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Lecture #1

1. Respiratory allergies

Respiratory allergies are common allergic diseases with predominant damage to the respiratory system.

Etiology

Allergosis develops as a result of sensitization by endogenous and exogenous allergens.

Exogenous allergens of non-infectious nature include: household - washing powders, household chemicals; epidermal - wool, skin scales of domestic animals; pollen - pollen of various plants; food - foodstuffs; herbal, medicinal. Allergens of an infectious nature include bacterial, fungal, viral, etc.

Classification

The classification is as follows.

1. Allergic rhinitis or rhinosinusitis.

2. Allergic laryngitis, pharyngitis.

3. Allergic tracheitis.

4. Allergic bronchitis.

5. Eosinophilic pulmonary infiltrate.

6. Bronchial asthma.

Symptoms and diagnostics

Allergic rhinitis and rhinosinusitis. Anamnesis - the presence of allergic diseases in parents and close relatives of the child, the relationship of diseases with allergens.

Symptoms are acute onset: sudden onset of severe itching, burning in the nose, bouts of sneezing, profuse liquid, often foamy discharge from the nose.

On examination, swelling of the mucous membrane of the nasal septum, lower and middle turbinates is revealed. The mucosa has a pale gray color with a bluish tint, the surface is shiny with a marble pattern.

An x-ray examination of the skull shows thickening of the mucous membrane of the maxillary and frontal sinuses, the ethmoid labyrinth.

Positive skin tests with infectious and non-infectious allergens are characteristic.

In laboratory diagnosis - an increase in the level of immunoglobulin E in the nasal secretion.

Allergic laryngitis and pharyngitis can occur in the form of laryngotracheitis.

It is characterized by an acute onset, dryness of the mucous membrane, a feeling of itching, soreness in the throat, bouts of dry cough, which later becomes "barking", rough, hoarseness of voice appears, up to aphonia.

With the development of stenosis, inspiratory dyspnea appears, the participation of auxiliary muscles in the act of breathing, retraction of pliable places of the chest, swelling of the wings of the nose, abdominal breathing becomes more intense and amplitude.

Bronchial obstruction develops due to edema, spasm and exudate and, as a result, obstructive ventilation failure.

The use of antibacterial agents does not have a positive effect, it may even worsen the condition.

Laboratory data - positive skin tests, increased levels of immunoglobulin E in the blood serum.

Allergic bronchitis occurs in the form of asthmatic bronchitis.

In the anamnesis there are data on the allergization of the body. Unlike true bronchial asthma, asthmatic bronchitis develops a spasm of large and medium-sized bronchus, so asthma attacks do not occur.

Eosinophilic pulmonary infiltrate develops with sensitization of the body.

The most common cause is ascariasis. In the general blood test, high eosinophilia (more than 10%) appears against the background of leukocytosis. Foci of infiltration appear in the lungs, homogeneous, without clear boundaries, which disappear without a trace after 1-3 weeks. Sometimes an infiltrate, having disappeared in one place, may occur in another.

2. Bronchial asthma

Bronchial asthma - an infectious-allergic or allergic disease of a chronic course with periodically recurring attacks of suffocation, caused by a violation of bronchial patency as a result of bronchospasm, swelling of the bronchial mucosa and accumulation of viscous sputum.

Bronchial asthma is a serious health problem worldwide. It affects from 5 to 7% of the population of Russia. There is an increase in morbidity and an increase in mortality.

Classification (A. D. Ado and P. K. Bulatova, 1969)

The form:

1) atopic;

2) infectious-allergic;

3) mixed. Type of:

1) asthmatic bronchitis;

2) bronchial asthma. Severity:

1) mild degree:

a) intermittent: attacks of bronchial asthma less than twice a week, exacerbations are short, from several hours to several days. Night attacks rarely occur - twice or less a month;

b) persistent: seizures do not occur every day, no more than two per week.

At night, asthma symptoms occur more than twice a month;

2) medium degree - manifests itself every day, requires daily use of bronchodilators. Night attacks occur more than once a week;

3) severe degree - bronchial obstruction, expressed to varying degrees constantly, physical activity is limited.

The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen with the occurrence of allergic inflammation in the mucous membrane of the bronchial tree.

When collecting an anamnesis from a patient, it is necessary to establish the nature of the first attack, the place and time of the year, the duration and frequency of attacks, the effectiveness of the therapy, the patient's condition during the non-attack period.

Pathogenesis

The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen and the occurrence of allergic inflammation.

Clinic

The main symptom is the presence of asthma attacks of the expiratory type with remote wheezing, paroxysmal cough. The forced position of the patient during an attack: the legs are lowered down, the patient sits on the bed, the body is tilted forward, hands rest on the bed on the sides of the body.

Symptoms of respiratory failure appear (participation of auxiliary muscles in the act of breathing, retraction of the intercostal spaces, cyanosis of the nasolabial triangle, shortness of breath). The chest is emphysematously swollen, barrel-shaped.

Percussion-box sound, the borders of the lungs are shifted down. Auscultatory - weakened breathing (short inhalation, long exhalation), an abundance of dry whistling rales, moist rales of various calibers. From the side of the cardiovascular system - narrowing the boundaries of absolute cardiac dullness, tachycardia, increased blood pressure.

On the part of the nervous system, there is increased nervous excitability or lethargy, a change in autonomic reactions (sweating, paresthesia).

Laboratory diagnosis

In the general history of blood - lymphocytosis, eosinophilia. In the general analysis of sputum - eosinophilia, epithelial cells, macrophages, or Charcot-Leiden crystals, and Kurshman spirals.

Instrumental research methods. On x-ray - emphysema (increased transparency, the boundaries of the lungs are shifted down). Spirography: a decrease in the rate of exhalation (pneumotachometry), a decrease in VC, hyperventilation at rest.

Allergological examination. Carrying out skin tests with bacterial and non-bacterial allergens gives a positive result. Provocative tests with allergens are also positive.

Immunological indicators. With atopic bronchial asthma, the level of immunoglobulins A decreases and the content of immunoglobulins E increases, with mixed and infectious asthma, the level of immunoglobulins G and A increases.

In the atopic form, the number of T-lymphocytes decreases, in the infectious-allergic form it increases.

In the atopic form, the number of suppressors is reduced and the content of T-helpers is increased. With sensitization by fungal agents, the level of CEC increases.

Patient examination

Questioning (collection of anamnesis, complaints). Inspection (palpation, percussion, auscultation). General blood analysis. Microscopy and culture of sputum.

X-ray of the chest organs. Study of indicators of external respiration. Allergological, immunological examination.

Differential diagnosis

The differential diagnosis of bronchial asthma is carried out with diseases manifested by a bronchospastic syndrome of a non-allergic nature, which are called "syndromic asthma"; chronic obstructive bronchitis, diseases of the cardiovascular system with left ventricular failure (cardiac asthma), hysteroid respiratory disorders (hysteroid asthma), mechanical blockage of the upper respiratory tract (obstructive asthma).

Differentiate with diseases of an allergic nature: polyposis, allergic bronchopulmonary aspergillosis with obstructive respiratory disorders.

It is necessary to take into account the presence of a combination of two or more diseases in a patient.

In contrast to bronchial asthma in chronic obstructive bronchitis, the obstructive syndrome persists stably and does not reverse development even when treated with hormonal drugs, and there is no eosinophilia in the sputum during the analysis.

With left ventricular failure, the development of cardiac asthma is possible, which is manifested by an attack of shortness of breath at night; a feeling of lack of air and tightness in the chest develops into suffocation.

It is combined with arrhythmia and tachycardia (with bronchial asthma, bradycardia is more common). Unlike bronchial asthma, both phases of breathing are difficult. An attack of cardiac asthma can be prolonged (until the use of diuretics or neuroglycerin).

Hysteroid asthma has three forms. The first form is similar to a respiratory cramp. The breath of the "driven dog" - inhalation and exhalation are strengthened. There are no pathological signs on physical examination.

The second form of suffocation is observed in hysterical people and is caused by a violation of the contraction of the diaphragm. During an attack, breathing is difficult or impossible, in the area of ​​​​the solar plexus - a feeling of pain.

The third form is associated with spasm of the glottis. The attack begins with a whistle when inhaling, at the height of the attack, respiratory arrest is possible.

To stop the attack, the patient is offered to inhale hot water vapor or give anesthesia.

Obstructive asthma is a symptom complex of suffocation, which is based on a violation of the patency of the upper respiratory tract.

The cause of obturation may be tumors, foreign body, stenosis, aortic aneurysm. The greatest value in the diagnosis belongs to the tomographic examination of the chest and bronchoscopy.

The combination of symptoms of shortness of breath and suffocation also occurs in other conditions (anemic, uremic, cerebral asthma, periarthritis nodosa, carcinoid syndrome).

Pollinosis, or hay fever, is an independent allergic disease in which the body is sensitized to plant pollen.

These diseases are characterized by: bronchospasm, rhinorrhea and conjunctivitis. The disease is characterized by seasonality. It starts with the flowering period of plants and decreases when it ends.

The stage of exacerbation is characterized by a persistent runny nose, pain in the eyes and tearing, coughing up to the development of an asthma attack.

Possible fever, arthralgia. In the general analysis of blood - eosinophilia (up to 20%). During the remission period, it does not manifest itself clinically.

Allergic bronchopulmonary aspergillosis - a disease caused by sensitization of the body to asperginella fungi. With this disease, damage to the alveoli, vessels of the lungs, bronchi, and other organs is possible.

The clinical sign is the symptom complex of bronchial asthma (obstructive syndrome, eosinophilia, increased immunoglobulin E).

Confirmation of the diagnosis is carried out by detecting skin sensitization to aspergillus allergens.

Diagnosis example. Bronchial asthma, atopic form, with frequent relapses, remission period, uncomplicated.

Treatment

The goal of treatment is to prevent the occurrence of asthma attacks, shortness of breath during physical exertion, coughing, and nocturnal respiratory failure. Elimination of bronchial obstruction. Maintain normal lung function.

The objectives of the therapy:

1) stop exposure to the body of the allergen - the cause of the disease. With pollen allergy, the patient is offered to move to another area during the flowering period of plants. With occupational allergies - change the place and working conditions. With food - strict adherence to an elementary diet;

2) carry out specific desensitization followed by the production of blocking antibodies (immunoglobulins G);

3) stabilize the walls of mast cells and prevent the secretion of biologically active substances;

4) limit the impact of irritants on the respiratory tract - cold air, strong odors, tobacco smoke;

5) rehabilitation of chronic foci of infection (teeth with inflammation, sinusitis, rhinitis);

6) to limit the developing allergic inflammation by prescribing glucocorticoids in inhaled form;

7) prevent the use of non-steroidal anti-inflammatory drugs.

Principles of treatment.

1. Elimination of the allergen (exclusion, elimination).

2. Bronchospasm therapy:

1) selective α-agonists (berotec, salbutalone, ventosin, terbutamol, fenotirol, guoetarin);

2) non-selective adrenomimetics (adrenaline, ephedrine, asthmapent, fulprenaline, isadrin, euspiran, novodrin);

3) phosphodiesterase antagonists, xanthines (theobramins, theophylline, eufilkin);

4) anticholinergics (atropine, ipratropine).

3. H blockers₂histamine receptors (tavegil, fenkarol, suprastin, atosinil, pipolfen, displeron).

4. Drugs that reduce bronchial reactivity (glucocorticoids, intal, betotifen).

5. Expectorants:

1) increasing the liquid phase of sputum (thermopsis, licorice root, marshmallow, potassium iodide, alkionium chloride);

2) mucolytic drugs (acetylcysteine ​​(ACC)), ribonuclease, deoxyribonuclease);

3) drugs that combine a mucoliptic effect with an increase in the level of surfactant (bromgesin, ambrocagn, lazolvan).

6. Antibiotics.

7. Vibration massage with postural drainage.

8. Physiotherapeutic procedures, reflexology (acupuncture, oxygen therapy).

9. Bronchoscopy, intranasal tracheobronchial sanitation.

10. Rehabilitation in the gnotobiological department.

11. Sauna therapy.

3. Acute bronchitis

Bronchitis is a disease of the bronchi, accompanied by a gradually developing inflammation of the mucous membrane, followed by involvement of the deep layers of the walls of the bronchi.

Etiology

More often it develops during activation, reproduction of the opportunistic flora of the organism itself with a violation of mucociliary clearance due to SARS.

A predisposing factor is cooling or sudden heating, polluted air, smoking.

Pathogens - viruses, bacteria, mixed, allergens.

Classification:

1) acute bronchitis (simple);

2) acute obstructive bronchitis (with symptoms of bronchospasm);

3) acute bronchiolitis (with respiratory failure);

4) recurrent bronchitis.

Pathogenesis

Viruses, bacteria, mixed or allergens multiply, damaging the epithelium of the bronchi, reduce the barrier properties and cause inflammation, impaired nerve conduction and trophism.

The narrowing of the bronchial passages occurs as a result of mucosal edema, excess mucus in the bronchi and spasm of the smooth muscles of the bronchi.

Clinic

The flow is undulating. By the end of the first week of illness, the cough becomes wet, the temperature returns to normal.

The main clinical symptom is cough with mucous or purulent sputum; subfebrile temperature, no symptoms of intoxication. Auscultatory - dry and wet, wheezing rales of medium caliber on exhalation, hard breathing are heard.

Wheezing is scattered, practically disappears after coughing. In the general analysis of blood - moderately pronounced hematological changes: increased ESR, monocytosis.

On radiography - strengthening of the broncho-vascular pattern, expansion of the roots, symmetrical changes.

Acute obstructive bronchitis is characterized by shortness of breath on exertion; agonizing cough with scanty expectoration.

Auscultatory - lengthening of the exhalation. With forced breathing - wheezing wheezing on exhalation. In the general blood test, hematological changes are more often leukopenia.

On the radiograph - emphysema, increased transparency of the lung tissue, expansion of the roots of the lungs.

Acute bronchiolitis (capillary bronchitis) is characterized by a generalized obstructive lesion of the bronchioles and small bronchi.

The pathogenesis is associated with the development of edema of the mucous wall of bronchioles, papillary growth of their epithelium.

Clinically manifested by severe shortness of breath (up to 70-90 breaths per minute) against the background of persistent febrile temperature; increased nervous excitability associated with respiratory failure within a month after normalization of temperature; perioral cyanosis; auscultatory heard small bubbling, cracking asymmetric rales. Cough dry, high-pitched. The chest is swollen.

In the general blood test - hematological changes: increased ESR, neutrophilic shift, moderate leukocytosis.

On the radiograph - the alternation of areas with increased density with areas of normal pneumatization; low standing of the diaphragm, sometimes total darkening of the lung field, atelectasis.

Recurrent bronchitis is diagnosed when there are three or more diseases during the year with a prolonged cough and auscultatory changes in bronchitis without an asthmatic component, but with a tendency to a protracted course. This disease does not cause irreversible changes and sclerosis. The pathogenesis is due to a decrease in the barrier function of the bronchial mucosa to resist infections.

Predisposing factors: immunity defects, heredity, predisposition, polluted air, damage to the bronchial mucosa by exogenous factors, bronchial hyperreactivity. Recurrent bronchitis develops against the background of clinical signs of SARS.

moderate fever. The cough is initially dry, then wet, with mucous or mucopurulent sputum. Percussion-pulmonary sound with a box shade. Auscultatory - hard breathing, dry, moist rales of medium and small caliber, scattered on both sides.

In the general blood test, hematological changes - leukocytosis or leukopenia, monocytosis.

On the radiograph - increased lung pattern, expansion of the roots, atelectasis, hypoventilation. Bronchological examination - signs of bronchospasm, delayed filling of the bronchi with contrast, narrowing of the bronchi.

Survey plan

The plan of examination of the patient is as follows.

1. Collection of anamnesis (earlier ARVI, premorbid background, concomitant diseases, frequency of ARVI, hereditary predisposition, allergy to something, assessment of the effect of the treatment).

2. Examination of the patient (assessment of cough, breathing, chest shape).

3. Palpation (the presence of emphysema, atelectasis).

4. Percussion - the mobility of the lungs during breathing, air filling.

5. Auscultation (vesicular breathing, hard, diffuse wheezing).

6. Blood test - increase in ESR, shift of the leukocyte formula.

7. General analysis of urine.

8. Analysis of sputum from the nasopharyngeal mucosa with the determination of sensitivity to antibiotics.

9. ECG.

10. The study of the ventilation function of the lungs.

11. Radiography - the study of the vascular and pulmonary pattern, the structure of the roots of the lungs.

12. Bronchoscopy and mucosal examination.

13. Tomography of the lungs.

14. Immunological study.

Differential diagnosis

Differential diagnosis is carried out with:

1) bronchopneumonia, which is characterized by local damage to the lungs, intoxication, persistent fever; X-ray changes characteristic of a focal lesion;

2) bronchial asthma, which is accompanied by asthma attacks, hereditary predisposition, contact with an infectious allergen;

3) with congenital or acquired heart disease, which are characterized by congestion in the lungs. Diagnosis example. Acute infectious-allergic obstructive bronchitis DN₂.

Treatment

Principles of treatment:

1) antibacterial therapy: antibiotics: ampicillin, tetracycline and others, sulfa drugs: sulfapyridazine, sulfomonolithaxin;

2) mucolytic drugs: acetlcysteine, bromhexine, trypsin, chymotrypsin;

3) expectorants: breast collection (coltsfoot, wild rosemary, marshmallow, elecampane), broncholithin;

4) bronchitis: amupect, berotene;

5) endobroncholitin: eufillin in aerosol;

6) vitamins of groups B, A, C (cocarboxylase, biplex);

7) immunostimulants (immunal, thymolin);

8) physiotherapy, massage, breathing exercises.

4. Respiratory failure

Respiratory insufficiency is a pathological condition of the body, characterized by insufficient provision of the gas composition of the blood, or it can be achieved with the help of compensatory mechanisms of external respiration.

Etiology

There are five types of factors leading to a violation of external respiration:

1) damage to the bronchi and respiratory structures of the lungs:

a) violation of the structure and function of the bronchial tree: an increase in the tone of the smooth muscles of the bronchi (bronchospasm), edematous and inflammatory changes in the bronchial tree, damage to the supporting structures of the small bronchi, a decrease in the tone of the large bronchi (hypotonic hypokinesia);

b) damage to the respiratory elements of the lung tissue (infiltration of lung tissue, destruction of lung tissue, dystrophy of lung tissue, pneumosclerosis);

c) decrease in functioning lung tissue (underdeveloped lung, compression and atelectasis of the lung, absence of part of the lung tissue after surgery);

2) violation of the musculoskeletal framework of the chest and pleura (impaired mobility of the ribs and diaphragm, pleural adhesions);

3) violation of the respiratory muscles (central and peripheral paralysis of the respiratory muscles, degenerative-dystrophic changes in the respiratory muscles);

4) circulatory disorders in the pulmonary circulation (lesion of the vascular bed of the lungs, spasm of the pulmonary arterioles, stagnation of blood in the pulmonary circulation);

5) violation of the control of the act of breathing (oppression of the respiratory center, respiratory neuroses, changes in local regulatory mechanisms).

Classification

The form:

1) ventilation;

2) alveolorespiratory.

Type of ventilation failure:

1) obstructive;

2) restrictive;

3) combined.

Severity: DN I degree, DN II degree, DN III degree.

Obstructive ventilation failure is caused by a violation of the gas flow through the airways of the lungs as a result of a decrease in the lumen of the bronchial tree.

Restrictive ventilation failure is the result of processes that limit the extensibility of lung tissue and a decrease in lung volumes. For example: pneumosclerosis, adhesions after pneumonia, lung resection, etc.

Combined ventilation failure occurs as a result of a combination of restrictive and obstructive changes.

Alveolorespiratory insufficiency develops as a result of a violation of pulmonary gas exchange due to a decrease in the diffusion capacity of the lungs, an uneven distribution of ventilation and ventilation-perfusion deposits of the lungs.

The main stages of diagnosis

Respiratory failure I degree. Manifested by the development of shortness of breath without the participation of auxiliary muscles, absent at rest.

Cyanosis of the nasolabial triangle is unstable, increases with physical exertion, anxiety, disappears when breathing 40-50% oxygen. The face is pale, puffy. Patients are restless, irritable. Blood pressure is normal or slightly elevated.

Indicators of external respiration: minute volume of respiration (MOD) increased, vital capacity (VC) decreased, respiratory reserve (RD) decreased, respiratory volume (OD) slightly reduced, respiratory equivalent (DE) increased, oxygen utilization factor (CIO)₂) is reduced. The gas composition of the blood at rest is unchanged, it is possible to saturate the blood with oxygen. The tension of carbon dioxide in the blood is within the normal range (30-40 mm Hg). Violations of the KOS is not determined.

Respiratory insufficiency II degree. It is characterized by shortness of breath at rest, retraction of compliant places of the chest (intercostal spaces, supraclavicular fossae), possibly with a predominance of inhalation or exhalation; P/D ratio₂ - 1,5:1, tachycardia.

Cyanosis of the nasolabial triangle, face, hands does not disappear when 40-50% oxygen is inhaled. Diffuse pallor of the skin, hyperhidrosis, pallor of the nail beds. Arterial pressure rises.

Periods of anxiety alternate with periods of weakness and lethargy, VC is reduced by more than 25-30%. OD and RD reduced to 50%. DE is increased, which is due to a decrease in oxygen utilization in the lungs. Blood gas composition, CBS: blood oxygen saturation corresponds to 70-85%, i.e., decreases to 60 mm Hg. Art. Normocapnia or hypercapnia above 45 mm Hg. Art. Respiratory or metabolic acidosis: pH 7,34 - 7,25 (at a rate of 7,35 - 7,45), base deficiency (BE) increased.

Respiratory insufficiency III degree. It is clinically manifested by severe shortness of breath, the respiratory rate exceeds 150% of the norm, aperiodic breathing, bradypnea occurs periodically, breathing is asynchronous, paradoxical.

There is a decrease or absence of respiratory sounds on inspiration.

The ratio of P / D changes: cyanosis becomes diffuse, generalized pallor is possible, marbling of the skin and mucous membranes, sticky sweat, blood pressure is reduced. Consciousness and reaction to pain are sharply reduced, skeletal muscle tone is reduced. Seizures.

Precoma and coma. Indicators of external respiration: MOD is reduced, VC and OD are reduced by more than 50%, RD is 0. Blood gas composition of COS: blood oxygen saturation is less than 70% (45 mm Hg).

Decompensated mixed acidosis develops: pH less than 7,2; BE more than 6-8, hypercapnia more than 79 mm Hg. Art., the level of bicarbonates and buffer bases is reduced.

The survey plan includes:

1) questioning and examination;

2) objective examination (palpation, percussion, auscultation);

3) determination of KOS, partial pressure O₂ and CO₂ in blood;

4) study of indicators of external respiration.

Differential diagnosis

Differential diagnosis of respiratory failure is based on a comparison of clinical symptoms and indicators of external respiration and tissue respiration. With the development of respiratory failure no more than II degree, it is necessary to find the cause of its development.

For example, in violation of alveolar patency, signs of depression of the central nervous system, a violation of the neuromuscular regulation of respiration and destructive processes are differentiated.

With the development of symptoms of obstruction, it is necessary to distinguish between diseases and conditions that cause high obstruction (acute stenosing laryngitis, tracheitis, allergic laryngeal edema, foreign body) and low obstruction (bronchitis, bronchiolitis, asthma attack and status asthmaticus). circulation).

Diagnosis example. Bronchopneumonia complicated by cardio-respiratory syndrome, acute course of II degree respiratory failure, obstructive ventilatory form.

Principle of treatment:

1) creation of a microclimate (ventilation of premises, humidification, aeronization);

2) maintenance of free airway patency (mucus suction, bronchodilators, expectorants, breathing exercises, vibration massage with postural drainage);

3) oxygen therapy (through a mask, nasopharyngeal catheter, oxygen tent, mechanical ventilation, hyperbaric oxygenation);

4) spontaneous breathing under constant positive pressure (CPAP);

5) normalization of pulmonary blood flow (eufillin, pentamine, benzohexonium);

6) CBS correction;

7) to improve the utilization of oxygen by tissues - a glucose-vitamin-energy complex (glucose 10-20; ascorbic acid, cocarboxylase, riboflavin, zeichrome C, calcium pantothenate, unition);

8) treatment of the underlying disease and concomitant pathological conditions.

5. Acute pneumonia

Pneumonia is an infectious lesion of the alveoli, accompanied by infiltration of inflammatory cells and exudation of the parenchyma in response to the invasion and proliferation of microorganisms in the usually sterile parts of the respiratory tract. One of the most common respiratory diseases; 3-5 cases per 1 people.

Etiology

The etiology of pneumonia may be due to:

1) bacterial flora (pneumococcus, streptococcus, staphylococcus, Escherichia coli, Proteus, etc.);

2) mycoplasma;

3) influenza, parainfluenza, herpes, respiratory sensitial, adenoviruses, etc.;

4) fungi.

Acute pneumonia is a common infectious disease of an inflammatory nature of microbial, viral or parasitic etiology. The etiology of acute pneumonia may be due to:

1) bacterial flora (pneumococcus, streptococcus, staphylococcus, Haemophilus influenzae, Friednender's bacillus, enterobacteria, Escherichia coli, Proteus);

2) mycoplasma;

3) influenza, parainfluenza, herpes, respiratory sensitial, adenoviruses, etc.;

4) fungi.

Classification

The form:

1) focal bronchopneumonia;

2) segmental pneumonia;

3) interstitial pneumonia;

4) croupous pneumonia.

Flow:

1) acute;

2) protracted.

The severity is determined by the severity of clinical manifestations or complications:

1) uncomplicated;

2) complicated (cardiorespiratory, circulatory, extrapulmonary complications).

Diagnostic criteria. Anamnestic:

1) the presence of respiratory diseases in the family (tuberculosis, bronchial asthma);

2) ARVI transferred the day before, adenovirus infection;

3) hypothermia.

Clinic

Complaints of cough, fever, weakness, sweating.

Signs of respiratory failure: breathing is groaning, rapid, the number of breaths is up to 60-80 breaths per minute, swelling of the wings of the nose, retraction of the pliable parts of the chest, violation of the rhythm of breathing, inhalation is longer than exhalation, cyanosis of the skin, nasolabial triangle is strongly pronounced, especially after exercise ; gray complexion, pallor of the skin of the face as a result of hypoxemia and hypercapnia, due to the exclusion of a more or less significant part of the alveoli from participating in normal respiratory gas exchange.

It is characterized by intoxication syndrome: fever, weakness, adynamia or agitation, sometimes accompanied by convulsions, sleep disturbance, loss of appetite.

Disorders of the cardiovascular system: muffled heart tones, tachycardia, expansion of the boundaries of the heart, pulse filling is reduced, blood pressure is sometimes increased, the emphasis of the second tone on the aorta. Slowing of cardiac function in severe pneumonia is a formidable symptom.

Changes in the gastrointestinal tract develop due to a decrease in secretory and enzymatic activity: nausea, vomiting, flatulence due to impaired peristalsis, abdominal pain due to irritation of the lower intercostal nerves innervating the diaphragm, abdominal muscles and abdominal skin.

Objective changes in the lungs: functional data are expressed in segmental (polysegmental) and confluent pneumonia, less pronounced in focal pneumonia and bronchopneumonia.

Minimal changes in interstitial pneumonia. Examination and palpation of the chest reveal swelling, more in the anterior sections, tension, which is a characteristic sign of lung enphysema.

During percussion, the percussion sound is variegated (dullness during percussion alternates with areas of tympanic sound); dullness of percussion sound in the lower back sections of the lungs is characteristic of confluent pneumonia.

It is possible with percussion that there are no changes due to the small size of the inflammatory focus.

During auscultation, respiratory failure is heard: hard, puerile, weakened, wet wheezing, small, medium and large caliber, depending on the involvement of the bronchi in the inflammatory process; wheezing can be dry, of a varied nature (whistling, musical). With a deep location of inflammatory foci in the lungs, there may be no percussion and auscultatory changes.

Research methods

X-ray examination: in the pictures, emphysematous changes are combined with foci of infiltration of the lung tissue. It is possible to damage the entire segment of the lung, including the root on the side of the lesion.

In the general blood test, hematological changes: in the peripheral blood, neutrophilic leukocytosis with a shift to the left, an increase in ESR. With a decrease in the reactivity of the body, the indicators may be within the normal range.

Examination plan:

1) general analysis of blood and urine;

2) biochemical study of blood serum (protein fractions, sialic acids, seromucoid, fibrin, LDH);

3) radiography of the chest in two projections;

4) ECG;

5) blood test for immunoglobulins, T- and B-lymphocytes;

6) bacteriological examination of mucus from the nasopharynx, sputum with the determination of the sensitivity of the isolated flora to antibacterial drugs;

7) assessment of the main indicators of external respiration;

8) study of pH and gas composition of blood;

9) radiography of the paranasal sinuses according to indications (complaints of pain when tilting the head, palpation in the projection of the sinuses, discharge from the nose).

Differential diagnosis

Differential diagnosis is carried out with bronchitis, bronchiolitis, acute respiratory viral infection, acute dissimilated pulmonary tuberculosis.

Diagnosis example. Focal bronchopneumonia uncomplicated, acute course.

Treatment

Principle of treatment:

1) the patient is prescribed bed rest, aerotherapy, a diet corresponding to the severity of the condition;

2) antibacterial drugs antibiotics (semi-synthetic penicillins, aminoglycosides, cephalosporins), sulfanilamide drugs (sulfadimezin, sulfoalopanetaxin, biseptol), nitrofuran drugs (furagin, furadonin, furazolidone);

3) treatment of respiratory failure, elimination of obstructive syndrome (removal of mucus from the upper respiratory tract, expectorants and mucolytics, bronchodilators);

4) antihistamines (diphenhydramine, fenkarol, kis-tin, telfast);

5) increase in the patient's immunological activity (immunoglobulin, dibazol, pentoxin, methyluracil, immunomodulators - immunal);

6) vitamin therapy.

6. Pleurisy

Pleurisy is an inflammation of the pleura, accompanied by a tension in the function and structure of the pleural sheets and changing the activity of the external respiratory system.

Etiology

The development of pleurisy may be associated with an infectious agent (staphylococcus, pneumococcus, tuberculosis pathogen, viruses, fungi); non-infectious effects - a complication of the underlying disease (rheumatism, systemic lupus erythematosus, pancreatitis).

Pleurisy may be of unknown etiology (idiopathic pleurisy).

Classification

The classification is as follows:

1) dry pleurisy (fibrous);

2) effusion pleurisy: serous, serous-fibrinous, purulent, hemorrhagic (depending on the nature of the exudate).

Diagnostic criteria

History of previously transferred infectious diseases, pneumonia, inflammation of the paranasal sinuses; frequent hypothermia of the body; the presence in the family or close relatives of tuberculosis or other respiratory diseases.

Clinical signs of pleurisy are manifested by a painful wet cough with a small amount of mucous sputum; the patient complains of pain in the chest (one half), which is aggravated by breathing.

There is a syndrome of respiratory failure: shortness of breath, pallor of the skin, perioral cyanosis, aggravated by physical exertion; acrocyanosis. It is characterized by intoxication syndrome: fatigue, poor appetite, lethargy, weakness.

An objective examination reveals asymmetry of signs: the forced position of the child on the affected side with fixation of the diseased half of the chest.

The side with the focus of inflammation looks smaller, lags behind in the act of breathing, the shoulder is lowered.

With the accumulation of exudate in the pleural cavity during percussion, there is a shortening of the percussion sound with an upper border that goes from the spine upwards outward and to the inner edge of the scapula (Damuazo line).

This line and the spine limit the region of clear lung sound (Garland's triangle). On the healthy side of the chest there is a triangular area of ​​percussion sound shortening (the Grocco-Rauhfus triangle).

Auscultatory: with exudative pleurisy, a sharp weakening of breathing is heard or there is no possibility to listen to it, with dry pleurisy - a pleural friction noise.

Additional research methods

On the radiograph there is an oblique darkening of the diseased lung (fluid level), mediastinal shift to the healthy side, infiltrates in the lung tissue.

The blood test has changes in the form of an increase in ESR, neutrophilic leukocytosis.

When examining the exudate of the pleural cavity, its nature is determined (serous, purulent, hemorrhagic), the specific gravity, the nature and number of formed elements, and the protein level are determined.

Inflammatory exudate is characterized by: the density is more than 1018, the amount of protein is more than 3%, a positive Rivalt test. In the cytological examination of the sediment at the beginning of the development of inflammation, neutrophils predominate.

With development, the number of neutrophils increases, and they can be destroyed. If eosinophils predominate in the sediment, then the patient has allergic pleurisy. The transudate is characterized by a sediment with a small amount of desquamated epithelium. With serous and hemorrhagic pleurisy, cultures on simple media do not give a result.

Tuberculous pleurisy can be established by inoculation on a special medium or infection of guinea pigs. Studies are supplemented with biopsy and morphological studies of altered areas of the pleura during thorocoscopy. In the presence of exudate in the pleural cavity, bronchoscopy is indicated.

Examination plan:

1) biochemical, general blood and urine tests;

2) examination of blood serum (protein, seromucoid, sialic acids, fibrinogen);

3) bacteriological studies of mucus from the pharynx and nose, sputum, fluid from the pleural cavity with the determination of the sensitivity of the isolated flora to antibiotics;

4) study of the immunological status with the determination of T- and B-lymphocytes;

5) radiography of the chest in two projections in a vertical position;

6) pleural puncture;

7) tuberculin diagnostics.

Differential diagnosis

Differential diagnosis is carried out between pleurisy of various etiologies (rheumatic pleurisy, with systemic lupus erythematosus, leukemia, lymphogranulomatosis, hemophilia, kidney disease, liver cirrhosis, liver amoebiasis, tumors, brucellosis, syphilis, mycosis), between effusion pleurisy and lower lobe atelectasis, lobar pneumonia .

Diagnosis example:

1) exudative pleurisy, purulent (pleural empyema, interlobar, pneumococcal);

2) dry pleurisy (fibrinous), effusion (purulent) pleurisy.

Treatment

Principle of treatment:

1) elimination of pain syndrome;

2) influence on the cause that caused pleurisy (antibiotics, anti-inflammatory therapy);

3) therapeutic pleural punctures;

4) symptomatic therapy;

5) physiotherapy, exercise therapy.

7. Chronic nonspecific lung diseases

Chronic nonspecific lung diseases are a group of diseases with different etiology and pathogenesis, characterized by damage to the lung tissue.

The classification is as follows:

1) chronic pneumonia;

2) malformations of the bronchopulmonary system;

3) hereditary lung diseases;

4) lung lesions in hereditary pathology;

5) bronchial asthma.

Chronic pneumonia is a chronic non-specific bronchopulmonary process, which is based on irreversible structural changes in the form of bronchial deformation, pneumosclerosis in one or more segments and is accompanied by inflammation in the lung or bronchi.

Etiology

Most often, chronic pneumonia develops as a result of recurrent or prolonged pneumonia of a staphylococcal nature, with destruction of the lungs.

Chronic secondary pneumonia is based on immunodeficiency states, aspiration of a foreign body, and malformations of the pulmonary system.

Classification

The form:

1) with deformation of the bronchi (without their expansion);

2) with bronchiectasis. Disease period:

1) exacerbation;

2) remission.

The severity of the disease depends on the volume and nature of the lesion, the frequency and duration of exacerbations, and the presence of complications.

Clinic

Chronic pneumonia: a history of repeated pneumonia with a protracted course and destruction of the lungs. Clinically manifested by a constant wet cough, aggravated during the period of exacerbation.

Mucopurulent sputum, more often in the morning. The symptoms of intoxication are pronounced: pallor of the skin, cyanosis of the nasolabial triangle, decreased appetite. Syndrome of chronic heart and lung failure; cyanosis, shortness of breath, tachycardia, nail phalanges in the form of "watch glasses" and "drumsticks".

The chest is deformed - flattening, asymmetry in the act of breathing; percussion - shortening of the sound over the affected area. Auscultatory - bronchial amphoric, weakened breathing. Wheezing varied, wet and dry.

Polycystic lung disease is characterized by a wet cough with purulent sputum, shortness of breath, swelling and retraction of individual parts of the chest. Percussion - shortening of the sound over the foci of inflammation. Auscultatory - amphoric breathing, moist rales.

Lung damage in primary immunodeficiency states. Characteristic frequent SARS, sinusitis, otitis media, hepatolienal syndrome. Decrease in immunoglobulins of a certain class. In the general blood test, lymphopenia; decrease in T- and B-lymphocytes.

Primary pulmonary hypertension. Clinical manifestations: cough may be absent, patients are severely emaciated, ECG shows right ventricular hypertrophy; on the radiograph - the expansion of the roots of the lungs, the expansion of the branches of the pulmonary artery.

Kartagener syndrome is characterized by a triad of symptoms:

1) reverse arrangement of internal organs;

2) bronchiectasis;

3) sinusitis.

Percussion - shortening of the sound above the lesion; auscultatory - moist rales. On the radiograph, the lung lesion is diffuse in nature with localization to a greater extent in the basal segments.

Idiopathic hemosiderosis of the lungs is characterized by damage to the lungs and the deposition of iron in them and anemia.

In sputum - macrophages with gynosiderin. In the blood, the content of indirect bilirubin is increased. On the radiograph - small cloud-like (1-2 cm) focal shadows, often symmetrical.

Lecture #2

1. Arrhythmias

Arrhythmias are heart rhythm disturbances caused by a violation of the activity of the sinus node or activation of the activity of heterotropic centers.

Etiology

Arrhythmias can occur with changes in the structure of the conduction system of the heart in various diseases or under the influence of autonomic, endocrine, electrolyte and other metabolic disorders, intoxication and other metabolic disorders.

The above causes affect the basic functions of the heart (automatism, conduction), the entire conduction system or its departments, determine the electrical inhomogeneity of the myocardium, which leads to arrhythmia.

Arrhythmia can be caused by congenital defects in the conduction system.

The severity of the arrhythmia depends on the severity of the underlying disease.

Diagnosis of arrhythmia is possible with auscultation and in the presence of appropriate changes in the ECG. There are arrhythmias of cardiac and extracardiac origin.

Cardiac arrhythmias can occur with myocarditis, congenital heart defects, cardiomyopathies, coronary heart disease, acute infectious diseases, drug poisoning.

Extracardial - with damage to the central nervous system, the presence of foci of chronic infections, emotional stress, endocrine changes, autonomic dysfunctions. An important role in the occurrence of arrhythmias is played by electrolyte disturbances (especially calcium, potassium, magnesium and sodium), hypoxia, acidosis, etc.

Classification

The classification is as follows.

I. Violation of the rhythm.

1. Nomotopic violations of automatism:

1) sinus tachycardia;

2) sinus bradycardia;

3) sinus arrhythmia;

4) migration of the pulse.

2. Heterotopic disorders of automatism:

1) passive heterotopia (popping antiventricular impulse, atrioventricular rhythm, coronary sinus rhythm, idioventricular rhythm, reciprocal rhythm);

2) active heterotopia (extrasystole, supraventricular tachycardia (sinus, atrial, atrioventricular), paroxysmal ventricular tachycardia, atrial fibrillation and flutter, ventricular fibrillation and flutter).

3. Combination of activity of two centers of automatism (parasystole):

1) parasystole with a focus in the atrium (isorhythmic dissociation);

2) parasystole with a focus in the ventricle; interfering dissociation (or dissociation with interference).

II. Impulse conduction disorders:

1) sinoauricular blockade;

2) intra-atrial blockade (atrial dissociation);

3) atrioventricular block I degree;

4) atrioventricular block II degree (Wenckenbach's periods);

5) atrioventricular blockade of the III degree (blockade 2: 1, 3: 1, etc.);

6) complete atrioventricular block;

7) intraventricular blockade;

8) aberant (deviating) pulse conduction;

9) syndrome of premature excitation of the ventricles (Wolf-Parkinson-White syndrome);

10) electrical alteration of the heart;

11) asystole.

Diagnostic signs

Anamnesis - it turns out the duration of the arrhythmia, its dynamics, possible causes of acute diseases, the influence of toxic factors, physical and mental injuries.

Clinic

In an objective study, it is necessary to pay attention to the presence of clinical lesions of the heart, chronic foci of infection, symptoms of circulatory disorders.

Laboratory and instrumental research methods. With arrhythmia on the ECG, you can determine the form of rhythm disturbance; on FKG, PCG, ECHO, various heart diseases (malformations, cardiomyopathies) are diagnosed, functional tests (Shantva and klikoortoproby) allow you to determine the vegetative status, latent heart failure.

Blood history data allow to exclude the inflammatory process.

A biochemical blood test makes it possible to judge mineral metabolism, the state of acid-base balance, and inflammatory changes in the body.

Nomotopic violations of automatism. Clinical manifestations are expressed in increased, slower pulse or irregularity (alternating quickening and slowing down).

On the ECG, sinus tachycardia is noted - a decrease in the distance between the P waves, the T - P interval is shortened; sinus bradycardia is characterized by an increase in the distance between the P waves and a prolongation of the T - P interval; sinus arrhythmia - the distance between the P waves is different, may decrease or increase.

Extrasystole - premature extraordinary contraction of the heart, due to the appearance of an impulse outside the sinus node. Extrasystole can appear with any heart disease.

Half of the cases of extrasystole are associated with psycho-emotional overstrain, drug intoxication, alcohol consumption, smoking, the use of stimulants, and the influence of internal organs on the heart.

Extrasystole may occur in physically trained people (athletes). Extrasystoles can occur in a row in two or more - paired or group. The rhythm of the heart, in which each normal systole is followed by an extraordinary contraction, is called extrasystole. Especially dangerous are early extrasystoles that occur along with the T wave. Polytopic extrasystoles occur in different foci and at different levels and differ in the form of the extrasystolic complex.

Such changes occur with severe pathology of the heart. Parasystomy - impulses follow in the correct (often sharp) rhythm, coincide with the refractory period of the surrounding tissue and are not realized.

Atrial extrasystoles on the ECG are manifested by a change in the shape and direction of the P wave and a normal ventricular complex.

The interval after extrasystole can be increased. It is associated with impaired atrioventricular and intraventricular conduction. Atrioventricular extrasystoles are characterized by close proximity or superimposition of the P wave on an unchanged ventricular complex. Possible violation of intraventricular conduction. The pause after the extrasystole is increased.

Ventricular extrasystoles are characterized by deformation of the QRST complex, the P wave is absent.

Intercalary extrasystoles are characterized by the absence of a post-extrasystolic pause on the background of bradycardia. Clinically manifested by a feeling of a sinking heart or a push. When examining the pulse, a loss of a pulse wave is felt, with auscultation - premature heart sounds.

Paroxysmal tachycardia - these are attacks of ectopic tachycardia, characterized by the correct rhythm with a frequency of 140-240 per 1 minute with a sudden onset and a sudden end. The heart rate increases by 2-3 times from the norm. There are supraventricular and ventricular forms.

Supraventricular or supraventricular (atrial) paroxysmal tachycardia characterized by strict rhythm, changes in ventricular complexes and a deformed P wave.

Atrioventricular tachycardia characterized by the presence of a negative P wave on the ECG, which follows the QRST complex. The rhythm is regular. Ventricular tachycardia is manifested by deformation of the QPST complex, the P wave is poorly distinguishable; the atria fire independently of the ventricles.

After an attack of paroxysmal tachycardia, negative T waves are recorded on the ECG, sometimes with ST shift. This phenomenon is called post-tachycardia syndrome. Clinically manifested by a feeling of palpitations from a few seconds to several days.

Vegetative manifestations: sweating, profuse urination, fever, increased intestinal motility. Patients complain of weakness, pressing pains in the region of the heart. Ventricular tachycardia may be a precursor to ventricular fibrillation.

Atrial fibrillation expressed in erratic incomplete contractions of the atria and the lack of a coordinated connection between the activity of the atria and ventricles. The muscle fibers of the atria contract randomly. The ventricles contract arrhythmically with a frequency of 100-150 per minute. Atrial flutter - regular atrial contraction with a frequency of 250-300 per minute.

Atrial fibrillation may be persistent or paroxysmal. Atrial fibrillation occurs with mitral heart disease, coronary artery disease, thyrotoxicosis, alcoholism. Transient atrial fibrillation occurs with myocardial infarction, intoxication with cardiac glycosides, alcohol.

It is clinically manifested by pain in the heart, palpitations, shortness of breath, anxiety, a pulse deficit is characteristic, an erratic rhythm is heard during auscultation. On the ECG, instead of P waves, there are F waves, the frequency of which ranges from 250 to 600 per minute, absolute randomness of the rhythm, QRS complexes without an R wave.

With atrial flutter, the waves are larger, like teeth, with a frequency of 250-200 per minute. The ventricular complexes are often deformed at irregular intervals. Persistent paroxysmal atrial fibrillation causes a tendency to thromboembolic complications.

Conduction disorder It is characterized by a violation of the conduction of excitation (up to a complete interruption in the conduction of excitation) along the conduction system and the myocardium and is called a blockade. Depending on the location of the conduction disturbance, blockades are distinguished: sinoauricular (an impulse is not formed at all or is not conducted), another cardiac complex appears on the ECG - a long pause equal to a double normal interval; intra-atrial (characterized on the ECG by splitting and widening of the P tooth) and atrioventricular blockade, intra-ventricular blockade.

Atrioventricular block is of two degrees; complete, incomplete.

Blockade of the first degree is characterized on the ECG by prolongation of the PQ interval more than the age norm. Blockade of the second degree with periods of Samoilov - Wenkenbach is characterized by a gradual increase in the PQ interval with the next loss of ventricular contraction, after which the PQ interval is restored to normal, then increases again.

Complete atrioventricular blockade is characterized by an independent rhythm of both the atria and the ventricles as a result of a violation of the connection between them.

The atria contract under the influence of an impulse from the sinus node, and the ventricles from places below the lesion: on auscultation - bradycardia, the first tone is muffled, periodically clapping; there may be attacks of Morgagni - Adams - Stokes, manifested by pallor, cyanosis, loss of consciousness, convulsions, with auscultation Strazhesko's cannon tone.

On the ECG, the P waves are not associated with the QRS complex, the distance between the Ps is equal, the intervals R - R are also equal, and the shape of the ventricular complex is determined by the impulse generation method; on FKG different amplitude of the first tone.

Intraventricular blockade is diagnosed using an ECG. The ECG shows a moderate notched QRS complex; the presence of a right- or left-hand image, depending on which leg is blocked; discordant arrangement of the R and T waves in the first and third leads.

Syndrome of premature ventricular excitation (WPW) - on the ECG, a shortening of the PQ interval, a widening of the QRS due to the presence of a wave.

Differential diagnosis

It is carried out between different types of arrhythmias based on the clinic and ECG studies.

Treatment:

1) elimination of the causes of arrhythmia;

2) impact on the disturbed electrolyte balance (potassium, magnesium preparations, polarizing mixtures);

3) antiarrhythmic drugs:

a) membrane stabilizing - suppressing the activity of ectopic foci (novocainamide, etmozin, atmanin, ritmodan, medocaine, difenin);

b) adrenergic blockers (obzidan, inderan, anaprilin, cordarone, amiodarone, atepolone, bisopropone, metopropone);

c) potassium antagonists reduce the rate of propagation of excitation in the atrioventricular junction (isoptin, finopetin);

4) mechanical (reflex) effect: pressure on the carotid sinuses, eyeballs, straining, etc.;

5) electrical impulse stimulation;

6) surgical treatment.

2. Vegetovascular dystonia

Vegetovascular dystonia is a condition based on a violation of the autonomic regulation of internal organs, blood vessels, endocrine glands, due to dysfunction of the central and peripheral nervous system.

Etiology

Hereditary and acquired factors predispose to the occurrence of vegetovascular dystonia. Hereditary factors:

1) genetic predisposition (constitutional features of the activity of the autonomic nervous system, hereditary dysautonomy - Riney-Day disease, congenital inferiority of the vestibular labyrinth, increased sensitivity of vascular muscles to humoral influences;

2) malformations of the central nervous system;

3) malformations of the endocrine glands;

4) personal characteristics.

Acquired factors affecting the state of suprasegmental vegetative centers:

1) asphyxia, hypoxia, in which the autonomic centers of the cerebral cortex, hypothalamus, choroid plexuses producing cerebrospinal fluid are damaged;

2) psycho-emotional overstrain;

3) acquired lesions of the central nervous system: skull injuries, infections, intoxications affecting the hypothalamus;

4) violation of the regime of the day, meteorological impact;

5) dysfunction of the endocrine system;

6) repeated infectious diseases, foci of chronic infection (tonsillitis, caries, sinusitis).

Classification

Type of vegetovascular dystonia:

1) with an increase in blood pressure;

2) with a decrease in blood pressure;

3) with cardialgia;

4) mixed. The nature of the flow:

1) latent;

2) permanent;

3) paroxysmal. Crisis nature:

1) symptomatic-adrenal;

2) vagoinsular;

3) mixed. Flow phase:

1) exacerbation;

2) remission.

Clinic

Clinic of vegetative-vascular dystonia with high blood pressure. An increase in blood pressure as a result of increased activity of the sympathetic part of the autonomic nervous system:

1) headache in the temporal or parietal region, often passing, short-term, occurs at the end of the day, after exercise, then becomes more frequent, lasts longer and disappears after taking analgesics or antihypertensive drugs; dizziness; rapid mood swings, anger, tearfulness, irritability, sleep disturbance, palpitations, arrhythmia;

2) with a sharp increase in blood pressure, it is complicated by sympathoadrenal crises: blood pressure 160/100 - 200/100, headache, fear, "tinnitus", "mesh before the eyes", nausea, vomiting, feeling hot, dry mouth, tachycardia, polyuria;

3) there are no changes in blood tests;

4) there are no changes in the fundus in the transient stage;

5) labile stage - unevenness and narrowing of the arteries of the retina, their sensitivity, expansion of venules;

6) on the ECG: smoothed or negative T wave, atrioventricular blockade, prolapse of atrioventricular nystagmus, rhythm disturbance (paroxysmal tachycardia);

7) on FCG, echocardiography, X-ray examination of the heart - no pathologies.

Vegetovascular dystonia with a decrease in blood pressure. The basis of arterial hypotension is a violation of the activity of the higher centers of the autonomic nervous system, which leads to a decrease in peripheral resistance (tonus of arterioles, precapillaries) and an insufficiently compensated increase in cardiac output.

Arterial hypotension is established at a systolic pressure of 102 mm and below, diastolic - 63 mm Hg. Art. and below, pulse pressure 30-35 mm Hg. Art. It is characterized by a headache of a pressing nature, dizziness. Symptoms first appear in the evening, in a stuffy room, sometimes a migraine-type headache, vomiting, intolerance to loud sounds, bright lights.

Deterioration in spring and autumn, altered circadian rhythm of well-being (in the morning - a decrease in working capacity, in the afternoon - improvement, in the evening - lethargy).

With an increase in the function of the parasympathetic autonomic nervous system (vagotonia) - a feeling of lack of air, tightness in the chest, sudden shortness of breath during exercise, deep sighs for no apparent reason, attacks of pseudoasthma at night, paroxysmal neurotic cough: pain in the region of the heart of a stabbing character that occurs more often with excitement; nausea, vomiting, belching, heartburn, abdominal pain, constipation, increased salivation; increased weakness, fatigue, isolation, drowsiness, mental exhaustion - memory loss, attention disorder. An objective examination of the skin easily reddens and turns pale, the hands are cold, wet, cyanotic; greasiness of the skin is increased on the face, acne is observed on the back; there may be an allergic rash; swelling on the face, limbs; hyperhidrosis, red persistent dermographism. Hypertrophy of lymphoid tissue (enlarged tonsils, thymus, peripheral lymph nodes).

"Vagus" heart - displacement of the left border outwards, muffledness of the first tone, the appearance of the third tone above the apex in a horizontal position; the number of heart sounds is reduced, respiratory arrhythmia, tachycardia during exercise; sometimes fainting (syncope) as a result of increased sensitivity α₂- adrenoreceptors of the vascular wall; vegetative paroxysms in vagotonia occur in the form of vagoinsular crises that occur during emotional or mental overstrain.

Last from several minutes to several hours (migraine-like headache, dizziness, lowering blood pressure up to fainting, hypothermia, nausea, vomiting, abdominal pain, suffocation, sweating, laryngeal spasms, asthma attacks, allergic rash, Quincke's edema); There is no pathology in the blood tests.

On the ECG: vagal heart - bradycardia, sinus arrhythmia, decreased amplitude of the P wave, prolongation of the PQ interval up to blockade of the I-II degree, high jagged T wave, shift of the ST segment above the isoline by more than 1 cm, myocardial dystrophy; Echocardiography - often an increase in the end diastolic volume of the left ventricle.

Vegetovascular dystonia with cardialgia. Blood pressure within physiological fluctuations; pain in the region of the heart with irradiation to the left arm, a feeling of tightness in the chest, lack of air, suffocation, paresthesia in the left arm, headache, dizziness, irritability, sweating are possible; heart rhythm disturbances are characteristic - paroxysmal and non-paroxysmal tachycardia, bradycardia, extrasystole. Complete blood count without pathologies.

On the ECG changes in the bioelectric activity of the myocardium, rhythm disturbance.

This condition is based on functional cardiopathy, which develops as a result of a violation of the neurohumoral regulation of the heart.

Vegetovascular dystonia of mixed type. The basis of this disease is damage to the hypothalamus: complaints and objective data characteristic of both sympathicotopia and vagotonia (headache, dizziness, fatigue, sleep disturbance, pain in the heart, palpitations); blood pressure indicators are labile (from hypertension to hypotension), blood pressure asymmetry is up to 10 mm Hg. Art.

Differential diagnosis

Differential diagnosis is carried out with the following diseases.

1. Vegetovascular dystonia with increased blood pressure: with symptomatic hypertension due to diseases of the kidneys, heart and large vessels, central nervous system (tumors, injuries), endocrine system, hypertension.

2. Vegetovascular dystonia with cardiopathy: with carditis of various etiologies, congenital disorders of the conduction system of the heart.

3. Vegetovascular dystonia with a decrease in blood pressure: with physiological hypotension of increased fitness (athletes), adaptive hypotension (in residents of the highlands, tropics), symptomatic hypotension, hypothyroidism, pituitary insufficiency, myocarditis, intoxication, infection.

Treatment

Characteristic for all types of vegetovascular dystonia:

1) elimination of etiological factors;

2) a rational day regimen, a calm emotional environment, a sufficient degree of physical activity and night sleep, outdoor walks, psychotherapy.

3. Hypertension

Hypertensive disease - primary arterial hypertension is an emergency - a disease that is manifested by a decrease in the adaptive mechanisms of the cardiovascular system, a violation of the mechanisms that carry out hemodynamics, an increase in speed, progressive changes in blood vessels and complications. Normal blood pressure in people 20-40 years old is below 140/90, in people 41-60 years old - below 145/90 mm, over 60 years old - below 160/90 mm Hg. Art. With violations of the daily regimen, the risk of hypertension increases.

High risk of developing hypertension in individuals with aggravated heredity; the risk is five times higher than in control groups. The development of hypertension depends on the salt regimen.

The more salt in the food, the greater the risk of developing hypertension. To reduce the incidence of hypertension lead to:

1) increasing the promotion of physical activity;

2) rational nutrition;

3) reduced salt intake;

4) reduction in the number of smokers;

5) effective treatment of patients with hypertension.

Classification of hypertension according to G. F. Lang (1950)

By stages:

1) neurogenic;

2) transitional;

3) nephrogenic.

By dominance:

1) cardiac;

2) cerebral;

3) renal.

By form or phase: malignant.

Classification of hypertension

By stages.

I - functional.

II - cardiac hypertrophy, vascular changes.

III - resistant to treatment. By forms:

1) malignant;

2) benign with a primary lesion: the heart, kidneys, coronary vessels, brain, eyes. Each stage is characterized by a certain level of blood pressure.

I degree - 160 (179) / 95 (104).

II degree - 180 (200) / 105 (114).

III degree - 210 (230) / 115 (129).

Clinic

The disease begins more often in people aged 30-60 years. An increase in blood pressure in people younger than 30 years is most often associated with recovascular hypertension. An increase in blood pressure in people over 60 years of age is associated with atherosclerotic vascular thickening. The progression of the disease can be slow (benign) or rapid (malignant).

Stage I (mild) is characterized by a slight rise in blood pressure. The level of arterial pressure is unstable, during the rest of the patient it gradually normalizes; the disease is fixed in contrast to borderline hypertension. Patients often do not experience any health problems.

Sometimes they worry about headaches, noise in the head, sleep disturbance, decreased mental performance, dizziness, nosebleeds.

There are no signs of left ventricular hypertrophy. ECG shows signs of hypersympathicotonia. Renal functions are not disturbed, the fundus of the eye is not changed.

Stage II (middle) is characterized by a higher level of blood pressure.

Patients often complain of headaches, dizziness, pain in the heart. Characterized by hypertensive crises.

Signs of organ damage appear: left ventricular hypertrophy, weakening of the first tone at the apex of the heart, emphasis of the second tone on the aorta; ECG signs of subendocardial ischemia.

From the side of the nervous system, signs of vascular insufficiency: ischemic transient attacks, cerebral strokes, encephalopathy.

On the fundus - narrowing of the arterioles, compression of the veins and their expansion, hemorrhages, exudates. The blood flow in the kidneys and the filtration rate are reduced.

Stage III is characterized by frequent vascular complications. The frequency of complications depends on the degree of stabilization of blood pressure, the progression of atherosclerosis. The level of increase in blood pressure reaches its maximum values.

Patients are often hospitalized with myocardial infarction, cerebral stroke, arrhythmia, hemophilia. On the part of the kidneys, dysfunctions are expressed - a decrease in renal blood flow and glomerular filtration.

There are several clinical forms of arterial hypertension. Hyperadrenergic manifests itself at the beginning of the disease, but may persist throughout the entire period of the disease.

It is characterized by sinus tachycardia, arterial pressure instability with a tendency to systolic hypertension, facial hyperhidrosis, eye glare; patients feel a pulsation in the head, palpitations, anxiety, chills. The hyperhydration form of hypertension is characterized by periorbital edema, puffiness of the face in the morning, swelling of the fingers, numbness and paresthesia.

Diuresis with a tendency to transient oliguria. Due to the rapid retention of sodium, water-salt hypertensive crises develop.

A malignant form of hypertension is a rapidly progressive form characterized by an increase in blood pressure to high levels, followed by the development of encephalopathy, visual impairment, pulmonary edema, and renal failure.

Treatment

Non-pharmacological principles include:

1) weight loss by reducing the amount of fats and carbohydrates;

2) reducing the amount of salt in the diet to 3 g;

3) the total amount of fluid consumed is 1,2-1,5 liters per day;

4) the fight against hypodynamia, physiotherapy exercises;

5) sanatorium treatment.

These methods are effective in the first stage of hypertension and serve as a background in the treatment of other forms. Medicinal principles - the method of titration is the selection of the dose until the optimal level of blood pressure is reached.

In the first stage of hypertension, an α-blocker or diuretic is prescribed. β-blockers are the drug of choice in the presence of concomitant arrhythmia and tachycardia. Diuretics are prescribed for reducing hypertension with bradycardia, obesity, bronchopulmonary pathology (indapamide 1 time per day in the morning).

In the second stage of hypertension, a combination of ACE inhibitors, β-blockers, calcium channel blockers, diuretics is used.

In the third stage, a combination of drugs is selected to normalize blood pressure and the dose of the above drugs is increased. Treatment of patients at the first and second stages is carried out on an outpatient basis. If difficulties arise in the selection of drugs, patients are hospitalized.

Forecast

The presence of a history of arterial hypertension in patients increases the risk of developing myocardial infarction, stroke, encephalopathy.

4. Angina

Angina pectoris is a disease characterized by an attack of sudden pain in the region of the heart and behind the sternum as a result of an acute lack of blood supply to the myocardium. Angina pectoris is a clinical form of coronary heart disease.

Pathogenesis

The disease is caused by atherosclerosis of the coronary arteries of the heart, which causes myocardial ischemia during physical or emotional overstrain. The onset of an attack is facilitated by a decrease in blood flow to the mouths of the coronary arteries (arterial distienic hypotension of medicinal origin, a decrease in cardiac output with tachyarrhythmia, venous hypotension; pathological effects from the organs of the gastrointestinal tract).

The main mechanisms for reducing pain at the time of an attack: a rapid and significant decrease in the level of work of the heart muscle (cessation of exercise, taking nitroglycerin), restoration of blood flow in the ischemic area.

The main conditions for slowing down and reducing the intensity of attacks are the adequacy of the patient's loads to the reserve capabilities of his coronary bed; development of blood circulation; decrease in blood viscosity; stabilization of systemic circulation; development of myocardial fibrosis in the area of ​​its ischemia.

Clinic

With angina pectoris at the time of an attack, the pain has a pronounced time of onset and cessation, remission; occurs under certain conditions, circumstances; begins to subside or decreases under the action of nitroglycerin 3-5 minutes after taking the drug sublingually. The occurrence of an attack can be associated with a load (acceleration of walking, when climbing uphill, with a sharp headwind, when lifting weights) or significant emotional stress.

When the load is increased, the pain intensifies and continues, and when the load is stopped, the pain decreases or stops within a few minutes.

Other signs complement the clinical picture, but their absence does not rule out this diagnosis:

1) localization of pain behind the sternum with irradiation to the left arm, under the shoulder blade on the left, to the neck;

2) the nature of the pain - pressing, squeezing, less often - burning (like heartburn), sometimes a sensation of a foreign body in the chest;

3) simultaneously with the pain syndrome, blood pressure rises, pallor of the skin is observed, and arrhythmia appears.

The equivalent of pain is shortness of breath (feeling short of breath). Rest angina pectoris occurs regardless of physical activity, more often at night, accompanied by suffocation, a feeling of lack of air.

In most patients, the course of angina pectoris is stable - attacks occur at a certain load at a certain time, do not change in strength and duration. The intensity of stable angina pectoris is classified by functional classes.

The functional class of the first type includes patients in whom angina pectoris manifests itself as rare attacks caused by heavy physical exertion.

The functional class of the second type includes persons who have seizures during normal exertion, but not always. The functional class of the third type includes persons whose seizures occur during mild physical exertion. The functional class of the fourth type includes persons who have seizures with minimal or no exercise.

Unstable angina - attacks become more frequent and intensify from the first weeks of illness; the course of angina pectoris loses stability; Seizures also occur during heavy exertion. On the ECG - a decrease in ST amplitude, T-wave inversion, arrhythmia. Increased ALT, AST.

Pre-infarction angina in 30% of cases ends with myocardial infarction. If the duration of angina pectoris exceeds 30 minutes and is not reduced by taking nitroglycerin, it is necessary to carry out a differential diagnosis with myocardial infarction.

Treatment

Relief of an attack: the patient is asked to calm down, take a sitting position, sublingual intake of nitroglycerin, repeated intake of nitroglycerin after 2-3 minutes in the absence of effect; valoserdin (valocardin) - 40 drops inside.

During the non-attack period, the patient must avoid stress that leads to an attack; nitroglycerin is indicated before the upcoming load; elimination of emotional stress; treatment of concomitant diseases; treatment of vascular atherosclerosis; expansion of physical activity.

In the interictal period with angina pectoris of the first functional class, nitrates are prescribed (kardiket, pektrol) in anticipation of significant loads.

With angina pectoris of the second functional class, long-term use of β-blockers (stenolone, metopronol, bisopronol) is prescribed under the control of heart rate (optimally 60-70 per minute).

Nitrates courses until the cessation of seizures and in the future before the loads.

With unstable angina, first of all, it is necessary to provide the patient with rest, to be hospitalized in a hospital; constant intake of nitrates; hyparinotherapy - subcutaneously in the abdominal wall 5000 IU 4 times a day; acetylsalicylic acid 100, 200 mg once a day; β-blockers; sedatives.

Calcium antagonists (nifedipine) are prescribed for angina at rest, with bradycardia (heart rate - 50-60 beats per minute).

The prognosis in the absence of complications is favorable.

5. Myocardial infarction

Myocardial infarction is a heart disease caused by acute circulatory failure and the occurrence of a focus of necrosis in the heart muscle. The most important clinical form of coronary heart disease.

Pathogenesis

The cause of a heart attack is:

1) coronary thrombosis - blockage of the lumen of the artery, which leads to the formation of an ischemia zone, and later - to necrosis - a macrofocal, often transanural infarction;

2) coronary stenosis - an acute narrowing of the lumen of the arteries by a swollen atherosclerotic plaque;

3) stenosing widespread coronary sclerosis - narrowing of the lumen of 2-3 arteries of the heart often leads to small-focal heart attacks.

Clinic

Myocardial infarction is characterized by a pronounced pain syndrome lasting more than 30 minutes, often many hours, not removed by taking nitroglycerin. Often patients complain of suffocation or pain in the epigastric region with asthmatic or gastric forms of myocardial infarction.

In the acute period, arterial hypertension appears (often pronounced), which decreases after the pain subsides; tachycardia, hyperthermia for 2-3 days. In the general analysis of blood - leukocytosis and increased ESR; the level of glycemia, fibrinogen, AST, ALT, LDH increases. Auscultatory - friction rub of the pericardium of the left edge of the sternum. On the ECG - a widening of the Q wave, a dome-shaped rise in the ST segment, a QS-form of the ventricular complex occurs, a decrease in the amplitude of R.

In 25% of cases, myocardial infarction is not accompanied by the use of EC. Complications of the acute period - left ventricular failure, cardiogenic shock, pulmonary edema, tachyarrhythmia with arterial hypotension, clinical death due to asystole.

The appearance of ventricular ectopic arrhythmias indicates thrombus lysis and venous artery patency.

Complications of the hospital period of myocardial infarction - agitation, inadequate attitude to one's condition, often mental disorders, resumption of pain behind the sternum, the appearance of fibrinous pericarditis, fluctuations in the heart rate, pulmonary infarction; paroxysms of tachycardia, early ventricular extrasystoles, atrioventricular block II-III degree; aneurysm of the left ventricle; acute heart failure, cardiogenic shock, thromboembolism in the pulmonary artery system; embolism of the arteries of the lower extremities (postinfarction syndrome).

For small-focal myocardial infarction, the same symptoms are characteristic as for extensive myocardial infarction, but to a lesser extent.

Differential diagnosis is carried out with pericarditis, pulmonary embolism, massive internal bleeding, acute pancreatitis, aortic aneurysm.

Treatment:

1) continuous exposure to nitrates;

2) the introduction of drugs that lyse the thrombus;

3) the introduction of β-blockers;

4) the introduction of potassium chloride in the form of a polarizing mixture. If the introduction of nitroglycerin does not give an analgesic effect, then it is advisable to introduce narcotic analgesics. Inhalation of nitrous oxide and oxygen (1:1).

Heparin is administered intravenously, starting with 1000 IU (effectively in the first hours (2-3) after a heart attack), infusion therapy with heparin is continued for 5-7 days. Stationary regimen for a patient who has had a myocardial infarction - at least 21 days. Congestion is stopped by the appointment of diuretics.

6. Carditis

Carditis is a lesion of the heart (endocardium, myocardium, pericardium), the substrate of which is inflammation in its classical form.

Etiology

Carditis can be of a different nature: viral (coxsackie enteroviruses A and B, ECHO, herpes simplex, rubella, cytomegaly); bacterial; yersinia; allergic (drug, serum, vaccine); idiopathic (of unknown etiology).

Classification

The classification is as follows:

1) the period of occurrence of the disease (congenital and acquired);

2) form (according to the predominant localization of the process);

3) severity of carditis: mild, moderate, severe;

4) course: acute (up to 3 months), subacute (up to 18 months), chronic (more than 18 months) (recurrent; primary chronic: congestive, hypertrophic, restrictive variant);

5) form and degree of heart failure: left ventricular I, IIA, IIB, III degrees; right ventricular I, IIA, IIB, III degrees; total;

6) outcomes and complications: cardiosclerosis, myocardial hypertrophy, rhythm and conduction disturbances: pulmonary hypertension, valvular lesions, constrictive myopericarditis, thromboembolic syndrome (N. A. Belokon, 1984).

Pathogenesis and clinic of acquired carditis

Extracardiac signs: connection with a previous acute respiratory viral infection or other infectious diseases.

Cardiac signs: an increase in the size of the heart, a change in the sonority of tones, shortness of breath, heart failure, pain in the region of the heart, systolic murmur at the top; on the ECG: violation of automatism, excitability and conduction; X-ray examination: moderate movement of the heart due to the left ventricle, a decrease in the depth of the pulsation; moderate or minimal laboratory activity (ESR, white blood cell count, protein fractions, DFA, C-reactive protein are normal or slightly elevated).

Chronic carditis occurs in the form of 2 forms:

1) primary chronic carditis (gradually developing carditis with a clinically asymptomatic initial phase);

2) chronic carditis develops in the acute or subacute period.

Extracardiac signs: fatigue, weakness, recurrent pneumonia, nausea, vomiting, abdominal pain.

The first cardiac symptoms are: shortness of breath, systolic murmur, sudden onset heart failure, tachy- and bradyarrhythmia.

Together with the general diagnostic criteria, it is possible to distinguish features for two variants of the course of chronic carditis (chronic carditis with an enlarged left ventricular cavity and chronic carditis with a normal and reduced left ventricular cavity). Chronic carditis with an enlarged left ventricular cavity is characterized by: a diffuse apex beat, a cardiac hump, the borders of the heart are sharply expanded, mainly to the left, muffled tones, systolic murmur of mitral valve insufficiency, tachycardia, shortness of breath, moderate enlargement of the liver; ECG: high voltage of arrhythmia teeth, moderate atrial overload, signs of left ventricular hypertrophy; X-ray examination: pulmonary pattern is moderately enhanced along the venous bed; heart shape mitral trapezoid, aortic; enlargement of the left heart; decrease in the amplitude of the pulsation along the contour of the left ventricle.

Chronic carditis with a reduced or normal left ventricular cavity is characterized by:

1) crimson cyanosis;

2) apex beat ascending, localized; the borders of the heart are expanded in both directions, the tones are loud, the I tone is clapping, a tendency to bradycardia;

3) ascites, significant enlargement of the liver, tachy- and dyspnea;

4) on the ECG: high voltage of the teeth, slowing of the atriventricular conduction and intraventricular conduction, signs of overload of both atria, more than the left one; signs of an increase in both ventricles, more than the right one;

5) during x-ray examination, the pulmonary pattern is enhanced along the venous and arterial bed; heart shape as in central and aortic stenosis; enlargement of the atria, right ventricle; pulsation amplitude is normal or increased.

Differential diagnosis

Differentiate with rheumatism, constrictive pericarditis, changes in storage diseases. Principles of treatment:

1) restriction of motor activity for 2-3 weeks;

2) good nutrition with sufficient content of vitamins, proteins, salt restriction, high potassium content;

3) antibiotic therapy (penicillin preparations);

4) non-steroidal anti-inflammatory drugs;

5) drugs that improve metabolic processes in the myocardium;

6) therapy of heart failure;

7) prednisolone;

8) in chronic carditis courses of depagin or voltaren 2-3 times a year. To prevent the damaging effect of cynics, anginin (prodectin), contracan for 1,5-2 months; glucocorticoids are prescribed individually, since chronic immune inflammations are often resistant to hormone therapy.

7. Circulatory failure

Acute and chronic circulatory insufficiency is a pathological condition consisting in the inability of the circulatory system to deliver to organs and tissues the amount of blood necessary for their normal functioning.

Etiology

Circulatory insufficiency accompanies not only heart disease, but also infectious diseases, metabolic diseases, surgical interventions, as well as diseases of the lungs, liver, kidneys and all diseases that lead to a decrease in myocardial contractility, to volume overload, pressure, to severe metabolic disorders in myocardium.

Classification

Form: heart failure, vascular insufficiency. Course: acute, chronic. Origin:

1) systolic, diastolic, mixed;

2) overload by pressure, volume, primary myocardial, disruption of rhythmic activity, combined.

Clinical variants: left ventricular I, II A, II B, III; right ventricular I, IIA, IIB, III degrees; total.

Vascular insufficiency

Downstream: acute, chronic, permanent, paroxysmal.

By origin: violation of the nervous and humoral regulation, changes in the sensitivity of the receptor apparatus, structural disorders of the vascular wall, thrombosis. Clinical variants: syncope, collapse, shock, various vascular dystonias (N. A. Belokon, 1987).

Criteria for the clinical picture. In the anamnesis, behavior and well-being are disturbed. The patient complains of fatigue, shortness of breath, cough, pain in the heart, palpitations, decreased diuresis, edema.

On physical examination: pale skin, cyanosis, dry skin, itching, seizures in the corners of the mouth, expansion of the venous network of the chest; shortness of breath, tachycardia, swelling of the lower extremities or general, enlarged liver, enlarged heart; on the ECG: symptoms of overload or hypertrophy of the heart, cardiac arrhythmias, metabolic processes; on the radiograph: a decrease in the contractility of the heart, expansion of the roots and an increase in the pulmonary pattern in the middle sections of the lungs, accumulation of transudate in the pleural cavity is possible; increase in ATC (more than 120-140 mm of water column), echocardiography makes it possible to distinguish compensated and de-compensated types of right and left ventricular failure.

With right ventricular failure, the size and volume of the ventricle prevail over the mass; with left ventricular - both volume and mass increase; sounding of the cavities of the heart allows you to assess the severity of heart failure: with right ventricular - increased systolic pressure, with left ventricular - diastolic.

Chronic heart failure

There are three degrees of circulatory failure.

NK I degree - hidden, there are no signs of circulatory disorders at rest, they appear after physical exertion in the form of fatigue, shortness of breath, tachycardia, pallor. Indicators return to normal after 10 minutes.

NK IIA - reversible stage, expressed mainly by insufficiency of the right or left heart at rest. The heart rate increases from the norm by 10-15%, the respiratory rate - by 15-30%, the edge of the liver is 2-4 cm below the costal arch.

There is pastosity of tissues, expansion of the boundaries to the right, swelling of the cervical veins with right ventricular failure. With left ventricular - shortness of breath, tachycardia, muffled wheezing in the lower parts of the lungs, congestive roots, bulging of the pulmonary artery arch.

NC IIB degree - total; shortness of breath is pronounced, the number of breaths increases by 30-70%, cyanosis, tachycardia (15-30% more than the norm), the liver protrudes from under the costal arch by 4 cm or more, peripheral edema, an increase in the borders of the heart in both directions, a decrease diuresis, a sharp decrease in appetite.

NK III degree - dystrophic, cachexic, characterized by a sharp decrease in body weight, atrophy of organs and tissues; the number of heartbeats increases by 50-60%, the number of breaths - 70 - 100%, anasarca, liver cirrhosis, pneumosclerosis; a total increase in the size of the heart, a violation of the heart rhythm.

Differential diagnosis

It is carried out between cardiac and vascular insufficiency.

Principle of treatment:

1) physical rest until decompensation is removed, a diet with fluid, salt restriction, Carrel's diet;

2) cardiac glucosides at a saturation dose, then maintenance (1/4 - 1/6 of the total dose);

3) diuretics;

4) regulation of metabolism in the myocardium (anabolic steroids, cocarboxylase, ATP, panangin);

5) B vitamins₆, AT₁₂, AT₅, E;

6) vasodilators (cardinet, pectron, nopochinava);

7) hormones;

8) elimination of arrhythmia;

9) treatment of the underlying disease.

Lecture #3

All diseases of the stomach are divided into functional and organic. Functional diseases include a violation of the secretory activity of the stomach, a violation of the motor activity of the stomach (cardiospasm, pylorospasm, reflux).

Organic diseases include gastritis, gastric ulcer. Diseases of the stomach include conditions after surgery (postoperative diseases) and tumors. The basis of functional disorders can be dietary disorders, improper food processing, insufficient number of first courses, dry food, poor chewing - alimentary reasons. The second reason is the presence of concomitant diseases of other parts of the gastrointestinal tract.

Clinically, functional disorders are manifested in dull, aching pains in the epigastric region. Pain can be cramping in nature and accompanied by a feeling of heaviness, nausea, vomiting. Vomiting brings relief.

The differential diagnosis should be carried out with food intoxication, which is accompanied by fever and dehydration.

Treatment consists in the normalization of the diet, the course appointment of enzyme preparations, herbal medicine (festal, creon, mezim-forte, marsh calamus).

The prognosis is favorable, but a transition to gastritis or peptic ulcer is possible.

1. Acute gastritis

Acute gastritis is an acute inflammation of the gastric mucosa of non-infectious origin. The cause of acute gastritis may be a malnutrition (change in diet, overload of the digestive tract with abundant food, smoked meats, marinades, cold food (ice cream)). Gastritis may occur due to the use of drugs (aspirin).

Clinically manifested a feeling of heaviness and pain in the epigastrium, accompanied by profuse vomiting. Bitter taste in the mouth. On palpation, swelling and pain in the epigastric region. The chair is unstable. With adequate treatment, the prognosis is favorable. Healed after three days.

Differential diagnosis carried out with toxicoinfection, helminthic invasion.

Treatment carry out the appointment of a diet (liquid cereals, jelly, vegetable puree, cottage cheese, boiled fish, meat, stale bread). Enzyme preparations (mezim-forte, inzistan, coenzyme, panzinorm).

2. Chronic gastritis

Chronic gastritis is a disease that is characterized by chronic inflammation of the gastric mucosa, impaired regenerative processes in the mucosa, followed by atrophy of the gastric glands.

Etiology

Exogenous factors - physical (cold, hot, rough food), chemical (pesticides, toxins, preservatives), biological (intake of allergens, microorganisms). Endogenous factors include: increased acidity, impaired mucus formation and regulation of digestion by hormones.

Classification

The classification is as follows.

I. By origin:

1) primary (exogenous gastritis);

2) secondary (endogenous).

II. By prevalence and localization of the process:

1) widespread gastritis;

2) focal (antral, fundal) gastritis.

III. By the nature of histological changes in the gastric mucosa:

1) superficial gastritis;

2) gastritis with lesions of the gastric glands without atrophy;

3) atrophic gastritis (moderately expressed with restructuring of the mucous membrane).

IV. According to the nature of gastric secretion:

1) with normal secretory function;

2) with reduced secretory function;

3) with increased secretory function.

V. Flow phases:

1) phase of exacerbation;

2) phase of incomplete remission;

3) remission phase.

Clinic

Clinically, chronic gastritis is characterized by the following symptoms: the patient complains of pain in the epigastric region during meals or immediately after meals. The tongue is coated at the root and on the back with a white or yellowish coating, on palpation there is pain in the epigastrium, Mallory's syndrome is positive. The duration of the disease is more than six months. In the anamnesis - in relatives of the disease of the stomach (chronic gastritis, peptic ulcer).

Diagnostics

Instrumental diagnostic criteria.

1. FGDS (fibrogastroduodenoscopy) - signs of inflammation in the stomach, hypersecretion.

2. Gastric sounding - an increase in acidity on an empty stomach, a change in acid formation in the basal and stimulated phases, both in the direction of hyposecretion and in the direction of hypersecretion.

3. X-ray studies: changes in folds, a large amount of contents on an empty stomach, spasm of the pylorus, duodenum, changes in the shape of the stomach (in the form of an hourglass, gastroptosis).

In terms of examining patients, there should be a history taking, examination, blood and urine tests, FGDS with biopsy, gastric fractional intubation, acid test, pH-metry, fluoroscopy of the stomach and duodenum.

Differential diagnosis

Differential diagnosis is carried out with gastric ulcer, esophagitis, pancreatitis.

Treatment chronic gastritis depends on the level of acidity. With increased acidity of the stomach are recommended:

1) diet number 1;

2) antacids, N₂- histamine blockers;

3) drugs that regulate the mucous membrane (venter, allaptoin, solcoseryl, actovegin);

4) physiotherapy (laser therapy, EHF, UHF).

With low acidity of the stomach are recommended:

1) diet number 2;

2) drugs that regenerate the mucous membrane;

3) stimulants or substitutes for the acid fraction (acidin-pepsin, pansinoris);

4) vitamins of group B;

5) physiotherapy (laser therapy, electrophoresis with vitamins B₁ and B₆).

When establishing the presence of Helicobacter pylori, it is advisable to prescribe Denol, antibiotic therapy (amoxicillin, metronidazole).

3. Biliary dyskinesia

Biliary dyskinesia is caused by impaired motility of the gallbladder and ducts, characterized by pain in the right hypochondrium.

Etiology

Primary JVP are associated with a functional change in biliary excretion as a result of a violation of neurohumoral regulatory mechanisms, endocrine disorders, allergic reactions, and neuroses. Secondary JVP occur reflexively in some diseases by the type of viscero-visceral reflex connections. Such diseases include viral hepatitis, dysentery, toxic infection.

Classification

There are the following types:

1) hypermotor, characterized by hypertension, hyperkenesia;

2) hypomotor, characterized by hypotension, hypokenesia;

3) mixed.

Clinic

Clinically manifested by pain: with hypertensive dyskinesia, the pain is paroxysmal in nature (cramping, stabbing, cutting); short-term pain can be caused by negative emotions, physical exertion.

Pain radiates to the right shoulder, epigastric zone. With hypotonic dyskinesia, the pain syndrome is manifested by constant, aching, periodically increasing pain or a feeling of fullness. Pain of an indefinite nature, pressing. Accompanied by nausea, sometimes vomiting, bitterness in the mouth, loss of appetite up to anorexia.

Diagnostics

Laboratory and instrumental studies to detect dyskinesia.

Fractional duodenal sounding (FDZ) reveals the hypertonicity of the sphincters of Oddi and Motkens (with an increase in the duration of the II and III phases of the FDD from 10 to 30 minutes). With hypotension - decrease to 13 minutes.

Hyperkenesia of the gallbladder is accompanied by rapid emptying, occurring immediately or in the first 3-5 minutes, the volume of servings (B) is not changed; probing may cause pain. With hypokenesia, the cystic reflex is normal or slowed down, the emptying time of the bladder is slowed down, the amount of bile in portion B is more than normal. With oral cholecystography, the hypertensive form of dyskinesia is characterized by accelerated or delayed emptying of the bladder, the gallbladder is ovoid. With hypotonic dyskinesia, the gallbladder is enlarged, its emptying is slowed down. Another research method for detecting dyskinesia is echocholecystography.

The survey plan includes:

1) fractional, duodenal sounding;

2) echocholecystography (ultrasound);

3) oral cholecystography;

4) general analysis of blood and urine.

Differential diagnosis

Differential diagnosis is carried out with duodenitis, gastritis, appendicitis, helminthic invasion.

Treatment

It is advisable to prescribe a diet according to Pevzner 5 and 5a - frequent fractional meals with a restriction of fatty, fried, salty, smoked dishes, egg yolks, pastry, cold dishes and drinks.

With hypomotor dyskinesia, drugs are prescribed that stimulate the secretion of bile (choleretics) - true choleretics (cholenzym, cholagon); drugs containing acids (allahol), synthetic drugs (nikodin, tsikvilon); herbal preparations (calamus, immortelle, corn, peppermint, dandelion, wild rose); drugs that cause an increase in the tone of the biliary tract (cholekinetics) - magnesium sulfate, sorbitol, xylitol, barberry.

With hypermotor dyskinesia: drugs that cause relaxation of the tone of the biliary tract (cholespasmolytics) - a group of M-cholinolytics, aminophylline; herbal preparations (St. John's wort, stinging nettle, chamomile).

Physiotherapy (inductotherapy, UHF, microwave, diadynamic currents). laser irradiation. Reflexotherapy (acu-, electro- and laser puncture). Physiotherapy.

Mineral water:

1) with a hyperkinetic form - low-mineralized waters (Slavyanskaya, Smirnovskaya);

2) with hypokinetic form - mineral waters of high and medium mineralization (Essentuki No. 17, Arzni, Akavan).

Spa therapy.

4. Acute cholecystitis

Acute cholecystitis is an acute inflammation of the walls of the gallbladder.

Etiology

The causative agent of inflammation is Escherichia coli, staphylococci and streptococci. The predisposing factor is stagnation of bile.

Clinic

It is clinically manifested by an acute onset: an increase in body temperature, cramping pains in the right half of the abdomen with irradiation under the scapula, collarbone; nausea and vomiting is observed in half of the patients; the pains intensify in the position on the right side, the tongue is coated with a coating, there is no appetite, stool retention, tachycardia. On examination and palpation, the abdomen is swollen, the muscles of the right side of the abdomen are stiff. Positive symptoms of Ortner, Murphy, increased ESR.

Differential diagnosis

Differential diagnosis is carried out with appendicitis, exacerbation of chronic cholecystitis, acute gastritis.

Treatment

Home regimen, antibiotics (ampioks, tseporin), antispasmodics, analgesics.

5. Chronic cholecystitis

Chronic cholecystitis (non-calculous) is a secondary chronic process that develops against the background of dyscholia and dyskenesia.

Etiology

There are infectious and non-infectious nature of inflammation of the walls of the gallbladder. The infectious process is caused by bacteria (usually autoflora) and viruses, the infectious process can be caused by duodenobiliary reflux, parasites, allergic reactions.

Predisposing factors: bile stasis, eating disorders, inflammatory diseases of the abdominal organs, acute cholecystitis, intestinal dysbacteriosis.

Classification

Localization: cholecystitis, cholangitis, cholecystocholangitis. Downstream: acute, chronic (latent, recurrent). By phase: exacerbation, subsidence, remission.

Clinic

It is clinically manifested by pain in the right hypochondrium and epigastric region; pains are of a different nature - aching, dull or sharp, paroxysmal; possible irradiation to the left shoulder blade, right shoulder, right half of the neck, subclavian region; duration of pain from several minutes to 2-3 hours - pronounced muscular protection, especially in the right hypochondrium; positive symptoms are determined: Kera (pain in the projection of the gallbladder during palpation on inspiration), Murphy (interruption of inspiration by patients with pressure on the gallbladder), Ortner (pain when tapping along the right costal arch); pain at Mussi's point (between the legs of the right sternocleidomastoid muscle), McKenzie's point (at the intersection of the right costal arch and the outer edge of the rectus abdominis muscle); dyspeptic syndrome: loss of appetite, nausea, sometimes vomiting, belching, feeling of heaviness in the epigastric region, unstable stool; intoxication syndrome: weakness, lethargy, fatigue from minor physical and mental stress, headache, dizziness, irritability, pallor of the skin, blue around the eyes; changes from other organs and systems.

An increase in the liver with cholecystitis is not permanent, there is a violation of its functions (lipid, carbohydrate, protein, pigment); dysfunction of the pancreas - a decrease in the activity of defects (amylase, lipase, trypsin); violation of the secretory function of the stomach - in the early period of the disease, normal or increased secretory function of the stomach is determined, in chronic forms - a reduced change in the cardiovascular system of a functional nature - tachycardia, arterial hypotension, muffled tones, soft systolic murmur at the apex and at the Botkin point.

Diagnostics

Laboratory data:

1) study of bile obtained by fractional duodenal sounding: changes in the physicochemical properties of bile - a decrease in specific gravity, a shift in pH to the acid side; sediment microscopy: a lot of mucus, an increase in the number of cholesterol crystals, bilirubin, the presence of Giardia cysts or opisthorchiasis eggs; biochemical study of bile - a change in the amount of bile acids, a decrease in the content of lysozyme, bilirubin and cholesterol;

2) immunological study: a decrease in the content of immunoglobulins A, G, M, lysozyme; bacteriological examination: sowing of bile on the flora (the norm is 1000 pieces in 1 ml);

3) complete blood count - leukocytosis, neutrophilia, increased ESR;

4) biochemical analysis of blood: an increase in sialic acids, an increase in the level of bilirubin, activity of transaminases, alkaline phosphatase.

Instrumental methods include:

1) oral cholecystography, intravenous cholegraphy;

2) retrograde endoscopic cholangiopancreatography;

3) echography;

4) thermal imaging research, radioisotope.

Differential diagnosis

Differential diagnosis is carried out with duodenitis, gastritis, pancreatitis, peptic ulcer, helminthic invasion, appendicitis, tuberculous mesadenitis.

Treatments

Purpose of diet No. 5b, 5a, antibacterial drugs, antiparasitic agents, desensitizing, choleretic and bile secretory agents, antispasmodics, biostimulants, herbal medicine, reflexology, physiotherapy, therapeutic exercises, spa treatment.

6. Gallstone disease

Gallstone disease (GSD) is a metabolic disease of the hepatobiliary system, accompanied by the formation of gallstones in the bile ducts (intrahepatic cholestasis), in the common bile duct (choledocholithiasis) or in the gallbladder (cholecystolithiasis). Stones are cholesterol, cholesterol-pigment-lime and pigment (bilirubin).

Etiology

The etiology is determined by factors that contribute to a change in the physicochemical properties of bile (lipsogenicity):

1) genetic predisposition;

2) malnutrition;

3) violation of the basic metabolism in the body;

4) hormonal dysfunction;

5) inflammatory diseases of the liver, biliary tract and gallbladder.

Classification

The first stage is physico-chemical; the second is latent, asymptomatic, stone-carrying. The third - clinical manifestations (calculous cholecystitis, cholelithiasis with chronic cholecystitis in the acute phase, incomplete remission and remission).

Clinically manifested pain syndrome in the third stage in the form of hepatic colic. Sudden acute pain in the right hypochondrium, often occurs at night with irradiation under the right shoulder blade, collarbone, upper jaw, in the epigastric region; simultaneously with colic, nausea and vomiting appear, which does not bring relief. On palpation, the defense of the muscles of the abdominal wall, a positive symptom of Ortner, Kera, Murphy.

Diagnostics

In the first stage - fractional duodenal sounding with microscopy of portion B, which leads to an increase in crystals of cholesterol, bilirubin; in the second stage - cholecystography reveals stones of any origin and ultrasound of the gallbladder reveals stones of a cholesterol nature; in the third stage - thermography, retrograde cholangiography, laparoscopy.

Differential diagnosis

Differential diagnosis is carried out with duodenal ulcer, gastroduodenitis, pankeratitis and adenitis, right-sided pyelonephritis.

Treatment

Treatment consists in prescribing diet No. 5 in the first and second stages with the exception of excesses in food, fatty, fried, smoked foods. Included in the diet are foods with the addition of bran, fiber. It is necessary to prescribe drugs for the synthesis and secretion of bile acids (phenobarbital). Suppression of the synthesis and secretion of cholesterol (ureodeoxycholic acid, lyopin). Shock wave lithotripsy (stones up to 3 cm, consisting of cholesterol, are exposed). In the third stage - radical surgical treatment (cholecystectomy).

7. Acute pancreatitis

Acute pancreatitis is an acute inflammatory disease accompanied by autolysis (due to the activation of its own enzymes) and pancreatic tissue degeneration.

Etiology

The cause may be viral infections, mechanical injuries of the abdomen, allergic reactions, malnutrition (an abundance of fatty, carbohydrate foods), the presence of diseases of the biliary tract, obstruction of the pancreatic duct, vascular pathology (atherosclerosis, severe hypotension), renal failure, diabetes, medications (glucocorticoids, estrogens), parasitic diseases.

Classification

The classification is as follows.

I.Shape:

1) interstitial;

2) hemorrhagic;

3) pancreatic necrosis;

4) purulent.

II. Disease period:

1) seizure;

2) reparative.

III. Clinical course:

1) type: acute, subacute, recurrent;

2) severity: light, moderate, heavy;

3) syndromic characteristics: pancreatic-hepatic, cerebral, cardiac syndromes, etc.

IV. The state of the function of the pancreas.

V. Complications and their nature: on the part of the gland: pseudocyst, abscess, diabetes; from other organs: bleeding, dysfunction of the cardiovascular system, liver, kidneys, central nervous system.

Clinic

The clinical picture consists of the following syndromes.

1. Pain syndrome is characterized by intense pain in the epigastrium with irradiation to the left, girdle character.

2. Dyspeptic syndrome is characterized by nausea, vomiting that does not bring relief, constipation or maldigestion.

3. Syndrome of intoxication - fever, headache, weakness, malaise, acute vascular insufficiency, DIC.

On examination, the tongue is coated with a white or yellowish coating, the abdomen is swollen, the muscles are defensive; Hodstel's syndrome (cyanosis of certain sections of the anterior abdominal wall, Gray-Turner syndrome (pigmentation on the lateral parts of the abdomen), Grunwald syndrome (petechiae around the navel), Mondor's syndrome (purple spots on the face and trunk), Ker's syndrome - pain in the transverse abdominal muscle above the navel in the projection of the pancreas (5-7 cm above the navel), Chauffard zone, Methot-Robson's zone, Desjardins' zone - pain on palpation, Voskresensky's syndrome (absence of pulsation of the abdominal aorta with pressure in the epigastrium).

Diagnostics

In the general blood test, leukocytosis, neutrophilia with a shift to the left. Amylase levels are high in the urine. In the biochemical blood test - dysproteinemia, increased amylase, lipase, transaminase, alkaline phosphatase, bilirubin (with secondary liver damage).

On ultrasound - an increase in the size of the gland with swelling of the tissues.

Differential diagnosis

Differential diagnosis is carried out with appendicitis, ulcer perforation, high intestinal volvulus, splenic infarction, pleurisy, acute cholecystitis, nephrolithiasis, acute gynecological diseases, aortic aneurysm, diabetic or hepatic coma.

8. Chronic pancreatitis

Chronic pancreatitis is a progressive inflammatory disease accompanied by sclerosis and destruction of the endocrine tissue of the pancreas. It is a consequence of acute pancreatitis. Diseases of the gallbladder contribute to the development of chronic pancreatitis; hemochromatosis (a combination of liver diseases with diabetes and pancreatic insufficiency; hyperparathyroidism; vascular lesions; exacerbation of chronic pancreatitis is provoked by errors in the diet, violation of the regimen, bacterial and viral infections.

Classification

The classification is as follows.

I.Shape:

1) recurrent;

2) with constant pain syndrome;

3) latent.

II. Disease period:

1) exacerbation;

2) remission.

III. Clinical course:

1) type: recurrent;

2) severity: light, moderate, heavy;

3) syndromic characteristics: pancreatic-hepatic, cerebral, renal syndromes.

IV. Stage of the disease: initial, advanced manifestations, final.

V. The state of the function of the pancreas: 1) the state of external secretion:

a) without manifestations of exocrine insufficiency;

b) with the phenomena of exogenous insufficiency;

2) the state of internal secretion:

a) without violations;

b) with a violation (hyper- and hypofunction of the insular apparatus). VI. Complications from the pancreas.

Clinic

It is clinically manifested by paroxysmal pains (aching, dull or stabbing), which are girdle in nature, radiate to the lower back, left arm. Decreased appetite, nausea, unstable stool, bloating, weight loss. In exacerbation of the defense of the muscles of the upper abdomen. Soreness at the Lito-Robson point, Desjardin's point. Positive symptoms of Chauffard, Grotto. Symptoms of intoxication: irritability, sometimes aggression, emotional lability, blue under the eyes, conjunctivitis, cracks in the corners of the mouth, hypovitaminosis phenomena.

Diagnostics

In the general blood test, neutrophilic leukocytosis with a shift to the left, lymphocytosis, eosinophilia, thrombocytopenia.

In the biochemical analysis of urine - an increase in amylase, peptidase. In the biochemical analysis of blood - an increase in amylase, lipase, hypo- and dysproteinemia. Coprogram - steatorrhea, creatorrhea, aminorrhea. On ultrasound - an increase in the gland or its department due to edema or sclerosis.

X-ray diagnostics - expansion of the duodenal arch, expansion of the relief of the medial wall.

Differential diagnosis

Differential diagnosis is carried out with nephroischiasis, invagination.

9. Nonspecific ulcerative colitis

Nonspecific ulcerative colitis is a chronic non-bacterial disease characterized by inflammatory and ulcerative lesions of the colon and manifested by continuous or recurrent hemocolitis with the development of anemia and malnutrition in more severe cases.

Etiology

The etiology remains unclear. This is an autoimmune disease. Provoking factors of the disease or causes of exacerbation can be:

1) viral or bacterial infection;

2) emotional stress reactions;

3) milk intolerance;

4) hereditary predisposition.

Classification

The classification is as follows.

1. According to the form of the disease: continuous, recurrent.

2. According to the severity of the disease: mild, moderate, severe.

3. According to the extent of the lesion of the colon: segmental colitis, total colitis.

4. Downstream: fulminant (2-3 weeks), acute (3-4 months), chronic (more than 3-4 months).

5. According to the phase of the disease: active process (exacerbation), remission.

Clinic

The severity of clinical manifestations depends on the severity of the disease. The onset of the disease is usually gradual, blood appears in the formed stool, after 2-3 months signs of colitis appear with an increase in stool up to 3-4 times a day. In some cases, hemocolitis is preceded by cramping pain in the left side of the abdomen, in the umbilical zone, or throughout the abdomen. Symptoms of intoxication accompany colitis with a rise in temperature from subfebrile to 38,5 - 39 ° C, appetite is sharply reduced. Anemia and malnutrition develop.

Complications - dematation, bleeding, perforation, stricture of the colon.

Diagnostics

In the general analysis of blood - anemia, leukocytosis with neutrophilia, increased ESR; coprogram: mucus, leukocytosis, erythrocytes; fecal bacal analysis for pathogenic intestinal flora is negative, there may be data indicating dysbacteriosis; fluoroscopy: hyperemia and swelling of the mucosa, bleeding on contact, erosion, ulcers, mucus, fibrin, pus; the number of pathological changes depends on the severity of the disease; irigography: deformity, absence of gaustra, serrated contours of the colon are detected; in severe form - filling defect; biochemical blood test - hypoproteinemia, dysproteinemia, increase - 1,2- and α-globulins, DFA, Hess test; a positive Boyden reaction with intestinal antigen is possible.

Differential diagnosis

Differential diagnosis is carried out with acute dysentery, Crohn's disease, intestinal tuberculosis, pseudomembranous colitis.

Treatment

The principles of treatment are as follows.

1. A diet with a high content of proteins and vitamins is prescribed, milk and dairy products are excluded, carbohydrates are limited.

2. Vitamin therapy.

3. Iron preparations (ferrum-lek, sorifer), albumins, plasma, hymeotransfusil.

4. Sanazosulfanilamides (sanozopyrin, sulfosanazine). In case of intolerance - enteroseptol, intestopan.

5. Biologicals, anabolic agents (nerabon, retabolin, intandrostepolone), therapeutic enemas with oil preparations and antispasmodics.

10. Esophagitis

Esophagitis is an inflammatory disease of the esophageal mucosa.

Etiology

The reasons for the development of esophagitis are:

1) alimentary factor (reception of hot, irritating food);

2) chemical factor (chemical substances - alkalis, acids, drugs, etc.;

3) injuries (food, household);

4) diseases of the stomach;

5) dysfunction of the sphincter apparatus.

Classification

Esophagitis is divided into:

1) by origin: primary, secondary esophagitis;

2) downstream: acute, (subacute), chronic;

3) by the nature of changes in the mucous membrane: catarrhal, erosive, ulcerative, hemorrhagic, necrotic;

4) by localization: diffuse (common), localized, reflux esophagitis;

5) according to the degree of remission: mild, moderate, severe;

6) complications: bleeding, perforation.

Diagnostics

It is characterized by pain syndrome with localization in the area of ​​the xiphoid process; dyspeptic syndrome (dysphagia, belching, heartburn).

Instrumental research methods: fibroscopy - signs of inflammation activity, the state of the sphincter apparatus; fluoroscopy: exclusion of congenital pathology, diaphragmatic hernia; pH-metry: reflux diagnostics; syanometry: determination of the functional state of the sphincter apparatus.

Differential diagnosis

Differential diagnosis is carried out with esophageal-gastric hernias, varicose veins of the esophagus.

Treatment

The principles of treatment are as follows.

1. A diet is prescribed (in the acute period, liquid or semi-liquid chilled food).

2. Antacids and astringents (gistal, almagel, maoloks, vikalin, bismuth, silver nitrate preparations).

3. Means that regulate the motility of the upper digestive tract (cerucal, regian, engonil).

4. Synthesis substitutes (venter, sucralfate).

5. Acid blockers (N₂-histamine blockers, N-anticholinergics).

6. Physiotherapy (EHF and laser therapy, diademic currents).

11. Peptic ulcer

Peptic ulcer (stomach or duodenal ulcer) is a chronic cyclically occurring disease, a characteristic feature of which is the formation of ulcers during an exacerbation in the areas of the digestive tract in contact with active gastric juice (stomach - fundus, antrum, duodenum).

Etiology

The following factors lead to the development of peptic ulcer:

1) hereditary predisposition;

2) neuropsychic;

3) alimentary;

4) bad habits;

5) medicinal effects;

6) infection (helicobacter pylori).

Classification

Peptic ulcer according to the following criteria.

1. Clinical and endoscopic stage - fresh ulcer; the beginning of the epithelialization of the ulcer; healing of an ulcerative defect of the mucous membrane with preserved duodenitis; clinical and endoscopic remission.

2. Phases: exacerbation, incomplete clinical remission, clinical remission.

3. Localization: fundus of the stomach, antrum of the stomach, duodenal bulbs, postbulbar region, double localization.

4.Shape:

1) uncomplicated;

2) complicated: bleeding, perforation, perivisceritis, penetration, pyloric stenosis.

5. Functional characteristics: acidity of gastric contents and motility: increased, decreased, normal.

Another classification.

I. General characteristics of the disease:

1) gastric ulcer;

2) duodenal ulcer;

3) peptic ulcer of unspecified etiology;

4) peptic gastrolocal ulcer after resection of the stomach.

II. Clinical form:

1) acute or newly detected;

2) chronic.

III. Flow:

1) latent;

2) mild or rarely recurrent;

3) moderate or recurrent (1-2 relapses or more within a year);

4) severe (3 relapses or more within a year) or continuously recurring, the development of complications.

IV. Phase:

1) exacerbation (relapse);

2) fading exacerbation (incomplete remission);

3) remission.

V. Characteristics of the morphological substrate of the disease:

1) types of ulcers:

a) acute ulcer;

b) chronic ulcer;

2) the size of the ulcer:

a) small (less than 0,5 cm);

b) medium (0,5-1 cm);

c) large (1,1-3 cm);

d) giant (more than 3 cm);

3) stages of ulcer development:

a) active;

b) scarring;

c) red scar stage;

d) stage of "white" scar;

e) not scarring for a long time;

4) localization of the ulcer:

a) stomach (cardia, subcardial region, body of the stomach, antrum, pyloric region; anterior wall, posterior wall, lesser curvature, greater curvature);

b) duodenum (bulb, postbulbar part, anterior wall, posterior wall, lesser curvature, greater curvature);

5) characteristics of the functions of the gastroduodenal system (only pronounced violations of the secretory, motor and evacuation functions are indicated).

Complications:

1) bleeding:

a) lungs;

b) moderate;

c) heavy;

d) extremely severe;

2) perforation;

3) penetration;

4) stenosis:

a) compensated;

b) subcompensated;

c) decompensated;

5) malignancy.

Clinic

Pain is the leading complaint. Pain depends on the state of the nervous system, endocrine system, individual characteristics, anatomical features of the ulcer, the severity of functional disorders. The pain is most often localized in the epigastric region, umblinkal region, diffused throughout the abdomen. The pain eventually becomes constant, more intense, takes on a "hungry" and nocturnal character. Characterized by nausea, vomiting, heartburn, belching, hypersalivation. Patients have decreased appetite. Emotional lability increases, sleep is disturbed, fatigue increases. Constipation or loose stools develop. Hyperhidrosis, arterial hypotension, bradycardia. On palpation, pain in the epigastrium or in the pyloroduodenal region, defense of the muscles of the anterior abdominal wall. Positive Mendel's syndrome, Oppenhovsky's syndrome (pain in the spinous processes of the XIII-XI thoracic vertebrae), Herbet's symptom (pain in the region of the transverse processes of the III lumbar vertebra). With bleeding ulcers, a positive reaction to occult blood. Has a value in the diagnosis of hereditary predisposition (especially in the male line).

Laboratory data. Study of gastric secretion (increase in volume, acidity, debit-hour of free hydrochloric acid and pepsin activity); complete blood count: there may be erythrocytosis, posthemorrhagic hypochromic anemia, leukopenia, with complications - an increase in ESR; positive stool test for occult blood.

Diagnostics

Instrumental research methods: fibrogastroduodenoscopy: detection of an ulcer;

X-ray examination with barium: direct signs - a niche, convergence of folds, etc.; indirect - fasting hypersecretion, bulb deformity, pyloroduodenospasm, spastic peristalsis; in a state of hypotension - with the use of pharmacological agents (atropine).

Cytological examination revealed Helicobacter pylori.

Differential diagnosis

Differential diagnosis is carried out with chronic gastritis (with high acidity) and gastroduodenitis (epozivny, antral, atrophic gastritis, erosive duodenitis).

Treatment

At the time of exacerbation, bed or semi-bed rest is prescribed. Diet No. 1a and 1b for a short time, then No. 1. Drug therapy is aimed at:

1) suppression of the aggressive properties of gastric juice; non-selective M-cholinolytics (atropine, platifillin, metacin); selective blockers M₁-cholinergic receptors (gastroepin, pyroncepin); H blockers₂histamine receptors (cisletidine, ranitidine, famotidine); calcium antagonists (verapamil, nifedipine); antacids (almagel, phosphamogel, gastrogel);

2) increasing the protective properties of the mucous membrane: whit-protectors (sodium carbenoxalone, sucralfate, collide bismuth); repair stimulants (sodium oxyferriscarbon, pyrimidines);

3) neurohumoral regulation: psychotropic (elenium, seduxen, sedatives); dopamine receptor blockers (cerucal, eglonil);

4) antibacterial action (metronidazole - in the presence of Helicobacter pylori). Physiotherapy - EHF, magnetic and laser therapy; electrophoresis of drugs, hyperbaric oxygenation.

Forecast

The prognosis for peptic ulcer disease depends on the individual characteristics of the organism, the regularity and adequacy of therapeutic measures. In most patients, the first course of intensive therapy leads to healing of the ulcer, but if the diet is not followed, it leads to a relapse of the disease and complications. Perhaps the development of perigastritis, periduodenitis, stenosis of the pyloroduodenal department, penetration (for example, into the pancreas), the development of bleeding and peritonitis.

Clinical examination

After discharge from the hospital, examination by a doctor quarterly, then 2 times a year (in spring and autumn). EGD is done 6 months after the onset of an exacerbation to assess the effectiveness of therapy. Anti-relapse treatment is carried out twice a year in spring and autumn for 3-4 weeks. Sanatorium treatment is carried out no earlier than 3-6 months after the disappearance of the pain syndrome and the healing of the ulcer in the sanatoriums of Essentuki, Zheleznovodsk, Borjomi, Druskinankaya.

12. Chronic hepatitis

Chronic hepatitis is an inflammatory destructive process in the liver that proceeds without improvement for at least 6 months, with relapses, clinically characterized by astheno-vegetative, dyspeptic syndromes, hepatomegaly, impaired liver function; morphologically - persistence of necrosis, inflammation, fibrosis while maintaining the overall architectonics of the liver.

Etiology

Chronic hepatitis can be caused by hepatitis B, C, D viruses or their combinations, herpes simplex, cytomegaly; chemical compounds - DDT, its analogues; medications - tuberculostatics, phenothiazine drugs; poisonous mushrooms; fatty hepatosis; intestinal dysbiosis.

Classification

The form:

1) chronic persistent (benign) hepatitis:

a) manifest;

b) oligosymptomatic (low active);

2) chronic active (aggressive) hepatitis:

a) highly active;

b) moderately active;

c) polystatic;

3) lupoid hepatitis.

Course: progressive, stable, latent. Phase: exacerbation, remission. Functional state of the liver: compensated, subcompensated, decompensated.

Clinic

Clinical signs:

1) pain syndrome: pain in the right hypochondrium, often dull, aching, not associated with food intake, after exercise; in some cases, there is no pain (chronic persistent hepatitis (CPH));

2) asthenovegetative syndrome; lethargy, fatigue, weakness, poor sleep, frequent headaches, irritability, tearfulness, weight loss, nosebleeds are possible in chronic aggressive hepatitis;

3) rispepsy syndrome: nausea, unstable stool (constipation, diarrhea), loss of appetite, flatulence, tongue covered with a brownish-yellow coating;

4) subicteric sclera; an increase in the size of the liver, the edge is rounded, of a dense consistency; the spleen can be palpated by 2-4 cm;

5) skin changes: pale, dryish, subicteric, with itching with scratching, hemorrhagic manifestations - hemorrhagic rash, ecchymosis, spider veins on the upper half of the body, "jellyfish head" on the skin of the abdomen and chest;

6) other changes: arthralgia, arthritis, allergic rashes, lymphadenopathy, kidney damage, fever, polyserositis.

Diagnostics

The first step is to establish the presence of liver damage:

1) blood serum bilirubin, activity of transaminases (ALT, AST), alkaline phosphatase, total protein, protein gram, sedimentary samples;

2) prothrombin time or index;

3) bilirubin and urobilirubininogen of urine;

4) bromsulfalein test (excretory-secretory function of the liver); altered sample readings may be the earliest sign of liver disease;

5) Ultrasound and scanning of the liver with AI-198 allow to determine the localization of the focal disease (abscess, echinococcus, tumor). With the help of screening methods, it is only possible to suggest liver disease, a specific diagnosis is not established.

The second stage is to clarify the nature or diffuse liver damage (i.e., nosological diagnosis):

1) laparoscopy with liver biopsy;

2) selective angiography;

3) ceniacography, hepatography for contrasting the arteries of the liver, veins and vessels of the spleen;

4) immunological study - determination of mitochondrial antibodies in liver biopsy specimens.

The third stage - detailing the diagnosis - determining the activity of the process, the stage of the disease, the presence or absence of complications (portal hypertension, its degree, liver failure). The nature of the disorders is assessed by indicators of biochemical and immunological tests (immunoglobulins, antibodies to smooth muscles, mitochondria, T-, B-lymphocytes). The main diagnostic method that verifies the diagnosis is morphological (puncture biopsy with histological examination of the biopsy).

Biochemical methods make it possible to distinguish four main syndromes in liver diseases:

1) cytolysis syndrome - increased direct bilirubin, ALT, AST activity;

2) cholestasis syndrome - increased cholesterol levels, alkaline phosphatase activity, conjugated bilirubin;

3) mesenchymal-inflammatory syndrome - an increase in the content of α-globulins, DPA samples, ESR, a decrease in sublimate samples;

4) hepatocrine syndrome: a decrease in the content of albumin, cholesterol, fibrinogen.

Chronic persistent hepatitis is characterized by: the absence of a bright clinic, liver function indicators are not impaired; morphologically - focal large cell infiltration without necrosis in the liver biopsy plate. In chronic aggressive hepatitis, the clinical picture is pronounced, liver parameters are sharply impaired (cytolysis, cholestasis, inflammation, hepatocrine syndrome); morphologically - lympho-macrophage infiltration in the portal tracts and inside the lobules, necrosis.

Differential diagnosis

Differential diagnosis is carried out with primary liver diseases (hepatosis pigmentosa, cirrhosis, tumors), metabolic disorders (fatty hepatosis, aminoidosis, hemochromatosis, glycogenosis, lipoidosis), circulatory disorders, secondary infiltrative processes in the liver (blood diseases, intoxication, polyagenoses ), diseases of the biliary tract (cholangitis, violation of the outflow of bile).

Treatment

The principles of treatment are as follows.

1. Mode sparing, diet, vitamin therapy, 5% glucose solution enterally.

2. Hepatoprotectors (Essentiale, Carsil, ATP, Essliver-Forte, LIV-52).

3. Glucocorticoids.

4. Cytostatics (imuran).

5. Pyrogenanotherapy + intestinal dialysis + oxygen.

6. Plasmaphoresis.

7. Antiviral drugs.

8. Immunocorrectors (T-activin).

13. Cirrhosis of the liver

Cirrhosis of the liver is a diffuse process characterized by a combination of fibrosis, nodular transformation of the parenchyma and the presence of fibrous septa; combination of necrotic changes.

Etiology

The development of cirrhosis is connected:

1) with infection (after viral hepatitis, brucellosis, cytomegaly);

2) with metabolic disorders (fermentopathy, galactodenia, glycogenous disease, hyperbilirubinemia);

3) with a violation of the outflow of bile (congenital anomalies of the bile ducts);

4) other causes (toxic-allergic, infectious-allergic, ulcerative colitis).

Classification

The classification is as follows.

I. By morphological features:

1) small-knot;

2) SKD;

3) biliary;

4) mixed.

II. By etiology:

1) infectious;

2) exchange;

3) due to a congenital anomaly;

4) other cirrhosis.

III. With the flow:

1) progressive:

a) active phase;

b) the phase is inactive;

2) stable;

3) regressive.

IV. Typical insufficiency: yes / no, portal hypertension (yes / no), hypersthenia (yes / no).

History: chronic hepatitis, acute viral hepatitis (B, C, D), contact with patients with acute viral hepatitis, delayed hospitalization, exposure to chemicals, mushroom poisoning, bowel disease.

Clinic

Clinical syndromes are as follows.

1. Astheno-neurotic syndrome: weakness, fatigue, weight loss.

2. Dyspeptic syndrome: decreased appetite, nausea, vomiting, aversion to fatty foods, intestinal dysfunction.

3. Abdominal syndrome: dull, aching pain in the right hypochondrium, not associated with eating.

4. Changes in the central nervous system - depression or excitation.

5. Hemorrhagic syndrome: ecchymosis, hemorrhagic rash, bleeding gums, nosebleeds.

6. "Spider veins", venous network on the anterior abdominal wall.

7. Liver smell from the mouth.

8. Arthralgia, arthritis, lymphadenopathy.

Diagnostics

Laboratory research:

1. Cytolysis - an increase in the content of bilirubin, activity of ALT, AST.

2. Cholestasis - an increase in the content of cholesterol associated with bilirubin.

3. Mesenchymal-inflammatory syndrome - an increase in α-globulins, a decrease in the sublimate test.

4. Hepatocrine syndrome - a decrease in the content of albumins, cholesterol, fibrinogen.

Differential diagnosis

Differential diagnosis is provided with acute viral hepatitis, chronic hepatitis, metabolic disorders, blood diseases, chronic heart failure, collagenoses.

Treatment

The principles of treatment are as follows.

1. Mode.

2. Diet.

3. Vitamin therapy.

4. Glucose 5% orally.

5. Hepatoprotectors.

6. Cytostatics.

7. Antiviral drugs (ribovarin, acyclovir).

Lecture number 4. Diseases of the urinary organs

Glomerulonephritis (acute glomerulonephritis) is a cyclic infectious and allergic kidney disease that develops 1-3 weeks after an infectious disease (usually streptococcal etiology). Chronic nephritis is a form of diffuse glomerulonephritis, in which changes in the urine (microhematuria and albuminuria) persist without significant dynamics for more than a year, or symptoms such as edema or hypertension are observed for more than 3-5 months.

Etiology

The etiology of glomerulonephritis is usually associated with infectious agents (streptococci, staphylococci); other "causal" factors (trauma, sun exposure, intolerance to foods, chemicals, drugs) are possible. Damage to the kidneys in diffuse glomerulonephritis can be caused by: antibodies to the renal tissue, antigen-antibody-complement complexes.

Classification

Glomerulonephritis is delimited.

I. Acute glomerulonephritis.

1.Shape:

1) with acute nephrotic syndrome;

2) with isolated urinary syndrome;

3) mixed form.

2. The activity of the renal process: the period of initial manifestations, the period of reverse development, the transition to chronic glomerulonephritis.

3. Status of kidney function: without dysfunction, with dysfunction, acute renal failure.

II. Chronic glomerulonephritis.

1.Shape:

1) nephrotic form;

2) hematuric form;

3) mixed form.

2. Activity of the renal process:

1) period of exacerbation;

2) a period of partial remission.

3. Kidney function status:

1) without impaired renal function;

2) with impaired renal function;

3) chronic renal failure.

III. Subacute (malignant) glomerulonephritis.

Kidney function status:

1) with impaired renal function;

2) chronic renal failure.

Clinic

Extrarenal symptoms: malaise, poor appetite, lethargy, nausea, pallor, temperature reaction; edematous syndrome; hypertension syndrome. Renal symptoms: oliguria, discoloration of urine (urine of the color of "meat slops"), abdominal pain of an unidentified nature, pain in the lumbar region, azotemia. urinary syndrome. The nature and severity are determined by the clinical form of the disease, the severity of functional and morphological disorders of the kidneys: high relative density of urine, oliguria; proteinuria; cylindruria, hematuria; microleukocyturia, absence of bacteria.

Differential diagnosis

Differential diagnosis is carried out with kidney diseases in diffuse connective tissue diseases, rheumatic diseases, systemic vasculitis; with hereditary nephritis, ditsmetabolic nephropathies, interstitial nephritis, anomalies of the urinary system.

Treatment

Principles of treatment.

1. Bed rest, diet (unloading, salt-free, with protein restriction).

2. Antibacterial therapy (1-1,5 - 2 months), nephrotoxic antibiotics are excluded.

3. Antihistamines (1-1,5 - 2 months).

4. Diuretics (furosemide, hypothiazide, veroshpiron).

5. Antihypertensive drugs.

6. Heparin.

7. Antiplatelet agents.

8. Glucocorticosteroids.

9. Immunosuppressants.

10. Quinoline drugs.

11. Non-steroidal anti-inflammatory drugs.

12. Membrane stabilizing drugs.

2. ​​Pyelonephritis

Pyelonephritis is a microbial-inflammatory disease of the tubulointerstitial tissue of the kidneys.

Etiology

The disease is caused by Escherichia coli, Proteus vulgaris, Pseudomonas aeruginosa.

Classification

The classification is as follows.

I. Form (by pathogenesis):

1) primary;

2) secondary:

a) obstructive;

b) with disembryogenesis of the kidneys;

c) non-obstructive - dysmetabolic, more often with tubulopathies.

II. Flow:

1) acute;

2) chronic (manifest and latent forms).

III. Period:

1) exacerbation (active);

2) reverse development of symptoms (partial remission);

3) remission (clinical and laboratory remission).

IV. Kidney function:

1) without impaired renal function;

2) with impaired renal function;

3) chronic renal failure.

Clinic

Pyelonephritis is characterized by general weakness, headache, loss of appetite, pain in the lower back of a constant, aching nature (often unilateral), abdominal pain, painful frequent urination, hyperthermia, chills, pale skin, pale mucous membranes, pasty face, Pasternatsky's symptom, more often with one On the other hand, blood pressure rises.

Diagnostics

In the general analysis of urine, an alkaline reaction, the density is reduced, the urine is cloudy, moderate proteinuria, severe leukocyturia, bacteriuria, cylindruria. The Nechiporenko test is characterized by a predominance of leukocyturia over erythrocyturia. Zimnitsky's test: decrease in density during the day.

In the general blood test: anemia, neutrophilic leukocytosis, increased ESR. Biochemical analysis of blood: increase in the content of sialic acids, α₂- and β-globulins, creatinine, urea, the appearance of C-reactive protein.

Plain radiography of the kidneys: an increase in the kidneys and hypotension of the ureters (in an acute process - a decrease in the thickness of the parenchyma, its heterogeneity).

Excretory pyelography: changes in the pelvicalyceal system.

Ultrasound examination of the kidneys: asymmetry in the size of the kidneys, deformation of the pelvicalyceal system, heterogeneity of the renal parenchyma.

Voiding cystourethrography: identification of anatomical and functional features, the presence of reflux.

Differential diagnosis

Differential diagnosis is carried out with cystitis, kidney tuberculosis, kidney tumor, urolithiasis, diffuse glomerulonephritis.

Treatment

The principles of treatment are as follows.

1. Antibacterial, nitrofuran drugs, sulfonamides.

2. Antispastic therapy (no-shpa, papaverine, baralgin).

3. Phytotherapy (diuretic, metholytics, antiseptics).

3. Acute renal failure

Acute renal failure is a sudden violation of kidney function with a delay in the excretion of nitrogen metabolism products from the body and a disorder of water and electrolyte, osmotic metabolism and acid-base status.

Etiology

The etiology is as follows:

1) prerenal acute renal failure is caused by shock, obstruction of the renal vessels, electrolyte metabolism disorder;

2) renal - due to the absence of a kidney, acute tubular or interstitial necrosis, intravascular hemolysis;

3) postrenal - due to urolithiasis, tumors, etc.

Classification

Acute renal failure is defined as follows.

I. Form (according to etiology and pathogenesis):

1) prerenal;

2) renal;

3) postrenal.

II. Clinical stages:

1) initial (shock);

2) oligoanuric;

3) recovery of diuresis;

4) recovery.

Clinic

The initial stage (duration 1-3 days) is characterized by the predominance of the clinic of the underlying disease, leading to acute renal failure; decrease in diuresis, low relative density of urine are registered.

The oligoanuric stage (duration 2-2,5 weeks) is characterized by worsening of the patient's condition, oliguria or anuria, development of azotemic coma, hyperkalemia.

The polyuric stage (restoration of diuresis, duration 1-6 weeks) is characterized by polyuria, hypo- and isosthenuria, hyposalia (decrease in sodium, potassium, magnesium, calcium in the blood serum), progression of anemia; at the same time, the infection is superimposed, which is one of the main reasons for the appearance of this stage.

Stage of recovery (duration - up to 2 years). Signs of recovery are: normalization of the concentration function of the kidneys, elimination of anemia.

Diagnostics

Urine: cloudy, dark brown or red, high proteinuria, hematuria, leukocyturia, cylindruria (granular and hyaline). In the general blood test: anemia, leukocytosis, neutrophilia with toxic granularity, an increase in ESR. In the biochemical analysis, azotemia (residual nitrogen more than 72 mmol / l, creatinine more than 1 mmol / l); hyperkalemiamagnesemia; decompensated metabolic acidosis.

Differential diagnosis

The differential diagnosis is carried out with chronic renal failure.

Treatment

Principles of treatment:

1) in the initial period: a decrease in the impact of the etiological factor; the formation of diuresis with osmodiuretics, water load, furosemide; prednisolone, heparin;

2) oligoanuric stage: protein and fluid restriction; antibacterial therapy; heparin; hemodialysis (with hypervolemia, persistent hyperkalemia, an increase in blood urea levels of more than 25 mmol / l per day);

3) polyuric stage: protein restriction; the diet is enriched with salts of potassium, calcium, magnesium, sodium, liquid is not limited; intravenous albumin, insulin-glucose therapy; hemodialysis (with persistent azotemia);

4) recovery periods: limitation of pharmacotherapy; phytotherapy.

4. Chronic renal failure

Chronic renal failure is a clinical symptom complex caused by a decrease in the number and a change in the function of the remaining active nephrons, which leads to a violation of the homeostatic function of the kidneys. Diagnosed with a decrease in glomerular filtration rate of less than 20 mmol/l per 1,73 m²lasting at least 3 months; increase in creatinine more than 177 mmol / l.

Etiology

The development of chronic renal failure is due to glomerulonephritis, obstructive pyelonephritis, hereditary nephritis, kidney dystrophy (hypoplasia, polycystic).

Classification

Stage, phase, name.

I. A, B, latent.

II. A, B, Azotemic.

III. A, B, uremic.

The laboratory criteria are as follows.

I. A. B: creatinine: normal - up to 0,18 mmol / l; filtration: norm - up to 50% of the due.

II. A: creatinine - 0,19 - 0,44 mmol / l; filtration - 20-50% of the due.

II. B: creatinine - 0,45 - 0,71 mmol / l and filtration: 10-20% of the due.

III. A: creatinine - 0,72 - 1,254 mmol / l; filtration - 5 - 10% of the due.

III. B: creatinine - 1,25 mmol / l and above; filtration - below 5% of the due.

Form: reversible, stable, progressive.

Indicators that are little dependent on the stage of chronic renal failure: biochemical - urea, residual nitrogen, electrolytes, KOS; clinical - blood pressure, anemia.

Differential diagnosis

The differential diagnosis is with acute renal failure.

Treatment

The principles of treatment are as follows.

1. In chronic renal failure of the first stage: treatment of the underlying disease, symptomatic therapy.

2. Second stage IIA: protein restriction to 1,5 g/kg, Giordano-Giovanneti diet, symptomatic therapy (hypotensive, diuretic, calcium preparations, vitamins), red blood cell transfusions.

3. The second stage IIB: regular hemodialysis is started at a creatinine level of more than 0,528 mmol / l, creatinine clearance - less than 10 ml / min per 1,73 m² 2-3 times a week.

4. Kidney transplantation.

5. Cystitis

Cystitis is an inflammation of the lining of the bladder.

Etiology

For the development of the disease, the anatomical feature of the urinary tract in women is important, non-compliance with hygiene-83

nic regimen, hypothermia, changes in hormonal levels. Perhaps the development of allergic or viral cystitis.

Classification

Cystitis is delimited as follows.

1. Primary; secondary.

2. Etiology: infectious (nonspecific, specific), chemical, toxic, medicinal, thermal alimentary, neurogenic, invasive, postoperative, parasitic.

3. Course: acute, chronic.

4. The prevalence of the inflammatory process: diffuse; focal (cervical, trigonitis - bladder triangle).

5. The nature and depth of morphological changes: acute, catarrhal, hemorrhagic, granulation, fibrinous, ulcerative-catarrhal, ulcerative, polypous, cystic, necrotic.

Clinic

Moderately expressed symptoms of intoxication, fever.

Symptoms of dysuria, polyapiuria, imperative urges, soreness over the pubis, aggravated after urination; terminal hematuria; urine is cloudy, macrohematuria, leukocyturia, erythrocyturia, bacteriuria are possible; in the general blood test: moderate leukocytosis and an increase in ESR.

Differential diagnosis

Differential diagnosis is carried out with acute and chronic pyelonephritis, acute appendicitis (with the pelvic location of the process).

Treatment

Principles of treatment:

1) strict bed rest, a diet with the exception of spicy and irritating foods;

2) broad-spectrum antibiotics in combination with nitrofurins or sulfonamides for at least 4 weeks;

3) herbal medicine to enhance diuresis (kidney tea, field horsetail, bearberry);

4) locally - heat on the area of ​​the bladder;

5) in chronic cystitis - treatment of complications (vesicoureteral reflux).

6. Urolithiasis

Urolithiasis (urolithiasis) is a large group of syndromes that are heterogeneous in etiology and pathogenesis, one of the clinical and morphological manifestations of which is the formation of stones in the organs of the urinary system.

Etiology

The presence of a urinary infection, stagnation of urine, a change in its normal composition, a metabolic disorder - uric acid diathesis, cystenosis, oxalosis leads to the development of urolithiasis.

Clinic

Extrarenal symptoms: moderate symptoms of intoxication, pain in the abdomen and lower back, constant dull pain with large stones, attacks of acute pain.

Renal symptoms: microhematuria - a constant symptom, leukocyturia (pyuria), increased excretion of salts.

Diagnostics

Radiographically, stones are determined on survey images or a filling defect against the background of a contrast agent.

Differential diagnosis

Differential diagnosis is carried out with glomerulonephritis, pyelonephritis, tuberculosis, anomalies of the urinary system.

Treatment

Principles of treatment:

1) dietary correction - a decrease in the concentration of salts in the urine, an increase in diuresis up to 2 liters;

2) drugs that inhibit the growth of stones (cystenal, rovatin, rovatinex, magnesium oxide, orthophosphates);

3) herbal medicine (metholytics);

4) mineral waters;

5) surgical treatment.

7. Nephrotic syndrome

Nephrotic syndrome is a clinical and laboratory symptom complex, including pronounced edema, massive proteinuria, impaired protein, lipid and water-salt metabolism.

Etiology

The cause of acquired nephrotic syndrome is hyaluronephritis, various diseases: diabetes mellitus, systemic lupus erythematosus, amyloidosis, neoplasms; drugs - nitrogen salts, penicillin, non-steroidal anti-inflammatory drugs.

The only clinical manifestation of nephrotic syndrome is characteristic of a genetically determined pathology - kidney microcystosis (Finnish type of nephrotic syndrome). In young people and adolescents, nephrotic syndrome develops as a result of primary kidney damage. The morphological feature of early nephrotic syndrome is the minimal change in the kidneys. Lipoid nephrosis is a disease in which there are only minimal changes in the kidneys, based on congenital immunological deficiency and morphological immaturity of the kidneys.

Classification

The classification is as follows.

1. Congenital nephrotic syndrome:

1) Finnish type;

2) familial nephrotic syndrome not associated with microcystic disease.

2. Primary nephrotic syndrome:

1) nephrotic form of glomerulonephritis, a hormone-sensitive variant, morphologically associated with minimal glomerulonephritis;

2) with other morphological forms of glomerulonephritis (nephrotic form of glomerulonephritis, hormone-resistant variant, mixed form of glomerulonephritis).

3. Secondary nephrotic syndrome:

1) with systemic connective tissue diseases, systemic vasculitis;

2) with renal disembryogenesis;

3) in metabolic diseases (pathology of tryptophan metabolism, cysticosis, glycogenosis);

4) with infectious diseases (malaria, cytomegaly, tuberculosis, syphilis);

5) with amyloidosis;

6) with thrombosis of the renal veins;

7) in case of poisoning, including reactions to medicinal substances;

8) with rare syndromes (sarcoidosis, sickle cell anemia).

Clinic

Extrarenal symptoms: increasing edematous syndrome, ascites, hydropericardium, hepatomegaly, pallor (pearl) of the skin.

Symptoms of hypoproteinemic cardiopathy: shortness of breath, tachycardia, systolic murmur at the apex, volemic shock.

Urinary syndrome: proteinuria, oliguria with high relative density of urine, cylindruria.

Hypoproteinemia, severe dysproteinemia (decrease in albumin and β-globulins, increase in α₂-globulins), hypersolesterolemia, high ESR.

Differential diagnosis

Differential diagnosis is carried out with primary, secondary and congenital nephrotic syndrome.

Treatment

The principles of treatment are as follows.

1. Bed rest, salt-free diet, fluid restriction (based on: previous daily diuresis + 15 ml/kg of body weight).

2. Glucocorticoids - 2-2,5 mg / kg (up to 5 mg / kg) for at least 4-6 weeks with a gradual decrease in dose upon the onset of remission. The maintenance dose is prescribed for a long time - up to 1,5 months.

3. Immunosuppressants (with hormone resistance - inefficiency of hormones for 2 months, or hormone dependence), azathiaprine, 6-mercaptopurine.

4. Diuretic (a combination of furosemide and veroshpiron, aminoride, hypothiazide).

5. Antibacterial therapy (penicillin, falosporin).

6. Heparin, antiplatelet agents.

7. Symptomatic therapy, vitamin therapy.

8. Methindon.

8. Polycystic kidney disease

Polycystic kidney disease is a congenital disease that is characterized by the formation of cysts in both kidneys, which increase and lead to atrophy of the functioning parenchyma. Polycystic is classified as a hereditary disease, and it occurs in members of the same family. The disease manifests itself and is diagnosed at the age of 20-40 years, but can manifest itself in adolescence and in old age.

Etiology and pathogenesis

The cause of the development of the disease is unknown. The pathogenesis is due to a violation of the embryonic development of the tubules, some of which turn into cysts. The kidneys increase in size, between the cysts there are layers of parenchyma or connective tissue. Possible suppuration of cysts.

Clinic

The disease can be asymptomatic for many years, it can be detected by chance during ultrasound and examination, surgery or autopsy.

In the early stages, it is asymptomatic. Due to a decrease in the mass of the parenchyma, the concentration function of the kidneys decreases. Patients complain of polyuria, thirst, loss of appetite, decreased ability to work, fatigue, dull pain and heaviness in the lower back, headache.

Diagnostics

Polyuria 3-4 l/day. Urine is colorless, low density. Nocturia. Isosthenuria. Proteinuria is small. The sediment contains erythrocytes. Perhaps a state when macrohematuria turns into profuse bleeding. Leukocyturia indicates an infection that leads to suppuration of the cysts. At the same time, fever appears, pain syndrome intensifies, intoxication increases.

On palpation, a bumpy, dense and painful kidney is felt.

Polyuria helps to eliminate toxins from the body, while azotemia may not be detected, but over time, kidney function is impaired, and azotemia develops.

The patient's condition becomes more severe, nausea, an unpleasant taste in the mouth appear. The deterioration of the condition is facilitated by surgical intervention, pregnancy, suppuration of cysts, trauma, arterial hypertension. In the later stages, anemia and other signs of kidney failure appear.

Differential diagnosis

Differential diagnosis is carried out with chronic glomerulonephritis and chronic pyelonephritis, a tumor of the kidneys. In cystic kidneys, the kidneys are greatly enlarged, and the function of both kidneys is impaired.

Treatment

Treatment is symptomatic. Gentle regimen (avoid physical exertion), sanitation of foci of chronic infection (colds, carious teeth).

When bleeding, bed rest must be observed. At accession of an infection purpose of antibiotics is reasonable.

It is necessary to follow a diet with restriction of protein and salt, but nutrition should be rational and rich in vitamins. With severe arterial hypertension, antihypertensive drugs are prescribed.

With suppuration of cysts, surgical intervention is performed. In the terminal stage of renal failure, hemodialysis or kidney transplantation is performed.

Forecast

More often, the disease leads to kidney failure.

9. Renal colic

Renal colic is a syndrome that appears with certain kidney diseases, the main characteristic of which is acute pain in the lumbar region.

Etiology and pathogenesis

The most common causes are: nephrolithiasis, hyperhidrosis, nephroptosis. These diseases are characterized by impaired urodynamics.

Renal colic can occur when the lumen of the ureter is obstructed by a blood vessel, stone, part of a tumor, caseous masses in tuberculosis. The main cause of pain is urinary tract spasm and ischemia, stretching of the fibrous capsule of the kidney and pelvic-renal reflux.

Clinic

The attack develops suddenly, characterized by severe pain in the lower back. Physical activity provokes colic.

An attack may be preceded by a feeling of discomfort in the lumbar region.

The strength of the pain increases, the patient cannot find a position in which the pain will be less pronounced.

The pain radiates to the groin and along the ureters. In the general analysis of urine: erythrocyturia, protein, calculi, blood clots. Colic may have a clinical picture of an acute abdomen and be accompanied by abdominal pain and intestinal paresis.

Differential diagnosis

Differential diagnosis is carried out with appendicitis, cholecystitis, intestinal obstruction and pancreatitis. If the stone is small or sand comes off, colic is manifested by frequent painful urge to urinate. The attack is accompanied by chills, fever, tachycardia, leukocytosis, increased ESR. The duration of the attack is from several minutes to many hours.

Diagnostics

Laboratory studies that confirm an attack of colic: chromocystoscopy, intravenous urography.

Treatment

Appointment of thermal procedures (heating pad, bath with water temperature of 37-39 ° C), spasmodic and analgesic drugs. It is good to stop the attack by intramuscular administration of baralgin and oral administration of 0,5 g of baralgin 3 times a day. Subcutaneous injections of atropine 1 ml and 1 ml of promedol or morphine. With prolonged colic, novocaine blockade of the spermatic cord is performed. With hyperthermia, it is advisable to hospitalize the patient in the urological department.

Forecast

The prognosis is favorable with adequate treatment.

10. Renal amyloidosis

In most cases, it is a systemic disease. It is characterized by changes leading to extracellular loss of amyloid (a complex protein-saccharide complex) in the tissue, which subsequently causes impaired renal function. The amyloid protein is perceived as an antigen.

Etiology and pathogenesis

Amyloidosis, as a rule, is accompanied by an infectious process in the body (tuberculosis, syphilis, osteomyelitis) - this is secondary amyloidosis. Secondary amyloidosis accompanies rheumatoid arthritis, ulcerative colitis, tumors, septic endocarditis. Primary amyloidosis develops with multiple myeloma, senile amyloidosis. The development of amyloidosis can lead to dysproteinemia, immunological failure of the body (inhibition of the T-system, changes in phagocytosis).

Clinic

The symptoms are varied and depend on the location of the amyloid, the degree of distribution in the organs, the duration of the course of the disease, and the presence of complications. Patients with amyloidosis of the kidneys do not complain for a long time. Then edema appears, increased general weakness, decreased activity, arterial hypertension, and renal failure.

Complications - vein thrombosis, pain syndrome, anuria, diarrhea. In the general analysis of urine, massive proteinuria up to 40 g per day. In the blood test - hypoproteinuria and dysproteinuria, hyperlipidemia.

The loss of protein calls for total edema. Characteristic signs of amyloidosis of the kidneys are massive proteinuria, hypoproteinemia, hypercholesterolemia and edema.

In the urine sediment - protein, cylinders, erythrocytes, leukocytes. Amyloidosis lesions affect the cardiovascular system.

Hypotension or hypertension develops, cardiac conduction disturbance and rhythm disturbance. Changes in the gastrointestinal tract - a syndrome of malabsorption develops.

The liver is enlarged, the spleen is enlarged (hepatomienal syndrome). Organ function may not be impaired. In the future, nephrotic syndrome and renal failure develop.

To clarify the diagnosis, a tissue biopsy is performed (kidney, intestinal mucosa, gum tissue, skin, liver).

Treatment

Prolonged dietary restrictions (salt, protein). Hypothermia, exposure to cold air and high humidity must be avoided. Patients with amyloidosis need a warm and dry climate. Sanatorium treatment in Central Asia, the southern coast of Crimea (Yalta). Bed rest during the period of massive edema or the development of heart failure and uremia. Vitamin therapy is required. Of great importance is corticosteroid therapy (prednisolone 1200-1500 mg per course of treatment). Patients with amyloidosis are recommended long-term (1,5-2 years) intake of raw liver (100-120 g / day).

In the initial stages, drugs of the 4-aminquinaline series (delagil 0,25 g 1 time per day under the control of leukopenia. Observation of an ophthalmologist, since deposition of drug derivatives in the refractive media of the eye is possible. Unitiol courses of 5-10 mg intramuscularly are used for 30-40 days. Sometimes colchidine is used, diuretics, antihypertensive drugs are used as symptomatic therapy, hemodialysis and kidney transplantation are possible.

11. Anomalies of the urinary system

Anomalies of the urinary system are the most common malformations. Some can lead to early death in childhood, others do not cause dysfunction of the urinary system and are found incidentally during an ultrasound examination or tomography, as well as an X-ray examination.

Some of the anomalies progress very slowly and can only become clinically apparent in old age. Some developmental anomalies can serve as a background for the development of another pathology (renal stones, chronic pyelonephritis, arterial hypertension).

The causes of anomalies may be hereditary predisposition, mother's diseases during pregnancy - rubella in the first months; ionizing radiation, syphilis, alcoholism, the use of hormonal drugs.

If an anomaly is found in one family member, then all family members should be examined.

Classification

There are the following groups of anomalies:

1) anomalies in the number of kidneys - bilateral agenesis (absence of kidneys), unilateral agenesis (single kidney), doubling of the kidneys;

2) anomalies in the position of the kidneys - momolateral dystopia (the lowered kidney is on its side); heterolateral cross dystopia (transfer of the kidney to the opposite side);

3) anomalies in the relative position of the kidneys (fused kidneys), horseshoe-shaped kidney, biscuit-shaped, S-shaped, L-shaped;

4) anomalies in the size and structure of the kidneys - aplasia, hypoplasia, polycystic kidney;

5) anomalies of the renal pelvis and ureters - cysts, diverticula, bifurcation of the pelvis, anomalies in the number, caliber, shape, position of the ureters.

12. Hydronephrosis

This disease develops as a result of a violation of the outflow of urine and is characterized by the expansion of the pelvis-calyx system, morphological changes in the interstitial tissue of the kidney and atrophic changes in the renal parenchyma. Hydronephrosis on the right or left occurs equally often, bilateral - in 6-10% of cases of the total number of the disease.

Etiology and pathogenesis

Hydronephrosis can be congenital or acquired. The cause of congenital hydronephrosis may be urinary tract dyskinesia; congenital malformations of the renal artery or its branches, compression of the ureter, ureterotia, congenital obstruction of the lower urinary tract, tumors of the urinary tract, tumors of the prostate gland, tumors of the retroperitoneal tissue, cervix, malignant metastasis of the retroperitoneal tissue and pelvic tissue, tumor metastasis to the retroperitoneal lymph nodes , traumatic injury to the spinal cord, leading to a violation of the outflow of urine.

If the obstruction to the outflow of urine is located distal to the ureteropelvic segment and the pelvis and ureter expand, hydroureteronephrosis develops. Hydronephrosis can be aseptic and infected.

If hydronephrosis is aseptic, then pathological changes depend on the degree of obstruction and the duration of the disease. In infectious hydronephrosis, changes in the kidneys depend on the degree of obstruction, the duration of the disease, and the virulence of the infectious agent. In the initial period of the disease, morphological changes are not very pronounced, expansions of the pelvis and calyces are found. Inside the pelvis, pressure rises and, as a result, there is a violation of kidney function. These changes are reversible, after the elimination of the cause of the dysfunction, a reverse development occurs. With a prolonged violation of the outflow of urine, organic changes develop that are irreversible - obstructive interstitial nephritis.

Partial restoration of kidney tissue and its function is possible. When infected with hydronephrosis - obstructive pyelonephritis.

Clinic

Hydronephrosis can be asymptomatic for a long time. Symptoms may appear when an infection is attached, the formation of a stone in the pelvis, traumatic damage to the kidneys. The first symptoms of the disease appear, which give rise to the study of the urinary system.

Hydronephrosis is characterized by pain syndrome - pain in the lumbar region in the form of renal colic with typical localization and irradiation along the ureters, in the groin, genital area, thigh, perineum. The initial stage of hydronephrosis is characterized by attacks of renal colic. At the next stage, the pelvis and calyces are replaced by connective tissue, the ability to actively contract is lost.

At this stage, hydronephrosis is manifested by dull pain in the lumbar region. Pain occurs both during the day and at night, regardless of the position of the patient. With nephroptosis, with which hydronephrosis is differentiated, patients sleep on their sore side. With upper urinary tract obstruction, dysuria occurs at the time of the attack. The most important symptom of hydronephrosis is hematuria. Macrohematuria in 20% of cases, microhematuria in most cases. Fever appears in case of infection.

Diagnostics

Methods of research:

1) palpation of a greatly enlarged kidney;

2) chromocystography, chronocystoscopy;

3) x-ray examination - the basis of the diagnostic method.

Plain radiography allows you to determine the size of the kidneys, the presence of kidney stones; urograms show expansion of the pelvis and calyces.

Differential diagnosis

Differential diagnosis is carried out with nephrolithiasis, nephroptosis, kidney tumors, polycystic kidney disease. The leading sign is a change on the radiograph.

Treatment

Treatment of hydronephrosis is only surgical. In case of infected hydronephrosis, antibiotic treatment is carried out under the control of urine cultures and a study of microflora for sensitivity to antibacterial drugs.

Forecast

Bilateral hydronephrosis leads to disruption of homeostasis and renal failure.

13. Pyelitis

Pyelitis is an inflammation of the renal pelvis. Acute inflammation of the mucous membrane of the upper urinary tract - the pelvis and calyces - is always accompanied by inflammatory changes in the kidney parenchyma.

Chronic inflammation of the pelvis and calyces is always supported by one of the factors that caused it - chronic inflammation of the interstitial tissue of the kidneys or a disease that prevents the elimination of the inflammatory process (stone, tumor, narrowing of the ureter).

First of all, it is necessary to diagnose the disease that caused pyelitis - chronic pyelonephritis, infected nephrolithiasis, hydronephrosis, tumor. There is practically no uninfected pyelitis, and it is always necessary to differentiate between acute and chronic pyelitis.

Mycobacteria enter the kidneys via the hematogenous route. For the development of the tuberculous process, a background state is necessary - the immunopathological state of the body and renal tissue. The spread of the process occurs through the urinary tract, through the lymphatic vessels.

Clinic

At the beginning of the disease - asymptomatic. Then there is weakness, fatigue, fever (subfebrile temperature), dull pain in the lumbar region. In the analysis of urine - pyuria, proteinuria, leukocyturia. In sowing, mycobacteria displace other flora; they do not grow on ordinary media. Dysuria.

Treatment

Conservative treatment is aimed at the use of anti-tuberculosis drugs (isoniazid 300 mg 1 time per day, rifampicin 300 mg 2 times a day in combination with ethambutol 400 mg 3 times a day).

Increasing the body's resistance. Treatment in an anti-tuberculosis dispensary or sanatorium. Polycavernous process must be treated surgically.

Forecast

The prognosis for early diagnosis and adequate treatment is favorable.

15. Nephroptosis

Nephroptosis (omission of the kidney) is a condition of the body in which the kidney is located lower than normal, shifts from its bed, the kidney becomes more mobile, especially in an upright position, and exceeds physiological norms.

Another name for nephroptosis is pathological mobility of the kidney.

Etiology and pathogenesis

Omission of the kidney occurs when the function of the ligamentous apparatus is impaired. Of great importance for maintaining the correct position of the kidney is its fatty capsule. Reducing the volume of this capsule contributes to the occurrence of nephroptosis. The correct position of the kidney is also determined by the renal fascia and fibrous cords in the region of the upper pole, as well as the dense fatty tissue between the adrenal gland and the kidney. There are a number of predisposing factors that contribute to nephroptosis: an infectious disease, sudden weight loss, a decrease in the muscle tone of the abdominal wall, trauma.

Nephroptosis is more common in women than in men. There are three stages of nephroptosis. Starting from the second stage, in addition to omission, rotation joins. Nephroptosis of the second and third stages leads to a violation of renal hypo- and urodynamics, which determine the clinical picture.

Clinic

In the first stage, a latent course or dull pain in the lower back, aggravated by exercise, can spread throughout the abdomen.

In the second stage, proteinuria and erythrocyturia appear. In the third stage, the pain is permanent and impairs ability to work. Nephroptosis is accompanied by a decrease in appetite, impaired bowel function, depression, neurasthenia.

Complications

Pyelonephritis, venous hypertension of the kidney, arterial hypertension.

Confirmation of the diagnosis is x-ray examination, excretory urography. Differential diagnosis is carried out with kidney dystopia, diseases of the abdominal organs and the female genital area.

Treatment

It consists in the use of an elastic bandage, a complex of physiotherapy exercises to strengthen the muscles of the anterior abdominal wall.

If the patient has lost a lot of weight, then a diet is prescribed to increase the adipose tissue around the kidney. Surgical treatment and supervision of the urologist is possible.

16. Interstitial nephritis

Interstitial nephritis (tubulointerstitial nephropathy) is an abacterial, non-destructive inflammation of the connective tissue of the kidneys with subsequent involvement of the entire nephron.

Etiology

Against the background of functional inferiority of the kidneys in the presence of dysplasia, abacterial damage to the interstitial tissue of the kidneys develops after an infectious disease (scarlet fever, diphtheria, tonsillitis), poisoning, burns, hemolysis and injuries, after drug therapy (penicillin, non-steroidal anti-inflammatory drugs).

Classification

Distinguish:

1) acute;

2) chronic interstitial nephritis.

Clinic

Pain syndrome - back pain, nausea, headache, chills, sweating, oliguria up to acute renal failure, hypertension.

In the analysis of urine: hypostenuria, proteinuria, erythrocyturia, increased salts, monocular and eosinophilic leukocyturia; early decrease in the secretory and excretory function of the tubules, preservation of glomerular filtration; in a chronic process, three syndromes develop: polyuria, arterial hypotension, weakness, stone formation.

Differential diagnosis

Differential diagnosis is carried out with pyelonephritis, glomerulonephritis, hereditary nephritis.

Treatment

The principles of treatment are as follows.

1. Complex of vitamins (A, B₆, E, P).

2. Antihistamines.

3. Antisclerotic drugs of the aminoquinoline series.

4. In acute renal failure - hemodialysis.

5. Phytotherapy (collection according to N. G. Kovaleva).

Lecture #5

1. Systemic lupus erythematosus

Systemic lupus erythematosus is a chronic polysyndromic disease that develops against the background of a genetically determined imperfection of immunoregulatory processes, leading to uncontrolled production of antibodies to one's own cells and their components with the development of autoimmune and immunocomplex inflammation of the connective tissue and blood vessels.

Etiology

The etiology has not been finally elucidated, a genetic predisposition is undoubted, and long-term persistence of the virus is not excluded.

Predisposing factors: insolation, infection, hypothermia, stressful situations, vaccination.

Classification

The classification is as follows:

1) the nature of the course of the disease: acute, subacute, chronic:

a) recurrent polyarthritis;

b) lupus syndrome;

c) Rebnaud's syndrome;

d) Werlhof's syndrome;

e) Sjögren's syndrome;

2) phase and degree of activity of the process: active phase: high (III), moderate (II), minimum (I); inactive phase (remission); 3) clinical and morphological characteristics of the lesion:

a) skin: butterfly symptom, capillaritis, exudative erythema, purpura, discoid lupus;

b) joints: arthralgia, acute, subacute and chronic polyarthritis;

c) serous membranes: polyserositis (pleurisy, pericarditis), effusion, dry; perihepatitis;

d) heart: pericarditis, endocarditis, mitral valve insufficiency;

e) lungs: acute and chronic pneumonitis, pneumosclerosis;

f) kidneys: lupus nephritis of nephrotic or mixed type;

g) urinary syndrome;

h) nervous system: meningoencephalopolyneuritis.

Clinic

The disease most often begins acutely, with an increase in body temperature and a violation of the general condition. This disease is characterized by a multisystemic lesion. Distinguish between major and minor diagnostic features.

Major diagnostic features:

1) "butterfly" on the face;

2) lupus arthritis;

3) lupus pneumonitis;

4) IE cells in the blood (normally absent) up to 5 per 1 leukocytes - single; 000 - 5 per 10 leukocytes - a moderate amount; more than 1000 - a large number;

5) ANF in large caption;

6) autoimmune Werlhof syndrome;

7) Coombs-positive hemolytic anemia;

8) lupus nephritis;

9) hematoxylin bodies in the biopsy material: swelling of the nuclei of dead cells with lysed chromatin; 10) characteristic pathomorphology in the removed spleen (bulbous sclerosis; clutches in sclerotic arteries and arterioles), skin biopsy (vasculitis, immunofluorescent luminescence of immunoglobulins on the basement membrane in the area of ​​the epidermal junction), kidneys (glomerular capillary fibrinoid, hyaline thrombi, phenomenon " wire bodies" - thickened basement membranes of giolarular capillaries impregnated with plasma proteins). Minor diagnostic signs:

1) fever over 37,5 °C for several days;

2) unmotivated weight loss (5 kg or more in a short time) and trophic disorders;

3) capillaries and on the fingers;

4) nonspecific skin syndrome (erythema multiforme, urticaria);

5) polyserositis - pleurisy, pericarditis;

6) lymphoidenopathy;

7) hepatosplenomegaly;

8) myocarditis;

9) damage to the central nervous system;

10) polyneuritis;

11) polymyoditis, polymyalgia;

12) polyarthralgia;

13) Rebno's syndrome;

14) increase in ESR (over 20 mm/h);

15) leukopenia less than 4 x 109 g/l;

16) anemia (hemoglobin less than 100 g/l);

17) thrombocytopenia (less than 100 x 109 g/l);

18) hypergammaglobulinemia (more than 22%);

19) ANF in low titer;

20) free IE bodies;

21) modified thromboenastogram.

The diagnosis of systemic lupus erythematosus is reliable with a combination of three major signs, with one mandatory: "butterfly", the presence of IE cells in large numbers or ANF in high titer, the presence of hematoxylin bodies. In the presence of only minor signs or in the combination of minor signs with lupus arthritis, the diagnosis of systemic lupus erythematosus is considered reliable.

Diagnostic criteria of the American Rheumatological Association:

1) erythema on the face ("butterfly");

2) discoid lupus;

3) Rebno's syndrome;

4) alopecia;

5) photosensitivity;

6) ulceration in the oral cavity and nasopharynx;

7) arthritis without deformation;

8) IE cells;

9) false positive Wasserman reaction;

10) proteinuria;

11) cylindruria;

12) pleurisy, pericarditis;

13) psychosis, convulsions;

14) hemolytic anemia and/or leukopenia and/or thrombocytopenia.

If four criteria are present, the diagnosis of systemic lupus erythematosus is considered sufficiently reliable.

Differential diagnosis

The differential diagnosis is carried out with rheumatism, rheumatoid arthritis, dermatomyositis, scleroderma, periarthritis nodosa, pheochromocytoma.

Treatment

Principle of treatment:

1) corticosteroids;

2) immunosuppressants;

3) non-steroidal anti-inflammatory drugs;

4) symptomatic means.

In systemic lupus erythematosus, prednisolone is prescribed immediately, followed by a switch to immunoregulatory therapy. For systemic lupus erythematosus among immunosuppressants, cyclophosphamide and isothioprine are considered the drug of choice.

2. Dermatomyositis

Dermatomyositis is a serious disease with a predominant systemic lesion of the muscles and skin, a mild but frequent organ pathology.

Etiology

The etiology has not been completely elucidated. Genetic predisposition matters, more often it is a secondary process, combined with a tumor (10-80%).

Predisposing factors: insolation, infection, hypothermia, vaccination, stressful situations.

Classification

Dermatitis is delimited according to the following criteria. Forms of the disease:

1) primary idiopathic:

a) dermatomyositis;

b) polymyositis;

2) secondary tumor:

a) dermatomyositis;

b) polymyositis.

The course of the disease: acute, subacute, primary chronic, chronic (previously occurring as acute or subacute), with one wave, undulating with continuous relapses.

Phase and degree of activity:

1) active phase:

a) maximum - I degree;

b) moderate - II degree;

c) minimal - III degree;

2) inactive phase.

Clinic and diagnostics

Skin and subcutaneous tissue: paraorbital purple erythema with edema, without edema; erythema-lilac elements under the area of ​​​​the joints; vascular stasis; telenangientasia, capillaritis; widespread edema, poikiloderma, bedsores.

Joints and muscles: skeletal muscle lesions; calcification (limited, diffuse); arthralgia, arthritis, tendon-muscle contractures.

Other organs and systems: vascular interstitial pneumonia, aspiration pneumonia; myocarditis, pericarditis, coronaritis; polyradiculoneuritis; erosive and ulcerative esophagitis; nephropathy.

The state of the musculoskeletal system:

1) functional insufficiency III degree (FN III);

2) functional insufficiency of II degree (FN II);

3) functional insufficiency of the I degree (FN I);

4) functional ability is fully preserved. Main clinical symptoms:

1) skin syndrome: purple paraorbital erythema with or without edema (dermatomyositis glasses), erythema over the extensor surfaces of the joints, sometimes with atrophic scars;

2) musculoskeletal syndrome: damage to symmetrical, predominantly proximal muscle groups (weakness, pain, swelling, hypertrophy, calcification);

3) visceral-muscular syndrome: damage to symmetrical, predominantly proximal muscle groups (weakness, pain, swelling, impaired breathing, dysphonia, dysphagia).

Additional clinical symptoms: irregular temperature curve, malaise, weight loss, poikiloderma (a combination of various skin changes), widespread swelling of the skin and subcutaneous tissue, vascular stasis, necrosis, arthritis, arthralgia, myocarditis, damage to the peripheral and central nervous system.

Diagnostics

Laboratory data:

1) increased activity of lactate dehydrogenase, creatinine phosphokinase, aminotransferases, aldoiosis, dysproteinemia;

2) accelerated ESR;

3) hypercreatinuria;

4) electromyographic: low-amplitude electrical activity up to bioelectric, highly sensitive fasciculations;

5) data from a morphological study (muscle biopsy): the development of sclerotic processes, atrophy of muscle fibers, calcification.

The diagnosis of dermatomyositis is considered reliable in the presence of 2-3 signs, and skin and muscle syndrome is mandatory.

The disease begins, as a rule, acutely, with a high temperature, a violation of general well-being. The most characteristic symptom: damage to the muscles and joints.

On examination, there is muscle stiffness, soreness, and progressive atrophy. Internal organs are involved (myocarditis, damage to smooth muscles, lungs, gastrointestinal tract). The disease is accompanied by high laboratory activity.

Differential diagnosis

Carried out with systemic lupus erythematosus, rheumatism, scleroderma, periarthritis nodosa, progressive muscular dystrophy, myasthenia gravis.

Treatment

The principles of treatment are as follows:

1) glucocorticoids, immunosuppressants;

2) non-steroidal anti-inflammatory drugs;

3) preparations of the aminoquinol group;

4) symptomatic treatment;

5) massage, physiotherapy treatment (electrophoresis with hyaluronidase, thermal procedures).

3. Nodular periarthritis

Periarthritis nodosa is an immunocomplex disease, which is based on damage to peripheral and visceral arteries, mainly of small and medium caliber, clinically characterized by fever, pain in the joints, muscles, various combinations of typical syndromes (skin, thrombotic, neurological, cardiac, abdominal, renal) .

Etiology

The etiology has not been sufficiently studied. Predisposing factors are: viral infection, vaccination. Small and medium-sized arteries are involved in the pathological process. The clinic is characterized by polymorphism. The onset of the disease is acute. The temperature is incorrect. Nodular periarthritis is most common in men and boys. The disease is accompanied by high laboratory activity.

Classification

Clinical option:

1) predominant damage to peripheral vessels;

2) predominant damage to internal organs;

3) an isolated lesion of the skin or internal organs.

Course: acute, subacute, chronic, recurrent.

Clinical syndromes: skin, thrombotic, muscular, articular, neurological, cardiac, renal (with arterial hypertension syndrome), abdominal, pulmonary.

Degree of circulation. D - no signs of discirculation.

DI - subcompensation stage (myalgia, arthralgia, local edema, nodules, pneumonitis, myocarditis, isolated urinary syndrome). DII - stage of decompensation:

A - causalgia, edema, cyanosis of the extremities, pulmonary infiltrates, coronaritis, pericarditis, abdominal crises, hepatomegaly, splenomegaly, high blood pressure;

B - necrosis of the skin, mucous membranes, distal gangrene, polyneuritis, cerebrovascular accident, myocardial infarction, lungs, kidneys, liver, spleen.

Complications

Hemorrhages in the brain, pulmonary hemorrhages, rupture of a coronary aneurysm; rupture of the liver, spleen, kidneys, perforation of intestinal ulcers, peritonitis.

Outcomes

Complete remission, relative clinical and laboratory remission, disability.

Clinic and diagnostics

The clinical syndromes of the disease are as follows.

1. Basic:

1) hyperthermia of the wrong type, debilitating muscle pain; subcutaneous or internal nodules; treelike livedo; dry gangrene of the fingers, necrosis of the mucous membranes and skin; asymmetric polyneuritis; central vascular crises; coronaritis, myocardial infarction; syndrome of hypereosinophilic bronchial asthma, abdominal syndrome; acutely developing arterial hypertension;

2) laboratory: leukocytosis, hypereosinophilia, Australian antigen;

3) biopsy of the skin and muscles: destructive - proliferative vasculitis with a predominant lesion of small arteries;

4) aortography: aneurysms of small and medium arteries of the kidneys, liver, spleen, mesentery, coronary and other arteries.

2. Auxiliary:

1) clinical: cachexia, hyperhidrosis, arthralgia, hyperesthesia, apolyradiculoneuritis, myocarditis or pericarditis, vascular pneumonia or volatile pulmonary infiltrates, enterocolitis, hepatosplenomegaly;

2) laboratory: an increase in ESR, hypergamiaglobulinemia, an increase in seromucoid, lipoproteins, fibrinogen, immunoglobulins M, G, a decrease in the level of T-lymphocytes and an increase in the content of B-lymphocytes;

3) skin and muscle biopsy;

4) capillaritis, lymphoid macrophage infiltration of the vascular wall;

5) aortography; deformation (stenosis, occlusion) of medium and small arteries, uneven contrasting of organs.

Differential diagnosis

It is performed with sepsis, rheumatism, systemic lupus erythematosus, JRA, dermatomyositis, pheochromocytoma, renovascular hypertension.

Treatment

The principles of treatment are as follows.

1. Corticosteroids.

2. Immunosuppressants.

3. Preparations of the aminoquinoline series.

4. Non-steroidal anti-inflammatory drugs.

5. Hemodialysis.

4. Rheumatism

Rheumatism (acute rheumatic fever) is a common infectious-allergic disease with a systemic lesion of the connective tissue with a predominant localization in the cardiovascular system, as well as the involvement of other internal organs and systems.

Etiology

The role of α-hemolytic streptococcus group A α-form in the etiology of rheumatism has been established.

Classification

Forms and degrees of activity:

1) active - I, II, III degree of activity;

2) inactive.

Clinical and anatomical characteristics of the lesion. Heart:

1) primary rheumatic heart disease without valve defects;

2) recurrent rheumatic heart disease with valvular disease;

3) rheumatism without obvious cardiac changes;

4) rheumatic myocardiosclerosis.

Other organs and systems:

1) polyarthritis, serositis (pleurisy, peritonitis, abdominal syndrome);

2) chorea, encephalitis, meningoencephalitis, cerebral vasculitis, neuropsychiatric disorders;

3) vasculitis, nephritis, hepatitis, pneumonia, skin lesions, iritis, iridocyclitis, thyroiditis;

4) consequences and residual effects of transferred non-cardiac lesions.

The nature of the course: acute, subacute, protracted, sluggish, continuously relapsing, latent.

Circulatory status: H0 - no circulatory failure; H₁ - I degree insufficiency; H₂ - II degree insufficiency; H₃ - III degree insufficiency.

Diagnostic criteria

Diagnostic criteria (Kisel - Jones - Nesterov).

Main: carditis, polyarthritis, chorea, rheumatic nodules, erythema annulare, effect of antirheumatic treatment.

Additional: previous streptococcal infection, fever, arthralgia, pneumonia, fatigue, epistaxis, abdominal pain, prolongation of the PQ interval, serological and biochemical parameters. For a reliable diagnosis, a combination of 2-3 main criteria (of which one is mandatory carditis) and 3-4 additional ones is necessary.

Criteria for the degree of activity of rheumatism.

I. Rheumatism with maximum activity (III degree).

1. Clinical syndrome: bright general and local manifestations of the disease with the presence of fever, the predominance of the exudative component of inflammation in the affected organs and systems:

1) pancarditis;

2) acute, subacute, diffuse myocarditis;

3) subacute rheumatic heart disease with severe circulatory failure;

4) subacute or continuously recurrent rheumatic heart disease in combination with symptoms of acute or subacute polyarthritis, pleurisy, peritonitis, rheumatic pneumonia, nephritis, hepatitis, subcutaneous rheumatic nodules, erythema annulare;

5) chorea with a pronounced manifestation of activity.

2. An increasing increase in the size of the heart, a decrease in the contractile function of the myocardium, pleuropericardial adhesions.

3. Clear dynamic changes in the ECG, FCG, depending on the localization of the rheumatic process.

4. Changes in blood parameters: neutrophilic leukocytosis above 10 x 109 g / l, ESR above 30 mm / h, C-reactive protein (+++), fibrinogenia above 9 - 10 g / l; α2-globulins above 17%; β-globulins - 23-25%; DPA test - 0,35 - 0,05 U, seromucoid above 0,6 U, antisterptolysin titer - 0 (ASL-0), anti-streptohyaluronidase (ASH), antistreptokinase (ASK) Ig 3 times higher than normal.

5. Permeability of capillaries II-III degree.

II. Rheumatism with moderate activity II degree.

1. Clinical syndrome: moderate clinical manifestations of a rheumatic attack with or without moderate fever, without a pronounced exudative component of inflammation in the affected organs:

1) subacute rheumatic heart disease in combination with circulatory failure of I-II degree, slowly responding to treatment;

2) subacute or continuously recurrent rheumatic heart disease in combination with subacute polyarthritis, rheumatic chorea, etc.

2. An increase in the size of the heart, pneumopericardial adhesions, decreasing under the influence of active antirheumatic therapy.

3. Dynamic changes in ECG and FCG under the influence of antirheumatic therapy.

4. Changes in blood parameters: neutrophilic leukocytosis within 8 - 109 g / l, ESR - 20-30 mm / h, C-reactive protein - 1-3 plus, α₂-globulins 11-16%, β-globulins - 21-23%, DFA test - 0,25 - 0,3 U, seromucoid - 0,3-0,6 U, increased ASL titers - 0, ASG - in 1,5, 2-XNUMX times compared to the norm.

5. Permeability of capillaries III degree.

III. Rheumatism with minimal activity (I degree).

1. Clinical syndrome: clinical symptoms of an active rheumatic process are mild, sometimes barely manifested; there are almost no signs of the exudative component of inflammation in organs and tissues; predominantly monosyndromic nature of inflammatory lesions:

1) protracted, continuously recurrent, latent rheumatic heart disease, difficult to treat;

2) protracted or latent rheumatic heart disease in combination with chorea, encephalitis, vasculitis, iritis, rheumatic nodules, annular erythema, persistent arthralgia.

2. X-ray changes depend on the presence of heart disease, without a clear dynamics during treatment.

3. ECG-, PCG-changes are mild, but persistent.

4. Indicators of the blood system are slightly changed or within the upper limit of normal.

5. Permeability of capillaries I-II degree.

Differential diagnosis

Depends on the severity of the main clinical symptoms. In the presence of articular syndrome, it is performed with JRA, reactive arthritis (yersiniosis, salmonellosis), infectious-allergic polyarthritis, hemorrhagic vasculitis. Rheumocarditis is differentiated from nonspecific carditis, functional cardiopathy, cardiac arrhythmias, artrioventricular blockade, infective endocarditis, congenital heart defects.

Treatment

The principles of treatment are as follows.

1. Semi-bed rest, with myocardial damage - strict bed rest.

2. Diet with limited content of salt and carbohydrates with a sufficient introduction of high-grade proteins and a high content of vitamins.

3. Benzylpenicillin sodium salt, then long-acting drugs (bicillin, bicillin-5). With intolerance to penicillins - replacement with cephalosporins.

4. Glucocorticoids.

5. Non-steroidal anti-inflammatory drugs (aspirin, indomethacin).

6. Aminocholine preparations.

The success of treatment depends on early recognition and treatment. All patients with active rheumatism are prescribed intramuscular injections of penicillin 1 IU (600 IU 000 times a day), and then bicillin-400, 000 IU, continuing every 4 days. In case of intolerance, erythromycin 5 mg 1 times a day is prescribed.

Anti-inflammatory therapy is carried out with prednisolone 20 (30) mg/day in 4 doses for two weeks, bringing the daily dose to 10 mg, and then decreasing by 2,5 mg every day.

At the III degree of activity, it is possible to prescribe non-steroidal anti-inflammatory drugs: acetylsalicylic acid up to 4 g / day, indomethacin 100-150 mg / day for 1 - 2 months. Ibuprofen is prescribed in outpatient practice at a dose of 400 mg 2-3 times a day.

The treatment of rheumatism is based on a system of staged treatment: a hospital - a polyclinic - a spa treatment. In the hospital, active anti-inflammatory therapy is carried out, after a decrease in the activity of the inflammatory process, the patient is discharged under the supervision of a rheumatologist, where they continue treatment, individually selected in the hospital, with bicillin-5, and aminoquinoline preparations. The third stage includes dispensary observation and preventive treatment of a patient with rheumatism. Primary prevention of rheumatism - organization of a set of measures aimed at eliminating the primary incidence of rheumatism: treatment of streptococcal infections (tonsillitis, pharyngitis, acute respiratory infections), improving living standards and improving living conditions. Secondary prevention should prevent recurrence and progression of the disease in patients who have had rheumatism, with the help of bicillin prophylaxis for 5 years. Regular monitoring by a rheumatologist is necessary.

5. ​​Rheumatoid arthritis

Rheumatoid arthritis is a systemic connective tissue disease characterized by chronic destructive polyarthritis. The term was proposed by Garrod in 1859.

Etiology

The etiology has not been elucidated. Destructive processes affect primarily the joints. Loose granulation tissue gradually destroys the cartilage and epiphyses of bones, followed by the development of ankylosis and joint deformity.

Classification

The disease is distinguished according to the following criteria:

1) articular shape;

2) articular-visceral form;

3) pseudo-septic form, characterized by lesions of many joints, visceritis, fever with chills and profuse sweats;

4) combined form with deforming osteoarthritis or rheumatism with heart disease;

5) seropositive;

6) seronegative process for rheumatoid factor. Course of the disease:

1) fast;

2) slow;

3) without noticeable progression.

The degree of activity of the process.

I degree - slight pain in the morning and stiffness, ESR no more than 20 mm / h, the content of fibrinogen, C-reactive protein is slightly increased.

II degree - pain in the joints during movement and at rest, exudative manifestations, morning stiffness, subfebrile body temperature, ESR up to 40 mm / h, the content of fibrinogen, C-reactive protein is significantly increased.

III degree - severe and prolonged morning stiffness, significant exudative changes in the joints, visceral lesions, high body temperature, ESR more than 40 mm / h, very high levels of fibrinogen, C-reactive protein.

X-ray examination, determination of the X-ray stage and the degree of functional disorders of the musculoskeletal system are necessary.

The main symptom is arthritis or polyarthritis, joint damage is symmetrical and persistent. Small joints of hands and feet, II and III metacarpal, phalangeal are more often surprised; morning stiffness, joint pain on motion and at rest. On examination, the joints are enlarged, painful on palpation, the contours are smoothed, there is exudate in the joint cavity, the skin is hyperemic over the joint, hot to the touch. General symptoms of intoxication: weakness, loss of appetite, weight loss, fever, sweating.

Clinic

Clinical options:

1) mono- or oligoarthritis (often the end joint);

2) the classic version - symmetrical and multiple lesions of the joints, polyarthritis, inflammation is progressive;

3) unstable polyarthritis with reversible joint damage;

4) polyarthritis with febrile syndrome;

5) polyarthritis with systemic manifestations is characterized by visceral lesions (heart, serositis). The advanced stage is characterized by deforming arthritis.

Extra-articular lesions in rheumatoid arthritis are common. The heart is most often affected (pericarditis with effusion, myocarditis).

The defeat of the lungs is manifested by dry, asymptomatic pleurisy. Pulmonary hypertension may develop. Kidney damage develops after 7-10 years from the onset of the articular symptom. There are signs of kidney aminoidosis, rheumatoid hyaluronephritis.

With rheumatoid arthritis, vasculitis often develops in the form of skin rashes, rheumatoid nodules. Eye damage in the form of scleritis, keratitis, iridocyclitis.

X-ray diagnostics - osteoporosis of the epiphyses of bones, narrowing of the joint gap, the formation of marginal usurs.

Distinguish stage IV.

I. Osteoporosis without destruction.

II. A slight narrowing of the joint space, multiple usu-ry.

III. Significant changes in the gap, single epiphyses.

IV. Ankylosis of the joints.

Diagnostics

Detection of high titer rheumatoid factor. Increase in fibrinogen, seromucoid, C-reactive protein, α₂-glo-bulins.

Treatment

The principles of treatment are as follows.

1. Non-steroidal anti-inflammatory drugs (indomethacin, brufen, naproxen, voltaren, metindol.

2. Basic funds:

1) aminoquinoline drugs (delagil) are used for a long time (for years);

2) gold salts (krizanol, sanocrisin), maintain doses for 1-2 years;

3) D-penicillamine in the early stages;

4) cytostatics are used for systemic and visceral manifestations.

3. Corticosteroids.

4. Immunomodulators (decaris, levmamizole, thymalin). A comprehensive rehabilitation program includes physiotherapy exercises, the fight against hypotrophic processes in the muscles, improving joint mobility, increasing the overall tone of the body, general and physical performance.

5. Teaching a new stereotype that prevents the development of pathological contractures.

6. Systemic scleroderma

Systemic scleroderma is a diffuse disease of the connective tissue, manifested by fibrosis of the skin, internal organs, vascular pathology of the type of obliterating endarteritis with the spread of vasospastic disorders.

Etiology

The etiology is not clear. A viral and hereditary disease is suspected.

Provoking factors: hypothermia, vibration, trauma, contact with certain chemicals, neuroendocrine disorders, allergization of the body.

Classification

The classification is as follows.

I. The nature of the course: acute, subacute, chronic.

II. Clinical forms:

1) typical (with a characteristic skin lesion);

2) atypical (with focal skin lesions);

3) predominantly visceral, articular, muscular, vascular.

III. Stage of development: initial, generalized, terminal.

IV. Degree of activity: minimal (I), moderate (II), high (III).

V. Clinical and morphological characteristics of lesions:

1) skin and peripheral vessels: "dense edema", induration, atrophy, hyperpigmentation, telangiectasia, Rebno's syndrome, focal lesion;

2) locomotor apparatus: arthralgia, polyarthritis (exudative or fibrous-indurative), polymyositis, calcification, osteolysis;

3) heart: myocarditis, cardisclerosis, heart disease (mitral valve disease often develops);

4) lungs: interstitial pneumonia, pneumosclerosis (compact or cystic), adhesive pleurisy;

5) digestive tract: eophagitis, duodenitis, colitis;

6) kidneys: true scleroderma kidney, hyaluronephritis;

7) nervous system: polyneuritis, vegetative changes, neuropsychiatric disorders.

Diagnostics

The diagnostic criteria are as follows.

I. Main:

1) peripheral:

a) vasomotor disorders (spasm of small vessels, especially fingers, from a slight feeling of chilliness to Rebno's syndrome with attacks of acroasphyxia and "white spot" phenomena);

b) scleroderma skin lesion (skin is tense, dense, thick, shiny, merging with the subcutaneous fat layer, not folded, amimic face);

c) osteolysis and calcification (Tibierge-Weissenbach syndrome);

d) musculoskeletal syndrome with contractures (disturbance of gait, reduction in the volume of active movements);

2) visceral:

a) basal pneumosclerosis (in X-ray examination, increased transparency of the lung tissue, increased vascular pattern or microcellularity of predominantly basal sections;

b) scleroderma kidney (sudden development of malignant hypertension with acute renal failure).

II. Additional:

1) peripheral: skin hyperpigmentation, telangiectasia, trophic disorders, Shepren's syndrome, polyectasia, polyarthralgia, myoalgia, polymyositis;

2) visceral:

a) lymphadenopathy, polyserositis, diffuse and focal nephritis, polyneuritis, damage to the central nervous system;

b) rapid weight loss, fever;

3) laboratory: increase in ESR more than 20 mm/h, hyperproteinemia (more than 85 g/l), hypergammaglobulinemia (more than 23%); antibodies to DNA or ANF; rheumatoid factor; an increase in hydroxyproline in plasma, urine.

The diagnosis is certain if there are three main criteria (or one of the main criteria if they are scleroderma kidney disease, osteolysis of the nail phalanges, or damage to the digestive tract) and three or more auxiliary criteria.

Differential diagnosis

The differential diagnosis is carried out with dermatomyositis, phenylketonuria, Butke's scleroma.

Treatment

The principles of treatment are as follows.

1. Glucocorticoids.

2. Immunosuppressants.

3. Rehabilitation therapy.

4. Massage, physiotherapy exercises.

To improve the rheological properties of blood, low molecular weight dextrans are introduced, with the development of calcification, disodium EDTA is used, external applications of a 50% solution of dimexide are effective, especially with the addition of vasodilators (nicotinic acid) in the affected skin area. The use of hyperbaric oxygenation, plasmapheresis is very effective.

Prevention

Limiting contact with chemical agents, allergenic factors, patients should avoid hypothermia, insolation, vibration.

In chronic and subacute course with minimal activity, sanatorium treatment is indicated: Evpatoria, Pyatigorsk. The appointment of physiotherapy exercises and physiotherapeutic procedures is mandatory - ultrasound with hydrocartisone, electrophoresis with hyaluronidase, paraffin applications, massage.

7. Gout

Gout is a disease characterized by the deposition of urate crystals in joints and other tissues, resulting from impaired metabolism of purine bases and uric acid.

Etiology and pathogenesis

Violation of the metabolism of purine bases (mainly included in the composition of nucleic acids) occurs as a result of congenital or acquired weakening of the activity of enzymes that regulate this process.

An increase in the level of uric acid in the blood (hyperuricemia), characteristic of gout, develops as a result of increased breakdown of purine bases or due to a decrease in the excretion of uric acid by the kidneys.

Gout can be a symptom of another disease (myeloid leukemia, heart disease). Hyperuricemia contributes to the accumulation and deposition of uric acid salts (urates) in the tissues in the form of microcrystals. The ingress of urate into the synovial fluid leads to inflammation. Hyperuricemia reduces the buffering properties of urine and promotes the deposition of urate in the urinary tract.

Clinic

The disease develops more often in middle-aged men. Recurrent acute mono- or oligoarthritis of the joints of the lower extremities is formed (the metatarsus of non-phalangeal joints, joints of the metatarsus of the ankle, knee joints are more often affected. Sometimes arthritis of the small joints of the hand develops.

Gouty arthritis has a number of features: it worsens at night, the intensity of pain increases rapidly and reaches a maximum in a few hours. The pain is pronounced, movements in the joint are impossible, the skin is hyperemic over the joint, fever is possible, arthritis can stop within a few days, leaving no changes. Provoking factors: eating foods high in purine bases (meat, alcoholic beverages), surgery, trauma, stress, taking diuretics, riboxin. Perhaps the development of chronic gouty polyarthritis with periods of exacerbation and remission. In 1/4 of patients with gout, urolithiasis and interstitial nephritis develop. Perhaps the deposition of crystals under the skin above the joints, in the cartilage of the auricles - tophi.

Treatment

In the treatment, non-steroidal anti-inflammatory drugs are used in maximum or even daily doses: voltaren, indomethacin (150-200 g / day), butadion.

With recurrent polyarthritis, tophi, urolithiasis, amipurinol is used (for life) in a daily dose of 0,3-0,4 g to normalize uric acid in the blood. In the absence of gouty kidney damage, urinosuric agents (anturac or etamide) are prescribed.

It is obligatory for patients to follow a diet: the exclusion of alcohol, the restriction of foods containing a large amount of purine bases (meat, fish), the amount of fat-117

the moat should be limited to 1 g / kg per day, the amount of proteins - up to 0,8 g / kg, salt - up to 3-4 g. Meat broths, liver, brains are excluded from the diet, sorrel, lettuce, spinach, legumes are limited ; fish and meat 1 time per week in boiled form. Plentiful drink with the inclusion of alkaline water, with urolithiasis or exacerbation of arthritis, the amount of fluid increases to 2-3 liters per day. Gouty tophi are characterized by spontaneous opening and the formation of fistulas with the release of uric acid crystals. In such cases, exercise therapy, physiotherapy, spa treatment (radon and sulfide baths) are used.

Treatment of patients with gouty crisis: abundant intake of alkaline waters, diet with purine restriction.

The drug for stopping the crisis: colchicine, autumn colchicum alkaloid.

Primary prevention consists in rational nutrition, in families where there are cases of gout, the prohibition of alcohol (especially red wines). Secondary prevention involves early detection and treatment of gout, prevention of recurrent gouty crises, and the fight against extra-articular manifestations of the disease.

8. Osteoarthritis

Osteoarthritis is a disease of the joints, in which the primary changes are mainly degenerative in nature and occur in the articular cartilage. In osteoarthritis, unlike arthritis, the inflammatory component is unstable, proceeds in the form of short-term exacerbations and is poorly expressed.

Etiology

The etiology is varied. There are primary and secondary osteoarthritis. Secondary is caused by dysplasia of the joints and bones, joint trauma, metabolic and endocrine disorders. This damages the articular cartilage. In cases where damaging factors are not identified, we should talk about primary osteoarthritis.

Pathogenesis

The pathogenesis is almost the same for the first and second forms of the disease. The initial degenerative changes in the cartilage lead to subsequent changes in other tissues of the joint: osteosclerosis (hardening) of the subchondral bone and the formation of osteophytes (growths). In the synovial membrane - reactive hyperemia, focal inflammation (synovitis) and subsequent fibrosis. All pathological processes that develop in the joint and bones are interconnected, which leads to the progression of the disease.

Clinic

The clinic depends on the localization of the pathological process. Most often, the metatarsophalangeal joints of the first toes, knee, hip joints, as well as distal and proximal interphalangeal joints of the hands are affected.

Osteoarthritis of the metatarsophalangeal joint develops as a result of an anomaly of the forefoot. Characterized by pain during prolonged walking, decreasing at rest, in the future, it is possible to limit movements in the joint, its thickening and deformation, and the development of bursitis.

Osteoarthritis of the knee joints (gonoarthrosis) is secondary and develops as a result of a change in the position of the axis of the legs - varus or valgus deformity. It is characterized by pain when walking, climbing stairs, kneeling, squatting. As the disease progresses, the time of painless walking decreases.

When joining synovitis, starting pain appears, pain when standing and at rest, at night.

In the later stages, deformity of the joint develops, flexion contracture, constant pain.

Osteoarthritis of the hip joint is most often the result of joint dysplasia. The clinic corresponds to the clinic of gonoarthrosis.

Diagnostics

The radiographic picture of osteoarthritis is characterized by narrowing of the joint space, sclerosis of the subchondral bone, and the development of osteophytes. There are no changes in the general analysis of blood and urine.

Treatment

The most important are preventive measures and the elimination of causative factors (correction of orthopedic defects, reduction of excess body weight). It is necessary to reduce the physical load on the affected joints, under certain working conditions - a change of profession.

Suggested appointment:

1) rumalon mukartrin, arteparon, slowing down the process of osteoporosis. Conduct two courses per year;

2) non-steroidal anti-inflammatory drugs (indomethacin);

3) intra-articular injection of corticosteroids (hydrocortisone, metipred 1-3 times in 5-7 days).

Exercise therapy is carried out in the supine and sitting position. Running, long walking are contraindicated, cycling, swimming are useful.

In the early stages of the disease, balneological treatment is recommended. With significant violations of the function of the joint, surgical treatment is advisable. Arthroscopy is indicated with frequent recurrence, persistent synovitis, and if chondromas are detected, they are removed.

Lecture #6

1. Anemia

Anemia is a polyetiological disease characterized by a change in external signs (pallor of the skin, mucous membranes, sclera, often masked by jaundice), the appearance of disorders in the muscular system (weakness, decreased tissue turgor), deviations in the central nervous system (lethargy, apathy, mild excitability) , functional disorders of the cardiovascular system (tachycardia, expansion of boundaries, the appearance of systolic murmur in Botkin's t. and the apex of the heart), the development of hepato- and splenomegaly, a change in the morphology of erythrocytes (a decrease in volume, a change in shape, osmotic stability), a change in the content of other cellular forms (leukocytes, platelets) bone marrow punctate, electrolyte metabolism and iron and magnesium content in blood serum.

The classification is as follows.

1. Deficiency anemia: iron deficiency, vitamin deficiency, protein deficiency.

2. Hypo- and aplastic anemias: Fanko-ni congenital anemia, Dabiond-Biekfen anemia, acquired anemias.

3. Hemolytic anemia: spherocytic, sickle cell, autoimmune.

By severity:

1) mild anemia: hemoglobin in the range of 90 - 110 g / l, the number of erythrocytes decreases to 3 minutes;

2) anemia of moderate severity: hemoglobin 70-80 g/l, erythrocytes up to 2,5 minutes;

3) severe anemia: hemoglobin below 70 g/l, erythrocytes below 2,5 min. According to the functional state of erythropoiesis:

a) regenerative anemia: retiulocytes more than 50%;

b) hypo- and regenerator anemias: low retilunocytosis, inadequate severity of anemia. Downstream: acute phase, subacute and chronic course.

Железодефицитная анемия

Iron deficiency anemia is a disease that is caused by iron deficiency in the blood serum, bone marrow and depot, which leads to the development of trophic disorders in tissues. The development of anemia is preceded by latent tissue iron deficiency. It is more common in women than in men, in 14% of women of childbearing age living in the middle lane.

Etiology: the causes of iron deficiency anemia are chronic blood loss, insufficient initial iron levels, which manifests itself during puberty; malabsorption and intake of iron with food. Most often, several unfavorable factors are combined. Agistral and entologic anemias are often accompanied by a deficiency of not only iron, but also vitamin B₁₂, folic acid, proteins.

Classification:

1) chronic posthemorrhagic;

2) due to hemoglobinuria and hemosiderinemia;

3) iron deficiency in donors (withdrawal of 400-500 ml of blood is accompanied by a loss of 200-250 mg of iron.).

Clinic. In anamnesis, insufficient, improper, unilateral nutrition, frequent diseases. Dryness, roughness of the skin, fragility of hair, pallor of mucous membranes, atrophy of the papillae of the tongue; functional changes in the gastrointestinal tract, leading to spasms of the esophagus, accelerated intestinal peristalsis, spleno- and hepatomegaly.

Changes in the morphology of erythrocytes and biochemical parameters of blood serum, anisocytosis, poikilocytosis, a decrease in the osmotic ability of erythrocytes, a decrease in the concentration of serum iron, an increase in the content of copper in the blood serum.

In the mechanism of development of clinical manifestations of iron deficiency anemia, tissue hypoxia and a decrease in the activity of most enzymes are of paramount importance.

Patients have severe weakness, darkening before the eyes with a change in body position, headaches, dizziness, fainting, shortness of breath, palpitations during slight physical exertion, increased tooth decay, smoothness of the papillae of the tongue. In severe cases - violation, discomfort when swallowing (Bekhterev's symptoms) of dry and solid food, crimson coloration of the tongue, atrophic changes in the pharynx and esophagus, spastic narrowing of the upper esophagus, fragility, the formation of longitudinal or transverse striation along the nail plate, koilonychia. Perversion of taste sensations (addiction to honey, tooth powder, chalk, dry cereals, coal, lime, ice, smells of gasoline, kerosene) indicates a violation of peripheral taste sensitivity. Patients may complain of muscle weakness, imperative urge to urinate, enuresis. Hyporegeneration of blood cells is caused by a decrease in the proliferative capacity of the bone marrow and ineffective hematopoiesis. Differential diagnosis is carried out with thalassemia, posthemorrhagic and infectious anemia.

Treatment

The principles of treatment are as follows.

1. Active mode.

2. Balanced diet.

3. Iron preparations in combination with ascorbic acid and copper.

4. Aerotherapy, massage, gymnastics.

5. Food enzymes.

6. Blood transfusion when the hemoglobin content is less than 60 g / l, iron preparations are administered orally between meals, since during this interval there is a better absorption. In case of iron intolerance (decreased appetite, nausea, vomiting, epigastric pain, dyspepsia, allergic dermatoses), iron preparations are administered parenterally to avoid damage to the gastrointestinal mucosa. Iron preparations include hemostimulin, ferroplex, sorbifer durulez, ferrum lek. Prevention of anemia should be carried out for donors, women with heavy menstruation, frequent pregnancies, girls during puberty, with frequently recurring bleeding.

vitamin deficiency anemia

Pernicious anemia (Addison-Birmer disease) is caused by vitamin B deficiency.₁₂, manifested by damage to the hematopoietic, digestive and nervous systems. It occurs more often in older age, with the same frequency in men and women.

Etiology. Vitamin deficiency is rarely exogenous, more often endogenous, associated with their increased consumption (helminthiasis) and impaired absorption of various nature (stomach disease, malabsorption syndrome). Vitamin B malabsorption₁₂ most often caused by atrophy of the gastric mucosa and the absence or decrease in the secretion of intrinsic factor, hydrochloric acid, pepsin. There is a hereditary predisposition associated with a violation of the secretion of the internal factor; violation of immune mechanisms (detection of antibodies to own cells). Pernicious anemia may occur after gastrectomy, resection.

Clinic

In patients with pernicious anemia, the skin acquires a lemon-yellow hue, the formation of mottled brown pigmentation is possible. Patients complain of weight loss caused by anorexia, possibly an increase in body temperature. Half of the patients have symptoms of glossitis, sometimes the mucous membranes of the cheeks, gums, pharynx, esophagus are affected, diarrhea develops, the liver enlarges, the spleen often enlarges - hepatosplenomegaly; shortness of breath, palpitations, extrasystole, weakness, dizziness, tinnitus. Characteristic of pernicious anemia is a rheumatic syndrome, which is caused by damage to the white matter of the spinal cord. In severe cases, there are signs of damage to the posterior columns of the spinal cord, unsteady gait, impaired coordination of movements, ataxia, hyperreflexia, tone of the feet. Rare, but dangerous symptoms are mental disorders, maximum outbreaks, paranoid states.

Differential diagnosis performed with familial megaloblastic anemia.

Survey plan.

1. General analysis of blood, urine, feces.

2. Examination of feces for occult blood.

3. Blood test for reticulocytes, platelets.

4. Determination of iron content in the blood (if iron deficiency anemia is suspected).

5. Fibrogastroduodenoscopy.

6. Colonoscopy (if irrigoscopy is impossible).

7. X-ray examination of the lungs.

8. Sternal puncture, myelogram study.

9. Biochemical analysis of blood (total protein and protein fractions, bilirubin, transaminases).

10. Study of the secretory function of the stomach.

Principles of treatment.

1. Diet therapy.

2. Appointment B₁₂ and folic acid.

3. Enzyme therapy.

4. Anabolic hormones and insulin.

5. Stimulating therapy.

Vitamin B treatment gives the best results₁₂ (cyanocobolamine). In severe cases, intravenous administration of the drug at 100-200 mcg during the week. The course dose is 1500-3000 mcg. In severe cases and in the presence of antibodies, the appointment of corticosteroids is indicated.

Hypo- and aplastic anemias

A group of diseases of the blood system, the basis of which is a decrease in the production of bone marrow cells, more often three-cell lines: erythrocyto-, leuko- and thrombocytopoiesis.

Diagnostic criteria. Congenital Fanconi anemia: in the analysis, a gradual increase in pallor of the skin and mucous membranes, weakness, lethargy, combined with a lag in physical development, strabismus, hyperreflexia.

In early childhood, melanin brown pigmentation of the skin appears, anomalies of the bones, forearms, thumbs, spinal deformity, dwarfism, combined with malformations of the heart, kidneys (heart, kidney failure), sensory organs, central nervous system (microcephaly) are detected; changes in the blood: a drop in hemoglobin, pancytopenia, a decrease in reticulocytes, a deficiency of glucose-6-phosphate dehydrogenase, a decrease in the activity of alkaline phosphatase, polysaccharides.

Congenital Estren-Dameshek anemia. In history: manifested at an early stage of development of children with the gradual development of pallor, irritability, apathy; peculiar appearance: blond hair, snub nose, wide-set eyes, thickening of the upper lip with a bright red border; slowing down the rate of ossification in the wrists; pronounced spleno- and hepatomegaly, changes in the blood; increasing iron deficiency anemia; in the bone marrow punctate: pallor of the brain due to the development of hypoplastic erythropoiesis.

Acquired hypo- and aplastic anemias. In history: develop after viral infections, with a predisposition to allergic reactions to drugs and toxins. It is distinguished by the rapid development of clinical symptoms; temperature reaction (subfebrile condition), pallor, rash on the skin, exanthema on the mucous membranes, stomatitis and tonsillitis, bloody stools, weakness, anorexia, shortness of breath, hemorrhages in the brain, adrenal glands are possible:

1) changes in the blood: pancytopenia, a sharp decrease in hemoglobin, hyperchromia and macrocytosis of erythrocytes, the content of iron in the blood serum is normal or increased;

2) in the bone marrow puncture: fatty degeneration, poverty in uniform elements, absence of young forms of megalocaryocytes.

Survey plan.

1. General analysis of blood, urine.

2. Blood test for reticulocytes, platelets.

3. Sterile puncture with myelography.

4. Fibrogastroduodenoscopy, colonoscopy, ultrasound examination of the liver, pancreas, kidneys (to exclude neoplasms).

differential diagnosis. Inhibition of hematopoiesis can occur in osteosclerosis and osteomyelofibrosis. It is also necessary to differentiate aplastic (hypoplastic) anemia from acute leukemia, Werlhof's disease.

Principles of treatment.

1. Transfusion of erythrocyte mass in acute forms.

2. Plasmaphoresis with the introduction of fresh frozen plasma, albumin or rheopolyglucin.

3. Impact on the vascular wall (dicinone, serotonin, rutin, ascorbic acid - ascorutin).

4. Glucocorticoids along with massive doses of antibiotics; B vitamins, folic acid.

5. Aminocaproic acid, anabolic hormones (reta-bolin).

6. Splenectomy.

Hemolytic anemia

These are anemias that develop as a result of the destruction of red blood cells.

Etiology - a group of acquired and hereditary diseases characterized by intracellular or intravascular destruction of red blood cells. Autoimmune hemolytic anemias are associated with the formation of antibodies to the erythrocytes' own antibodies.

Diagnostic criteria: hereditary microspherocytic anemia (Minkowski-Schauffir disease):

1) in history: the first symptoms are detected at any age, they begin as a result of an existing congenital defect in the lipoid structures of the erythrocyte membrane, therefore, it is important to identify relatives suffering from anemia;

2) pallor with a lemon-yellow tint, congenital stegein (tower skull, wide bridge of the nose, high palate, lethargy, weakness, loss of appetite up to anorexia, dizziness);

3) changes in the cardiovascular system, palpitations, shortness of breath, systolic murmur;

4) changes in the gastrointestinal tract: abdominal pain, colic and a significant increase and induration of the liver and spleen;

5) ulcers on the legs - changes in the blood: a drop in the number of erythrocytes to 2,5 minutes, hemoglobin to 70 g / l, an increase in retinulocytes to 30-50%, a decrease in the minimum osmotic resistance of erythrocytes with an increased maximum, an increase in the level of indirect bilirubin, urobillinogen urine, stercobillin in the skin;

6) in the bone marrow punctate - inhibition of the erythroid germ.

sickle cell anemia

Anemia develops at an early age. A family history matters, the identification of abnormal hemoglobin in relatives:

1) pallor or yellowness of the skin, mucous membranes, sclera, asthenia of the body; characteristic appearance: short torso, long thin limbs, narrow shoulders and hips, towering skull, large abdomen, ulcers on the limbs, hepatosplenomegaly, expansion of the borders of the heart, arrhythmia, systolic murmur;

2) changes in the blood: normochromic anemia 2,5-3 minutes, hemoglobin S or its combination with hemoglobin F, anisocytosis, poikilocytosis, target erythrocytes, deficiency of the enzyme glucose-6-phosphate dehydrogenase.

Autoimmune anemia:

1) in history: anemia develops acutely or gradually after viral, bacterial infections, against the background of rheumatism, cirrhosis of the liver, lymphogranulomatosis, etc.;

2) pallor of the skin and mucous membranes, jaundice in 75% of cases, fever, weakness, drowsiness, irritability, headaches, pain in the abdomen, back, splenomegaly, hematuria;

3) changes in the blood: a decrease in the level of hemoglobin, erythrocytes, reticulocytes, bilirubinemia, an increase in the concentration of serum iron; positive Coombs reaction (detection of antibodies to erythrocytes);

4) in urine: hemoglobinuria;

5) in the bone marrow punctate: irritation of the erythrocyte process.

Survey plan.

1. General analysis of blood, urine, feces.

2. Blood test for reticulocytes, platelets.

3. Urinalysis for urobilin and bilirubin.

4. Biochemical analysis for urea, creatinine, transaminases (AIT, AST), bilirubin, total protein and protein fractions.

5. Study of the osmotic stability of erythrocytes.

6. Fibrogastroduodenoscopy.

7. Ultrasound examination of the liver, pancreas and gallbladder.

8. Coulibs reaction (with suspicion of autoimmune anemia).

differential diagnosis. It is carried out with acute leukemia, Werlhof's disease, sepsis, other hemolytic anemias, in which spherocytosis is not detected and the osmotic resistance of erythrocytes increases (thalassemia, etc.).

Principles of treatment.

1. Diet.

2. Transfusions of erythrocyte mass, ear blood.

3. Corticosteroids.

4. Glucose 5% with insulin and vitamins B, B₂, AT₁₂, AT₆, FROM.

5. In the absence of effect - immunosuppressants, splenectomy, laser irradiation.

2. Hemorrhagic diathesis

Hemorrhagic diathesis is a group of diseases characterized by impaired hemostasis (vascular, platelet or plasma) and manifested by an increased tendency to bleeding and hemorrhage.

Etiology

The heredity of hemorrhagic conditions is determined by abnormalities of megakaryocytes and platelets, a defect in plasma coagulation factors, and inferiority of the cervical blood vessels.

Acquired hemorrhagic diathesis is caused by DIC, toxic-infectious conditions, liver diseases, and the action of drugs.

Classification

Diets are limited.

I. Disease caused by impaired vascular hemostasis (vasopathy).

1. Shenein's disease - Henoch (simple, rheumatoid, abdurative and fulminant purpura):

1) simple form;

2) chronic form.

2. Hereditary-familial simple purpura (Davis).

3. Anular telangiectatic purpura of Mabocca.

4. Necrotic purpura of Sheldon.

5. Hyperglobulinemic purpura of Waldenström.

6. Hereditary hemorrhagic telangiectasias.

7. Louis-Barr syndrome (capillary telangiectasia of the conjunctiva with ataxia and chronic pneumonia).

8. Kazabakh's syndrome - Merritt.

9. Scurvy and Mimer-Barny's disease.

II. Diseases caused by a violation of the platelet mechanism of hemostasis (thrombocytosis, thrombocytopenia):

1) hemorrhagic thrombocytopathy, Werlhof's disease:

a) acute form;

b) chronic form (continuous and recurrent);

2) amegakaryocytic thrombocytopenic purpura (Landolt);

3) autoimmune thrombocytopenia of various origins;

4) thrombocytopenic hymiphragic purpura with acquired autoimmune hemolytic anemia (Fimer-Evans syndrome);

5) thrombocytopenic purpura with chronic purulent tint and exudative diathesis (Ondrich's syndrome);

6) thrombotic thrombocytopenic purpura of Moshkovich;

7) thrombocytopenia in heangiomas (Kazabakh-Merritt syndrome);

8) hereditary properties of thrombopathy:

a) Glanuman's thrombasthenia;

b) Willibrand's thrombopathy;

9) thrombocytopathy in combination with impaired coagulation factors.

III. Diseases caused by a violation of blood clotting factors (quagulopathy):

1) hemophilia A (factor VIII deficiency):

a) hereditary;

b) family;

c) sporadic;

2) hemophilia B (lack of factor IX):

a) hereditary;

b) family;

c) sporadic;

3) hemophilia C (lack of factor XI);

4) pseudohemophilia due to hypoprothrombinemia:

a) idiopathic hypoprothrombinemia;

b) secondary hypoprothrombinemia (hemorrhagic disease of the newborn, malabsorption of vitamin K, liver disease, poisoning with chloroform, phosphorus, arsenic);

5) Ouren's pseudohemophelia:

a) congenital form;

b) acquired form;

6) pseudohemophilia due to lack of factor VII:

a) congenital form;

b) acquired form;

7) pseudohemophilia due to lack of fibrinogen (afibrinogenemia):

a) congenital form;

b) acquired form (DIC);

8) pseudohemophilia due to lack of factor X;

9) pseudohemophilia due to lack of fabrinase;

10) pseudohemophelia due to an excess of anticoagulants:

a) idiopathic;

b) immunoallergic;

c) acquired forms.

3. Hemorrhagic vasculitis

Hemorrhagic vasculitis (Shenein-Genoch disease, capillary toxicosis, anaphylactic purpura) is an infectious-toxin-allergic disease, which is based on generalized hyperemic inflammation of the vessels.

Etiology

The cause of the acute inflammatory process of small joints of the skin, joints of the digestive tract and kidneys has not been fully elucidated.

Degree of activity - I, II, III.

Course: acute, subacute, chronic, recurrent.

Outcome: recovery, transition to a chronic form, outcome in chronic nephritis (A. S. Kalinichenko, 1970).

Diagnostic criteria

Clinical:

1) hemorrhagic skin syndrome: the rash is usually located symmetrically, characterized by stages of the rash, localized on the extensor surfaces of the limbs, around the ankle and knee joints, in the feet, less often in the hips; rashes, as a rule, polymorphic: hemorrhagic papules, erythritic papules, spots; at the beginning of the disease, the rashes are urtical in nature, later they become hemorrhagic, up to necrosis, relapses are characteristic;

2) articular syndrome: joint lesions have a migratory polyatric character with predominant localization in the ankle, ankle, elbow, wrist joints, and joint damage is rarely symmetrical;

3) abdominal syndrome: cramping abdominal pain of varying intensity; pain may be accompanied by intestinal and renal bleeding.

Laboratory research: hematological changes: leukocytosis, neutrophilia, eosinophilia, accelerated ESR, platelet count is sometimes slightly reduced; retraction of the blood clot, the duration of bleeding and the time of blood clotting are not disturbed; hypercoagulability is often detected; urinalysis: in the acute period of the disease, morning proteinuria, hematuria are often detected; in the feces with abdominal syndrome there may be an admixture of blood.

Examination plan:

1) general analysis of blood, urine, feces;

2) study of platelet clotting time;

3) definition of coagulogram;

4) examination of feces for occult blood (Gregersen's reaction).

Differential diagnosis

It is carried out with thrombocytopathy, thrombocytopenia, coagulopathy, toxic drug-induced vasculitis, allergic and infectious diseases.

Principles of treatment

1. Hospitalization and bed rest for at least three weeks.

2. Diet with the exception of cocoa, coffee, citrus fruits, strawberries, etc.

3. Heparin therapy.

4. Nicotinic acid in combination with heparin.

5. Prednisolone.

6. Plasmapheresis (for chronic vasculitis).

4. Thrombocytopathies

Thrombocytopathy is a quantitative and qualitative insufficiency of the platelet link of hemostasis, clinically manifested by hemorrhagic syndromes.

Etiology

Depending on the genesis, two groups are distinguished:

1) thrombocytopenia - a decrease in the number of platelets (Verlhof disease, Wilbrand-Yurgens, Frank, Kazabakh-Merrit disease);

2) thrombocytopathy - a violation of the properties of platelets. In the vast majority of cases, thrombocytopenia is observed, which are based on an immunoallergic conflict.

Classification

By type: primary (idiopathic) and secondary (symptomatic) thrombocytopenia.

Nosological forms: isoimmune, transimmune, heteroimmune, autoimmune.

Werlhof disease

Classification of idiopathic thrombocytopenic purpura (Werlhof's disease)

Course: acute (up to 6 months); chronic: with rare relapses, with frequent relapses, continuously relapsing.

The clinical picture of purpura: dry purpura (skin syndrome); wet purpura (skin syndrome and bleeding).

Immunological tests: positive, negative.

Period: exacerbation, clinical remission, clinical and gamotological remission.

Complications: uterine, gastric, intestinal bleeding, posthemorrhagic encephalopathy, etc.

Diagnostic criteria

Clinical: pallor of the skin and immune membranes:

1) hyperplastic syndrome: enlargement of the spleen, less often - the liver;

2) hemorrhagic syndrome: hemorrhages in the skin, mucous membranes (asymmetrically located, of various shapes and sizes from petechiae to ectomoses, bleeding from various organs (nasal, uterine, intestinal, etc.), positive endothelial tests (symptoms of tourniquet, pinch).

Laboratory Criteria:

1) in the general blood test, a decrease in the number of platelets, changes in the morphology of the plates and their functional properties (adhesion, aggregation); violation of blood clot retraction; an increase in the duration of bleeding, a slowdown in blood clotting; decrease in the number of erythrocytes, raticunocytes during the period of bleeding;

2) change in the myelogram: hyperplasia of the megakaryocytic germ with a violation of the functional activity of megapariocytes;

3) immunological: the presence of antiplatelet antibodies. Survey plan.

1. General analysis of blood, urine, feces.

2. Blood clotting time, bleeding time, platelet count.

3. Coagulogram.

4. Feces for occult blood (Gregersen's reaction).

5. Examination of bone marrow punctate (myelogram).

6. Immunological studies for the presence of antiplatelet antibodies.

Differential diagnosis

It is necessary to distinguish idiopathic thrombocytopenic purpura from allergic anemias, primary liver diseases in combination with splenomegaly, systemic lupus erythematosus, genetically determined thrombocytopenia.

Treatment

Principles of treatment of thrombocytopenia:

1) prevention of bruises and injuries;

2) antibiotics for bacterial infections;

3) transfusion of plasma and large doses of γ-globulin;

4) corticosteroids;

5) splenectomy;

6) immunosuppressants (azothiopril, vancristine). Principles of treatment of thrombocytopathies:

1) E-aminocaproic acid, synthetic contraceptives, (bisekurin, microfollin), magnesium sulfate 25% IM, magnesium thiosulfate inside;

2) topically, s / c or / m adrenochrome monosemicarbazone (adroxon, chromadron, adrenoxyl), dicionon;

3) intravenous administration of platelet mass.

5. Coagulopathy

Coagulopathy - disorders of hemostasis, which are based on a deficiency of certain plasma coagulation factors.

Etiology

Hereditary coagulopathy (correctly called hemophilia) is caused by a genetically determined decrease or change in the plasma components of hemostasis. Acquired coagulopathy occurs in infectious diseases, liver and kidney diseases, severe enteropathies, rheumatoid arthritis, etc.

Classification

Classification of hereditary coagulopathy.

1. Hemophilia: A-deficiency of factor VIII (syntihemophilic globulin); B-deficiency of factor IX (Christmas); C-deficiency of factor XI (the precursor of plasma thromboplastin); D-deficiency XII (Hagemani).

2. Parahemophilia: deficiency of factor V (proaccelerin); factor VII deficiency (proconvertin); factor II deficiency (pro-trolobin); factor X deficiency (Stuart-Prawer).

3. Violation of fibrin formation, deficiency of factor I (fibrinogen). Forms of flow: light, heavy, hidden.

Diagnostics

Clinical diagnostic criteria - pallor of the skin and immune membranes; hemorrhagic syndrome: hamarthrosis, hemorrhage into soft tissues in case of trauma to the skin and mucous membranes (extensive hematomas); hematuria; internal hemorrhages.

Laboratory diagnostic criteria - hematological: anemic syndrome (decrease in the number of erythrocytes and hemoglobin, hypochromia, reticulocytosis with bleeding), hypocoagulation syndrome of blood clotting disorders (according to Lee-White more than 10 minutes), an increase in recalcification time (more than 250 s), an increase in plasma tolerance to heparin (more than 180 s), a decrease in plasma factors.

Survey plan.

1. General analysis of blood, urine.

2. Determination of blood clotting time and platelet count.

3. Coagulogram, determination of antihemophilic globulin (AGG).

4. Radiography of the affected joints.

Differential diagnosis

Carried out with thrombocytopathies, hemorrhagic vasculitis, with hemarthrosis with rheumatism.

Treatment

The principles of treatment are as follows:

1) an increase in the blood level of AGG: the introduction of AGG concentrates, fresh frozen plasma, concentrates containing factor IX; desmopressin (increasing the level of factor VIII);

2) transfusions, venipuncture against the background of the introduction of epsilon-aminocaproic acid;

3) prevention of injuries and the use of drugs containing aspirin.

Lecture #7

1. Liver failure

Liver failure (LF) is a pathological condition in which a discrepancy develops between the needs of the body and the ability of the liver to meet these needs. Liver failure can be major (precoma and coma) and minor (any abnormal liver function without encephalopathy). Hepatic coma is a clinical and biochemical metabolic syndrome that develops with a short degree of liver failure against the background of severe functional and morphological changes in the liver.

Etiology

The reasons for the development of PN can be:

1) liver disease (acute, chronic hepatitis, cirrhosis of the liver);

2) obstruction of the bile ducts (cholelithiasis, tumors of the liver or common bile duct);

3) chronic diseases of other organs and systems (heart, connective tissue vessels, endocrine and infectious diseases);

4) poisoning with hepatotropic toxic substances (carbon tetrachloride, benzene, halothane); medications (antibiotics, aminosine, tuberculostatics); poisonous mushrooms (pale toadstool, fly agaric);

5) extensive injuries, burns, tissue decomposition, prolonged compression syndrome, surgical interventions;

6) electrolyte disturbances.

Classification and clinic

Classification of major liver failure:

1) sign - hepatogenic encephalopathy (as a result of the toxic effect on the brain of ammonia, phenol, phenylalanine, tryptophan, tyrosine, fatty acid methionine);

2) a sign - a decrease in the level of indicators of the hepatoprival syndrome (procoagulants, cholinesterase, cholesterol, albumins, an increase in the content of bilirubin, transaminase activity, severe hemorrhagic syndrome);

3) a sign: an increase in the level of gluntation (ammonium, phenylanine, tyrosine, methionine, bilirubin, transaminases). Forms of major liver failure:

1) hepatocellular (endogenous, true);

2) portal-hepatic (shunt);

3) mixed.

Precoma: characterized by the presence of 3 signs:

1) mental disorders are distinct;

2) there is no unconscious state;

3) reflexes are preserved. Coma stages.

I stage:

1) mental disorders are distinct during the period of recovery of consciousness;

2) the unconscious state is unstable;

3) reflexes are alive.

II stage:

1) there are no mental disorders;

2) the unconscious state is permanent;

3) reflexes are preserved.

III stage:

1) there are no mental disorders;

2) the unconscious state is permanent;

3) there are no reflexes.

Minor liver failure: present with chronic liver damage (chronic hepatitis, cirrhosis, hepatosis, tumors, slow intoxication), with intercurrent diseases, surgical interventions, adverse effects of environmental factors on the body.

Small liver failure can develop into a coma, but stabilization of the pathological process can also occur. Clinical signs correspond to the underlying disease.

Diagnostics

Laboratory Criteria:

1) indicators of hepatoprival (hepatodepressive) syndrome: a decrease in the content of albumins, cholesterol, procoagulants;

2) stress tests: study of hepatic clearance (volume of blood plasma that the liver can clear within 1 min);

3) bromsulfalene test - determination of the mass of a functioning liver parenchyma using radionuclide methods (determining the rate of excretion of compounds, labeled radioactive carbons), computed tomography;

4) general blood and urine tests.

Major liver failure.

Clinical criteria:

1) malnutrition syndrome - loss of appetite, nausea, intolerance to fatty and protein foods, abdominal pain, unstable stools, weakness, weight loss; skin changes - dryness, exhaustion, wrinkling; development of neuritis: anemia. At the heart of this syndrome is a violation of metabolic processes;

2) fever syndrome (temperature 38-40 ° C, but more often subfebrile), caused by liver necrosis, the entry of toxic products into the blood, bacteremia;

3) jaundice syndrome - due to massive neuroses;

4) syndrome of endocrine disorders (hair loss, atrophy of the endocrine glands, uterus, testicles), due to the accumulation of estrogens and biogenic amines due to a violation of their inactivation in the liver;

5) syndrome of disturbed hemodynamics; vasodilation due to the accumulation of histamine-like and other vasoactive substances. Hypotension due to a decrease in peripheral resistance with an increase in cardiac output;

6) edematous-ascitic syndrome (usually with cirrhosis of the liver) is associated with a decrease in albumin synthesis and a drop in oncotic pressure, hyperaldosteronism, sodium retention, and a decrease in potassium;

7) the liver smell is due to the release of methylmercaptan, which is formed from methionine, which does not go through the process of demethylation in a diseased liver;

8) syndrome of hyporrhagic diathesis; occurs due to a decrease in the synthesis of coagulation factors, which leads to the spread of thrombosis and DIC. Bleeding often occurs;

9) a decrease in the size of the liver.

Laboratory criteria: indicators of hepatoprival syndrome; a significant decrease in the content of albumins, cholesterol, blood coagulation factors, a drop in the dynamics of transaminases (after a significant increase), an increase in the content of phenol, ammonia, bilirubin (bound and unbound, vitamin B₁₂, iron).

Portal hepatic (shunt) coma

Clinical criteria: develops gradually, slowly:

1) the liver is enlarged, dense, the stars do not fade for a long time, the liver palms are preserved;

2) jaundice is not expressed;

3) hemorrhagic syndrome occurs early;

4) persistent smell of sulfur.

Laboratory criteria: high activity of transaminases (AST, ALT), the content of ammonia is sharply increased. Survey plan.

1. General analysis of blood, urine.

2. Biochemical blood test (ammonia, tryptophan; methonine, tyrosine, phenol, phenylalanine, proteinogram, cholesterol, bilirubin, alkaline phosphatase, transaminase activity (ALT, AST), fibrinogen, prothrombin).

3. Ultrasound of the liver.

4. Radionuclide research.

5. Determination of hepatic clearance, the mass of the functioning liver parenchyma (bromsulfalene test, computer gammagraphy).

6. Histological examination of the liver biopsy.

Differential diagnosis

It is carried out with comatose states of another genesis: with diabetes mellitus (hyperglinic and gynoglinic coma), uremia, severe damage to the heart and brain.

Treatment

The principles of treatment are as follows.

1. A sharp restriction of protein, its exclusion from the diet.

2. Regular bowel lavage (intestinal dialysis solution, manganese, 2% soda).

3. Antibiotics (kanamycin, biomizin) orally (in enemas, through a probe) to suppress intestinal microflora.

4. Gamma-aminocaproic acid, vitamins K, C, calcium genopapit - in hemorrhagic syndrome.

5. 5 - 10% glucose solution (intravenously, enterally), 0,1-0,3% potassium chloride solution in combination with the introduction of low molecular weight blood substitutes (hemodez, neocompensan). The total volume of liquid - no more than 2 liters.

6. Control of diuresis, with fluid retention - spironolactone.

7. Correction of acidosis (every 2 hours in / in a 4% sodium bicarbonate solution in combination with / m and / in the introduction of cocarboxylase).

8. Vitamin therapy.

9. Oxygen through a mask or nasal tube.

10. Cardiotonics.

11. Sedatives excreted by the kidneys (haloperidol, butyrofenn, droperidol, sodium hydroxybutyrate).

12. L-glutamine for neutralization of ammonia.

13. Coenzymes - coenzyme A.

14. Antiprosthetic drugs (trasimone, counterpal, Gordox).

15. Precursors of catecholamines - L - DOPA.

16. Glucocorticoids.

17. Intraportal infusion of medicinal substances.

18. Plasmapheresis, peritoneal dialysis, extracorporeal connection of homo- and hetero-liver, hemosorbulia.

19. Colectomy (disconnection of the colon).

20. Drainage of the thoracic lymphatic duct.

21. Liver transplantation.

2. Portal hypertension

Portal hypertension is a condition characterized by increased pressure in the portal vein system. There are 3 types of portal hypertension:

1) adrenal form - develops as a result of complete or partial blockade of the hepatic veins, which leads to the development of Budd-Chiari syndrome or disease: more often formed in women as a result of prolonged use of oral contraceptives, after septic abortions, in men who suffer from erythremia;

2) the intrahepatic form develops as a result of narrowing of the venous bed in the liver, mainly in the area of ​​the sinusoids; so, for the most common cause of this form of hypertension - cirrhosis of the liver - postsinusoidal blockade is characteristic;

3) the subhepatic form occurs as a result of a complete or partial blockade of the portal vein and its large branches (splenic vein, etc.), a more common cause of the development of this form of sinus blockade is a severe lesion of the pancreas (possibly with a cardiocyte or cyst formation). The adrenal form of portal hypertension occurs in 2-5% of cases, intrahepatic - in 80-85%, subhepatic in 10%. Often there are mixed forms of portal hypertension. Clinical picture: most often with portal hypertension appears varicose veins of the esophagus and stomach (diagnosed by endoscopic or radiological method), splenomegaly (diagnosed by palpation, percussion, ultrasound, scintigraphy). Ascites may develop. Diagnosed by ultrasound and computed tomography. Esophageal-gastric bleeding is possible from varicose veins of the esophagus and stomach. In these cases, angiographic examination, venokavagrafiya is necessary.

The main hepatological syndromes: when examining a patient with a liver disease, along with a nosological and ethnological diagnosis, it is necessary to establish:

1) the activity of the pathological process in the liver;

2) the degree and nature of liver failure;

3) the severity and nature of portal hypertension.

These indicators have a decisive influence on the prognosis and nature of treatment.

Lecture #8

1. Chronic eating disorders

Chronic eating disorders (dystrophies) develop in patients with chronic diseases of the gastrointestinal tract, in violation of the absorption of nutrients, after severe and prolonged infectious diseases, with endocrine pathology. They are characterized by a violation of the absorption of nutrients by body tissues. There are dystrophies: with a lack of body weight - malnutrition; with a body weight corresponding to height - paratrophy; overweight - obesity.

The classification is as follows.

1. Type of dystrophy (according to the ratio of body weight and length): malnutrition (lag behind body weight from height); hypostatura (lag in weight and in growth); paratrophy:

1) with a predominance of body weight over height;

2) with uniformly overweight and height;

3) with normal body weight and height.

2. Degree of severity - I, II, III.

3. Period: initial, progression, stabilization, convalescence.

4. Origin: prenatal, postnatal, prenatal-postnatal.

5. Etiology:

1) exogenous:

a) alimentary: unbalanced diet;

b) infectious;

c) toxic;

d) violation of the regime and other adverse factors;

e) mixed;

2) endogenous:

a) malformations;

b) endocrine and non-endocrine disorders;

c) primary (hereditary or congenital) enzyme pathologies.

Hypotrophy

Hypotrophy is a chronic eating disorder with a lack of body weight, which develops under the influence of various factors.

Diagnostic criteria.

Clinical:

1) the thickness of the subcutaneous fat layer with malnutrition of the first degree - depletion in all parts of the body, except for the face; at II degree - disappearance on the stomach, sometimes on the chest, but the preservation of a thinned layer on the limbs; at III degree - absence everywhere;

2) assessment of changes in body weight and height - weight-height coefficient;

3) change in body weight: with malnutrition of I degree - below the norm by 10-20%, with II degree - 20-30% below the average values ​​in people of the same height, with III degree - a decrease of 30% or more (in relation to to growth)

4) manifestation of hypovitaminosis C, A, group B on the skin and mucous membranes;

5) development of foci of infection (pneumonia, pyelonephritis, otitis media, etc.) with an asymptomatic course;

6) decreased appetite and food tolerance, intestinal disorders: mealy stools (with excessive consumption of carbohydrates) - liquid, yellow-green in color with mucus; protein stools (with an excess of protein products in the diet) - not abundant, dense, gray-putrefactive in color, with a putrid odor, with an increase in green color and with an admixture of mucus; hungry stool - scanty, dry, discolored, with a putrid smell, quickly turning into dyspeptic.

Laboratory indicators:

1) hypoproteinemia (due to insufficient intake of proteins from food, hypocholesterolemia, dysglobulinemia (increased α₁-globulins), a decrease in the albumin-globulin ratio;

2) intestinal dysbiosis (Proteus and associations of various microorganisms);

3) violation of membrane digestion (slowdown of hydrolysis and absorption of starch, maltose);

4) the development of metabolic acidosis (increase in the content of lactic acid and pyruvate in the blood serum);

5) decrease in the immunological activity of the body (immunoglobulins A, M, antibody titer, phagocytosis, lysozyme).

Differential diagnosis

Hypotrophy is differentiated from all diseases that can be complicated by chronic eating disorders. Hypostatura is differentiated from dwarfism and constitutional hyposomia. The main criterion for the diagnosis of malnutrition and degree is the thickness of the subcutaneous fat layer.

Treatment

The principles of treatment are as follows.

1. Ensuring the correct diet.

2. Diet therapy under the control of the body weight curve, the amount of liquid and food drunk per day, the frequency of stools, the nature of the stool and the presence of pathological impurities.

3. Enzyme preparations (pancreatin, panzinorm, festal).

4. Vitamin therapy (group B, C, PP, A, E).

5. Anabolic hormones (nerabol, systandrostenedione).

6. Biological products (lactobacterin, bifidumbacterin, bacti-subtil).

7. Adaptogens (ginseng, pantocrine, saparan, apilac).

8. With severe metabolic disorders, a sharp decrease in food tolerance, parenteral nutrition is used (polyamine, alvuem, friamin, mepofundin, intralipid, lipozan, glucose).

In patients with malnutrition, treatment should be comprehensive and include:

1) identification of the causes of malnutrition and attempts to correct or eliminate them; diet therapy;

2) organization of a rational regimen, care, massage, gymnastics;

3) identification and treatment of foci of chronic infection, other complications and concomitant diseases;

4) enzyme-vitamin therapy, stimulating and symptomatic treatment.

Diet therapy is the basis of proper nutrition for patients with malnutrition. The degree of weight loss and appetite may not correspond to the severity of malnutrition as a result of damage to the gastrointestinal tract and central nervous system. The main principle of diet therapy for malnutrition is two-phase nutrition:

1) the period of clarification of tolerance to food;

2) a period of enhanced nutrition.

A large food load, which is introduced abruptly and out of time, can cause a breakdown and dyspepsia. It is possible when a patient with malnutrition, even with excess nutrition, does not have an increase in the curve of weight gain, and a decrease in the caloric content of food leads to an increase in body weight. An increased food load should be introduced gradually, with the control of the coprogram.

The most important principles of diet therapy in patients with malnutrition are:

1) the use in the early stages of treatment of only easily digestible food (sour-milk products, steamed vegetable dishes, meat soufflé, steamed or boiled fish), since intestinal dysbacteriosis and intestinal lactose deficiency are often detected in patients with malnutrition;

2) frequent meals in small portions (seven with hypotrophy of the I degree, eight - hypotrophy of the II degree, ten meals - with hypotrophy of the III degree);

3) adequate systematic monitoring of nutrition (keeping a diary with notes on the amount of food eaten at each feeding), stool, diuresis, the amount of fluid drunk and given parenterally, salt intake, etc .; regular, every 5-7 days, calculation of the food load for proteins, fats and carbohydrates; a coprogram should be performed twice a week).

The daily volume of food for malnutrition of the first degree should usually correspond to height and age, calorie content - 120 kcal / kg / day. With malnutrition II and III degree, the initial daily volume of food should not exceed 2/3 - 1/2 of the due, and the calorie content of food should be 100/95 kcal per kg / day. With very severe malnutrition, begin with a daily amount of food no more than 60 mg / kg. Then add 20 mg/kg/day. The amount of protein is 0,6 g/kg. The missing amount of liquid in severe cases is administered parenterally in the form of a 5% glucose solution, glucose-salt solutions. With persistent vomiting, diarrhea, obstruction of the gastrointestinal tract, it is necessary to use the parenteral method of administration. It should be borne in mind that the daily amount of potassium should not exceed 1,5 times the norm, sodium - no more than 2,5 mmol / l. Restoring the normal volume of circulating blood and maintaining and correcting disturbed electrolyte exchanges, stimulating protein synthesis are the main tasks of the first days of therapy for severe malnutrition. With parenteral nutrition, amino acid solutions or albumins are added.

During the period of enhanced nutrition with malnutrition of the I degree, the calorie content of food should be 200 kcal / kg per day. The amount of protein should be 10-15% of the total calories. The increase in protein is carried out by increasing the amount of cottage cheese, meat. An increase in fats - the introduction of cream, an increase in the amount of butter. An increase in carbohydrates - the introduction of sugar syrup, compote, cereals.

Qualitative signs of the effectiveness of treatment are an increase in the emotional state, normalization of appetite, improvement in the condition of the skin and muscle tone, a daily increase in body weight by 25-30 g, and improvement in digestion according to the coprogram.

Patient care is as follows. Patients with malnutrition should be in a spacious, regularly ventilated room, avoid overheating and hypothermia. Warm baths (38 °C), massage and gymnastics are obligatory. It is necessary to carry out prevention and sanitation of chronic foci of infection.

Replacement enzyme therapy (mezim-forte, abomin, gastric juice).

Vitamin therapy, especially vitamins of group B, alternating courses of vitamins A, PP, B₁₅, AT₅, E, B₁₂. Appointment of adaptogens (apilac, dibazol, pentonam, rosehip, ginseng, anabolic steroids - nerabol, retabolin).

Symptomatic therapy consists in the appointment of iron preparations (for anemia) and folic acid.

The prognosis for alimentary and alimentary-infectious malnutrition is favorable.

Obesity

Obesity is a disease that is manifested by an excess of adipose tissue in the body (more than 20% in men and 25% in women), as well as an increase in body weight by more than 25-30 kg/m².

Pathogenesis. The main cause of obesity is an energy imbalance between the calorie content of food and the body's energy expenditure.

This condition develops as a result of errors in nutrition: excessive intake of calories from food and reduced energy consumption, poor nutrition (excessive amounts of carbohydrates or fats), violation of the diet - the main meal occurs in the evening hours. Excess energy that comes from food is deposited in fat cells, resulting in an increase in the size of adipocytes and an increase in body weight.

Excess body weight may be the result of a violation of energy consumption in the body due to metabolic, enzymatic disorders. In healthy people, with an increase in the calorie content of food, the rate of metabolic processes increases, which helps to maintain a constant body weight. In obese patients, adaptation of the basal metabolism to changes in the calorie content of food does not occur.

Obesity is a genetically determined disease. In persons whose family has relatives with overweight, there is an increase in body weight even with rational nutrition.

Distinguish between brown and white adipose tissue. White adipose tissue contains cytochrome. With excess nutrition, brown adipose tissue converts excess energy into heat and prevents its deposition in fat depots. Insufficient physical activity creates an excess of energy in the body, which contributes to weight gain. The likelihood of developing obesity persists throughout life. There are several factors that cause obesity (age, gender, professional, physiological conditions - pregnancy, lactation, menopause).

In all forms of obesity, the central regulatory mechanisms are disrupted. Violation in one of the links of regulation leads to changes in nutrition, deposition and breakdown of fat, and further to the development of obesity.

The pathogenesis of obesity depends on its cause. With exogenous-constitutional obesity, excessive intake of carbohydrates from food leads to hyperinsulinism. Insulin causes the synthesis of triglycerides in adipose tissue and causes dysfunction of the hypothalamus, the development of secondary diencephalic syndrome, which contributes to the progression of obesity.

Diencephalic (hypothalamic obesity develops as a result of primary, organic damage to the nuclei of the hypothalamus as a result of trauma, tumors, meningitis, encephalitis, anesthesia, hypoxia). Secondary obesity in endocrine pathology is a consequence of hyperinsulinemia, insulin overdose in diabetes mellitus, lack of hormones with a lipolytic effect (hypothyroidism, hypogonadism).

Classification.

1. Alimentary-constitutional obesity.

2. Hypothalamic obesity.

3. Endocrine obesity.

Clinic. Patients with obesity present a variety of complaints: the more pronounced the degree of obesity, the more patients present complaints.

With the I degree of obesity, there may not be any complaints. At the II degree - there is weakness, reduced performance, fatigue, headaches, lability of the nervous system, irritability, apathy, insomnia periodically disturb. During physical exertion, shortness of breath, palpitations, aching pains in the heart area, swelling of the feet and legs, pain in the spine, joints, caused by metabolic disorders and increased stress due to high body weight, appear. Patients complain of heartburn, flatulence, heaviness in the epigastrium, constipation, pain in the right hypochondrium, belching, bitterness in the mouth.

With hypothalamic obesity, intracranial pressure is increased and, as a result, headaches, visual disturbances, neurological disorders, mental disorders (frequent mood swings, increased appetite, thirst, hunger at night) appear.

In women, menstrual disorders, sexual function, primary or secondary infertility, fibrocystic mastopathy are possible. In men - impotence, gynecomastia, reduced hair growth on the face and body.

In the hypothalamic form of obesity, trophic skin disorders, small pink striae on the abdomen and thighs, hyperpigmentation, increased blood pressure, lymphostasis of the lower extremities, heart and respiratory failure come to the fore.

In a laboratory study, hyperlipidemia, hypercholesterolemia, hyperinsulinemia, elevated ACTH, impaired glucose tolerance are detected.

Complications. Decrease in life expectancy, risk of cardiovascular diseases (myocardial infarction, stroke), vascular atherosclerosis, risk of developing diabetes mellitus, hypertension, diseases associated with impaired function of the musculoskeletal system, muscle atrophy, impaired renal function, reproductive system, infertility, increased risk of developing cancer of the prostate, rectum, in women - cancer of the mammary glands, endometrium, ovaries.

The most dangerous complication is Pickwick's syndrome (an obese syndrome characterized by hypoventilation, a violation of the sensitivity of the respiratory center to hypoxia, hypercapnia with a violation of the rhythm of breathing and periods of apnea, pulmonary hypertension, cardiopulmonary insufficiency, damage to the central nervous system (sleep disturbance, depression).

Treatment. The basic principle is to reduce body weight and prevent its increase. Decrease in calorie content of food, increase in physical activity. It is necessary to prescribe a low-calorie balanced diet.

With obesity of I-II degrees, caloric content is limited by 20-30%; at III-IV degree - by 45-50%. Reducing the calorie content of food is carried out by reducing the amount of easily digestible carbohydrates and fats. Flour products, muffins, pasta, cereals (semolina), confectionery, sugar, potatoes are excluded from the diet. Allowed rye bread, sweetener, fructose, butter and vegetable oil - 10-15 g per day - meat, fish, low-fat dairy products. The total protein content is not limited within the normal range. Especially shown is the use of foods high in fiber, which promotes rapid satiety, accelerates the passage of food through the intestines and reduces the absorption of nutrients.

Fasting days are recommended: fruit, vegetable, fish, meat, kefir and rice. Meals should be at least 5-6 per day. The last meal - no later than 19 hours. On an outpatient basis, weight loss should be 800 - 1000 g per week. Complete fasting is carried out only in a hospital under the supervision of a doctor due to the possibility of developing complications: a decrease in the body's defenses, infection, exacerbation of chronic diseases, vegetovascular disorders, anemia, nervous, emotional disorders, impaired liver and kidney function, loss of protein by muscle tissue. The first decrease in body weight occurs due to an increase in carbohydrate metabolism and fluid loss. Subsequently, weight loss occurs due to the acceleration of fat metabolism.

The combination of diets with exercise is considered effective, which contribute to the mobilization and enhancement of fat metabolism, the preservation and slight increase in protein synthesis in skeletal muscles.

Medications are prescribed in addition to diet and exercise. Anorexic drugs (fepranone, teronac, reginon) are prescribed to reduce appetite. These drugs belong to amphetamines, so the course should not exceed 1-1,5 months due to the possibility of addiction, arousal. With caution should be prescribed for arterial hypertension, diseases of the cardiovascular system. Side effects: agitation, insomnia, nausea, dry mouth, allergic reactions, increased blood pressure. In some cases, sinocarb is prescribed 1-2 times a day. In case of violation of ovarian function, treatment is carried out under the supervision of a gynecologist.

Patients with secondary obesity are treated for the underlying disease.

The prognosis for long-term and proper treatment is favorable.

2. Vitamin deficiency (hypovitaminosis and beriberi)

Vitamin deficiency is a pathological condition of the body, which is caused by a lack of a vitamin or a complex of vitamins in the body. Allocate stage III vitamin deficiency.

Stage I - prehypovitaminosis (subnormal supply of vitamins). The lack of vitamins at this stage can be detected only with the help of laboratory tests.

Stage II - hypovitaminosis, is the result of a relative lack of vitamins.

Stage III - beriberi, or an extreme degree of vitamin deficiency. Currently, in socio-economically developed countries, it is rarely diagnosed.

Hypovitaminosis is common, especially in the elderly, pregnant, lactating, people with heavy physical work, athletes, in patients with chronic pathology of the gastrointestinal tract, children. Vitamins cannot be synthesized in the body, but must come from outside with food.

Vitamins are involved in the form of coenzymes in the biochemical processes of the body.

Intense physical activity, work in hazardous industries, pregnancy, lactation, climatic conditions, infectious diseases, intoxication, endocrine pathology increase the need for vitamins.

Avitaminosis and hypovitaminosis develop gradually.

Hypo- and beriberi are divided into:

1) exogenous (primary, alimentary) associated with a deficiency of vitamins in food;

2) endogenous (secondary), caused by impaired absorption, transport, metabolism of vitamins in the body. Endogenous hypovitaminosis often accompanies: chronic diseases of the gastrointestinal tract (chronic enteritis, dysbacteriosis, helminthiases, chronic pancreatitis), cancer, protracted infectious process, systemic connective tissue diseases.

In the development of avitaminosis, a combination of exogenous and endogenous factors is possible.

The modern classification of vitamin deficiency is based on 3 provisions:

1) etiological;

2) pathogenetic;

3) clinical.

Vitamin deficiency can be exogenous (primary) and endogenous (secondary). According to clinical manifestations, hypovitaminosis and avitaminosis are distinguished.

All vitamins are divided into III large groups.

I - fat-soluble: vitamins A, D, E, K.

II - water-soluble vitamins: C, P, B₁, AT₂, AT₆, RR, V₁₂, folic acid, pantothenic acid, biotin.

III - vitamin-like compounds: choline, inositol, vitamin V, lipoic acid, orotic acid, pangamic acid (B₁₅).

When diagnosing beriberi, it is necessary to carefully collect an anamnesis (age, presence of chronic diseases, occupational hazards, pregnancy, dietary habits).

Treatment should include oral vitamins, a diet rich in vitamins, sufficient protein. In the spring it is shown to carry out prophylactic intake of vitamins. In severe vitamin deficiency, the administration of vitamins is carried out parenterally.

Vitamin A deficiency characterized by visual impairment - hemeronopia ("night blindness"), eye damage, dry mucous membranes and skin, skin hyperkeratosis. Tendency to diseases of the intestines and respiratory tract. Vitamin A comes from food in the form of provitamin - carotene. Foods high in vitamin A: animal fats, meat, fish, eggs, milk, dairy products.

Treatment consists in the appointment of retinol per os. A diet rich in vitamin A.

Vitamin B deficiency₁ manifested by a change in the function of the nervous system, heart, intestines. The extreme degree is beriberi disease. With a deficiency in₁ metabolic products accumulate. Manifested by a decrease in appetite, nausea, constipation, impaired sensitivity, paresthesia in the lower extremities, decreased performance, emotional lability.

On examination, the abdomen is swollen, the skin is dry, the tongue is dry, tendon reflexes and sensitivity are reduced, muscle weakness, tachycardia, the borders of the heart are expanded, liver enlargement, systolic murmur at the apex, swelling of the legs and feet.

Violation of peripheral circulation, polyneuritis.

Treatment carried out on an outpatient basis: a diet rich in vitamin B is prescribed₁, and oral intake of vitamin 50 - 100 mg / day or parenteral cocarboxylase 1 ml.

Vitamin B deficiency₂ - this is a pathological condition that develops with a deficiency in the body of riboflavin; characterized by damage to the mucous membranes of the mouth, eyes and skin. The most common vitamin B deficiency₂ appears with viral hepatitis, chronic colitis, cirrhosis, alcoholism, etc. It also accompanies chronic conjunctivitis, blepharitis, dermatitis, skin cracks, trophic ulcers. Vitamin B deficiency₂ causes tissue hypoxia, since this vitamin is involved in the system of respiratory enzymes.

Clinic: an early sign is angular stomatitis (jamming) in the form of cracks, crusts, maceration in the corners of the mouth. Cheinosis in the form of hyperemia with transverse striation, cracked lips. Glossitis - hyperemia, a clear pattern of the taste buds of the tongue, a burning sensation in the tongue, later a "polished tongue" is formed.

Laboratory diagnosis: decrease in riboflavin in the urine to 100 mcg / day (N - 300 - 1000 mcg / day).

Treatment is to prescribe a diet with a high content of vitamin B₂. Orally appoint 5 - 10 mg of riboflavin for 14-30 days. In case of malabsorption, riboflavin injections are prescribed.

Nicotinic acid deficiency (niacin, PP, vitamin B₃) is a pathological condition of the body, which is caused by a lack of vitamin B₃. There are two forms of deficiency: pellagra - with severe deficiency, hypovitaminosis PP - with slight deficiency. This condition is manifested by a violation of the function of the nervous system, the gastrointestinal tract, a violation of the trophism of the skin and mucous membranes. The disease develops with alimentary insufficiency, in the presence of chronic pathology of the gastrointestinal tract, nervous system, poisoning with berries. Nicotinic acid affects many types of metabolic processes. You need a constant supply of vitamin B₃ with food. Deficiency can be mild, moderate, severe. The severe form is accompanied by cachexia, psychosis, extensive skin lesions.

Clinic. Manifested by dark red erythema of the lips, nose, hands, feet, face, sometimes blisters appear; on the mucosa - cracks. Patients complain of pain, burning sensation in the oral cavity. Diarrhea. Appears asthenic, delirious syndrome. Seizures are possible. In bright sunlight, the disease worsens.

Laboratory diagnostics: a decrease in the content of the vitamin and its metabolites in the blood and urine indicates its deficiency.

Differential diagnosis carried out with systemic lupus erythematosus, sprue, dysentery. A combination of three syndromes (dermatitis, diarrhea, dysfunction of the central nervous system) is necessary.

Treatment. It is necessary to provide adequate nutrition. Vitamin B content₃ - 20-25 mg. Nicotinic acid is prescribed orally 50 mg per day. Injections of a 1% solution are administered in 1 ml intramuscularly. The course of treatment is 1 month. It is necessary to combine with the intake of vitamin C, thiamine and riboflavin.

Vitamin B deficiency₆ is a pathological condition associated with vitamin B₆ (its deficiency). It is manifested by damage to the oral mucosa and the functions of the central nervous system. Most often, hypovitaminosis is secondary, observed during pregnancy, alcoholism, polyneuritis, Parkinson's disease, epilepsy, anemia, rheumatism, hepatitis. Forms of hypovitaminosis: mild, moderate, severe.

Laboratory diagnosis: reduction of pyridoxine to a level of less than 50 mcg.

Treatment. Balanced diet. Assign per os 0,002 - 0,005 g per day for prevention, and for treatment - 0,05 - 0,1 g for 30 days.

Vitamin B deficiency₁₂ characterized by damage to the hematopoietic system, digestive and nervous systems. Pernicious anemia and funicular myelosis develop. Accompanied by paresthesia in the extremities, burning of the oral mucosa. It is more common in people who eat large amounts of meat and dairy products. It is found in large quantities in the liver of fish and cattle, kidneys, meat, eggs, milk, soybeans. Synthesized by intestinal microflora. The daily requirement is 3 mg. Vitamin B deficiency₁₂ can be endo- and exogenous.

In the endogenous form, there is an increased consumption of vitamin B₁₂ (pregnancy, helminthiases). In the endogenous form, absorption is impaired. Three main symptoms are diagnosed: hypochromic anemia, gastric achlohydria, funicular myelosis and polyneuropathy. It is also possible to reduce appetite, diarrhea, pallor of the skin and mucous membranes, paresthesia. Prescribe vitamin B supplements₁₂ 100-500 mcg daily intramuscularly for 10 days. Nutrition should be rational, with regular consumption of milk and meat.

Ascorbic acid deficiency is due to its deficiency in the body. The extreme form of insufficiency is scurvy. Hypovitaminosis of vitamin C appears with prolonged use of aspirin, hyperthyroidism, and hemodialysis. Vitamin C is necessary for the implementation of redox processes in the body. With a deficiency of vitamin C, the permeability of the vascular wall is disturbed, immunity is reduced, which leads to the development of infectious diseases. Classification.

At stage I, moderate weakness, pain in the legs, bleeding gums, purpura, gingivitis, and increased fatigue appear. In stage II, hemorrhages become common, hyperthermia, hymarthrosis, gingivitis and stomatitis are pronounced. Stage III is manifested by a severe general condition, exhaustion of patients, increased bleeding, the appearance of trophic ulcers, infectious diseases against the background of a decrease in immunity.

Laboratory diagnosis

Excretion of vitamin A in the urine is determined. Differential diagnosis is carried out with hemorrhagic diathesis, vasculitis.

Treatment

Rational nutrition rich in vitamins. For prevention, an infusion of wild rose, lemon is prescribed. Treatment is carried out on an outpatient basis. Rutin is administered orally at a dose of 100-150 mg/day. With a lack of vitamin C II and III degree, treatment is carried out in stationary conditions. The diet should be enriched with proteins 120-150 g/day. The daily dose of vitamin C at stage II is 500 mg, at stage III - 1000 mg. The course of treatment is at least 1 month.

Author: Kuznetsova Yu.V.

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