waves of antiperistalsis (a sign of intestinal obstruction) are detected.

When examining the abdomen, the characteristics of the respiratory movements of the abdominal wall are of some importance. Increased participation of the abdominal muscles in breathing in women may be a consequence of chest pathology. A complete absence of movement of the abdominal wall during breathing most often occurs with diffuse peritonitis, and unilateral - with local inflammatory processes in the abdominal cavity (cholecystitis, appendicitis, etc.).

When examining the abdomen, you should pay attention to possible hernial protrusions on the anterior abdominal wall.

Examination of the abdomen can reveal an important sign of portal hypertension - the presence of an expanded venous network on the anterior abdominal wall - "caput Medusae". On the diagnostic significance of the development of collateral circulation on the abdominal wall - see the methodological development “Questioning and examining patients with diseases of the hepatobiliary system”

6. Percussion of the abdomen. The nature of percussion sound. Percussion of the abdomen according to Mendel.

Conditions for topographic percussion of the abdominal cavity are very unfavorable, since the stomach and intestines produce a loud tympanic sound, creating a large resonance. Therefore, it is necessary to use quiet percussion, which makes it possible to better identify pathological processes in the abdominal cavity. Although the tympanic sound obtained over the intestinal area is higher than over the stomach area, it is only in rare cases that it is possible to determine the boundary between the stomach and intestines using percussion.

With pneumoperitoneum (accumulation of free gas in the abdominal cavity), which occurs when a gastric or duodenal ulcer is perforated, the percussion sound becomes loud, tympanic and completely uniform over the entire abdomen. The gas usually occupies the highest position and is also located between the anterior surface of the liver and the inner surface of the lower ribs, so percussion hepatic dullness disappears.

The same uniform loud tympanic sound is detected during flatulence.

With pneumoperitoneum and flatulence, as the amount of gases in the abdominal cavity or intestines increases, the tension of the dense elements increases, in the first case - the abdominal wall, in the second - the intestinal walls. As a result, their ability to vibrate increases and their participation in the formation of percussion sound increases.

When the gas content in the intestines decreases or when it is overfilled with liquid or solid feces, the percussion sound may be dull or completely dull. A dull percussion sound can be heard with a very thick abdominal wall, since in this case the percussion blow does not penetrate the gas contained in the intestines and stomach.

Limited areas of dullness to percussion or areas of complete dullness may be observed over tumors or inflammatory infiltrates in the abdominal cavity if they are large enough and located close to the anterior abdominal wall.

Percussion according to the Mendelian method, which is used to determine local areas of pain in the abdominal cavity, is of diagnostic value. It is performed with a percussion hammer or the middle finger of the right hand, which strikes the upper parts of both rectus abdominis muscles. With a stomach or duodenal ulcer, pain occurs over the site of localization, sometimes sharp. The cause of pain in this case is the increased sensitivity of the parietal layer of the peritoneum in the place corresponding to the diseased organ (viscerosensory reflex).
7. Method of percussion palpation (succussion) of the stomach according to the method of V.P. Obraztsova. Diagnostic value.

Percussion palpation (succussion) of the stomach according to the method of V.P. Obraztsova. It is used to determine the size of the stomach, the location of its greater curvature, and the state of the tone of its walls. The splashing noise can be caused if there is liquid and air in the stomach, and the air is located in front of the liquid. To detect the splashing noise, use the elbow edge of the slightly bent left hand to press in the area of ​​the xiphoid process. In this case, the air of the gas bubble will be distributed over the surface of the liquid. Next, with four half-bent fingers of the right hand, short points are made in the epigastric region, slightly below the xiphoid process, and, gradually moving down, they cause a splashing noise until the fingers slide off the greater curvature of the stomach. The cessation of the splashing noise indicates the location of the lower border of the stomach. Normally, the splashing noise does not occur below the line connecting the upper spines of the iliac crests (linea biiliaca). If the splash is determined below this line, prolapse of the lower border of the stomach should be recognized (gastroptosis, gastric dilatation).

In healthy people, splashing sounds are produced shortly after eating. If a loud splashing noise is detected on an empty stomach or 6-7 hours after a meal, then the motor function of the stomach is reduced or its evacuation ability is impaired. This may be due to spasm or pyloric stenosis. A splashing sound to the right of the midline of the abdomen is detected when the prepyloric part of the stomach expands (Vasilenko's symptom).
8. Diagnostic value of the auscultatory afriction method.

To determine the lower border of the stomach, you can use the method of stetoacoustic palpation (auscultatory affriction). The stethoscope is placed under the left costal arch, under the area of ​​Traube's space. Using the index finger of the right hand, make light rubbing movements along the abdominal wall from top to bottom towards the navel. While the finger is above the stomach, a rustling sound is heard in the stethoscope, which disappears or sharply weakens when the finger goes beyond its limits. Sometimes this method gives inaccurate results.
9. Determination of free and encysted fluid in the abdominal cavity.

Methods for determining free and encysted fluid in the abdominal cavity.

1. Determination of free fluid in the abdominal cavity.

With the patient positioned on his back, quiet percussion is performed from the navel towards the lateral abdomen. If there is free fluid in the abdominal cavity, it accumulates in the flanks. As a result, during percussion in the center of the abdomen (in the navel area), a tympanic sound is detected, and a dull sound is detected above the flanks. If you then ask the patient to turn on his side, the free fluid will move to the appropriate side, and above the flank, which is at the top, the dull sound is replaced by a tympanic sound.

Even more convincing results are obtained by percussion when determining free fluid in the abdominal cavity when the patient is in an upright position. Percussion is performed from top to bottom along the midline. If there is fluid in the lower abdomen, a dull sound is caused.

To determine small amounts of liquid, it is recommended to perform percussion in the patient’s knee-elbow position. In this case, dullness of percussion sound in the navel area is detected.

Large quantities of liquid can be detected by fluctuation. To do this, the left hand is placed flat on the lateral surface of the abdominal wall, and short blows are applied to the abdominal wall from the opposite side with the fingers of the right hand. These impacts cause vibrations in the fluid, which are transmitted to the other side and are perceived by the left hand in the form of the so-called “wave symptom”.

In order to make sure that the fluctuation is transmitted through the fluid and not along the abdominal wall, it is recommended that the research assistant place the edge of the hand in the middle of the abdomen and thereby eliminate the transmission of the wave along the anterior abdominal wall.

1. 
   Determination of encysted fluid in the abdominal cavity.

Enclosed fluid in the abdominal cavity is characteristic of limited peritonitis with the formation of adhesions or cysts, most often emanating from the ovary or pancreas.

During percussion, a dull sound is detected above the encysted fluid, which, unlike free fluid, does not change its localization depending on changes in the patient’s position. With large abdominal cysts, the zone of dull percussion sound is located in the middle of the abdomen, and tympanitis is detected in the lateral parts due to the intestines being pushed back there.
10. Auscultation of the abdomen. Diagnostic value of listening to peristaltic sounds and friction sounds of the peritoneal layers.

Above the abdominal cavity in healthy people, intestinal peristalsis is usually heard in the form of a slight splashing or rumbling. It is listened to using a stethoscope or directly to the ear.

Loud rumbling occurs when there is stenosis of the intestine, inflammatory processes in it, accelerated movement of liquid contents through the intestines, etc.

The absence of sound phenomena over the abdominal cavity can serve as a sign of intestinal paresis and occurs with peritonitis.

With inflammation of the serous cover of the liver and spleen (perihepatitis, perisplenitis), as well as in patients with fibrinous peritonitis, you can listen to the friction noise of the peritoneal layers.

DISEASES OF THE GASTROINTESTINAL TRACT AND BILITAL TRACT

CHRONIC HEPATITIS

It is a common disease - 50% of all diseases. It was isolated from liver cirrhosis when a new research method appeared - laparoscopy and the method of intravital targeted biopsy. This is an inflammatory-dystrophic disease. For more than 6 months, progression to varying degrees. The criterion for diagnosis is the undisturbed lobular structure of the liver.

Etiology

I. In 50% - acute viral hepatitis. The transition to chronic is facilitated by:

late diagnosis

insufficient treatment

eating disorders, diets

drinking alcohol

early discharge

early start of physical activity after illness

against the background of gastrointestinal diseases.

But even if all of the above factors are excluded, viral hepatitis becomes chronic in 5% of cases.

II. Toxic effect on the liver:

alcohol (50-80% of patients are alcoholics)

benzene, carbon tetrachloride, DDT

drug-induced hepatitis (when taking anti-tuberculosis, sedative, hypotensive (dopegit), cytostatic, narcotic drugs, tetracycline antibiotics)

aniline dyes

heavy metal salts

metabolic hepatitis associated with metabolic disorders and long-term malnutrition.

Pathogenesis

Long-term persistence of the virus in the body. Blood with Australian antigen is contagious. Intrauterine infection of the fetus through the placenta is possible. The hepatitis virus belongs to the group of slow viruses.

Inclusion of immunological reactions in the process. HRT-type reactions are especially important. The integrity of the hepatocyte membrane is disrupted, membrane lipoprotein is released, which stimulates T-lymphocytes. Antigens can enter the blood through a series of trabeculae - the production of antibodies begins. Histio-lymphocytic infiltration appears.

Activation of mesenchymal tissue is possible during acute hepatitis. Proliferation proceeds so quickly that the mesenchyme begins to rob hepatocytes and take away their nutrients - the so-called “stealing phenomenon.” Hepatocytes begin to die off as entire islands, and their failure occurs.

Morphology

The liver increases in size. It starts out as a large white liver, then turns into a large motley liver. Along the portal fields there is inflammatory infiltration. There may be fields of necrobiosis. Intrarenal ducts and choleostasis may be affected. Morphological definition: chronic hepatitis is an inflammatory-dystrophic lesion of the liver with histiolymphocytic infiltration along the portal tract with hypertrophy of Kupffer cells, atrophic changes in the parenchyma and preservation of the lobular structure.

Classification

1. By etiology:

a) viral

b) toxic

c) toxic-allergic (for collagenosis)

d) alcoholic.

2. According to morphology:

a) persistent - histological changes are minimal: moderate fibrosis, sometimes histiolymphocytic infiltration, no dead cells. Slow benign course, no dead cells. When the etiological factor is eliminated, it ends in fibrosis, but not cirrhosis.

b) active (aggressive) hepatitis - a malignant form with pronounced intoxication. There is autogression, destruction and necrosis. Sharp changes in the mesenchyme. Progresses quickly, after 4-6 years it turns into cirrhosis in 30-60%. One of the options - lipoid hepatitis was recently considered an independent nosological form, but this is an extremely severe case of chronic aggressive hepatitis. It happens more often in young women.

c) cholestatic - as a rule, intrahepatic cholestasis is observed, the symptoms of cholemia dominate. This is one of the very malignant hepatitis. Primary biliary cirrhosis is more common.

Asthenovegetative syndrome: associated with impaired detoxification function of the liver. It manifests itself in general weakness, increased irritability, decreased memory, and interest in the environment.

Dyspeptic syndrome: especially with cholestatic hepatitis. Decreased appetite, changes in taste, in chronic alcoholism - decreased tolerance to alcohol: a feeling of bitterness in the mouth, flatulence is especially characteristic, a dull aching pain in the right forecourt, a feeling of heaviness: belching with bitterness, air, vomiting, stools are often loose.

Cholestatic syndrome: dark urine, light stool, itching, jaundice.

Minor liver failure syndrome: in 80%, the transit function of the liver suffers, hepatic jaundice develops, in addition, the synthesis of proteins by the liver and the inactivation of aldosterone are disrupted - this leads to edema, and there may be a hemorrhagic syndrome due to a disruption in the synthesis of blood proteins.

Objectively

Hepatomegaly.

Changes in the skin: 50% yellowness, sometimes with a dirty tint due to excess deposition of melanin and iron, secondary hematochromatosis (more often in alcoholics), itching of the skin - scratching, acne, sometimes urticaria, sometimes accumulation of fat - xanthomatosis of the sclera; spider veins are a manifestation of hyperastrogenism: there may be phenomena of hemorrhagic diathesis, liver palms are bright red (they also occur in healthy people).

Splenomegaly - more often with active hepatitis.

In addition, there may be fever, allergic rash, pericarditis, nephritis (more often with lupoid hepatitis).

Diagnostics

An increase in the level of bilirubin in the blood is especially high in the cholestatic variant, with a sharp exacerbation of the chronic process.

Enzymes:

a) ALT (GPT) are indicator enzymes, the increase in activity of which is accompanied by the destruction of hepatocytes and reflects the degree of necrobiotic processes in the liver. But we must remember that some increase in these enzymes also occurs during myocardial infarction

b) milk phosphatase - activity increases when the outflow of bile is impaired (cholestasis): normally 5-7 units

c) aldolase, lactate dehydrogenase.

Cholesterol - increases to 1000-1200 mg%.

Blood protein fractions:

a) hypoalbuminemia, especially with the active form (N 56.6-66.8%)

b) hypogammaglobulinemia - reflects the activity of immunological processes during inflammation (normal 21%)

c) hypofibrinogenemia (2-4 g/l)

d) decrease in prothrombin (absorption of vitamin K is impaired).

Hyperglycemia.

Tests to assess the antitoxic functions of the liver: Kwik's test - determination of hypuric acid in the urine after the introduction of sodium benzoate into the body. A violation is indicated if less than 30% of sodium benzoate taken orally is excreted.

Tests for assessing protein spectrum disorders: Weichtmann coagulation tape, Tokata-ara reaction, (N-), sublimate tests, veronal-thymol test (in N - 5 units).

Immunological reactions: determination of immunoglobulins and liver. antibodies.

Tests to assess the excretory function of the liver: test with bromsulfalein - after an hour, 60-80% of the substance should be excreted.

Radioisotope study with *** gold, Bengal rose.

Puncture liver biopsy.

Laparoscopy.

Cholangiography.

Features of the clinic

Persistent hepatitis: Australian antigen is often detected. Outside of exacerbation, there may be no clinical manifestations, with the exception of an enlarged liver. This is a benign form, but patients are virus carriers. Liver tests were slightly changed; protein fractions of the blood changed extremely late.

Active hepatitis. Antigen independent, bright clinic:

a) fever, jaundice

b) splenomegaly, sometimes with manifestations of hypersplenism

c) thrombocytopenia

d) hypergammoglobulinemia

e) excess enzyme activity

f) increase in immunoglobulin titer

g) sometimes antinuclear antibodies are detected, sometimes there are blastotransformations of lymphocytes.

Lupoid variant: duration of course is about 1 year

a) young women get sick more often

b) often have atralgia

c) allergic manifestations, urticaria

d) lymphadenopathy (B-lymphocytes participate in reactions)

e) sometimes thyroiditis

e) changes in the heart.

The cholestatic variant is more common in older women, closer to menopause; Severe skin itching, severe jaundice with hyperbilirubinemia, increased alkaline phosphatase activity, impaired absorption of vitamin D ® osteoporosis, pathological fragility of bones gradually increase.

Chronic alcoholic hepatitis has a long history, men are more often affected; Previously it was 10: 1, now 4: 1. At first they can occur like other forms, but then there is tremors, loss of interest in the environment, a feeling of humiliation, impotence, gynecomastia, hair loss, secondary hemachromatosis, severe anemia, usually hyperchromic - the influence of ethanol on bone marrow, hyperleukocytosis, hypoalbuminemia.

Differential diagnosis

Chronic hepatitis sometimes occurs as acute. Anamnesis helps to recognize. In addition, in acute hepatitis, enzyme activity reaches very high levels; in chronic hepatitis, enzyme activity increases moderately. In acute hepatitis, according to the proteinogram, there are no disturbances in the protein fractions of the blood.

In chronic hepatitis, unlike liver cirrhosis, there are no signs of portal hypertension. The biopsy method also helps: in chronic hepatitis, the lobular structure is preserved.

Dubin-Jones syndrome: benign hyperbilirubinemia. Another name is juvenile intermittent jaundice. In this case, there is a defect in the enzyme that transports bilirubin. Unlike chronic hepatitis, there is no enlargement of the liver; enzymopathy is inherited in an autosomal dominant manner. The disease appears for the first time after puberty. Complaints of heaviness and dull pain in the liver, epigastrium, unknown dyspeptic disorders. There is no splenomegaly, moderate jaundice, total bilirubin is usually 2-6 mg% and constantly fluctuates around the same average value. Bound bilirubin is increased and accounts for 60-80% of the total. Constant bilirubinuria is observed, urobilin bodies remain normal. One of the characteristic signs is an increase in the retention of bromine***phalein after 30 minutes of its administration. An increase in urine coproporphyrin -1 of more than 80% is pathognomonic for the disease. Almost every patient with the syndrome is hospitalized with suspected acute viral hepatitis. The disease has almost no effect on ability to work and there is no special treatment other than diet. does not require.

Eliminate the damaging etiological factor.

In case of exacerbation - hospitalization, bed rest. Diet: sufficient protein, carbohydrates, limited fat, moderate amount of salt.

Pathogenetic treatment

a) Corticosteroids - prednisolone 30-40 mg/day

b) cytostatics: imuran 100-200 mg/day, 6-mercaptopurine, plaquenil 0.5 - 1 time/day.

Of the cytostatics, preference is given to imuran (azothioprotein). The duration of such combination therapy is several months, and in the lupoid variant - several years. Doses of drugs are reduced slowly and no earlier than after 2-3 months, switching to maintenance doses - prednisolone 20 mg/day, Imuran 50 mg/day - given for a year.

Indications: active cholestatic hepatitis, persistent in the acute phase. Contraindications: detection of Australian antigen. Together with prednisolone, delagil 0.25-0.5 can be prescribed.

Symptomatic treatment

a) Glucose orally, and in severe cases intravenously, at the rate of 50 g/day - reduces intoxication

b) vitamins of group B, C, etc.: C - in the presence of signs of hemorrhagic diathesis, k - in case of hemorrhagic diathesis and decreased prothrombin, D - in case of cholestasis, because their absorption is impaired. B1, -2, -6, -12.

Liver hydrolysates: sirepar 2.0 IV for a course of 50 injections. In case of protein metabolism disorders: albumin solution 10% 50-100 ml; protein hydrolysates + anabolic steroids (cautiously) - retabolil, plasma infusion. Glutamic acid.

For intrahepatic cholestasis:

Phenobarbital 0.01 x 3 (improves the structure of the bile micelle), choleretic (caution) - better herbal ones: corn silk and others. Cholestyramine is an ion exchange resin that forms insoluble complexes with bile acids in the intestine, which leads to increased absorption of cholesterol in the intestine, reducing itching and jaundice. Give 10-15 g/day.

CIRRHOSIS OF THE LIVER

Liver cirrhosis is a chronic disease with degeneration and necrosis of the hepatic parenchyma, with the development of enhanced regeneration with a diffuse predominance of the stroma, the progressive development of connective tissue, a complete restructuring of the lobular structure, the formation of pseudo-lobules, with impaired microcirculation and the gradual development of portal hypertension.

Liver cirrhosis is a very common disease and in the vast majority of cases develops after chronic hepatitis.

Etiology

Viral hepatitis, chronic alcohol intoxication, drug intoxication, cholestasis.

Morphology

As liver cells die, their accelerated regeneration begins. The peculiarity of false lobules is that they do not contain normal triads - there are no central veins. Vessels develop in connective tissue cords - portal shunts. The efferent veins are partially compressed and destroyed, and microcirculation is gradually disrupted. Blood flow in the hepatic artery is also disrupted. When blood flows into the portal vein, portal hypertension increases. The death of liver cells progresses. As a result of the described processes, the surface of the liver becomes rough and lumpy.

Classification

According to morphology: micronodular, micro-macronodular (mixed), macronodular, septal (with damage to the interlobar septa). According to the clinic, taking into account the etiology: viral alcoholic, toxic (drug), cholestatic, storage cirrhosis.

Astheno-vegetative syndrome.

Dyspeptic syndrome.

Cholestatic syndrome.

Portal hypertension.

Violation of the antitoxic function of the liver - hepatocellular insufficiency, inactivation, binding, defatting, and removal of chemical compounds are impaired: hyperestrogenism. Manifested by spider veins, red “liver palms” (palmar erythema), gynecomastia and impotence in men, amenorrhea in women, hair loss; changes in hemodynamics; hypotension due to a sharp change in peripheral resistance, changes in blood volume, hyperaldosteronism; sodium retention in the body, increased excretion of potassium with the ensuing consequences; a gradual increase in ammonia, indole, skatole in the blood - hepatic coma may develop; increased histamine ® allergic reactions; increased serotonin; decreased protein synthesis by the liver; hypoalbuminemia, hypoprothrombinemia, hypofibrinogenemia, decreased angiotensin levels; iron, which is normally bound by proteins, ends up in tissues; disturbance of the metabolism of magnesium and other electrolytes; bilirubin retention (bound bilirubin-glucuronide is not released), the binding of indirect bilirubin is impaired, there may be hyperbilirubinemia, but jaundice is observed only in 50% of cases.

Portal hypertension: desolation of veins, new formation of blood vessels, and arteriovenous shunts occur. All this leads to poor circulation. Within 1 minute, 1.5 liters of blood under high pressure pass into the portal vein, the pressure in the portal vein system increases - the vessels dilate (hemorrhoidal veins, veins of the esophagus, stomach, intestines, splenic artery and vein). Dilated veins of the stomach and lower third of the esophagus can cause gastrointestinal bleeding. During digital examination, hemorrhoidal veins are found in the form of nodes; they can fall out and become pinched, causing hemorrhoidal bleeding. The subcutaneous peri-umbilical veins expand - the “head of the jellyfish”.

Mechanism of ascites formation:

a) fluid leakage into the abdominal cavity due to increased pressure in the portal vein

b) hypoalbuminemia also contributes, due to which the oncotic pressure of blood plasma sharply decreases

c) lymph formation is disrupted - lymph begins to sweat immediately into the abdominal cavity.

Other signs of portal hypertension: gastrointestinal disorders, flatulence, weight loss, urinary retention, hepatolienal syndrome: splenomegaly, often with symptoms of hypersplenism (leukopenia, thrombocytopenia, anemia).

Objectively: examination of hemorrhoidal veins, dilation of the esophageal veins (fluoroscopy, fibrogastroscopy). Changes in the reticuloendothelial system: hepato- and splenomegaly, polylymphoadenopathy, immunological changes and an increase in antibody titer - with exacerbation of cirrhosis; enlargement of the parotid salivary glands; trophic disorders; Dupietren's contracture (degeneration of the tissue of the palmar aponeurosis into fibrous tissue, contracture of the fingers). Pronounced changes in the nervous system.

Features of the clinic:

Viral cirrhosis (posthepatitis).

More often associated with viral hepatitis. Characterized by focal liver damage with areas of necrosis (the old name is postnecrotic cirrhosis). This is a large-nodular form of cirrhosis, clinically resembling active hepatitis. Hepatocellular insufficiency, symptoms of impairment of all liver functions, comes to the fore. Portal hypertension appears. Life expectancy is 1-2 years. The cause of death was hepatic coma.

Alcoholic cirrhosis. It proceeds relatively benignly. Early portal hypertension is characteristic. Often the damage is systemic - not only the liver suffers, but also the central nervous system, peripheral nervous system, muscular system, etc. Peripheral neuritis appears, and intelligence decreases. There may be myopathy (atrophy of the shoulder muscles is especially common). Sudden weight loss, severe hypovitaminosis, myocardiopathy. The stomach and pancreas are often affected (gastritis, stomach ulcers, pancreatitis). Anemia.

Causes of anemia:

a) a large deficiency of vitamins (often hyperchromic anemia, macrocytic anemia, lack of vitamin B12

b) iron deficiency

d) toxic effect of ethanol on the liver

e) bleeding from varicose veins of the gastrointestinal tract. In addition, hyperleukocytosis and slow ESR are often observed, but it can also be accelerated; hypoproteinemia.

Biliary cirrhosis. Associated with stagnation of bile - cholestasis. It occurs more often in women aged 50-60 years. Relatively benign course. It occurs with skin itching, which can appear long before jaundice.

Cholestasis can be primary and secondary, like cirrhosis: primary is the outcome of cholestatic hepatitis, secondary is the outcome of subhepatic cholestasis.

In addition to skin itching, other signs of cholemia are also characteristic: bradycardia, hypotension, greenish coloration of the skin.

Signs of hypercholesterolemia: xanthomatosis, steatorrhea. Cholestasis also leads to osteoporosis, increased bone fragility. Alkaline phosphatase activity increases. Direct bilirubin up to 2 mg%. The liver is enlarged and dense. In secondary biliary cirrhosis - previous or recurrent pain syndrome (usually a stone in the bile ducts). There are also chills, fever, and other signs of inflammation of the bile ducts. Enlarged painless liver, finely nodular. The spleen never enlarges.

Drug-induced cirrhosis. Depends on the duration of use of drugs and their intolerance: tubazid, PAS, GINK drugs and other anti-tuberculosis drugs; aminazine (causes intrahepatic cholestasis), iprazide (MAO inhibitor - causes liver damage in 5%), dopegide, nerabol, etc.

It most often occurs as cholestatic. Portal hypertension. Indicators of cirrhosis activity: increased temperature, high enzyme activity, progressive metabolic disorders, increased alpha-2 and gamma globulins, high content of sialic acids.

Differential diagnosis

Adrenal block. Associated with impaired blood outflow in the hepatic vein (thrombosis, congenital narrowing). Portal hypertension develops. Batkiari syndrome. Clinical manifestations depend on how quickly portal hypertension progresses.

Subhepatic block. Associated with damage to the portal vein (thrombosis, external compression). Clinic - severe pain, fever, leukocytosis, rapid impairment of liver function.

Intrahepatic portal block - liver cirrhosis. If there is no clear etiological factor, then splenography is used (a contrast agent is injected into the spleen and after 6-7 seconds it is removed from the liver). If biliary cirrhosis occurs, the level of cholestasis (primary or secondary) must be established. Cholangiography is used.

Accumulation cirrhosis (hemochromatosis) - pigmentary cirrhosis, bronze diabetes, is associated with a deficiency of the enzyme that binds iron to protein and, thereby, regulates its absorption. With this defect, iron is intensively absorbed in the intestine and, not sufficiently binding to protein, begins to be intensively deposited in the liver, skin, pancreas, myocardium, and sometimes in the adrenal glands. In the liver, iron accumulates in the RPE cells - a large, finely nodular liver is observed. Inactivation of sex hormones is often disrupted. Signs of portal hypertension dominate. The skin has a gray-dirty pigmentation, the same on the mucous membranes, the skin becomes especially dark if iron is deposited in the adrenal glands - a symptom of adrenal insufficiency. When the pancreas is damaged - diabetes mellitus syndrome. With myocardipathies, severe irreversible rhythm disturbances. For diagnosis, the level of iron in the blood is determined and a puncture biopsy of the liver is performed.

Wilson-Konovalov disease is another storage cirrhosis (hepatolenticular degeneration). The disease is based on a copper metabolism disorder associated with a birth defect. The normal concentration in blood plasma is 100-120 mcg%, with 93% of this amount being in the form of ceruloplasmin and only 7% associated with serum albumin. Copper in ceruloplasmin is tightly bound. This process takes place in the liver. Ceruloplasmin is an alpha-2 globulin, and each molecule contains 8 copper atoms. Radioisotope methods have established that in hepatolenticular failure, the disorder is associated with a genetic defect in the synthesis of ceruloplasmin, due to which its content is sharply reduced. In this case, copper cannot be stably bound and is deposited in tissues. In some cases, the content of ceruloplasmin remains normal, but its structure changes (the ratio of fractions changes). In Wilson-Konovalov syndrome, copper is especially tropic to the liver, brain nuclei, kidneys, endocrine glands, and cornea. In this case, copper begins to act as a toxic agent, causing typical degenerative changes in these organs.

It is a set of syndromes characteristic of damage to the liver and extrapyramidal nervous system. According to the course, acute and chronic forms are distinguished. The acute form is characteristic of an early age, develops at lightning speed and ends in death, despite treatment. The chronic form with a slow course and gradual development of symptoms is more common. The first to appear is extra pyramidal muscular rigidity of the lower extremities (impaired gait and stability). The picture of parkinsonism gradually forms, then the psyche changes (paranoid reactions, hysteria). Sometimes liver failure comes to the fore: liver enlargement, the picture resembles cirrhosis or chronic active hepatitis.

The differential sign is hypocupremia below 10 mcg% or the copper level is at the lower limit of normal, a lot of copper is excreted in the urine - over 100 mcg/day. There may be a positive thymol test. An important symptom is the Kayser-Fleischer ring (bluish-green or brownish-green at the periphery of the cornea due to copper deposition). Treatment is aimed at binding copper and removing it from the body: cuprenil (D-penicillinamine) is used, as well as unitol + a diet excluding copper (chocolate, cocoa, peas, liver, rye bread).

Complications of liver cirrhosis

Bleeding.

Attachment of infection.

The appearance of a tumor.

Liver failure

MAJOR LIVER FAILURE

It is based on the entry into the bloodstream of large quantities of toxic products of protein metabolism, which are not sufficiently neutralized by the liver (ammonia, phenol, methionine, tryptophan, indole, skatole). There are two types of hepatic coma:

Hepatocellular coma (more severe variant).

Porta-caval form.

The first is associated with progressive necrosis of liver cells, with the formation of additional toxic products, hence the more severe clinical picture. Porto-caval forms occur in conditions of a sharp increase in pressure in the portal vein - shunts open, blood begins to be dumped, bypassing the liver, and liver cells suffer. Clinical signs are associated with the accumulation of cerebrotoxic products in the blood. The alkaline-acid balance in the blood is disturbed, the ratio of lactic and pyruvic acids is disturbed. A shift to the acidic side leads to intracellular acidosis, which manifests itself in edema of the brain and liver.

Acidosis also promotes potassium influx and intracellular hypokalemia. Secondary hyperaldosteronism occurs, which further aggravates hypokalemia. Microcirculation is disrupted. Damage to the central nervous system is associated with mental status disorders: unmotivated actions, increasing adynamia, hallucinations and delusions, psychotic state, tremors of the limbs, weakness, malaise. Next, clinical convulsions occur, spreading to individual muscle groups, and in severe cases, involuntary urination and defecation. Gradual transition into coma. Jaundice increases and the temperature increases. Hemorrhagic syndrome occurs, the liver often decreases in size (yellow liver atrophy), skin itching disappears (cessation of bile acid synthesis).

Hepatic coma is provoked by:

Bleeding from esophageal varices (anemia, hypoproteinemia).

Absorption of blood breakdown products from the intestines - intoxication increases even more.

Taking medications, especially hepatotoxic ones (barbiturates, morphine group).

Intercurrent infection.

Violation of diet (excess protein - ammonia intoxication).

Heavy surgical interventions.

Alcohol consumption.

80% of patients die in comas.

Treatment of cirrhosis

Elimination, if possible, of the etiological factor.

Diet: table No. 5 - elimination of indigestible fats, a sufficient amount of B vitamins, limiting table salt. reasonable protein restriction. Protein is limited to a level at which there are no signs of encephalopathy due to ammonia intoxication.

Symptomatic therapy

a) If liver failure predominates - glucose, vitamins B, C, etc., sirepar.

b) For portal hypertension and ascites - saluretics in combination with veroshperon, plasma expanders, anabolic hormones, salt-free diet.

c) For signs of cholestasis - phenobarbital, cholestyramine up to 15 mg/day orally, fat-soluble vitamins A and D, calcium gluconate.

d) For intercurrent infections, broad-spectrum antibiotics.

Pathogenetic therapy

Prednisolone 20-30 mg/day, cytostatics; Imuran 50-100 mg/day, poaquenil, delagil.

Indications:

a) acute phase, active phase with signs of increased immunological reactivity

b) primary biliary cirrhosis.

Treatment of liver failure

Diet with protein restriction to 55 g/day.

Daily bowel cleansing with laxatives or enemas.

Suppression of intestinal microflora: drugs are administered orally or through a tube: kanamycin sulfate 0.5x2, ampicillin, tetracycline 1g/day,

To improve liver function: cocarboxylase 100 mg/day, pyridoxine solution 5% 2.0, cyanocobamine solution 0.01% 1.0, ascorbic acid solution 5% 20.0, glucose, potassium preparations.

To restore acid-base balance - sodium bicarbonate 4% w/v.

Panangin 30.0, prednisolone 120-150 mg IV, drip. Morphine and diuretics should not be administered.

For psychomotor agitation: GABA 100 mg/kg of patient’s weight, haloperidol, chloral hydrate in enema 1.0.

To neutralize ammonia: 1-argin 25-75 g/day in a 5% glucose solution; glutamic acid 30-40 mg.

Levodopa 1-3 g/day.

Coenzyme A 240 mg.

A-lipoic acid 65 mg.

CHRONIC GASTRITIS

The most common internal disease. Chronic gastritis is a clinical and anatomical concept.

Morphological changes in the mucous membrane are nonspecific, the inflammatory process is focal or diffuse.

Structural restructuring of the mucosa with impaired regeneration and atrophy.

Nonspecific clinical manifestations.

Disturbances of secretory, motor, and partially endocrine functions.

The incidence of chronic gastritis is increasing every year. At 1.4 ® by the age of 70, anyone can have a polyetiological disease, but the true cause is unknown. 2 groups of so-called etiological factors:

Exogenous.

Long-term violation of the diet and rhythm; prolonged consumption of food of a special quality that irritates the stomach; long-term alcohol consumption; long-term smoking; long-term use of drugs that cause gastritis (sulfonamides, reserpine, potassium chloride); prolonged contact with occupational hazards (dust, vapors of alkalis and acids) is an acute gastrogenic factor. Now he is being questioned.

Endogenous.

Prolonged nervous tension; endocrine (diabetes mellitus, thyrotoxicosis, hypothyroidism); chronic deficiency of vitamin B-12, iron; chronic excess of toxins in chronic renal failure; chronic infections, allergic diseases; hypoxia in heart failure and pulmonary failure.

Usually a combination of endo- and exofactors is important.

Pathogenesis

Common pathogenic mechanisms:

Damage, breakthrough of the protective mucous barrier of the stomach.

The central link is the blockade of regeneration of the glandular epithelium; poorly differentiated cells appear. The reasons for the blockade are not known. As a result, the functional activity of the glands decreases and the rapid rejection of defective cells. New cell formation lags behind rejection. Ultimately, this leads to atrophy of the main and parietal cells.

Restructuring of epithelial glands according to the intestinal type - enteralization.

Immunological disorders - antibodies to parietal cells, intrinsic Castle factor and even to chief cells.

Types of chronic gastritis according to Strickland McKay:

1. Condition of the antral mucosa

Usually normal

Usually gastritis

2. Condition of the fundic mucosa

Usually gastritis

Usually normal

3. Antibodies to parietal cells

4. Blood gastrin level

5. Link to pernicious anemia

Absent

Private mechanisms. Features of gastritis caused by exofactors:

Changes in the gastric mucosa are of a primary inflammatory nature, infiltration, swelling, hyperemia.

The lesion begins in the antrum and spreads throughout the stomach (antral expansion).

Slow progression.

Associated with endogenous factors:

Changes of a non-inflammatory nature occur primarily; the inflammatory component is secondary and weakly expressed.

It starts from the body of the stomach.

Atrophy and achylia develop early.

Features of the antrum (pyloroduodenitis, painful gastritis).

The pathogenesis is close to peptic ulcer disease:

Hyperplasia of the fundic glands.

Increased secretory activity.

Acidotic damage to the mucosa.

Helicobacter pilori is of great importance in the etiology of gastritis. Its features:

Actively breaks down urea, surrounds itself with a cloud of ammonium, thus protecting itself from hydrochloric acid.

Retains viability at pH=2.

High catalase activity and phosphatase activity ® protection against phagocytosis.

We have the classification of S.M. Ryssa. By etiology: exo- and endogenous.

According to morphology:

Surface.

With damage to the glands without atrophy.

Atrophic (moderate, pronounced, with enteralization).

Hypertrophic.

Antral.

Erosive.

Functionally:

With normal secretory function.

With secretory insufficiency.

With increased function.

according to the clinical course:

Remission phase.

Aggravated.

Fading exacerbation.

Special types: rigid, giant hypertrophic - Menetrier's disease. Polypous.

There are no specific clinical symptoms, which leads to overdiagnosis of the disease. May occur without clinical manifestations. The role of gastroscopy and targeted biopsy is great.

There are 7 main syndromes:

Gastric dyspepsia syndrome. When hyper - more often heartburn, sour belching; with hypo - nausea, bitter rotten belching.

Pain syndrome, 3 types:

a) early pain immediately after eating

b) late, hungry after 2 hours; characteristic of antral duodenitis.

c) 2-wave, occur when duodenitis attaches.

Intestinal dyspepsia syndrome, with secretory insufficiency.

Dumping-like - after eating, weakness, dizziness.

Polyhypovitaminosis. Burning of the tongue, teeth marks remain on it. Sticking in the corners of the mouth, peeling skin, hair loss, brittle nails.

Anemic: iron and B12.

Asthenoneurotic. Often happens in women.

An objective examination reveals little; upon palpation there is slight pain in the epigastric region. There may be a deficiency of K+ (visible on the ECG: decreased ST and negative T), calcium deficiency, there may be alkalosis, enzymatic changes, polygranular endocrine insufficiency syndrome (sexual dysfunction, moderate adrenal insufficiency).

Examination:

Clinical blood test.

Feces to Gregersen's reaction.

Histamine test.

X-ray (there are no radiological signs of gastritis) is necessary for differentiation from peptic ulcer disease and cancer.

FGS targeted multiple, stepwise biopsy.

Thermography detects in 100% of cases.

5 groups of complications:

Anemia - occurs with erosive and atrophic.

Bleeding - with erosive.

Pancreatitis, cholecystitis, enterocolitis.

Pre-ulcerative condition and ulcer, especially with piluroduodenitis.

Stomach cancer.

It has been proven: patients with a primary lesion of the antrum and antrocardial expansion (on the border between healthy and diseased cardiac expansion (on the border between healthy and diseased tissue). Family history of cancer - 4 times higher probability of the disease. Absence of immunological reactions, blood group II Rh+. Signs of early cancer include a change in the nature of a pre-existing symptom, the appearance of minor signs syndrome, causeless weakness, rapid satiety with food, and loss of appetite.

As a rule, it is outpatient, without sick leave.

Indications for hospitalization:

Presence of complications.

The need for differential diagnosis, first of all, with stomach cancer.

Treatment depends on secretory activity, the phase of the disease, and in endo-on the underlying disease.

Principles of diet: mechanical, chemical, temperature sparing; meals 4-5 times a day. Eating in a strictly gentle diet is harmful - disabled by the diet. In case of secretory insufficiency, table No. 2 has a sufficient sonic effect. With preserved and increased secretion - table No. 1. With exacerbation - 1-B.

9 main groups of drugs:

For secretory insufficiency: natural gastric juice, 1 tbsp. Spoon while eating. Dilute HCl 10-15 drops in 1/4 glass of water during meals. Acedin-pepsin - 1 tablet. Dissolve in 1/2 glass of water, also during meals.

Enzymatic preparations: pancreatin, festal, panzinorm, cholenzyme, mexaza, etc.

Antispasmodics: anticholinergics (for hypersecretion): platifilin, metacin, atropine, myotropic (halidor, no-shpa, papaverine).

Antacids: for increased secretion, for poloroduodenitis: almagel, Bourget's mixture (its composition: Na bicarbonate 8.0, Na phosphate 4.0, Na sulfate 2.0 - in 0.5 l of water) - drink throughout the day. Vikalin, vikair, almagel 1 and 2.5 hours after meals, 1-2 tablespoons (with 3 meals a day) + 1 spoon before bed, a total of 7 spoons per day.

Bitters are used to improve appetite, often with reduced secretory activity: delicious tea, pomegranate juice, dandelion root (1 teaspoon per glass of boiling water, leave for 20 minutes, cool, strain and 1/4 cup 30 minutes before meals) .

Anti-inflammatory. The best is De-Nol.

Agents that improve regeneration: vitamins, metacil, pentoxyl, sea buckthorn oil, 1 teaspoon 3 times a day, nerabol, retabolil.

Glucocorticoids are used mainly for pernicious anemia.

Antibacterial therapy: metanidazole, amoxicillin, nalidixic acid preparations.

Physiotherapy with great caution: absolutely not at the slightest suspicion of malignancy.

Evolution of chronic gastritis:

Increased atrophy and achylia.

Transformation into peptic ulcer.

Transformation into cancer.

Recovery can also be allowed.

ULCER DISEASE

This is a common chronic relapsing disease, characterized mainly by seasonal exacerbations with the appearance of ulcers in the wall of the stomach or duodenum. But over the past 10 years, seasonality has become blurred - exacerbations began to occur even in the warm season. Based on localization, they are divided into pyloroduodenal and mediogastric.

Etiology

Neuropsychic stress.

Eating disorder.

Biological defects inherited at birth.

The role of hereditary predisposition is undoubted, especially in pyloroduodenal localization.

External contributing factors:

Nutritional. Negative erosive effect on the mucous membrane and food that stimulates active secretion of gastric juice (normally, mucosal injuries heal in 5 days). Hot, spicy, smoked foods, fresh baked goods (pies, pancakes), large amounts of food, cold food, most likely the same irregular diet, dry eating, refined foods, coffee.

Smoking is reliable.

The direct ulcigenic effect of alcohol has not been proven, although it has a powerful sonic effect and does not have an antacid effect.

Libra Neck: defense/aggression. If defense and aggression are equal, then there will be no peptic ulcer. Pathology occurs as soon as any of them is disrupted.

Factors influencing pathogenesis (internal):

Acid-peptic - increased secretion of HCl, increased 6-cells involved in the production of HCl.

Reduced intake of alkaline duodenal-pancreatic juice.

Impaired coordination between the secretion of gastric juice and the secretion of alkaline duodenal contents.

Disturbed composition of the mucous coating of the gastric epithelium (mucoglycoproteins that promote repair of the mucous membrane. This substance is called gastric surfactant, it covers the mucous membrane with a layer and protects it from burns).

Secretion of the ulcirogenic fraction of pepsinogens.

Protective factors:

Adequate capillary blood flow in the submucosal layer.

Production of protective PG by stomach cells.

Stimulation of mucus secretion by the cells of the stomach and duodenum and the production of bicarbonates. It is carried out reflexively (promotes alkalization of the environment).

In 1983, Warren and Marshall isolated a Gram(-) spiral-shaped bacterium from the mucous membrane of Campilobacter pilori; this bacterium should not be considered as a cause; it contributes to the chronicity of the process, reduces the protective properties of the membrane, and has mucinase and urease activity:

Urease - breaks down urea and surrounds itself with a cloud of ammonium, which reproduces the bacterium from the acidic contents of the stomach. Mucinase manifests itself in the fact that it breaks down mucin, while reducing the protective properties of mucus.

Campilobacter has also been found in healthy people. It is often detected with pyloroduodenal ulcers, but not always, which means its presence is not the main factor in the formation of ulcers. The microbe is rarely found in the bottom, walls and body of the stomach; it is more often found between the cells of the gastric mucosa. Secretion of histamine by mast cells of the gastric mucosa. The secretion of histamine by mast cells increases, which disrupts microcirculation ® and creates conditions for ulceration.

More often, the ulcer occurs against the background of type B gastritis and is localized at the junction between the changed and healthy mucous membrane. Peptic ulcer disease is not realized without the participation of other organs and systems, for example, the influence of n. vagus, although its role has recently been exaggerated. Central nervous system - with a pyloroduodenal ulcer, anxiety, egocentrism, increased demands, anxious-phobic, hypochondriacal symptoms.

Classification

By localization: pre-, subcardial, prepyloric section, duodenal bulb. By stages: pre-ulcerative condition (duodenitis, gastritis B) and ulcer.

By phase: exacerbation, subsiding exacerbation, remission.

According to acidity: high, normal, low, with achlorhydria.

By age of disease: juvenile, elderly.

By complications: bleeding, perforation, pervisceritis, stenosis, malignancy, penetration.

Signs of a pre-ulcerative condition with a mediogastric ulcer:

Chronic gastritis, especially over the age of 35-40 years.

Severity and increase in pain syndrome.

Vomiting of sour contents and heartburn, after vomiting the pain subsides.

For duodenum:

Ulcerative hereditary history, these are often young (up to 35-40 years), thin, with vegetative lability.

Severe dyspeptic syndrome, heartburn - sometimes preceded by a year or two. It is provoked by fatty, salty foods, and dry eating. 1-2 hours after eating, pain appears, there may be pain on palpation, and the acidity level in the juice is increased. X-ray for a pre-ulcerative condition: motor-evacuation dysfunction, pylorospasm, there may be deformation that disappears after the administration of atropine. Vr FGS is often erosion, signs of gastritis, dysfunction of the pyloric sphincter (spasm or gaping).

With a stomach ulcer, pain in the epigastrium on the left, with a duodenal ulcer in the epigastrium on the right, sometimes in the right hypochondrium. Irradiation (lesser curvature) - up and to the left, sometimes imitating cardialgia, when localized in the body of the stomach there is usually no irradiation, 12/p in the hypochondrium, back under the scapula (irradiation is more typical for perivisceritis - not a fresh process). The severity of the pain depends on the depth of the ulcer, especially for penetrating ulcers, here the pain is very intense. Callous ulcers are practically painless.

With a stomach ulcer, pain appears after 2-3 minutes and lasts 1.5-2 hours, but this is not absolutely true. Ulcers 12/p are characterized by true hunger pains at night, which subside after eating.

Trigan, spazgan, no-spa, atropine and other antispasmodics, as well as a heating pad, relieve pain: traces of it indicate a peptic ulcer. An additional mammary gland in men is a genetic marker of peptic ulcer disease.

Dyspeptic phenomena:

Heartburn. Equivalent to pain. Immediately or 2-3 hours after eating, most typical for 12/p. Reflux esophagitis.

Belching, more typical of a stomach ulcer, is often air, and rotten - a sign of stenosis.

Nausea - for antral ulcers.

Vomiting - with functional or organic pyloric stenosis, and rarely with uncomplicated ulcers.

Usually appetite is preserved or increased, especially with a ulcer of the 12th intestine, but there is stenophobia - fear of food due to expected pain.

Bowel functions:

Constipation for 3-5 days is typical for the localization of the ulcer in the bulb of the 12th intestine, “sheep” stool, spastic dyskinesia of the large intestine. Changes in the central nervous system - poor sleep, irritability, emotional lability - with an ulcer of the 12th intestine.

When collecting anamnestic data, take into account: the duration of the disease with the appearance of pain and heartburn and all other signs, when a “niche” was discovered - RG or FGS, the frequency and duration of exacerbations, seasonality. What stops it, ask about black stools and other complications. What and how was it treated, heredity, the last exacerbation, what was associated with it, regularity of food intake, visits to canteens, to see if all the teeth are intact. Stressful conditions, shift work, business trips, etc. Smoking, alcoholism. Among the hazards: microwave, vibration, hot shop, military service.

Objectively: thin, asthenic - 12/p. But weight loss is not always typical. If the edge of the tongue is sharp, the papillae are hypertrophied - the secretion of HCl is increased. If the abdomen is retracted and painful - perivisceritis, perigastritis, periduodenitis, penetration. Pronounced red dermographism, wet palms.

Laboratory diagnostic methods

In a clinical blood test, you can find hypochromic anemia, but it can also be the other way around, a slow ESR - bulb 12/p. But erythrocytosis also often occurs.

Feces to Gregersen's reaction. If, warn before the FGS or not do it at all, because dangerous.

Study of the acid-forming function of the stomach. Assessed on an empty stomach and with various modulations of acid-forming function.

Bottomless method (acidotest) tab. Per os - they interact with HCl, change, and are excreted in the urine. Based on the concentration upon release, one can indirectly judge the amount of HCl. The method is very crude, used when it is impossible to use sounding, or for screening the population.

Leporsky method. The volume is assessed on an empty stomach (normally 20-40 ml). The qualitative composition of the fasting portion is assessed: 20-30 mmol/l is the norm for total acidity, up to 15 is free acidity. If free acidity is zero - the presence of lactic acid, a tumor is possible. Then stimulation is carried out: cabbage broth, caffeine, alcohol solution (5%?), meat broth. The volume of breakfast is 200 ml, after 25 minutes the volume of gastric contents (residue) is studied - normally 6080 ml, then every 15 minutes in a separate portion. The volume for the next hour is the hourly voltage. Total acidity 40-60, free acidity 20-40 is normal. Assessment of the type of secretion. When is maximum (excitable or inhibitory type of secretion).

Parenteral stimulation with histamine (there will be a feeling of heat, hypotension. Be careful with hypertension, coronary artery disease, bronchial asthma). The criterion is the HCl flow rate/hour - this is the volume of acid produced per hour. Next, basal secretion is assessed: 1.5-5.5. Histamine 0.1 ml/10 kg body weight is administered. After an hour, the volume should be 8-14 mmol/hour. The maximum secretion is estimated with the maximum dose of histamine (4 times more) - after an hour the volume is 16-24 mmol/hour.

It is better to use pentagastrin instead of histamine.

pH-metry is a change in acidity directly in the stomach using a probe with sensors: pH is measured on an empty stomach in the body and antrum (6-7), normally in the antrum 4-7 after the administration of histamine.

2. Assessment of the proteolytic function of gastric juice. They examine it by immersing the probe inside the stomach, and it contains the substrate. After a day, the probe is removed and the changes are studied.

3. X-ray changes:

“Niche” - accessibility of verification of at least 2 mm.

Convergence.

Ring-shaped inflammatory cushion around the niche.

Cicatricial deformities.

Indirect signs:

Extreme gastric peristalsis.

Retraction along the greater curvature is a “finger” symptom. Local pain on palpation.

X-ray localization of ulcers of the 12th intestine is most often found on the anterior and posterior walls of the bulb.

Preparation according to Gurvich is carried out if there is swelling of the gastric mucosa: 1 g of amidopyrine is dissolved in a glass of water + 300 mg of anesthesin x 3 times a day + 1 ml of 0.1% solution of adregalin 20 drops, dilute and drink. Within 4-5 days. FGS must be done. The absolute indications are decreased secretion and achylia + suspicion of an ulcer. They do a biopsy.

Contraindications: IHD, esophageal varices, esophageal diverticula, bronchial asthma, recent bleeding.

Features of peptic ulcer disease in old people: if the ulcer forms after 40-50 years, it is necessary to exclude atherosclerosis of the mesenteric vessels. The course is erased, there is no pain, no dyspeptic disorders. It is often combined with abdominal angina, which manifests itself during hard work: patients have atherosclerosis of the mesenteric vessels and aorta.

Complications

Periduodenitis, perigastritis, pervisceritis - a change in the nature of pain, the rhythm of pain disappears, becomes constant, intense, especially during physical work, and after eating can radiate to different places.

In 10-15% there is bleeding. Vomiting occurs with or without blood. Tarry stools (melena) are often accompanied by hemodynamic disorders, changes in the content of hemoglobin and red blood cells, and acute anemia is formed. Do FSH carefully.

Penetration 6-10% - acute girdling pain appears, especially when penetrating into the pancreas.

Perforation - stabbing pain, vomiting, etc. Peritonitis develops. Perforation can be subacute if the omentum covers the perforation. RG - subdiaphragmatic gas accumulation.

Degeneration of an ulcer into cancer. Elderly and senile people are prone to this. The pain becomes constant, loss of appetite, nausea, aversion to meat, weight loss, decreased gastric secretion up to achlorhydria, persistent positive Gregersen reaction, increased ESR and anepization.

Cicatricial pyloric stenosis:

stage - episodic vomiting due to food retention, once every 2-3 days.

stage - a constant feeling of heaviness, daily vomiting, the masses contain food eaten the day before.

stage - pronounced stenosis, water passes with difficulty, gastric peristalsis and splashing noise are visible. Vomiting is artificially induced, vomit with a putrid odor.

1 The patient should eat like a normal person; 3-4 times a day - 7 doses of antacids per day (2 x 3 + 1 at night). Amount of antacids according to tolerance (aluminum - constipation, magnesium - diarrhea). Almagel, phospholugel.

2 Drugs that reduce HCl production: primarily H2 histamine blockers: reduce basal secretion by 80-90%, reduce stimulated acidity by 50%, do not affect gastrointestinal motility, reduce gastric juice production.

Preparations:

Cimetidine 800-1000 mg per day (1 tablet 200 mg). Take 3 times after meals + 1 at night for 6 weeks, then perform FSH; if remission - reduce the dose by 200 mg every week, or a week to 400 mg at night, they need to be continued for another 2 weeks, then 2 weeks, 1 tablet at night and cancel. You can generally use 200-400 at night for years to prevent exacerbations.

Another method: 800-1000 mg once at night, cancel as with the previous method.

Ranitidine (ranisan, zantac) 2 tablets. (150 mg each) for 2 doses, after 4-6 weeks reduce to 1 tablet at night (per week), and so on for 2 weeks and cancel.

Another option: 300 mg at night. There have not yet been cases where the ulcer did not heal, but 10-15% of patients are resistant to H2 histamine blockers. We must remember this! Resistance, if after a week the pain syndrome does not disappear, but there is only a decrease in its intensity, then the drug still works.

Famotidine(gastrosedin, ultrafamide) 80 mg or 40 mg - daily dose.

Nizatidine(axid) we don’t have it yet.

1000 mg cimetidine + 300 mg ranitidine + 80 mg famotidine. Since these drugs can cause withdrawal symptoms, they should not be stopped abruptly; at the onset of the disease, make sure that the patient has enough of them for the course of treatment.

Side effects:

Withdrawal syndrome.

Colonization of the stomach with nitrozonephritis flora, which produces carcinogens.

Only cimetidine is characterized by: dizziness, weakness, can cause mental changes - never prescribe to patients with schizophrenia!

Cimetidine also has an antiandrogenic effect - a man becomes sterile during use.

If the size of the ulcer is up to 5 mm, then it can be treated on an outpatient basis, and with erosion, too.

Proton pump blockers: Omeprazole(spoons). 20 mg 1 time per day in capsule. Very fast and reliable action. Ulcer scarring is 100%. Has no side effects.

Increased protection factors: De-Nol(tribimol). In the presence of even small amounts of HCl, it forms a protective film over an erosion or ulcer. Destroys Campilobacter pilori (bactericidal + bacteriostatic effect). It is almost not absorbed and acts in the lumen of the gastrointestinal tract. 120 mg (1 tablet > 4 times a day 40-60 minutes before meals). The chair is painted black. Can be used for monotherapy or with H 2 histamine blockers, but the formation of insoluble compounds is possible; to avoid this, use at intervals of 1.5-2 hours.

Sucralfate(Venter, Corafate) contains aluminum, forms an aluminum-protein complex, fills the ulcer + has antacid properties. 4 g per day for 40-60 minutes. Before meals + at night. Effect on mediogastric ulcers. The effectiveness may be slightly lower than that of De-Nol, perhaps depending on the specific forms. Gastrozepine.

Solcoseryl- This is a non-specific drug. Stimulates metabolic processes in all tissues; there is no convincing data on the effect on ulcers.

DISEASES OF THE URINARY TRACT

ACUTE GLOMERULONEPHRITIS

This is a disease of infectious-allergic nature with primary damage to the capillaries of both kidneys. Distributed everywhere. They are most often affected at the age of 12-40 years, somewhat more often in men. It occurs more often in countries with cold and humid climates and is a seasonal disease.

Etiology

The causative agent is group A beta-hemolytic streptococcus, nephritogenic strains 1, 3, 4, 12, 49. Evidence of streptococcal etiology is:

connection with streptococcal infection (tonsillitis, odontogenic infection, sinusitis, sinusitis, etc.), as well as skin diseases - erysipelas, streptoderma;

A). Hemolytic streptococcus is often cultured from the throat;

b). Streptococcal antigens are detected in the blood of patients with acute glomerulonephritis: streptolysin 0, streptokinase, hyaluronidase;

V). then the content of antistreptococcal antibodies in the blood increases;

G). experimental nephritis is possible.

Pathogenesis

Various immunological disorders play a role in pathogenesis.

Formation of conventional antibodies. The antigen-antibody complex can settle on the renal membrane, since it has rich vascularization, predominantly large deposits settle. The antigen-antibody reaction takes place on the renal membrane itself, while complement and biological active substances are present: histamine, hyaluronidase, and the capillaries of the whole body may also suffer.

With streptococcal infection, streptococcal antigen can damage the endothelium of the renal capillaries, the basement membrane, and the epithelium of the renal tubules - autoantibodies are formed, and an antigen-antibody reaction occurs. Moreover, damaged cells act as antigens.

The basement membrane of the kidneys and streptococcus have common antigenic structures, so normal antibodies in streptococcus can damage the basement membrane at the same time - a cross-reaction.

Proof that the pathogenesis is based on immune processes is that between streptococcal infection and the onset of acute nephritis there is always a time interval during which the accumulation of antigens and antibodies occurs and which is 2-3 weeks.

Morphology

It is determined by lifelong biopsy followed by electron microscopy and immunofluorescence: deposition of immune complexes in the form of humps is found.

A). Intracapillary glomerulonephritis - changes affect the endothelium, its proliferation occurs, the basement membrane thickens, and its permeability increases.

b). Extracapillary glomerulonephritis - changes affect not only the vessels, but also the visceral layer of Bowman's capsule proliferates, as a result of which the glomerulus dies. This is a severe form of damage.

The disease begins with a headache, general malaise, sometimes nausea, and lack of appetite. There may be oliguria and even anuria, manifested by rapid weight gain. Very often, against this background, shortness of breath and attacks of suffocation appear. In the elderly, manifestations of left ventricular heart failure are possible. In the very first days, swelling appears, usually on the face, but can also be on the legs, and in severe cases on the lower back. Hydrothorax and ascites are extremely rare. In the very first days of the disease, blood pressure reaches 180/120 mm Hg.

Syndromes and their pathogenesis

Urinary syndrome - according to urine analysis:

A). Hematuria: changed + unchanged red blood cells, 20% have gross hematuria, urine the color of meat slop.

b). Proteinuria, rarely high, often moderate up to 1%. High proteinuria indicates significant membrane damage.

V). Moderate leukocyturia (with pyelonephritis, leukocyturia is the leading syndrome).

G). Cylindruria - hyaline casts (casts of protein), in severe cases blood casts made of red blood cells.

d). Specific gravity, creatinine are normal, azotemia is absent.

Edema, its causes:

A). a sharp decrease in renal filtration - Na and H20 retention.

b). secondary hyperaldosteronism;

V). increased permeability of capillaries of all vessels as a result of an increase in the content of histamine and hyaluronidase in the blood;

G). redistribution of fluid with predominant retention in loose fiber.

Hypertension, its causes:

a) increased cardiac output as a result of overhydration (hypervolemia);

b). increased renin production due to renal ischemia;

V). sodium retention in the vascular wall - its swelling and increased sensitivity to catecholamines;

G). reduction in the release of depressor humoral factors (prostaglandins and kinins).

Hypertension can last 3-4 months. Based on the nature of the clinic, there are reservoir and monosymptotic ones.

Laboratory diagnostics

Urinary syndrome.

Rehberg's test - a sharp decrease in filtration.

The blood side is normal.

There may be an acceleration of ESR.

The ECG shows signs of left ventricular hypertrophy approximately 2 weeks after the onset of the disease.

X-ray of increased heart size.

Complications

They can develop from the first days of the disease and are the main cause of mortality in acute glomerulonephritis.

Acute left ventricular failure: more often in old age, especially in previous cardiovascular pathology. Its causes: sudden volume overload of the ventricles, sudden rapid increase in blood pressure (the heart is not ready); damage to the myocardium itself (dystrophy, toxic damage). Manifested by shortness of breath, cough, congestive wheezing, cardiac asthma, pulmonary edema.

Renal eclampsia: caused by a sharp increase in intracranial pressure against the background of hypertension. Swelling of the brain and optic nerve occurs. Clinical manifestations: severe headache, deterioration of vision up to complete blindness (swelling of the nerve nipple, retinal detachment, sometimes hemorrhage into it); speech impairment, clonic convulsions, then tonic. Epileptiform seizures are typical (tongue biting, dilated pupils, unconsciousness for several hours).

Uremia occurs against the background of complete anuria for > 3 days. Rarely seen.

Acute and chronic renal failure: nausea due to oliguria, vomiting, itching; increase in biochemical parameters.

Differential diagnosis

Toxic kidney: signs of intoxication, toxemia, presence of infection.

Acute pyelonephritis: history of abortion, hypothermia, diabetes mellitus, childbirth. Higher temperature: 30-40o C. often chills, initially there is no increase in blood pressure. No swelling. Severe leukocyturia. Severe pain in the lumbar region on one side (with glomerulonephritis, 2-sided damage).

Hemorrhagic vasculitis (renal form): the leading symptom is hematuria; there are skin manifestations.

Exacerbation of chronic glomerulonephritis. The course of the disease depends on:

A). severity of the process;

b). timing of diagnosis and length of hospitalization: up to 10 days - 80% recovery, after 20 days - 40% recovery;

V). age: after 50 years the prognosis is more severe;

G). correctness of treatment.

Criteria for cure.

Complete cure.

Recovery from a defect.

Recovery can take up to 2-3 years, sometimes becoming chronic. In this case, a kidney biopsy is indicated. Persistent proteinuria is an indicator of chronicity (30%).

Aimed at the etiological factor and at preventing complications.

Bed rest: improves renal blood flow, increases renal filtration, reduces blood pressure. When standing up, hematuria and proteinuria increase. Bed rest for at least 4 weeks.

Diet: in severely developed form - a regime of hunger and thirst (only rinse the mouth, small children can be given a little sweet water). After the proposal of such a diet, acute left ventricular failure and renal eclampsia almost did not occur. They keep this diet for 1-2 days, then give 100-150 g of sugar with water, fruit juices, semolina porridge; Mineral waters and vegetable juices are not allowed due to hyperkalemia, table salt is sharply limited. Protein up to 0.5 g/kg body weight, after a week up to 1.0 g/kg. Only boiled fruits, only raw juices.

Antibiotics: penicillin 6 times a day, all nephrotoxic antibiotics are contraindicated.

Anti-inflammatory drugs: indomethacyl (metindole) 0.025 * 3 - helps improve the reabsorption of protein in the tubules; proteinuria decreases.

Desensitizing agents: tavegil 0.001 * 2; suprastin 0.25 * 3; pipolfen; diphenhydramine 0.03 * 3; calcium gluconate 0.5 * 3.

For oliguria: furosemide 40 mg; lasix 1% 2.0 IV (in the first days of illness), glucose 40% 10.0 IV with insulin mannitol.

For eclampsia: bloodletting; aminazine 2.5% 2.0 IM; magnesia 25% 20.0 IM (dehydration and sedative); reserpine 0.1 mg * 2-3 times; dextran 10% 100.0.

For heart failure: bloodletting; lasix; drugs.

CHRONIC GLOMERULONEPHRITIS

This is a bilateral inflammatory disease of the kidneys of immune origin, which is characterized by gradual but steady death of the glomeruli, shrinkage of the kidney, gradual decrease in function, development of arterial hypertension and death from chronic renal failure.

The frequency is about 4 per 1000 autopsies. The incidence of men and women is the same. It is found in all countries of the world, but more often in cold ones.

Etiology

It is not completely clear, some have a history of acute glomerulonephritis, other cases are not clear. Sometimes the provoking factor can be repeated vaccination, drug therapy - for example, antiepileptic drugs.

Pathogenesis

It is based on an immunological mechanism. Morphologically, deposits of immune complexes consisting of immunoglobulin and complement are found in the area of ​​the basement membrane. The nature of immune deposits can be different: if there are a lot of them, coarse deposits, severe damage. Sometimes the protein composition of the membrane itself may change.

Classification

Clinical:

A). Latent form - nephritis with isolated urinary tract.

b). Chronic glomerulonephritis with a nephrotic component (nephrosonephritis). The main manifestation is nephrotic sm.

V). The hypertensive form occurs with an increase in blood pressure and progresses slowly.

G). Mixed form.

Histological (arose with the advent of intravital biopsy followed by electron microscopy.

A). Chronic glomerulonephritis with minimal lesions. At el. microscopy reveals changes in the basement membrane, mainly in podocytes - cells of the visceral layer of the Shumlyansky-Bowman capsule. The outgrowths of podocytes merge, representing a single system with immune deposits. Clinic: often in children (65-80%). Previously it was called lipoid nephrosis, but this is incorrect, since nephrosis is a lesion of the renal tubules, and here the glomeruli are affected. Corresponds to chronic glomerulonephritis with nephrotic syndrome: severe proteinuria (high selectivity) can be up to 33%; hypoproteinemia (hypoalbuminemia); edema due to a decrease in plasma ocotic pressure (hypoxia), due to edematous fluid, the amount of blood proteins decreases even more - hypovolemia, secondary hyperaldosteronism, increased edema; hypercholesterolemia, as well as an increase in triglycerides (up to 3-5 thousand mg). Previously, it was believed that hypercholesterolemia compensatory increases oncotic pressure. It has now been established that oncotic pressure increases slightly due to lipids. The reason for hypercholesterolemia is a decrease in the lipolytic activity of the liver. In general, this is a benign form. It almost never leads to death, but infection, hypertension, and hematuria may result in a shriveled kidney.

b). Membranous variant of nephritis: the basement membrane is affected more deeply. With conventional microscopy, there is thickening, membrane ruptures, and large deposits of immunoglobulins and complement. The clinical picture is most often based on the type of nephrosonephritis. The course is more malignant. Slight hematuria, gradual increase, outcome in a secondary shriveled kidney.

V). Fibroplastic variant: processes on the basement membrane occur quickly, the mesangium is activated, the membrane continues to grow, the growth of the glomeruli occurs more slowly. Clinic: hypertension, urinary syndrome is mild, sometimes there are only periodic changes in the urine, there is no edema at the beginning; then real glomerulonephritis appears with edema and hypertension. This form is favorable in terms of the duration of the disease, but almost always results in a secondary wrinkled kidney and chronic renal failure.

G). Proliferative variant: there is a massive proliferation of mainly the vascular endothelium (endocapillary type), less often proliferation is of the extracapillary type - from the side of Bowman’s capsule. More often it is a mixed form, the clinical manifestation is arterial hypertension.

d). Membranous-proliferative: b) + d). The hypertensive form of chronic glomerulonephritis with the clinic of the classical form of hypertension is specially distinguished, but there are changes in the urine. The degree of change in the fundus may be greater than in HD.

Differential diagnosis

Acute glomerulonephritis: anamnesis is important, the time from the onset of the disease, the specific gravity is high throughout the disease, and with chronic glomerulonephritis there may be a decrease in the specific gravity of urine. Left ventricular hypertrophy may be pronounced. Hypertension. Histological examination is of decisive importance - the presence of hyperplastic processes.

A malignant form of hypertension: now extremely rare. Persistent high blood pressure 260/130-140 or more. Significant changes in the fundus. Then, urinary syndrome may also occur.

Chronic pyelonephritis: a history of often gynecological diseases, abortions, cystitis. There is a tendency to low-grade fever. Pyuria. Bacteriouria, early decrease in urine specific gravity. The presence of radiological signs of pyelonephritis (the calyces become sclerotic early and change their shape).

Polycystic kidney disease: appears at 30-40 years of age. The presence of enlarged kidneys on both sides. X-ray - the presence of an uneven scalloped edge of the kidneys, a cyst. Hypertension, azotemia. Early causes chronic renal failure.

Renal amyloidosis: usually a picture of nephrotic syndrome. Occurs against the background of long-term chronic inflammation. Often combined with amyloidosis of the liver and spleen, there may be intestinal amyloidosis (diarrhea, exhaustion, weight loss). There may also be primary amyloidosis - there is no history of suppurative diseases. May occur in very old people; the tongue becomes very large (does not fit in the mouth), enlargement of the heart. Diagnostics is helped by a test with Congo-r. Biopsy of the oral mucosa or, preferably, the rectum with a test for amyloid (with iodine).

Diabetic glomerulosclerosis: occurs when diabetes is unrecognized or severe and poorly treated. Hyalinosis of the renal vessels and death of the renal glomeruli occurs.

Clinic: only neurotic syndrome, and only in the later stages are hypertension and renal failure added.

Multiple myeloma with myeloma kidney: nephrotic syndrome is often associated with kidney damage. Diagnostics is helped by a picture of the blood and bone marrow, an increase in protein fractions of the blood, and the appearance of paraproteins in the blood - Ben-Jones protein.

For glomerulonephritis with minimal changes - good. Recovery may be defective - small but progressive proteinuria. Most often the course is progressive and results in chronic renal failure.

Complications

1. In the hypertensive form - cerebral hemorrhage, retinal detachment.

2. With nephrosclerosis - the addition of various infections.

3. Chronic renal failure.

1. In case of exacerbation of streptococcal infection - penicillin.

2. For hypertension - antihypertensives, saluretics - furosemide, lasix. Doses should be moderate, because due to kidney damage there may be cumulation. Veroshpiron.

3. Impact on autoimmune processes: corticosteroids and cytostatics are advisable only for glomerulonephritis with minimal lesions - this is an absolute and justified indication, the effect is 80-100%: prednisolone 40-60 mg/day. 3 weeks. If the treatment is effective, then a positive effect will appear at week 4; if there is a positive effect, they switch to maintenance doses of 5-10 mg/day. during a year. It is better to carry out therapy in courses, as side effects are reduced: a/4+3 (4 days prednisolone, 3 days rest) 6/7+7, you can combine hormones with cytostatics - imuran 100 mg. cyclophosphamide 150-200 mg/day. In fibroplastic forms, cytostatics are futile.

4. To reduce proteinuria: indomethacin 0.025.

5. Anabolic agents: retabolil (increases protein synthesis).

6. Anticoagulants: heparin - improves microcirculation in capillaries, anti-complementary effect, but can increase hematuria.

7. Vitamins in large doses, especially vitamin C.

8. Glucose 40% IV solution.

9. Diet therapy: water-salt regimen (since the amount of water and salt decreases with edema): for hypertension, heart failure - water restriction: in the absence of azotea, the amount of protein is 1 g/kg of weight: for nephrotic syndrome, food protein in adults is raised to 2 g/kg per day. Protein loss is determined in the daily amount of urine - proteinuria over 5 g/day is considered massive.

10. Normal mode. Bed rest - in the most severe cases.

11. Spa therapy.

12. Physiotherapy: diathermy, heat.

13. Sanitation of foci of chronic infection.

CHRONIC PYELONEPHRITIS

Nonspecific infectious and inflammatory disease of the mucous membrane of the urinary tract: pelvis, calyces and interstitial tissue of the kidneys. Essentially interstitial bacterial nephritis, 60% of all kidney diseases.

Etiology

Always infectious. Pathogens in descending order of frequency: Escherichia coli, Proteus vulgaris, staphylococcus, streptococcus, enterococcus, microbial associations, mycoplasmas and viruses, L - forms of bacteria. But in 30% of cases the pathogen is not cultured - this does not exclude an infectious process.

Pathogenesis

1. Hematogenous from the source of infection

2. Urinogenic in vesicoureteral reflux, - ascending route.

Required components:

1. Presence of infection.

2. Violation of urodynamics, increased intrapelvic pressure.

3. Initial damage to the kidneys and urinary tract.

Predisposing factors:

1. Gender - more often in women, 2-3 times, 70% of women get sick before the age of 40, and men - after. Women have 3 critical periods:

a) childhood: girls during this period get sick 6 times more often than boys:

b) beginning of sexual activity:

c) pregnancy.

2. Hormonal imbalance: glucocorticoids and hormonal contraceptives.

3. Diabetes mellitus, gout.

4. Anomalies of the kidneys and urinary tract.

5. Drug-induced injuries such as abacterial interstitial nephritis (sulfonamides, anti-tuberculosis drugs, vitamin D in large doses, phenacetin, analgesics, nephrotoxic antibiotics.

There is no single classification. Highlight:

I a) Primary - without previous disorders of the kidneys and urinary tract.

I b) Secondary - based on organic or functional disorders (obstructive), preceded by urological diseases. Primary 20%, secondary 80%.

II. Single and double sided.

III. Along the route of infection spread: hematogenous, often primary, and urinogenic, often secondary.

IV. According to the course: rapidly progressing, recurrent and latent.

V. According to clinical forms:

V.1. Latent.

V.2. Recurrent.

V.3. Hypertensive.

V.4. Anemic.

V.5. Hematuric (associated with venous hypertension and disruption of the integrity of the vessels of the fornix).

V.6. Tubular with loss of Na+ and K+.

V.7. Azotemic. Clinic

May leak under masks.

1. Latent form - 20% of patients. Most often there are no complaints, and if there are, then - weakness, increased fatigue, and less often low-grade fever. Women may experience toxicosis during pregnancy. A functional study reveals nothing, except for a rare unmotivated increase in blood pressure and mild pain when tapping the lower back. Laboratory diagnosis. Repeated tests are of decisive importance: leukocyturia, moderate, no more than 1 - 3 g/l proteinuria + Nechiporenko test. Stengheimer-Malbin cells are doubtful, but if there are more than 40% of them, then it is characteristic of pyelonephritis. Active leukocytes are rarely detected. True bacteriuria *****> 10 5 bacteria in 1 ml.

To prove it, 30 g of prednisolone IV and evaluate the indicators (increase in leukocytes by 2 or more times, active leukocytes may appear).

2. Recurrent almost 80%. Alternation of exacerbations and remissions. Features: intoxication syndrome with fever, chills, which can occur even at normal temperature, leukocytosis in a clinical blood test, increased ESR, shift to the left, C-reactive protein. Pain in the lumbar region, usually 2-sided, in some like renal colic: the pain is asymmetrical! Dysuric and hematuric syndromes. Hematuria syndrome now occurs more often, there may be micro- and macrohematuria. Increased blood pressure. The most unfavorable combination of syndromes: hematuria + hypertension - > after 2-4 years, chronic renal failure.

3. Hypertensive form: the leading syndrome is an increase in blood pressure, which may be the first and only one, the urinary syndrome is not pronounced and is not constant. It is dangerous to do a provocation, as there may be an increase in blood pressure.

4. Rarely anemic. Persistent hypochromic anemia may be the only sign. Associated with a violation of erythropoietin production, urinary syndrome is not expressed and is not constant.

5. Hematuric: recurrence of macrohematuria.

6. Tubular: uncontrolled urinary losses of Na + and K + (salt - losing kidney). Acidosis. Hypovolemia, hypotension, decreased glomerular filtration, may be acute renal failure.

7. Azotemic: appears for the first time already. honor disadvantage

Establishing diagnosis

1. X-ray examination is crucial. Excretory urography (retrograde is not used in therapy). Asymmetry is functional and structural. Assess: size, contours, deformation of the cups, tone disturbance, detection of pyelorenal reflux, shadows of stones. Normal sizes: for men: right 12.9 * 6.2 cm, left 13.2 * 6.3 cm, for women: right 12.3 * 5.7 cm: left 12.6 * 5.9 cm Evaluation rules: If the left one is 0.5 cm smaller than the right one, this is almost pathognomonic for its wrinkling; if the difference in the length of the kidneys is 1.5 cm or more, this is a wrinkling of the right kidney. With the help of intravenous urography, the following is detected: In the initial stage, a slowdown in the removal of contrast, deformation of the cups and pelvis, spreading of the cups due to edema and infiltration, then their bringing together due to wrinkling.

2. Radioisotope methods. Asymmetry and degree of functional damage are identified. Statistical and dynamic scintigraphy is used.

3. Ultrasound diagnostics.

4. Computed tomography.

5. Renal angiography - a picture of “burnt wood” due to obliteration of small vessels.

6. Kidney biopsy. Indications: suspicion of mixed forms of glomerulus and pyelonephritis and clarification of the nature of the increase in blood pressure; a negative result does not exclude pyelonephritis, since it is focal in nature + biopsy: focal interstitial sclerosis and infiltration of lymphoid-histiocytic elements and neutrophils.

Mode depending on phase. During an exacerbation, stay in bed for 1 - 2 weeks, or at home. Focus on lowering the temperature. Expanding the mode only when the temperature normalizes. Outside of an exacerbation, physical activity is not significantly limited. For intercurrent infections, bed rest. Nutrition: acute phase - limiting spicy foods, canned food, alcoholic beverages and coffee. Salt is limited to 5 - 8 g/day. for 2 - 3 weeks, for hypertension up to 2 - 4 g (with the exception of salt - a losing kidney in the tubular form). Drinking regime is not limited, 2 - 3 l/day. definitely, cranberry juice is especially useful due to its bacteriostatic effect. Remission: 10 - 12 g/day, with an increase in blood pressure 6 - 8 g. For renal failure, special nutrition.

Drug treatment. During an exacerbation, active antibacterial therapy: antibiotics, sulfonamides, nitrofurans, nalidixic acid preparations, PALIN, combination drugs.

In the first two weeks, antibiotics + sulfonamides or antibiotics + nalidixic acid. Requirements for antibiotics:

1) effectiveness against most pathogens of pyelonephritis:

2) absence of nephrotoxicity: chloramphenicol, ceparin, tetracycline, gentamicin. Of the sulfonamides - long-acting, due to reabsorption: sulfopyridazine and sulfadimethoxine.

Nitrofurans for E. coli and Gr (+), Gr (-): furadonin, furagin, solafur intravenously. They are recommended to be combined with cranberry extract. Nalidixic acid should not be combined with nitrofurans.

Palin acts on Gr(+) and Gr(-). It has a peculiarity: it causes a photosensitizing effect -> do not sunbathe.

Combined drugs: 5-NOK (5 - nitroxyquinoline) - consists of nitrofuran and hydroxyquinoline. Biseptol.

In the remission phase, 2 approaches:

1. Constant, continuous treatment for up to a year or longer, all drugs in minimal doses, with a gradual change of medications.

2. Intermittent treatment: in spring and autumn + during exacerbation.

Ryabov's regimen during remission: First week: 1 - 2 tablets. biseptol at night. Second week: uroseptic of plant origin: birch buds, lingonberry leaf, chamomile. Third week: 5-NOK 2 tablets. for the night. Fourth week: chloramphenicol 1 tablet. for the night.

After this, the same sequence, but change the drugs to similar ones from the same group.

For anemia + iron supplements, vitamin B12, erythropoietin. For nephrolithiasis CISTINAL. For unilateral lithiasis, remove it. For high blood pressure, use conventional antihypertensive drugs. with the exception of ganglion blockers. It is theoretically believed that 35% of patients can be cured this way.

CHRONIC RENAL FAILURE

CRF is a pathological condition of the body characterized by constant progressive impairment of kidney function.

Etiology

1) Chronic glomerulonephritis.

2) Chronic pyelonephritis (it is believed that the main reason).

3) Polycystic kidney disease.

4) Malignant hypertension with outcome in nephrosclerosis.

5) Kidney amyloidosis.

6) Various urological pathologies (urolithiasis, etc.).

7) Diabetic glomerulosclerosis.

8) Adenoma and prostate cancer (consequence of urostasis). Chronic renal failure is a common cause of disability and death in young people.

Pathogenesis

1. Accumulation of nitrogenous wastes:

a) urea > 40 mg% (8 mmol/l), but blood nitrogen can be both endogenous and exogenous - from food, therefore it is better to determine kidney function by creatinine.

b) creatinine 1.0-1.2 mg% - excreted by filtration, not reabsorbed, therefore filtration is judged by the level of creatinine.

c) uric acid (but it can increase with gout).

2. Violation of water and electrolyte balance:

a) excess sodium - reduction -> hyponatremia:

b) excess potassium - cut -> hypokalemia (but in the terminal stage of chronic renal failure with severe oliguria there may also be hyperkalemia). The norm is 3.6 - 5.0 mmol/l.

c) changes in the excretion of calcium and phosphorus: calcium is washed out of the bones - osteoporosis, osteomalacia; hyperphosphatemia; the blood Ca/P ratio changes - there may be a picture of secondary parathyroidism.

d) magnesium retention;

e) water metabolism changes: first, dehydration due to polyuria, then hyperhydration - edema, left ventricular heart failure.

3. Changes in acid-base balance: acidosis: in the terminal stage, vomiting, diarrhea - loss of sodium and chlorides -> hypochloremic alkalosis occurs.

The clinical picture for chronic renal failure develops gradually and is often assessed retrospectively. In the initial stages it is scanty. From the nervous system: weakness, increased fatigue, loss of interest in the environment, memory loss, drowsiness during the day, insomnia in the evening, decreased appetite, sometimes persistent vomiting, headaches, sometimes itchy skin. From the cardiovascular system: hypertension up to 200 - 140/130 - 140 mm Hg. Art.

Objectively

1) The skin is pale, yellowish in color (due to the accumulation of urochrome in it). Puffiness of the face. Scratching, especially on the legs, due to itchy skin.

2) From the cardiovascular system: hypertension, intense pulse, dull first tone, emphasis of the second tone on the aorta, with prolonged hypertension, increased apical impulse; There are often vascular murmurs, their causes: hypertension, myocardial dystrophy - in this case, a gallop rhythm and an increase in the size of the heart are possible. In the terminal stage, the pericardial friction rub due to fibrous pericarditis (deposition of nitrogenous wastes on the pericardium) is the death sound of the uremic or the death sound of Breitig.

ECG: sometimes they find a prolongation of the PQ interval, but more often arrhythmias, a tendency to bradycardia, but sometimes tachycardia. The ECG is used to judge the level of potassium in the blood: low T for hypokalemia, high for hyperkalemia (in the terminal stage of chronic renal failure). Heart failure often accompanies CNP and significantly worsens the prognosis.

3) From the respiratory system: cough (uremic pneumonitis), asthma attacks, up to cardiac asthma, pulmonary edema (and the cause of pulmonary edema is not left ventricular failure, but a violation of water metabolism - hyperhydration of the lungs - uremic pulmonary edema. Hyperhydration is treated with forced diarrhea). The x-ray picture of the lungs is characteristic - in the form of a butterfly. Tendency to infection (bronchitis, pneumonia).

4) From the gastrointestinal tract: coated tongue, anorexia, there may be weight loss, the formation and release of ammonia - an unpleasant taste in the mouth, ammonia is released through the upper respiratory tract --> increased aversion to food. Diarrhea. In the terminal stage, ulceration occurs.

5) From the nervous system: in severe cases, an increase in apathy - “silent uremia”. Uremic poisons (ammonia, indole, skatole) have a toxic effect on the brain -> headaches, twitching of individual muscle groups. Eclampsia (associated with increased intracranial pressure - “noisy uremia”).

6) From the urinary system: renal filtration decreases, urinary sediment is scanty, few red blood cells 2-10 in the field of view, hypoisosthenuria, maybe polyuria, in the terminal stage - oliguria. Creatinine clearance can be up to 5 ml/min. Residual urea nitrogen increases. Increased uric acid.

7) From the musculoskeletal system: x-ray osteoporosis (associated with loss of calcium), osteomalacia, secondary hyperparathyroidism.

Laboratory data

Blood test: anemia, sometimes very severe and persistent, more often in the terminal stage, normal or hypochromic. Causes of anemia: toxic impact of nitrogenous waste on the bone marrow, decreased production of erythropoietin, increased bleeding. There may be neutrophilic leukocytosis. Sharply accelerated ESR to 50-60 mm/hour. Changes in coagulogram towards hypocoagulation.

In the terminal stage, vomiting, diarrhea occurs, loss of sodium and chlorides occurs - hypochloremic alkalosis occurs. Violation of the production of a number of hormonally active substances: a decrease in erythropoietin (with chronic renal failure there can be very persistent anemia), in 80% of patients there is hyperreninemia - an increase in blood pressure. Uroninase (fibrinolysin) normally ensures normal microcirculation, preventing intravascular blood coagulation. In chronic renal failure, various thrombohemorrhagic complications are often observed due to impaired urokinase.

Dysfunction of various organs and systems: cardiovascular, respiratory, nervous, skin - impaired production of vitamin D3.

Morphology

The size of the kidney is reduced due to the death of nephrons. Compensatory mechanisms are great: at 50% of nephron death, chronic renal failure does not yet develop. The glomeruli become empty, the tubules die, and fibroplastic processes occur: hyalinosis, sclerosis of the remaining glomeruli.

Regarding the preserved glomeruli, there are 2 points of view:

1) They take over the function of those nephrons that died (1:4) - the cells increase in size, the diameter of the capillaries increases - these are compensatory processes.

2) The theory of intact nephrons: some nephrons are not damaged and normal nephrons take over the function of the remaining ones. At the same time, there are no compensatory hypertrophies.

Classification

1. By creatinine level:

1st degree: 2.1 - 5.0 mg% (0.19 - 0.44 mmol/l).

2nd degree: 5.1 - 10.0 mg% (0.45 - 0.88 mmol/l).

3rd degree: 10.1 - 15.0 mg% (0.89 - 1.33 mmol/l).

Grade 4: more than 15.0 mg% (more than 1.33 mmol/l).

2. Clinical classification (S.I. Ryabov)

1st degree - pre-azotemic, no clinical manifestations:

“A” - no disturbances in filtration and reabsorption (Rehberg test):

“B” - latent, there are disturbances in filtration and concentration.

2nd degree - azotemic:

“A” - latent, azotemia is present, but there is no clinical manifestation (0.19-0.44);

“B” - initial clinical manifestations (0.45-0.71).

3rd degree - uremic:

“A” - moderate clinical manifestations (0.72-1.24);

“B” - pronounced clinical manifestations. Uremia, filtration less than 55 from normal, creatinine > 1.25 mmol/l.

Differential diagnosis

It is necessary to differentiate from renal failure caused by loss of chlorides. Hypochloremic alkalosis develops. Azotemia is caused by the breakdown of tissue proteins. There are no pathological changes in the urine. Oliguria, anuria. Treatment: IV fluid infusion with the addition of chlorides. In chronic pyelonephritis, chronic renal failure develops more benignly and more slowly, since hypertension occurs relatively late. Chronic renal failure is very severe in malignant hypertension; the heart and blood vessels are involved early.

Treatment of chronic renal failure is pathogenetic, but not etiological. Drug doses should be approximately halved, especially for drugs excreted by the kidneys. Avoid nephrotoxic drugs. Antibiotics not allowed - kanamycin, monomycin, barbiturates, drugs of the morphine group, opium, salicylates, oral antidiabetic agents.

1. To correct acidosis: sodium bicarbonate 3 - 5% 100.0 IV, calcium carbonate 1.0 - 2.0 * 4-8 times a day (can cause intestinal atony).

2. For alkalosis, sodium chloride.

3. To correct phosphorus-calcium metabolism: vitamin D - 3, calcium gluconate, almagel (favorably affects phosphorus metabolism).

4. For anemia: nerabol 0.005 * 3 times a day, retabolil 5% oil solution 1.0 IM once a week, iron supplements for parenteral administration, large doses of vitamins C and B, blood transfusion once a week.

5. Diuretics: Lysix 1% - 2.0 IV, furosemide, uregit.

6. For hypertension, the optimal rauwolfia preparations are: reserpine 0.0001; dopegyt 0.25 0.5 tab. or 1 tablet 3 times a day.

7. For heart failure: digoxin, since it is excreted by the kidneys, doses should be small. Strophanthin should not be taken due to the danger of intoxication.

8. Regular bowel cleansing reduces the amount of nitrogenous waste in the body: sorbitol 100 - 700 ml. magnesium sulfate 100 ml (before diarrhea), cleansing enemas, gastric lavage through a thin tube.

9. To remove nitrogenous waste through the skin - hot baths.

10. Drugs that enhance renal excretory function; Lespenefril (flaronin) 1-2-4 teaspoons orally - improves the functioning of the renal glomeruli.

11. Diet therapy: high-calorie, low-protein foods; with stage 1 chronic renal failure, there is no need to limit protein. Exclude meat and fish. Eggs, vegetables and fruits in large quantities. There is little fluid restriction due to compensatory polyuria. Limit table salt to 1 - 1.2 g/day.

12. In the 3rd stage of chronic renal failure it is necessary: ​​program dialysis, decision on the issue of kidney transplantation.

13. Spa therapy in dry and hot climates.

Prognosis: always difficult. Death may occur suddenly. At the 1st degree, the ability to work is preserved.

CHRONIC NON-SPECIFIC

LUNG DISEASES

About 7% of the total adult population has COPD.

Classification:

Chronic diseases genetically determined pulmonary dysplasia chronic also

Acquired diseases

a) with predominant damage to the bronchi

b) with predominant damage to the parenchyma.

Tracheobronchial dyskinesia. During exhalation, stenosis of the bronchus occurs with a prolapsed membrane (expiratory suffocation) during coughing or physical effort.

Mounier-Kuhn disease. At 8-10 years of age, the trachea is excessively dilated and practically devoid of cartilaginous cover. This is an extreme degree and is rare. Closure of the trachea by 15-20% - 1st degree, 20-30% - 2nd degree, more than 30% - 3rd degree of tracheobronchial dyskinesia. Surgical treatment methods are not perfect enough (transplantation of costal cartilage or synthetic atraumatic tube, which is worse). Tracheobronchial dyskinesia occurs with long-term chronic bronchitis during an exacerbation, but rarely more than 1 degree.

Polycystic lung disease. Symmetrically or asymmetrically located cavities. They may not show any clinical signs for years; clinical manifestations during infection then resemble bronchiectasis with saccular bronchiectasis. Since in most cases the pathology is 2-sided, it is unfavorable for surgical treatment.

Cartagena syndrome. There are polycystic lungs. This is characterized by situs wiscerus inwersus + bone defects - additional ribs, spina bifidum. Currently, about 70 dysplasias are known, but the rest are extremely rare.

Genetically determined:

1) Cystic fibrosis (7% of all congenital). This is a change in the viscosity of the secretion of all externally secreting glands (saliva, sweat, bronchial glands, etc.). The secret is more viscous. In a pronounced variant, death occurs in the first days of life, since the intestines cannot clear meconium. (Such cases are in the homozygous variant). In milder cases, symptoms of chronic obstructive bronchitis, the inability to provide forced breathing during physical activity. The 2nd symptom is cough, very tense, since the eyelashes do not work due to thick secretions, intensifies with physical activity. 3rd symptom: rapid development of emphysema. Infection quickly sets in, and severe purulent obstructive bronchitis develops. The sputum has a peculiar appearance; it cannot be shaken out of the spittoon, as it is very sticky. It is necessary to find out the genetic history. Digestive defects are often associated: loss of appetite, tendency to diarrhea, poor digestion of food, and such children have stunted height and weight.

Diagnosis: sweat analysis and other special methods are carried out in special centers. Restrictions in choosing a profession: no dust, in a warm place. Treatment: mucolytic drugs, bronchodilators, acetylcysteine ​​inhalations. Without treatment, cor pulmonale will develop. Alpha-1 antitrypsin deficiency (1%).

PROTECTIVE SYSTEMS

The proteolytic system of the lungs is needed for the proteolysis of inhaled foreign protein. Oxidant system. Phagocytosis and mucocellular clearance.

Alpha-1-antitrypsin acts as an antiproteolytic system. It is synthesized in the liver. With its deficiency, proteolysis of its own connective tissue structures occurs and preseptic pulmonary emphysema develops. There is practically no treatment yet, only a lung transplant.

Generalized hypoxia and hypoxemia develop. shortness of breath, first with exertion, then at rest. “Drumsticks” and “watch glasses”, diffuse cyanosis. The only therapeutic measure: permiator - enriches the air with oxygen up to 40%.

Congenital immune deficiency - Bruton's disease (0.1%). Boys get sick and it is hereditary. Clinic: purulent inflammatory diseases of the lungs: pneumonia, purulent bronchitis, empyema. It is very difficult to treat.

Most acquired diseases have underlying genetic predisposition. 2 groups of acquired diseases: acute and chronic.

Acute - with acquired damage to the bronchi - acute bronchitis and acute tracheitis; acute with damage to the parenchyma; acute pneumonia, acute lung destruction.

Chronic with acquired damage to the bronchi - chronic bronchitis, bronchial asthma, bronchiectasis. Chronic with damage to the parenchyma: pulmonary emphysema, chronic pneumonia - 1.5% of all COPD.

Chronic pneumonia is a chronic, recurrent inflammatory process in a limited area of ​​the pulmonary parenchyma, leading to the formation of focal pneumosclerosis. Most often the 9th - 10th segment is on the right, but it also happens on the left, also the middle lobe of the right lung, and the lingular segments of the left lung. Chronic pneumonia often occurs at the site where there is a “bad bronchus.” It is necessary to differentiate from bronchial cancer; bronchoscopy, cytological examination of sputum, and tomography are required. In chronic pneumonia, cylindrical or spindle-shaped bronchiectasis occurs. There is little sputum, but bleeding is frequent. They can be radically cured surgically.

CHRONICAL BRONCHITIS

According to bronchial patency: obstructive and non-obstructive. According to the level of damage: proximal - up to 5 - 6 generations of bronchi. Purulent and catarrhal.

Obstructive bronchitis. If distal, then the main symptom is associated with an air trap (when you inhale, air enters the alveoli, during exhalation the bronchi shorten, take on the appearance of a corrugated tube and the air does not pass back, the volume of residual air increases, the pressure rises. This occurs until the pressure will not be sufficient to overcome the resistance of the shortened bronchi. Ischemia and dystrophic changes develop, emphysema develops early. The main symptom is shortness of breath. Cough is not typical for distal bronchitis. This is 5% of all COPD.

Smoking and aeropolutants (occupational hazards) are considered as the etiological factors.

Cough for at least 3 months a year, at least 2 years in a row. If other diseases that are characterized by cough are excluded - chronic bronchitis.

The bronchi become infected, and pneumococcus, Haemophilus influenzae, and pneumotropic virus become the supporting factor.

Proximal bronchitis. The main symptom is cough. Obstructive bronchitis is characterized by paroxysmal cough. Dyspnea. Tracheobronchial dyskinesia may develop. The number of goblet cells increases. Mucin is very viscous, evacuation is difficult, and mucocellular clearance is impaired. The load on the right chambers of the heart gradually increases. Blood pressure in the pulmonary artery increases to 35 - 40 mm Hg. Art. First, hypertrophy, then dilatation of the right ventricle. Epigastric pulsation, in severe cases, tricuspid insufficiency and systolic murmur over the right chambers, before this accent of the ll tone (or splitting) over the pulmonary trunk. The outcome of chronic bronchitis is decompensated cor pulmonale.

Pain and heaviness in the right hypochondrium (liver), swelling, ascites. Cor pulmonale develops with increased load on the right ventricle; due to the reduction of blood vessels in the pulmonary artery system, blood pressure in it increases to 30-40 mm Hg. This is already enough to cause hypoxia. Purely distal bronchitis is very rare. On auscultation, nothing is heard, only weakening of breathing.

At the proximal stage there is a lot of wheezing, a box sound on percussion. A decrease in FEV 1 is the first indication of obstruction. The MOS of inhalation and MOS of exhalation are also reduced, as well as the MVL. Study: 2 breaths of Berotek or salbutamol, after 15 minutes. record the spirogram again. If it increases by 20 - 25%, bronchospasm occurs.

Obstruction:

2. Swelling of the bronchial mucosa.

3. Accumulation of secretions in the bronchi. This happens with inflammation.

4. Transudation into the lumen of the bronchus is less significant, for example, with pulmonary edema (heart failure), a lot of moist rales.

5. Sclerosis of the bronchial wall. The sign is that the chest is stubborn and cannot be treated yet.

In chronic bronchitis, the initial etiology is non-infectious; infection occurs later. Mainly pneumococcus, hemophilus influenzae, there may be viruses of the respiratory group - they persist, the epithelium sloughs off - the way opens for bacteria. There may also be yeast and fungi. Now this is a common occurrence.

Clinical signs of active infectious inflammation in the bronchi (exacerbation):

1. Increased cough.

2. The appearance or increase in the amount of green or yellow sputum.

3. Scattered wheezing, dry, sonorous, can be wet, small and medium in caliber.

4. Evening chills.

5. Night sweats; localization - back, neck, back of the head - a symptom of a “wet pillow”.

6. Accumulation of bacteria in a cough smear.

7. Cultures: if pneumococcus grows in a dilution of 10-6-10-7 - the diagnostic value is undoubted, if only in 10-2 - it is doubtful. Cytological examination of sputum, you need to know the percentage of sputum cells. X-ray gives almost nothing - it only enhances the pulmonary pattern. Interstitial pneumonia is essentially complicated bronchitis. It is necessary to differentiate from allergic inflammation - there is no chills or sweating with it. In allergic sputum, eosinophils predominate (up to 70%), neutrophils are few.

If there is an increase in cough and sputum without other signs, there are few purulent cells in the sputum - catarrhal bronchitis. The most severe chronic purulent obstructive bronchitis in the acute phase. The easiest is chronic catarrhal non-obstructive. Non-obstructive catarrhal disease lasts for decades without any significant consequences. In others, secondary bronchiectasis, cylindrical and fusiform, may form. These are subsegmental bronchi, maybe smaller ones. Clinic: cough stabilization. There is not a lot of sputum, “dry bronchiectasis.” They often bleed, often with blood-streaked sputum. Bronchial cancer is 8 times more common in smokers. Emphyema is also an outcome.

Secondary chronic bronchitis occurs secondarily, where there is, for example, fibrous-cavernous tuberculosis, that is, where drainage is impaired. Described in individuals after removal of areas of the lungs, in areas of pneumosclerosis, especially in the lower lobes. May be due to lung carcinoma.

Treatment of chronic bronchitis

If the patient smokes all his life, and irreversible changes have already occurred, then prohibiting smoking is useless - it will no longer help. But if you have been smoking for less than 20 years in a row, that is, there are no irreversible changes yet, then definitely quit smoking. If the profession is harmful, change it. Hardening. Start with rubbing, back massage with a terry towel between the shoulder blades. Bronchospasmolytic drugs. If it is non-obstructive, during an exacerbation, euphilin tablets 2 times a day are enough. If it is obstructive, then stronger drugs, better selective ones. If there is also coronary artery disease, it is better not to take sympathomimetics; it is better to take anticholinergics, for example, Atrovent; if there is concomitant glaucoma, it is the other way around. Mucolytic drugs. Breast preparations, other herbal medicine (sage, chamomile, string, Icelandic moss). If there is very little sputum, they are not needed. If the cough is unproductive, explain that there is no need to try to cough a lot.

Antibiotics (synthetic penicillins), after 10 days switch to long-acting sulfonamides (up to 3 weeks). Chopped garlic, squeeze out the juice, dilute 3 times, apply through a water inhaler. Before inhalation, take 2 breaths of Berotek. Inhale 2 ml in the morning and evening. It is especially useful for bacterial infections, candidiasis. (Garlic loses its medicinal properties from mid-March). Therapeutic bronchoscopy is allowed. During the acute phase, aspirin 250 mg. * 3 times a day after meals. Antioxidants are indicated for almost everyone; use for months: vitamin “C” 300 mg per day, also in 3 doses. From physiotherapy to the acute phase, cupping, massage.

BRONCHIAL ASTHMA

The reason is genetically determined internal defects formed in the prenatal period, during childbirth or in subsequent life. But there is definitely an altered sensitivity of the bronchial mucosa with a pathological reaction to acetylcholine, even if there are no clinical manifestations yet, + changes at the preclinical stage in other systems, for example, an increase in IG E, there may be changes in the endocrine system - detected during the desamethasone test. Characteristic changes in the central nervous system. All this creates heterogeneity of pathogenesis while the clinical picture is uniform.

Desquamation eosinophilic bronchitis, but 20% have non-eosinophilic bronchitis. For internal reasons, see above. External causes are environmental factors that reveal disturbed systems. 1% of the adult population suffers from bronchial asthma. The state of pre-asthma occurs in 60% of patients. Legally, a diagnosis of clinically significant bronchial asthma can be made after the first attack.

Causes of death: ischemic heart disease, oncology and others, but few die from the attack of suffocation itself.

Preasthma is not yet a mosological form. Her criteria:

1. Acute or chronic lung diseases with bronchial obstruction. These are asthmatic and obstructive bronchitis, acute pneumonia with obstruction, acute respiratory infections with obstruction.

2. Extrapulmonary manifestations of altered reactivity.

3. Eosinophilia of blood and (or) sputum.

4. Hereditary predisposition.

If all this is present, then within 3 years clinically pronounced bronchial asthma occurs in 70%. The fewer these signs, the less likely it is to develop.

There is no diagnosis of preasthma in the nomenclature of diseases. Bronchial asthma begins with the first attack of suffocation.

1. Most people have an aura.

2. Attack.

3. Recovery.

Aura - tickling in the nose, throat, trachea, behind the sternum, fluid from the nose, anxiety, coughing, the beginning of wheezing when exhaling. All this in 2-3 minutes. and even faster. For some, the attack begins with coughing and difficulty breathing.

“Mute lung” syndrome, when there is not enough air to form noise. It's very hard. Boxed tone on percussion. In some patients, the attack is accompanied by skin itching, rarely rhino-conjunctival syndrome (itching in the eyes).

3 degrees of severity:

1. Light. No more than 1-2 times a year, they can be stopped without injections.

2. Moderate severity, exacerbations up to 5-6 times a year. Injections are required (euphyllin).

3. There are statuses.

Phases: remission and exacerbation - when a series of attacks occurs, every day, cough, shortness of breath, sometimes there are individual attacks of suffocation outside the exacerbation phase.

Previously, atopic and infectious-allergic were distinguished.

1. Atopic bronchial asthma.

a) Occurs only during the flowering season, not in winter; patients feel worse in sunny, windy weather, better in rain, and also at home with the windows closed. Usually there is rhino-conjunctival syndrome, sometimes the temperature is up to 37.5 degrees C, rarely higher, sometimes nausea and diarrhea. The reaction is more often to cereals (weeds), poplar, nightshade, less often to conifers.

b) Dust atopy. Night attacks 1 - 1.5 hours after going to bed - due to carpets, shelves with dusty books. Pillow causes feather allergy. Ask if you used dichlorvos, chlorophos, etc. If a patient, leaving home, feels better on the first day, the reason is home.

Composition of household dust: mites from the genus dermatophagoides, up to 0.2 mm long. Their feces have high allergenic properties. There are especially many mites in old feather pillows. They can live on eyelashes. Food allergens - the appearance of respiratory discomfort, up to an attack of suffocation after eating (citrus fruits, nuts, honey, red fruits and vegetables, fish, especially sea fish, fresh milk (lactalbumin, there is more of it in foam), eggs, chocolate, coffee). Often food allergy sufferers have chronic urticaria and eczema. As a rule, there are changes in the oral mucosa: bleeding gums - periodontal disease. Gastritis, duodenitis with dyskinesias, enteritis, recurrent hemorrhoids. Food allergies are forever, they do not go away with time.

If the patient does not know what he is reacting to, then the listed obligate allergens are first eliminated for 2-3 weeks: if this does not clarify the cause, vegetables, including bread and plant products, are excluded. After the reaction disappears, gradually return the products and notice what exactly the reaction is to. If there is no result, then on the contrary, exclude meat or milk, also for 2-3 weeks. The patient should write a food diary: how he feels after each meal. No store-bought confectionery: there are many allergens there: no canned food, sausages.

DRUG INTOLERANCE

Before prescribing a drug, always ask whether you have used it before and with what results. For penicillin and streptomycin, perform tests. In general, for an allergic person, the first dose of any drug is 1/4 of the usual dose, regardless of how you tolerated it before. If there are no local and systemic signs of allergy, then the next day take the usual dose.

Occupational allergies. When it doesn't work, there are no manifestations. Often there are manifestations in those working in similar conditions. Most often damage to open parts. The diagnosis is made by an occupational pathologist. History + diagnostics in vitro et in vitro (up to intracosal administration), IG E study - informativeness of at least 60-70%.

Type 1: allergen --> macrophages --> Ts, Tx, Vl --> plasma cells --> IG E (IG G 4) --> Tk --> BAS --> chemotactic factors (hychtamine, slow-reacting substance , leukotrienes, etc.) --> bronchial obstruction.

Histamine is an immediate reaction, chemotactic factors - after a few hours.

Type 3: immunocomplex. Receptors for immune complexes are present on almost all bronchial cells (nonspecific).

Type 4: sensitized lymphocytes, reaction within a day or a little later.

Mast cells of allergy sufferers have an increased affinity for immune complexes. They secrete biologically active substances when they shouldn't. Membrane-stabilizing substances (intal) help. Action of euphilin: represses phosphodiesterase --> restoration of cAMP --> strengthening of the action of the sympathetic system.

Aspirin asthma: aspirin intolerance, bronchospasm and polyps. Since acetylsalicylic acid interferes with the metabolism of arachidonic acid. If there is a defect in the enzyme that triggers the cyclooxygenase pathway, the lipoxygenase pathway will go - the production of leukotrienes and a slow-reacting substance.

Intolerance to wild grass pollen is often combined with intolerance to cotton products. Intolerance to birch + berries, fruits.

Infectious dependence of the disease: The action of infection in three ways:

1) Often, especially viral ones, they are accompanied by exacerbations of bronchial asthma, since this increases sensitivity to the infectious agent.

2) There can be a reaction to bacteria, viruses, candida in itself. This is practically impossible to establish.

3) Changes the epithelium of the upper respiratory tract and increases their sensitivity to chemicals.

History: connection between the onset of bronchial asthma and inflammatory disease of the upper respiratory tract, connection between exacerbations and active infection. Microsymptoms: contact with infectious patients, recognized as ARVI. If tank. infection - its own characteristics, for example, the “wet pillow” symptom, blood changes. Fungal infection (less commonly) - usually there is onychomycosis, intolerance to yeast-containing products.

1-2% of all asthmatics have an autoimmune variant: antibodies to their own cells. This is the most severe version of bronchial asthma 3 and 4 path. Diagnosis: the patient’s own lymphocytes are injected into the skin. Hyperemia, edema, even point necrosis.

DISHORMONAL BRONCHIAL ASTHMA

a) With glucocorticoid deficiency. It is most often formed iatrogenically, that is, during hormone therapy. It is safer for people over 50 years of age to prescribe hormones for the first time. If cortisol in the blood is 25 - 30% less than normal, replacement therapy is necessary. If the cortisol level is normal, but there are manifestations of deficiency, check tissue sensitivity (incubation with lymphocytes). If tissue resistance is bad, you will have to give hyperdoses. If the level and sensitivity are normal, but upon withdrawal signs of deficiency appear, psychotherapy is necessary.

b) Disovarial asthma: 2 - 3 days before menstruation, an exacerbation of bronchial asthma occurs. There is a defect in bronchodilating progesterone with excess estrogen. Rectal temperature is more than 1 degree higher than body temperature.

Severe adrenergic imbalance: The activity of the alpha receptor apparatus predominates -> normal levels of adrenaline cause a pathological reaction (rarely). Often with an overdose of adrenergic agonists. If more than 5 inhalations of 2 inhalations of adrenergic agonists are taken per day, this is dangerous due to the rebound phenomenon.

There is also a cholinergic variant (rare). Atropine helps.

Group 1 of symptoms: conditioned reflex mechanism of bronchial asthma (a classic example is an artificial paper rose). There may also be a conditional reflex cessation of the attack. Often 70% odor intolerance is not allergic, but a conditioned reflex mechanism. It is possible to treat by suggestion.

Group 2: Dominant theory. Minor irritations add up and create attacks. If another very strong dominant arises, it can temporarily extinguish the dominant of bronchial asthma. If the temperature is above 380C, then there will be no attacks.

Vagal mechanism (in the 2nd half of the night). This is due to a deficiency of the non-adrenergic nervous system. It contains the mediator VIP, which has a powerful bronchodilator effect.

10-20% suffer from asthma as a result of inadequate adaptation to the microsocial environment. The child attracts attention with respiratory syndrome, he takes advantage of it. In adulthood - infantilism.

Cholinergic variant 1%. There is a lot of coating here 1/2 - 1 cup. There is a history of peptic ulcer disease, bradycardia, hypotension, wet, sweaty palms.

Primary altered sensitivity and reactivity of the bronchi is diagnosed by excluding the rest. This is a disease after 40 years of age, the majority of patients are smoking men with occupational hazards, with obstructive bronchitis. This also includes exercise-induced asthma. Also intolerance to cold air, intolerance to strong odors (varnishes, paints). A special place is aspirin asthma. Right here.

The diagnosis begins with “bronchial asthma”, then clinical and pathogenetic variants, indicate the phase, then concomitant pathology, primarily adjacent to bronchial asthma.

Differential diagnosis

1) Tracheobronchial dyskinesia. Occurs at the height of coughing, physical activity, etc.

2) Hysteria. Here the whistle does not come from the lungs, but from the vocal cords.

3) Periarteritis nodosa (this is vasculitis), combines nephritis with hypertension, chronic pneumonia. Expiratory shortness of breath may occur. Mostly men get sick: fever, POPs. This is a systemic disease and is rare.

4) Carcinoid syndrome (intestinal, pulmonary, mixed). This is a tumor that produces serotonin. Facial hyperemia, increased blood pressure, intestinal colic. Associated with physical activity. This is also a rare disease.

6) Cardiac asthma. Here the suffocation is inspiratory, there are a lot of moist rales in the lungs. But in older people there may also be a component of bronchial asthma. It is better to administer prednisolone; Euphilin is dangerous.

7) Entry of foreign objects into the upper respiratory tract.

Elimination therapy is very important. Stage of tactical therapy - during an exacerbation, patients are treated more or less the same. Hormones 3 - 4 - 5 days, cancel immediately. Methylxanthine group. Adrenergic agonists: berotec, salbutamol, 2 breaths at intervals of 10 - 15 seconds. After this, inhale one breath 4 times a day. Ditek (intal + berotec). For ischemic heart disease and hypertension, anticholinergics are better: Atrovent, duodenal. For concomitant cardiac pathology, calcium antagonists, vitamin C 300 mg/day: with meals 3 times a day for months.

Antilymphocytic IG in the atropic form. Barotherapy with reduced pressure (up to an altitude of 3500 m) - this stimulates the adrenal glands, etc. Inhalation of small crystals of NaCl (halochamber). Training in the volitional method of breathing, except for patients with neuropsychiatric disorders and respiratory failure. The inhalation is very shallow. maximum breath holding - exhale, gradually increase to 7 - 8 breaths per minute. Acupuncture.

In case of infection-dependent in the attenuation phase, sanitation of foci of infection + specific hyposensitization against bacterial allergens. Thymalin (thymogen, T - activin) 5 - 6 times.

Sputum autolysate. In the acute phase, receive, treat with carbolic acid, in the remission phase, administer at a high dilution intravenously and then subcutaneously. Hyperbaric chamber, back massage. Therapeutic bronchoscopy to clear away mucus.

For autoimmune asthma, treat in a special department. In case of overdose of Berotek, etc., use glucocorticoids. In case of glucocorticoid deficiency, their determination in blood plasma. Intermittent regimen of glucocorticoids. With them potassium preparations, anabolic steroids 1 - 2 times a month. Watch Gregersen's reaction. Beclomed (bikatide) is an inhaled glucocorticoid. Less resorptive effect. 4-5 times a day, 2 breaths, after inhalation of a bronchodilator. Possible candidiasis. If there is a pronounced neuropsychic variant, psychotherapy, especially pathogenetic. Family psychotherapy. Gestalt therapy is training for rational solutions to problems in the microsocial sphere.

CHRONIC PULMONARY HEART

Chronic cor pulmonale refers to right ventricular hypertrophy secondary to a disease affecting lung function or structure, or both, unless these pulmonary changes are the result of left heart disease or congenital heart defects.

More often associated with chronic bronchitis, emphysema, bronchial asthma, pulmonary fibrosis and granulomatosis, tuberculosis, silicosis, with conditions that impair the mobility of the chest - kyphoscoliosis, ossification of the costal joints, obesity.

The disease primarily affects the pulmonary vessels: thrombosis and embolism of the pulmonary artery, endarteritis.

Mortality from chronic pulmonary heart disease came in 4th place. In the early stages it is difficult to diagnose clinically. In 70 - 80% of cases, the cause is chronic bronchitis, especially destructive bronchitis.

Pathogenesis.

Pulmonary hypertension -> right ventricular hypertrophy -> right ventricular decompensation. But some patients do not have a significant increase in blood pressure in the pulmonary artery. Normally up to 30 systolic, 12 - 15 mm Hg. diastolic. In patients with chronic pulmonary heart disease 40 - 45 to 50 mm Hg. But attempts to make an early diagnosis of pulmonary hypertension failed. Indirect data on the value of blood pressure in the pulmonary artery can be obtained by determining the speed function of the heart - Doppler echocardiography is the only thing that can be recommended.

Right ventricular hypertrophy can be determined using ultrasound. Spasm of small capillaries due to arterial hypoxia and hypoxemia (reflex), emptying of blood vessels, increased minute volume due to hypoxemia, increased blood viscosity; often this is also accompanied by reflex erythrocytosis. Bronchopulmonary anastomoses. Primary increases during physical exertion and exacerbations - crises of pulmonary hypertension.

Diagnostics

Usually, already decompensated cor pulmonale is diagnosed. Signs. Dilatation of the right parts of the heart: displacement of the apical impulse without displacement into the 6th intercostal space, emphasis of the 2nd tone on the pulmonary artery, cardiac impulse, epigastric pulsation, Graham-Still murmur, increased 1st tone in the region of the 3-leaf valve. These signs are clear when the pressure rises above 50 mm Hg. Emphysematous lungs make diagnosis very difficult.

Initial signs of decompensation of the right heart:

Complaints: shortness of breath of an expiratory nature also becomes inspiratory. Stability of shortness of breath appears, its duration increases after a cough attack, fatigue, cyanosis, changes in vibrations of the neck veins, heaviness or a feeling of pressure in the right hypochondrium, a positive Plesch test - swelling of the neck veins when pressed (hepatojugular reflux). Watchel's test with strophanthin: 1 - 2 days measure diuresis and urine output, then 1 - 2 days drip 0.5 ml of strophanthin 1 time per day. Measure diuresis and weight. With pathology, diuresis increases by 500 ml. weight loss is somewhat less indicative.

3 degrees of right ventricular decompensation:

1. Latent, assessed during physical activity, not at rest.

2. There is at rest, but there are no organ changes.

3. Dystrophic. Persistent pronounced changes in organs are very difficult to treat.

With 2A: moderate but constant enlargement of the liver, the appearance of edema in the evening, disappearance in the morning, more pronounced hepatojugular reflux.

2B: already large painless liver, persistent and significant swelling in the legs.

In the 3rd degree there is swelling up to anasarca, congestive kidneys, etc. But patients with pulmonary pathology rarely survive to stage 3.

For more accurate ECG diagnosis. Diagnosis if in V 1 the internal deviation time is more than 0.03, or in I standard R is almost equal to S, mmm in V 5 R/S< 1, или неполная блокада правой ножки пучка Гисса при ORS не более 0,12". Диагноз: если есть 2 и более этих признаков.

Differential diagnosis with cardiosclerosis, which leads to left ventricular failure, congestion in the right circle and ultimately to decompensation.

PULMONARY HEART

CARDIOSCLEROSIS

1. puffiness

Swelling and pulsation of the neck veins

diffuse

expiratory

inspiratory

Cough with phlegm

absent

"Drumsticks", "watch glasses"

may not be

fingertips

cold

Orthopnea

Lung congestion

Cardiac asthma

Pain in the heart area

less often, removed with oxygen

Atrial fibrillation

Circulatory failure

right ventricular type

left ventricular type

Arteriosclerosis of cerebral arteries

Concomitant arteriosclerosis of peripheral vessels

Erythrocytosis

May be

absent

Increased blood pressure

exists only with concomitant headache, but there are conditions for its faster development

absent

X-ray

small size of the heart, the diaphragm lowers, it stretches

heart enlarged upward

Configuration

close to mitral or normal

close to the aorta

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