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1. Respiratory allergies

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

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.

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.

2. Bronchial asthma

Bronchial asthma is 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)

1. By shape:

1) atopic;

2) infectious-allergic;

3) mixed.

2. By type:

1) asthmatic bronchitis;

2) bronchial asthma.

3. By 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 twice a 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 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).

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

3. Allergic bronchopulmonary aspergillosis

Allergic bronchopulmonary aspergillosis is 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.

Principles of treatment.

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

2. Bronchospasm therapy:

1) selective β-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. Histamine H2 receptor blockers (tavegil, fencarol, 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.

4. 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.

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.

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. Dry and wet, wheezing rales of medium caliber on exhalation, hard breathing are auscultated.

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

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

Clinically manifested by severe shortness of breath (up to 70-90 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.

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.

Principles of treatment:

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

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

3) expectorants: breast collection (coltsfoot, bogulnik, 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.

5. Etiology and classification of respiratory failure

Respiratory insufficiency is a pathological condition of the body, characterized by insufficient provision of the gas composition of the blood, 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

1. By shape:

1) ventilation;

2) alveolorespiratory.

2. By type of ventilation failure:

1) obstructive;

2) restrictive;

3) combined.

3. By severity:

1) DN I degree;

2) DN II degree;

3) DN III degree.

6. Diagnosis and treatment of respiratory failure

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.

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; ratio P / D2 - 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%.

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.

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.

7. 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.

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:

1) focal bronchopneumonia;

2) segmental pneumonia;

3) interstitial pneumonia;

4) croupous pneumonia.

Clinic

Complaints of cough, fever, weakness, sweating.

Signs of respiratory failure: breathing is groaning, rapid, the number of breaths is up to 60-80 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.

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

8. 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.

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).

The classification is as follows:

1) dry pleurisy (fibrous);

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

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: a forced position 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 area 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 opportunity to listen to it, with dry pleurisy - a pleural friction noise.

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.

9. 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.

Classification:

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.

Chronic pneumonia: in history - 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: pale 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.

10. 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.

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.

Classification I. Rhythm disturbance.

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, atriventricular 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.

11. Extrasystole. Tachycardia

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. Parasystole - 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.

Insertion extrasystoles are characterized by the absence of a post-extrasystolic pause against 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 is an attack of ectopic tachycardia, characterized by a regular rhythm with a frequency of 140-240 per 1 min 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 is characterized by strict rhythm, changes in ventricular complexes, and a deformed P wave.

Atrioventricular tachycardia is 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.

12. Atrial fibrillation

Conduction disorder

Atrial fibrillation is expressed in erratic incomplete atrial contractions and the absence 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 beats per minute. Atrial flutter - regular atrial contraction with a frequency of 250-300 beats 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 beats per minute, absolute randomness of the rhythm, QRS complexes without an R wave.

Conduction disturbance is characterized by a violation of the conduction of excitation (up to a complete interruption in the conduction of excitation) through the conduction system and the myocardium and is called a blockade. Depending on the place of conduction disturbance, blockades are distinguished: sinoauricular (an impulse is not formed at all or is not carried out), 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 wave) and atrioventricular blockade, intraventricular blockade.

Atrioventricular blockade 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. Second-degree blockade with periods of Samoilov-Wenckenbach 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 deaf, 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 RR intervals 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.

13. 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.

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 of vegetovascular 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) a 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: BP 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) there are no pathologies on FCG, echocardiography, X-ray examination of the heart.

14. Classification of 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 40-60 years old - below 145/90, 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)

1. By stages:

1) neurogenic;

2) transitional;

3) nephrogenic.

2. By predominance:

1) cardiac;

2) cerebral;

3) renal.

3. By form or phase: malignant.

Classification of hypertension

1. By stages:

1) functional;

2) cardiac hypertrophy, vascular changes;

3) resistant to treatment.

2. By forms:

1) malignant;

2) benign with a primary lesion of 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 (130).

15. Clinic and treatment of hypertension

Hypertension begins more often in people 30-60 years old. 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.

On the part 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 in a hospital with myocardial infarction, cerebral stroke, arrhythmia, hemophilia. On the part of the kidneys, functional disorders are expressed: a decrease in renal blood flow and glomerular filtration.

Treatment

In stage I hypertension, a β-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 II stage of hypertension, a combination of ACE inhibitors, β-blockers, calcium channel blockers, diuretics is used. In stage III, a combination of drugs to normalize blood pressure is selected and the dose is increased.

16. 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.

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.

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.

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.

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 per minute).

17. 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.

The cause of a heart attack is:

1) coronary thrombosis - blockage of the lumen of the artery, which leads to the formation of an ischemic zone, and later - to necrosis, 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. Treatment:

1) continuous exposure to nitrates;

2) the introduction of drugs that lyse the thrombus;

3) 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.

18. Carditis

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

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).

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, IB, III degrees; right ventricular I, IIA, IB, III degrees; total;

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

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 18b liver; on the ECG - high voltage of the teeth of arrhythmias, 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 - the left one; signs of an increase in both ventricles, more - right;

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

19. 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.

Forms of circulatory failure

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.

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.

NK IB 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.

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) vitamins B6, B12, B5, E;

6) vasodilators (cardinet, pectron, nopochinava);

7) hormones;

8) elimination of arrhythmia;

9) treatment of the underlying disease.

20. Gastritis

Acute gastritis is an acute inflammation of the gastric mucosa of non-infectious origin. The cause of acute gastritis may be malnutrition.

Clinically manifested by 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.

Treatment is carried out by the appointment of a diet. Enzyme preparations (mezim-forte, inzistan, coenzyme, panzinorm).

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.

Classification

1. By origin:

1) primary (exogenous gastritis);

2) secondary (endogenous).

2. According to the prevalence and localization of the process:

1) widespread gastritis;

2) focal (antral, fundal) gastritis.

3. 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).

4. By the nature of gastric secretion: 1) with normal secretory function;

2) with reduced secretory function;

3) with increased secretory function. 5. Flow phases:

1) phase of exacerbation;

2) phase of incomplete remission;

3) remission phase.

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

1) diet number 1;

2) antacids, H2-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 de-nol, antibiotic therapy (amoxicillin, metronidazole).

21. 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.

The classification of JVP is as follows. Allocate:

1) hypermotor, characterized by hypertension, hyperkenesia;

2) hypomotor, characterized by hypotension, hypokenesia;

3) mixed.

Clinically manifested by pain. With hypertensive dyskinesia, the pains are paroxysmal in nature (cramping, stabbing, cutting); short-term pains 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.

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); medicines 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).

The following are prescribed: physiotherapy (inductotherapy, UHF, microwave, diadynamic currents), laser irradiation, reflexology (acu-, electro- and laser puncture), physiotherapy exercises, mineral waters.

22. Cholecystitis

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

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.

Treatment

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

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

It is clinically manifested by a pain syndrome 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, Murphy, Ortner; soreness at Mussi's point, McKenzie's point; 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 top and at the Botkin point.

Treatment

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.

23. 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 - latent, asymptomatic, stone-carrying; the third - clinical manifestations (calculous cholecystitis, cholelithiasis with chronic cholecystitis in the acute phase, incomplete remission and remission).

Clinically manifested by pain syndrome of 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 do 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 at the first and second stages of diet No. 5 with the exception of excesses in eating 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). At the third stage - radical surgical treatment (cholecystectomy).

24. Acute pancreatitis

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

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

1.Shape:

1) interstitial;

2) hemorrhagic;

3) pancreatic necrosis;

4) purulent.

2. Period of illness:

1) seizure;

2) reparative.

3. Clinical course:

1) type: acute, subacute, recurrent;

2) severity: mild, moderate, severe;

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

4. The state of the function of the pancreas.

5. Complications and their nature

1) from the side of the gland: pseudocyst, abscess, diabetes;

2) from other organs: bleeding, dysfunction of the cardiovascular system, liver, kidneys, central nervous system.

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; Hodstell'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's zone, Methot-Robson's point, Desjardins' point - pain on palpation; Voskresensky's syndrome (lack of pulsation of the abdominal aorta with pressure in the epigastrium).

25. 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

1.Shape:

1) recurrent;

2) with constant pain syndrome;

3) latent.

2. Period of illness:

1) exacerbation;

2) remission.

3. Clinical course:

1) type: recurrent;

2) severity: mild, moderate, severe;

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

4. Stage of the disease: initial, extended manifestations, final.

5. 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.

6. Complications from the pancreas.

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 Lito-Robson's 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.

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.

26. 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.

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

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.

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 there are signs of colitis 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.

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 (ferrumlek, sorifer), albumins, plasma, hymeotransfusil.

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

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

27. 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

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, moalox, vikalin, preparations of bismuth, silver nitrate).

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

4. Synthesis substitutes (venter, sucralfate).

5. Acid blockers (H2-histamine blockers, N-cholinolytics).

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

28. Classification of peptic ulcer

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

Classification

1. 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.

2. Clinical form:

1) acute or newly detected;

2) chronic.

3. Current:

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.

4. Phase:

1) exacerbation (relapse);

2) fading exacerbation (incomplete remission);

3) remission.

5. 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) white scar stage;

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).

29. Clinic and treatment of peptic ulcer

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. In patients, appetite decreases, emotional lability increases, sleep is disturbed, and fatigue increases. Constipation or unstable stools, hyperhidrosis, arterial hypotension, bradycardia develop. On palpation, pain in the epigastrium or in the pyloroduodenal region, defense of the muscles of the anterior abdominal wall are observed. 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. Examination of gastric secretion (increased 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.

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 of M1-cholinergic receptors (gastroepin, pyroncepin); histamine H2 receptor blockers (cisletidine, ranitidine, famotidine); calcium antagonists (verapamil, nifedipine); antacids (almagel, phosphamogel, gastrogel);

2) increasing the protective properties of the mucous membrane: uitoprotectors (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.

30. 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 asthenic-vegetative, dyspeptic syndromes, hepatomegaly, impaired liver function; morphologically - persistence of necrosis, inflammation, fibrosis while maintaining the overall architectonics of the liver.

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.

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

30b, 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. 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).

31. 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.

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

1. By morphological features:

1) small-knot;

2) SKD;

3) biliary;

4) mixed.

2. By etiology:

1) infectious;

2) exchange;

3) due to a congenital anomaly;

4) other cirrhosis.

3. Downstream:

1) progressive:

a) active phase;

b) the phase is inactive;

2) stable;

3) regressive.

4. Typical insufficiency (yes, no), portal hypertension (yes, no), hypersthenia (yes, no).

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.

The principles of treatment are as follows: regimen, diet, vitamin therapy, glucose 5% orally, hepatoprotectors, cytostatics, antiviral drugs (ribovarin, acyclovir).

32. Glomerulonephritis

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.

Classification

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.

33. ​​Pyelonephritis

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

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

Classification

1. Form (by pathogenesis):

1) primary;

2) secondary:

a) obstructive;

b) with disembryogenesis of the kidneys;

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

2. Current:

1) acute;

2) chronic (manifest and latent forms).

3. Period:

1) exacerbation (active);

2) reverse development of symptoms (partial remission);

3) remission (clinical and laboratory remission).

4. 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.

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 study of blood: an increase in the content of sialic acids, β2- 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.

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.

The principles of treatment are as follows.

1. Antibacterial, nitrofuran drugs, sulfonamides.

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

3. Phytotherapy (diuretic, metholytics, antiseptics).

34. 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.

Classification

1. Form (according to etiology and pathogenesis):

1) prerenal;

2) renal;

3) postrenal.

2. 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; Simultaneously, the infection accumulates, 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. 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 the level of urea in the blood 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; intravenously - albumin, insulin-glucose therapy; hemodialysis (with persistent azotemia);

4) recovery periods: limitation of pharmacotherapy; phytotherapy.

35. 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 m2, lasting 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%.

II. B: creatinine - 0,45-0,71 mmol / l; filtration - 10-20%.

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

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

Forms: 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. The second stage of NA: protein restriction to 1,5 g/kg, Giordano-Giovanneti diet, symptomatic therapy (antihypertensive, diuretic, calcium preparations, vitamins), red blood cell transfusions.

3. The second stage of IB: 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.

36. 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, non-compliance with the hygienic regimen, hypothermia, and changes in hormonal levels are important. Perhaps the development of allergic or viral cystitis.

Classification

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). 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).

37. Nephrotic syndrome

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

Classification

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).

37b 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.

The principles of treatment are as follows.

1. Bed rest, salt-free diet, fluid restriction.

2. Glucocorticoids.

3. Immunosuppressants.

4. Diuretic.

5. Antibacterial therapy.

6. Heparin, antiplatelet agents.

7. Symptomatic therapy, vitamin therapy.

8. Methindon.

38. 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.

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.

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.

39. Renal colic

Renal amyloidosis

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

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.

Treatment

Appointment of thermal procedures (heating pad, bath with a 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.

Renal amyloidosis in most cases 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.

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.

Treatment

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 the oculist, since the deposition of derivatives of the drug in the refractive media of the eye is possible. Apply unithiol courses of 5-10 mg intramuscularly for 30-40 days. Sometimes colchidine is used. From symptomatic therapy, diuretics, antihypertensives are used. Hemodialysis and kidney transplantation are possible.

40. Hydronephrosis

Hydronephrosis develops as a result of a violation of the outflow of urine and is characterized by the expansion of the pelvic-cup 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 causes of congenital hydronephrosis can 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.

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 40b course of 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, gross hematuria - in 20% of cases, microhematuria - in most cases. Fever appears in case of infection.

Methods of research:

1) palpation of a greatly enlarged kidney;

2) chromocystography, chronocystoscopy;

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

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.

41. 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.

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:

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:

a) active phase: high (III), moderate (II), minimal (I);

b) 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.

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.

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.

42. Dermatomyositis

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

Classification:

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) I degree - maximum;

b) II degree - moderate;

c) III degree - minimal;

2) inactive phase.

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. 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).

43. 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) .

Classification Clinical variant:

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.

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.

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.

44. Classification of rheumatic affection

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.

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 - insufficiency of the II degree; H3 - III degree insufficiency.

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

1. Rheumatism with maximum activity (III degree).

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.

2. Rheumatism with moderate activity (II degree). 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.

3. Rheumatism with minimal activity (I degree).

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.

45. Diagnosis and treatment of rheumatism

Rheumatism 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.

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 the administration for 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. Active anti-inflammatory therapy is carried out in the hospital, 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.

46. ​​Rheumatoid arthritis

Rheumatoid arthritis is a systemic connective tissue disease characterized by chronic destructive polyarthritis. The term was proposed by Harrod in 1859.

Classification

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 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.

47. 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.

The etiology is unclear. A viral and hereditary disease is suspected.

Provoking factors: hypothermia, vibration, trauma, contact with certain chemicals, neuroendocrine disorders, allergization of the body.

Classification

1. The nature of the course: acute, subacute, chronic.

2. Clinical forms:

1) typical (with a characteristic skin lesion);

2) atypical (with focal skin lesions);

3) predominantly visceral, articular, muscular, vascular.

3. Stage of development: initial, generalized, terminal.

4. Degree of activity: minimal (I), moderate (II), high (III).

5. 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, cardiosclerosis, 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.

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.

48. 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 (which are mainly part 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 (metars of non-phalangeal joints, joints of the metatarsus of the ankle, knee joints are more often affected). Sometimes arthritis develops in the small joints of the hand.

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.

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 mandatory for patients to follow a diet.

49. 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.

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.

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.

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.

50. 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 at the Botkin point 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 the content of iron and magnesium in the blood serum.

Classification

1. Deficiency anemia: iron deficiency, vitamin deficiency, protein deficiency.

2. Hypo- and aplastic anemia: Fanconi congenital anemia, Dabiond-Biekfen anemia, acquired anemia.

3. Hemolytic anemia: spherocytic, sickle cell, autoimmune.

By severity:

1) mild anemia: hemoglobin in the range of 90-110 g / l, the number of red blood cells 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 minutes.

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.

vitamin deficiency anemia

Pernicious anemia (Addison-Birmer's disease) is caused by vitamin B12 deficiency, which manifests itself in damage to the hematopoietic, digestive and nervous systems. It occurs more often in older age, with the same frequency in men and women.

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 of three cell lines: erythrocyto-, leuko- and thrombocytopoiesis.

Hemolytic anemia

These are anemias that develop as a result of the destruction of red blood cells. sickle cell anemia

Anemia develops at an early age. A family history is important, the identification of abnormal hemoglobin in relatives.

51. 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

1. A disease caused by a violation of vascular hemostasis (vasopathy).

1) Shenein-Genoch disease (simple, rheumatoid, abdurative and fulminant purpura);

2) hereditary-familial simple purpura (Davis);

3) anular telangiectatic purpura of Mabocca;

4) necrotic purpura of Sheldon;

5) Waldenstrom's hyperglobulinemic purpura;

6) hereditary hemorrhagic telangiectasias;

7) Louis-Barr syndrome (capillary telangiectasia of the conjunctiva with ataxia and chronic pneumonia);

8) Kazabakh-Merritt syndrome;

9) scurvy and Mimer-Barny's disease;

2. Diseases caused by a violation of the platelet mechanism of hemostasis (thrombocytosis, thrombocytopenia):

1) hemorrhagic thrombocytopathy, Werlhof's disease;

2) amegakaryocytic thrombocytopenic purpura of Landolt;

3) autoimmune thrombocytopenia of various origins;

4) thrombocytopenic hymiphragic purpura with acquired autoimmune hemolytic anemia (Ivens-Fischer syndrome);

5) thrombocytopenic purpura with chronic purulent tint and exudative diathesis (Ondrich's syndrome);

6) thrombotic thrombocytopenic purpura Mogmkowitz;

7) thrombocytopenia in heangiomas (Kazabakh-Merritt syndrome);

8) hereditary properties of thrombopathy (Glanuman, Willibrand);

9) thrombocytopathy in combination with impaired coagulation factors.

3. Diseases caused by a violation of blood coagulation factors (quagulopathy):

1) hemophilia A due to lack of factor VIII;

2) hemophilia B due to lack of factor IX;

3) hemophilia C due to lack of factor XI;

4) pseudohemophilia due to hypoprothrombinemia;

5) Ouren's pseudohemophilia;

6) pseudohemophilia due to lack of factor VII;

7) pseudohemophilia due to lack of fibrinogen (afibrinogenemia);

8) pseudohemophilia due to lack of factor X;

9) pseudohemophilia due to lack of fabrinase;

10) pseudohemophilia due to an excess of anticoagulants.

52. Hemorrhagic vasculitis

Hemorrhagic vasculitis (Schönein-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.

Activity level 1, 2, 3.

Course: acute, subacute, chronic, recurrent.

Outcome: recovery, transition to a chronic form, outcome in chronic nephritis.

Clinical criteria for diagnosis:

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 studies: 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.

Differential diagnosis

It is carried out with thrombocytopathy, thrombocytopenia, coagulopathy, toxic drug 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).

53. 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, Wilbrand-Jurgens, 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.

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 mega-karyocytic germ with a violation of the functional activity of megapariocytes;

3) immunological: the presence of antiplatelet antibodies.

Principles of treatment of thrombocytopenia:

1) prevention of bruises and injuries;

2) antibiotics for bacterial infections;

3) transfusion of plasma and large doses of d-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% intramuscularly, magnesium thiosulfate inside;

2) locally, subcutaneously or intramuscularly monosemi-carbazone of adrenochrome (adroxon, chromadron, adrenoxyl), dicyonon;

3) intravenous injection of platelet mass.

54. 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 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 (protrolobin); factor X deficiency (Stuart-Prower).

3. Violation of fibrin formation, deficiency of factor I (fibrinogen). Forms of flow: light, heavy, hidden.

Clinical diagnostic criteria: pale 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

It is carried out with thrombocytopathies, hemorrhagic vasculitis, with hemarthrosis with rheumatism. 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.

55. 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.

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 is 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.

Small liver failure is present in chronic liver damage (chronic hepatitis, cirrhosis, hepatosis, tumors, slow intoxication), with intercurrent diseases, surgical interventions, and 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.

56. 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.

Classification

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) enzymopathies.

Hypotrophy is a chronic eating disorder with a lack of body weight, which develops under the influence of various factors.

3. Enzyme preparations (pancreatin, panzinorm, festal).

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.

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.

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