Internal illnesses. Lecture notes: briefly, the most important

Lecture notes, cheat sheets
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Internal illnesses. Lecture notes: briefly, the most important

Lecture notes, cheat sheets

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LECTURE No. 1. The subject of internal diseases, history and tasks

Internal diseases is a field of clinical medicine that studies the etiology, pathogenesis, semiotics, treatment, prognosis and prevention of diseases of internal organs.

Internal medicine is the most important section of practical medicine, covering most human diseases. The term "internal diseases" came into practice in the XNUMXth century. and supplanted the more general term "therapy".

From the point of view of a clinician, any disease is a change in the normal functioning of the body, characterized by a violation of the functional activity of a particular system, a limitation of the adaptive, compensatory and reserve capabilities of the body as a whole and a decrease in its ability to work.

Disease is a dynamic process in which dynamism is determined by the coexistence of damage and repair reactions. The ratio between these reactions reflects the direction of the disease towards either recovery or progression. Elucidation of this direction makes it possible to assess the outcome of the disease, to predict the fate of the patient.

Diagnosis of a disease (from the Greek. diagnosis - "recognition") - a brief definition of the essence of the pathological process, reflecting the cause of its occurrence, the main mechanisms that led to the development of changes in the body, and the characteristics of these changes. Every diagnosis that a doctor makes is (ultimately) a differential diagnosis - weighing each individual symptom, evaluating and differentiating it.

In the early stages of development, medicine was not a science and was purely empirical knowledge based only on observations. For the first time, a representative of ancient Greek medicine, Hippocrates, when examining a patient, used palpation, listening, and compiled a description of many symptoms and syndromes of diseases. The doctrine of the pulse was created by the representative of the Alexandrian school Herophilus, the description of some signs of pleurisy, stomach ulcers, meningitis was presented by the Tajik scientist Abu-Ali Ibn-Sina (Avicenna).

In the XVIII-XIX centuries. questions of internal medicine were developed in detail by Auenbrugger, Laennec, G. I. Sokolsky, M. Ya. Mudrov, G. A. Zakharyin.

The scientific clinical school of internal medicine was created by S. P. Botkin, subsequently developed by many brilliant clinicians: I. M. Sechenov, V. P. Obraztsov, N. D. Strazhesko, B. E. Votchal, A. M. Myasnikov, N S. Molchanov, E. M. Tareev, V. Kh. Vasilenko, etc.

At the present stage of development of internal medicine, a great contribution was made by domestic scientists E. I. Chazov, P. E. Lukomsky, F. I. Komarov, G. I. Dorofeev, A. G. Chuchalin, A. I. Vorobyov and others.

The final diagnosis of the disease should include information about the etiology (etiological diagnosis), its pathogenesis (pathogenetic diagnosis), morphological changes (morphological diagnosis) and functional state (functional diagnosis) of the affected organ or system. The final diagnostic formula accumulates all types of diagnoses, and reflects the doctor's view of the pathological process by highlighting the underlying disease, complications and concomitant diseases. In the future, the doctor determines the direction of the development of the pathological process, possible outcomes and consequences of the disease. The assessment of all these changes is carried out as a result of observation of the patient, the use of special additional studies, the treatment used.

LECTURE No. 2. Neurocirculatory asthenia

Neurocirculatory asthenia (NCA) is most common in young people during the period of hormonal changes in the body. NCA is a functional disease, which is based on a failure of adaptation or a violation of the neuroendocrine regulation of the cardiovascular system.

Etiology. The reasons for the development of NCA can be external and internal factors.

External factors: psycho-emotional, physical overstrain, violation of the regime of work and rest. Internal factors: congenital or acquired inferiority of the nervous and humoral systems of regulation of vascular tone, features of the protective and adaptive mechanisms of the body (such as higher nervous activity, the state of the endocrine system).

Pathogenesis. The formation of the disease occurs against the background of a genetic or acquired inferiority of the neurohormonal system.

There is a formation of neurosis and visceral disorders, while the internal organs are involved in emotional arousal selectively.

The type of NCA is formed depending on the nature and severity of dysfunctions of the sympathoadrenal and cholinergic systems, as well as on the relationship between adreno- and cholinergic processes.

With an increase in the activity of the sympathoadrenal system and a relative decrease in the activity of the cholinergic system, the formation of hypertensive and cardiac types of NCA occurs (central or peripheral or combined dysfunction of the cardiovascular system). With an increase in the activity of the cholinergic system and a relative insufficiency of the sympathoadrenal system, the formation of the hypotensive type of NCA occurs.

Classification. In the clinic, the most common classification of NCA is according to N. N. Savitsky (1956) and V. P. Nikitin (1957), distinguishing the following types:

1) cardiac;

2) hypertensive;

3) hypotensive;

4) mixed.

Clinic. Main syndromes: neurotic, cardiac (algic or arrhythmic variants), hypertensive, hypotonic, respiratory distress syndrome, hyperkinetic, asthenic, vascular.

It is characterized by the presence of a large number of various subjective signs of the disease with the insignificance of objective data. There are complaints of pain in the region of the heart, which differs from coronarogenic ones - they are localized in the region of the apex of the heart, have a dull, aching, stabbing character. There may be a feeling of heaviness and pressure. Physical stress often does not increase pain, but relieves it (it is noted in half of the patients). Pain is often associated with excitement and emotional stress, can be short-term or long-term. They can radiate to the left arm and scapula, be accompanied by hyperalgesia in the region of the apex of the heart, the left shoulder, and are not removed by nitroglycerin, which is also poorly tolerated.

Perhaps the appearance of complaints that characterize the disorder of breathing - a periodic deep breath (dreary breath), frequent shallow breathing, leading to a state of hyperventilation (dizziness, darkening in the eyes).

There may be sensations of heat, hot flashes to the head, a short-term fainting state. Perhaps the presence of acrocyanosis, sweating, pronounced red or white dermographism, "play" of vasomotors of the skin.

There may be signs of peripheral circulatory disorders (such as Raynaud's syndrome), temperature asymmetries, lability of the pulse, blood pressure, a tendency to tachycardia, respiratory arrhythmia due to dysfunction of the respiratory center, extrasystole, group extrasystoles, attacks of paroxysmal tachycardia.

There are general weakness, fatigue, irritability, headache, unstable sleep, a tendency to rapid mood swings. Distracted attention, memory loss, dizziness, a feeling of fear are noted.

The boundaries of the heart do not change, the tones are clear, at the apex, a functional systolic murmur can sometimes be heard, associated with an acceleration of blood flow and a change in the tone of the capillary muscles. The nature of the noise changes with a change in the position of the body. Noise is not conducted into the left armpit, decreases or disappears during exercise.

The dynamics of changes in blood pressure depends on the type of NCA. Arterial hypotension is considered pressure figures: at the age of 25 years - 100/60 mm Hg. Art. and less, over the age of 30 - below 105/65 mm Hg. Art.

For NCA by cardiac type characteristic: persistent sinus (sometimes paroxysmal) tachycardia, extrasystole, an increase in minute blood volume. Severe tachycardia and a decrease in pulse pressure are noted during functional tests (orthostatic and with physical activity).

For NCA for hypertensive type characteristic: lability of blood pressure with a tendency to systolic hypertension, an increase in stroke and minute blood volumes, good tolerance of the orthostatic test with an increase in mean hemodynamic pressure.

For NCA by hypotensive type fainting or collaptoid states, lability of blood pressure with a tendency to hypotension, muffled heart tones, a tendency to increase cardiac output, poor tolerance of an orthostatic test with a drop in mean hemodynamic pressure, tachycardia, an increase in minute blood volume during exercise (immediately after its completion is possible sudden drop in blood pressure).

Additional diagnostic study. Of diagnostic importance are studies of the level of catecholamines in the blood and urine, 17-hydroxycorticosteroids (increased amounts), estrogen levels (decreased amounts), and studies of thyroid function (radioimmunological determination of T3, T4 and TSH).

The indicators of central hemodynamics are studied: in the cardiac type, there is an increase in minute volume and a decrease in specific peripheral resistance, the average hemodynamic pressure remains unchanged.

A study of blood pressure indicators is carried out with the determination of residual pressure (pressure measured 10-15 minutes after a random, single dose) and basal pressure (pressure measured in the morning under basal metabolic conditions).

The average hemodynamic pressure is investigated (the integral value of the pressure variables during one cardiac cycle) is measured by the tachiooscillographic method according to Savitsky, normally 80-90 mm Hg. Art., with NCA of the hypertensive type - does not exceed 90 mm Hg. Art.

Functional stress tests are widely used: Master's test, step test, bicycle ergometry in NCA by cardiac type, test with dosed physical activity (20 squats in 30 seconds), hyperventilation test, breath holding test. In NCA for hypertensive and hypotensive types, active and passive orthostatic tests are performed.

If there are negative T waves on the ECG, stress pharmacological tests are performed: a test with inderal, potassium chloride, atropine, adrenaline. When performing an electrocardiographic study, the following can be detected: sinus tachycardia, bradycardia and arrhythmia, impaired atrioventricular conduction, displacement of the RS-T segment below the isoelectric line, flattening and the appearance of a negative T wave, ventricular extrasystoles are more often detected.

Echocardiographic examination allows to confirm the functional nature of the changes. Be sure to consult specialists: ophthalmologist, endocrinologist, nephrologist, neuropathologist, psychiatrist.

Complications. The development of arrhythmias, acute vascular insufficiency (fainting, collapse), autonomic crises, and angioedema is possible.

Treatment. Includes elimination of etiological factors. Sanitation of hidden foci of chronic infection should be carried out. The normal mode of physical activity must be restored, the duration of sleep increased to 10 hours per day. Non-drug methods are widely used in treatment: acupuncture, hypnosis. Physical therapy is prescribed. Spa treatment is used.

Preference is given to local sanatoriums and rest houses. In the summer, staying in a hot climate is not shown.

Sedatives are used according to indications, hypnotics are used only for severe sleep disorders. Tranquilizers are used in small doses, short courses. β-blockers are used in the hypertensive type of NCA with tachycardia. With an increase in the activity of the cholinergic system, anticholinergic agents are used. Of the agents that increase the activity of the central nervous system, tinctures of ginseng, eleutherococcus, Chinese magnolia vine, etc. are used.

Forecast. The prognosis is favorable, performance is restored.

LECTURE No. 3. Hypertension

A chronically occurring disease, the main manifestation of which is the syndrome of arterial hypertension, not associated with the presence of pathological processes in which an increase in blood pressure is due to known causes.

Etiology. The development of the disease is caused by neuropsychic overstrain and dysfunction of the gonads.

Pathogenesis. The biosynthesis of sympathetic amines is disrupted, resulting in an increase in the tone of the sympathoadrenal system. Against this background, the pressor mechanisms of the renin-angiotensin-aldosterone system are activated and the depressor factors are inhibited: prostaglandins A, E, and the kinin system.

Classification. In clinical settings, the disease is divided according to the severity of arterial hypertension, the degree of risk of developing damage to target organs, and the stage of development of hypertension.

Definition and classification of blood pressure levels

Normal BP:

1) optimal - less than 120 and less than 80 mm Hg. Art.;

2) normal - less than 130 and less than 85 mm Hg. Art.;

3) high normal - 130-139 and 85-89 mm Hg. Art.

Arterial hypertension:

I degree (soft) - 140-159 and 90-99 mm Hg. Art.;

subgroup: borderline - 140-149 and 90-94 mm Hg. Art.;

II degree (moderate) - 160-179 and 100-109 mm Hg. Art.;

III degree (severe) - more than 180 and more than 110 mm Hg. Art.

Hypertension isolated:

1) systolic - more than 140 and less than 90 mm Hg. Art.;

2) subgroup: borderline - 140-149 and less than 90 mm Hg. Art.

Definition of risk group

Table 1. Risk stratification

Note: FR - risk factors, POM - target organ damage, ACS - associated clinical conditions.

Table 2. Criteria for risk stratification

Risk levels (risk of stroke or myocardial infarction in the next 10 years): low risk (1) - less than 15%, medium risk (2) - 15-20%, high risk (3) - 20-30%, very high risk ( 4) - above 30%.

Determining the stage of hypertension:

Stage I: no changes in target organs;

Stage II: the presence of one or more changes in the target organs;

Stage III: the presence of one or more associated conditions.

Clinic. With hypertension stage I there are periodic headaches, tinnitus, sleep disturbance. Mental performance decreases, dizziness, nosebleeds are noted. Possible cardialgia.

In the left thoracic branches, the presence of high-amplitude and symmetrical T waves is possible, the minute volume of the heart remains normal, increasing only during exercise. Hypertension crises develop as an exception.

With stage II hypertension there are frequent headaches, dizziness, shortness of breath during physical exertion, sometimes angina attacks. Possible nocturia, the development of hypertensive crises.

The left border of the heart shifts to the left, at the top of the first tone is weakened, an accent of the second tone is heard over the aorta, sometimes a pendulum-shaped rhythm. Cardiac output at rest is normal or slightly reduced, with dosed physical activity it increases to a lesser extent than in healthy individuals, the speed of propagation of the pulse wave is increased.

With stage III hypertension two options are possible:

1) there is a development of vascular accidents in target organs;

2) there is a significant decrease in minute and stroke volumes of the heart at a high level of peripheral resistance, the load on the left ventricle decreases.

With malignant hypertension extremely high blood pressure figures are noted (diastolic blood pressure exceeds 120 mm Hg), leading to the development of pronounced changes in the vascular wall, tissue ischemia and impaired organ functions. Renal failure progresses, vision decreases, weight loss, symptoms from the central nervous system, changes in the rheological properties of the blood appear.

Hypertensive crises

Sudden sharp increase in blood pressure. Crises are of two types.

Crisis type I (hyperkinetic) is short-lived. It develops against the background of good health, lasts from several minutes to several hours. Manifested by a sharp headache, dizziness, blurred vision, nausea, rarely vomiting. Excitation, palpitation and trembling throughout the body, pollakiuria are characteristic, by the end of the crisis there is polyuria or copious loose stools. Systolic blood pressure rises, pulse pressure rises. It is necessary to immediately lower blood pressure (not necessarily to normal).

Type II crisis (eu- and hypokinetic) is severe. It develops gradually, lasts from several hours to 4-5 days or more. Caused by circulatory hypoxia of the brain, characteristic of the later stages of hypertension. Manifested by heaviness in the head, severe headaches, sometimes paresthesia, focal disorders of cerebral circulation, aphasia. There may be pain in the heart of an anginal nature, vomiting, attacks of cardiac asthma. Significantly increased diastolic pressure. Blood pressure should be reduced gradually over several hours.

Additional diagnostic study. The examination includes 2 stages: a mandatory study and a study to assess target organ damage.

Mandatory studies include: a general blood and urine test, determination of potassium, fasting glucose, creatinine, total blood cholesterol, electrocardiography, chest x-ray, fundus examination, ultrasound examination of the abdominal organs.

Additional studies include: echocardiography (as the most accurate method for diagnosing left ventricular hypertrophy), ultrasound examination of peripheral vessels, determination of the lipid spectrum and triglyceride levels.

Complications. The development of hemorrhagic stroke, heart failure, grade III-IV retinopathy, nephrosclerosis (chronic renal failure), angina pectoris, myocardial infarction, atherosclerotic cardiosclerosis is possible.

Differential diagnostics. It is carried out with secondary hypertension: diseases of the kidneys, adrenal glands (Itsenko-Cushing syndrome, Conn syndrome), pheochromocytoma, Itsenko-Cushing disease, organic lesions of the nervous system, hemodynamic arterial hypertension (aortic coarctation, aortic valve insufficiency, sleep-disordered breathing syndrome), iatrogenic arterial hypertension.

Treatment. At high and very high risk levels, immediate medication is prescribed. If the patient is classified as an average risk group, the question of treatment is decided by the doctor. Observation with blood pressure control is possible from several weeks to 3-6 months. Drug therapy should be prescribed if blood pressure remains above 140/90 mm Hg. Art. In the low-risk group, longer observation is possible - up to 6-12 months. Drug therapy is prescribed when blood pressure levels remain above 150/95 mm Hg. Art.

Non-drug treatments include smoking cessation, weight loss, alcohol restriction (less than 30 g per day for men and 20 g for women), increased physical activity, and reduction of salt intake to 5 g per day. A comprehensive change in diet should be carried out: it is recommended to eat plant foods, reduce fat, increase potassium, calcium contained in vegetables, fruits and grains, and magnesium contained in dairy products.

Drug treatment is carried out by the main groups of drugs:

1) the central mechanism of action: central sympatholytics, imidazoline receptor agonists;

2) antiadrenergic, acting on adrenergic receptors of various localization: ganglionic blockers, postganglionic adrenergic blockers, non-selective α-adrenergic blockers, selective α₁-blockers, β-blockers, α- and β-blockers;

3) peripheral vasodilators: arterial myotropic action, calcium antagonists, mixed, potassium channel activators, prostaglandin E₂ (prostenon);

4) diuretics: thiazide and thiazide-like, potassium-sparing;

5) ACE inhibitors (angiotheisin converting enzyme inhibitors);

6) neutral endopeptidase inhibitors;

7) angiotensin II (AII) receptor antagonists.

Antihypertensive drugs of the 1st line include ACE inhibitors, β-blockers, diuretic drugs, calcium antagonists, AII receptor antagonists, α-blockers.

Effective drug combinations:

1) diuretic and β-blocker;

2) a diuretic and an ACE inhibitor or an angiotensin II receptor antagonist;

3) a calcium antagonist from the group of dihydropyridones and a β-blocker;

4) calcium antagonist and ACE inhibitor;

5) α-blocker and β-blocker;

6) a drug of central action and a diuretic. In uncomplicated hypertensive crisis, treatment can be carried out on an outpatient basis, oral β-blockers, calcium antagonists (nifedipine), clonidine, short-acting ACE inhibitors, loop diuretics, prazosin are prescribed.

With a complicated hypertensive crisis, vasodilators (sodium nitroprusside, nitroglycerin, enaprilat), antiadrenergic drugs (phentolamine), diuretics (furosemide), ganglioblockers (pentamine), antipsychotics (droperidol) are administered parenterally.

Flow. The course is long, with periods of remission; progression depends on the frequency and nature of exacerbations, the duration of periods of remission.

Forecast. The prognosis of the disease is determined by the stage of its course. At stage I - favorable, at stages II-III - serious.

Prevention. Prevention of the disease should be aimed at treating patients with neurocirculatory dystonia, monitoring those at risk, and using active recreation. When a diagnosis of hypertension is made, continuous comprehensive treatment is carried out.

LECTURE № 4. Myocarditis

Myocarditis is an inflammatory disease of the heart muscle of an infectious, allergic or toxic-allergic nature.

Etiology. The main factors in the development of the disease are bacterial infections, purulent-septic diseases (pneumonia, cholangitis, tuberculosis, sepsis), viral infections (Coxsackie viruses, influenza, ECHO), allergic factors, intoxications (thyrotoxicosis, uremia, alcohol).

Pathogenesis. Myocardial damage leads to the development of dystrophic-necrobiotic changes in muscle cells. The activity of cells in the inflammatory infiltrate increases due to hydrolases: acid phosphatase, β-glucuronidase, aminopeptidase. During a viral infection, viruses replicate in the myocardium. Against this background, the nucleic acid metabolism of cardiomyocytes is disrupted, collagen synthesis increases with the development of fibrous tissue.

Clinic. The main clinical variants are: pain (not accompanied by heart failure, recovery after 1-2 months), arrhythmic (with severe myocardial damage), circulatory failure (severe diffuse myocardial damage in combination with rhythm and conduction disorders), mixed (pain with arrhythmic , arrhythmic with circulatory failure, etc.), Abramov-Fiedler (severe idiopathic myocarditis).

The disease begins during the period of convalescence or 1-2 weeks after recovery from infection. An inexplicable low-grade fever appears, rarely - fever, weakness, malaise, sweating. There are cardialgias: from non-intense short stabbing pains to severe angina pectoris pains, a feeling of palpitations, interruptions in the work of the heart, shortness of breath. Objectively noted tachycardia, low filling of the pulse, in severe cases - altered pulse. In severe cases, the size of the heart increases, blood pressure is normal or reduced. The heart sounds are muffled, splitting of the I tone is possible, the appearance of additional III and IV tones, the "gallop rhythm", a muscular systolic murmur appears above the apex of the heart, there may be a pericardial rub.

With Abramov-Fiedler's myocarditis, increasing symptoms of progressive heart failure, thromboembolism of the kidneys, lungs, and spleen suddenly appear.

Additional diagnostic study. A general blood test is performed to determine the presence of leukocytosis and an increase in ESR. Biochemical studies are being carried out which indicate dysproteinemia, an increase in the content of α- and β-globulins, an increase in the level of sialic acids, the appearance of C-reactive protein, an increase in the activity of AST and CPK (in severe forms), a virological study, an immunological study (a decrease in the activity of the nonspecific component of the immune system). response, increase in the content of IgA, IgJ, IgM, CEC, appearance of anticardiac antibodies).

Scintigraphy is performed with Ga67, while radioactive gallium accumulates in inflammatory infiltrates.

An ECG study reveals the following changes: ST segment displacement, T wave changes - flat, biphasic, negative, (expansion of the QRST complex, decrease in voltage; there may be atrioventricular blockade, blockade of the legs of the His bundle; atrial, ventricular tachycardia; with Abramov's myocarditis- Fiedler changes may be similar to myocardial infarction.

Echocardiography is not very specific. Hypo- and dyskinesia of the myocardium, accumulation of a small amount of fluid in the pericardium, an increase in the left ventricle and left atrium are revealed, with Abramov-Fiedler's myocarditis, dilatation of the cavities, to a lesser extent, myocardial hypertrophy.

Complications. Complications of the disease include arrhythmias, circulatory failure, angina pectoris, myocardial cardiosclerosis, thromboembolism.

Differential diagnostics. Should be carried out with neurocirculatory dystonia, coronary heart disease, thyrotoxic myocardial dystrophy, primary rheumatic heart disease.

Treatment. In treatment, the appointment of bed rest is mandatory (for 1-2 months, depending on the severity of the condition). Conducted etiotropic therapy, which is effective in infectious myocarditis, and in viral myocarditis is ineffective.

NSAIDs are prescribed: salicylates, pyrozolone derivatives (butadione, reopyrin), indolacetic acid (indomethacin, metindol), phenylpropionic acid (brufen, naproxen, phenylacetic acid (voltaren).

In the treatment of effective immunosuppressants, which include corticosteroids, rarely cytotoxic drugs. Treatment with prednisolone is carried out for 1,5-12 months with an initial dose of 30-60 mg / day.

Symptomatic therapy is also carried out with cardiac glycosides, antiarrhythmic drugs, diuretics, and metabolic agents.

Flow. It can be acute, abortive, recurrent, latent, chronic.

Forecast. With most myocarditis, the prognosis is favorable, and with Abramov-Fiedler myocarditis, it is serious.

Prevention. The primary measures to prevent the disease include prevention, timely treatment and sanitation of foci of infections, after acute infections - limiting physical activity. Measures of secondary prevention is dispensary dynamic monitoring of ill persons.

LECTURE № 5. Infective endocarditis

It is a peculiar form of sepsis, characterized by the localization of the pathogen on the heart valves or parietal endocardium, followed by damage to many organs and systems.

Etiology. The causative agents of the disease include microbial flora: cocci (Staphylococcus aureus, viridescent streptococcus, S. Epidermidis, enterococci), gram-negative bacteria (E. coli, Proteus, Pseudomonas aeruginosa, Klebsiella), fungi such as Candida, rickettsia, viruses, Brucella.

Pathogenesis. Of great importance in the development of the disease are risk factors that reduce the immunobiological resistance of the body. These include: acquired and congenital heart defects (ventricular septal defect, open aortic disease), minor surgical and dental operations, parenteral drug administration, heart valve replacement, urinary tract infection, prolonged use of catheters, abortions, program hemodialysis.

Damage to the valvular apparatus of the heart occurs with malformations of the heart muscle, microtrauma, impaired hemodynamics and microcirculation. Interstitial valvulitis and thrombotic vegetations develop. The reactivity of the endocardium changes, the pathogenic flora is activated. Thromboembolic complications (heart attacks and abscesses of the myocardium, brain, lungs, and other organs), bacterial damage to the valves (endocarditis) with bacteremia, and focal nephritis are formed. Immune generalization of the process is accompanied by the development of immunocomplex nephritis, vasculitis, myocarditis, hepatitis, splenomegaly. At the final stage, dystrophic changes in internal organs are formed: the heart, blood vessels, kidneys, liver, and other organs (dystrophic phase).

Pathological anatomy. With this pathology, the aortic valve is most often affected, less often the mitral valve. On the affected valves, tendon chords, sometimes parietal endocardium, ulcerative defects are formed, covered with massive polyp-like thrombotic deposits. There may be perforations or aneurysms of the leaflets. Inflammatory infiltrates consist of lymphoid cells and histiocytes. In the future, wrinkling of the maturing granulation tissue occurs, deformation of the valve leaflets.

Classification. When making a diagnosis, the following points should be considered:

1) clinical and morphological form: primary (on unchanged valves) and secondary (against the background of rheumatic, syphilitic, atherosclerotic, lupus, traumatic defects, arteriovenous aneurysms, prosthetic valves);

2) the nature of the course (acute, subacute, chronic (recurrent));

3) the degree of activity of the process: I degree - minimal (ESR up to 20 mm/h), II degree - moderate (ESR 20-40 mm/h), III degree - high (ESR more than 40 mm/h).

Clinic. The main manifestations of the disease include:

fever (from subfebrile to high), which persists for a long time, is accompanied by chills, profuse sweating. Muscle weakness, pain in muscles and joints appear, appetite decreases.

At the onset of the disease, chills, profuse cold sweats, high fever, severe intoxication may occur, which is typical for primary endocarditis. The onset of the disease may be imperceptible with the development of malaise, weakness, weight loss, subfebrile condition.

The skin is pale with an icteric tint, petechial rashes appear, especially on the skin of the lower eyelid (Lukin-Libman symptom), painful nodules on the palms and soles (Osler's nodules). The fingers are like drumsticks, the nails are like watch glasses.

Valve damage begins with the appearance of a systolic murmur over the aorta due to narrowing of the aortic orifice. This occurs a few weeks after the onset of the disease. Less often, the presence of systolic murmur over the apex of the heart can be determined; later, with the development of aortic insufficiency, diastolic murmur appears over the aorta. There are: tachycardia, muffled heart sounds, rhythm and conduction disturbances, which is typical for developing myocarditis. From the side of the vessels, the development of thrombosis, aneurysms, vasculitis, developing in the internal organs, can be observed. Diffuse glomerulonephritis may develop in the kidneys.

The criteria for remission of the disease are repeated negative blood cultures, the disappearance of clinical manifestations, the disappearance of vegetations with repeated echocardiography.

Additional diagnostic study. A general blood test is performed, in which anemia, leukopenia, thrombocytopenia, and an increase in ESR can be detected. A biochemical blood test can determine the presence of dysproteinemia, hypergammaglobulinemia, and a positive formol test.

Immunological study determines the inhibition of the non-specific link of the immune response, the activation of its humoral link (increased IgA, IgM, CEC).

Bacteriological examination of blood is carried out with three blood cultures. In this case, the pathogen must be detected in two crops.

An ECG study reveals a rhythm and conduction disturbance, a decrease in the voltage of the teeth. An echocardiographic study reveals the presence of vegetations on the cusps of the affected valve, signs of a formed heart disease in the form of insufficiency, ruptures of the chords, perforation of the cusps can be established.

Complications. Complications include pulmonary infarction, pulmonary edema, myocardial infarction, heart failure, kidney infarction, cerebrovascular accidents, splenic infarction, and retinal embolism.

Differential diagnostics. Should be carried out with rheumatic heart disease, acute and subacute SLE, brucellosis, patent ductus arteriosus, aortic lesions of syphilitic or atherosclerotic origin, myeloma, visceral form of lymphogranulomatosis, some tumors, serum sickness.

Treatment. Treatment should be as early as possible, it must be carried out in a hospital. It is necessary to introduce an anti-staphylococcal penicillinase-resistant antibiotic oxacillin, 2 g every 4 hours (12 g / day). After clarifying the type of pathogen, further selection of antibiotics is carried out. Antistaphylococcal plasma is administered intravenously (5 infusions per course).

The duration of the first course of antibiotic therapy is at least 4-6 weeks; with a late start of treatment - up to 8-10 weeks. Antibiotics should be changed every 2-4 weeks, their administration can be both intravenous and intramuscular.

After discharge from the hospital, further prophylactic antibacterial courses are carried out for 2-3 weeks, then after 1, 3 and 6 months with an antibacterial drug that produced the greatest effect.

With pronounced immunological manifestations, the following are used: prednisolone (40-60 mg / day), non-steroidal anti-inflammatory drugs.

In the dystrophic phase, cardiac glycosides, potassium preparations, diuretics are prescribed, for anemia - iron preparations in combination with vitamins of groups B and C.

Perhaps a blood transfusion or red blood cells.

Indications for surgical treatment are: progressive heart failure, lack of effect from conservative therapy, repeated embolism, fungal endocarditis.

Flow. In the acute form, the course can be rapidly progressive, in the subacute form - protracted, in the chronic form - recurrent.

Forecast. In the acute form, the prognosis is unfavorable, life expectancy is not more than 2 months. In subacute and chronic forms, the prognosis is relatively favorable, up to 60% of patients are cured.

Prevention. It consists in preventing the development of bacterial infections, active treatment of acute infections, rehabilitation of foci of chronic infection, hardening of the body, and secondary prevention in people who have had infective endocarditis.

LECTURE No. 6. Pericarditis

Pericarditis is an inflammatory disease of the pericardium, which is more often a local manifestation of a certain disease (tuberculosis, rheumatism, diffuse connective tissue diseases) or a concomitant disease of the myocardium and endocardium.

Etiology. The disease is caused by various pathogens (bacteria, viruses, fungi, rickettsiae, mycobacteria, typhoid and dysenteric bacillus).

It is possible to develop aseptic pericarditis with allergies, systemic connective tissue lesions, traumatic injuries, autoimmune processes (post-infarction, post-commissurotomy, blood diseases, hemorrhagic diathesis, radiation injuries, hemodialysis, malignant tumors, deep metabolic disorders (uremic, gouty).

There is a group of idiopathic pericarditis.

Pathogenesis. The infection penetrates into the pericardial cavity by the hematogenous or lymphogenous route. Ex-sudative processes intensify in the pericardium. In the pericardial cavity, fibrinogen is released, fibrin is formed. Fibrous pericarditis develops. Under the fibrin layer, the mesothelium is destroyed, the fibrinous masses fuse with the underlying tissue. With the total involvement of the pericardium in the inflammatory process, the development of exudative pericarditis is possible.

The accumulation of a large amount of exudate in the pericardial cavity is manifested by the syndrome of cardiac tamponade. Diastolic filling of the cavities of the heart with blood is difficult with the development of congestive insufficiency of the right ventricular type.

Pathological anatomy. Pericarditis are fibrinous, serous, serous-fibrinous, serous-hemorrhagic, hemorrhagic, purulent, putrefactive.

The adhesive process is not limited to the pericardial cavity, it can go beyond it, lead to the formation of adhesions with the pleura, mediastinum, diaphragm, with the anterior chest wall, the vena cava and hepatic veins can be affected.

Clinic. Dry (fibrinous) pericarditis there are pains in the region of the heart of varying strength. The pains are usually localized in the lower sternum or in the region of the apex of the heart, radiating to the left shoulder blade, neck, epigastrium, to the left arm.

Borders and heart sounds are not changed. A pericardial friction rub is heard, which is more often determined on the sternum and to the left of the parasternal line. Noise is heard in any phase of the cardiac cycle, sometimes it can be heard only in the sitting position or in the knee-elbow position. The murmur is heard better on inspiration, has a scratchy tone, higher than other heart murmurs. It may last for several hours or months.

With effusion (exudative) pericarditis, which develops after the stage of dry pericarditis or without it, appear: shortness of breath, decreasing in the sitting position, when the torso is tilted forward; cough (usually dry), vomiting possible. The body temperature rises, the boundaries of the heart increase in all directions, the apical impulse decreases or disappears, the cervical veins swell (pulsation is not visually determined). Heart sounds are sharply muffled, sinus tachycardia is possible, pericardial friction rub (with a small amount of exudate), which weakens with the accumulation of exudate.

With a large effusion, the pulse decreases, especially on inspiration (paradoxical pulse), blood pressure decreases, especially systolic.

With cardiac tamponade there are severe pain behind the sternum, collapse, tachycardia, paradoxical pulse. With compression of the superior vena cava, the formation of a "consular" head, Stokes collar, is possible. With compression of the inferior vena cava appear: hepatomegaly, premature ascites, Breitman's position, periodic disturbance of consciousness.

With adhesive (adhesive) pericarditis an adhesive process develops due to purulent, tuberculous and hemorrhagic pericarditis and may be asymptomatic. Pain in the region of the heart, dry cough, aggravated by physical exertion, are more often noted. Perhaps the retraction of the apex beat (symptom of Saly-Chudnovsky), its combination with Friedreich's diastolic venous collapse and the prodiastolic tone of the throw, obliteration of the cavities and fusion of the pericardium with the anterior abdominal wall) the boundaries of relative and absolute dullness merge. During auscultation, the three-term nature of the rhythm is determined (an additional click at the end of systole, which does not change from inhalation or exhalation). Perhaps the appearance of systolic non-conductive noise over the anterior surface of the heart.

With constrictive (compressive) pericarditis in the early stages, shortness of breath develops, which occurs first during exertion, then at rest, a slight cyanosis of the lips and the tip of the nose. In the extended stage, Beck's triad appears: high venous pressure, ascites, "small quiet heart".

The cervical veins swell, puffiness of the face, cyanosis appears. The position of the patient in orthopnea. Trophic disorders develop. The apex beat disappears, is not detected by palpation. The pulse is rapid, small amplitude, atrial fibrillation, blood pressure is reduced, especially systolic, venous pressure is increased. The size of the heart may not be increased, the heart sounds are muffled. There may be a low systolic murmur, anasarca, hydrothorax, ascites are noted.

This variant of pericarditis is more often observed in men, the main cause of its development is tuberculosis.

Additional diagnostic study. A general blood test is performed, in which leukocytosis is detected with a shift of the formula to the left, an increase in ESR. The severity of the indicators depends on the inflammatory manifestations.

To detect changes in the configuration of the heart shadow, effusion, pulsation of the contours of the heart in chronic pericarditis, thickening of the pericardium, lime deposits, an X-ray examination is performed.

An ECG study is required. With dry pericarditis in all leads, the ST segment is elevated above the isoline with gradual normalization, a negative T wave may appear. The ECG picture resembles an acute myocardial infarction, since the Q wave and the QRS complex do not change, ST segment changes are never discordant.

With exudative pericarditis, there is a decrease in the voltage of all teeth, extrasystole, atrial fibrillation.

EchoCG study visualizes changes in the heart, while probing the heart, the pressure in the cavities is measured. A diagnostic puncture is carried out with a mandatory subsequent cytological, bacteriological, biochemical, immunological study of the punctate.

Differential diagnostics. Should be carried out with nonspecific myocarditis, myocardial infarction, dry pleurisy, cardialgia of various origins.

Treatment. In the acute period, bed rest, a diet with enough protein, vitamins C and K, and salt restriction are prescribed. The underlying disease is being treated - etiotropic therapy.

Of the means of pathogenetic therapy, NSAIDs are used (not indicated for secondary pericarditis, with myocardial infarction), glucocorticoids for 1-1,5 months (with a tumor nature not prescribed), antihistamines, vitamin C.

If necessary, symptomatic therapy is used.

With squeezing pericarditis, surgical treatment (pericardectomy) is indicated. The consequences of operations are serious. For the treatment of heart failure, diuretics are used for a long time (sometimes years) in small doses.

Flow. The course can be acute (pass within 1-2 months), long-term, progressive.

Forecast. determined by the underlying disease. In acute forms, the prognosis is often favorable, in chronic forms it is serious.

LECTURE No. 7. Rheumatism (Sokolsky-Buyo disease)

Rheumatism is a systemic toxic-immunological inflammatory disease of the connective tissue with a predominant localization of the process in the cardiovascular system. The disease develops at any age, mainly among adolescents and children (7-15 years). Women get sick more often than men.

Etiology. The disease is caused by group A β-hemolytic streptococcus.

Pathogenesis. The secreted streptococcal antigens (streptolysin-O, streptokinase, streptohyaluronidase) lead to the development of an acute phase of inflammation with cell exudation and phagocytosis. In the connective tissue, reparative processes develop: cell proliferation, stimulation of the formation of mucopolysaccharides. The work of the immune system is activated through the enhancement of the functioning of the complement system, lysosomal enzymes. Gradually, chronic inflammation is formed with the transfer of activity to immune mechanisms, collagen formation with the formation of fibrosis processes.

Pathological anatomy. There are 4 phases of development of morphological changes, the duration of each is 1-2 months.

Phase I - mucoid swelling of the interstitial tissue and collagen fibers.

Phase II - fibrinoid changes with disorganization of collagen fibers, formation of structureless fields impregnated with fibrin.

Phase III - the formation of Ashoftallaev granulomas with the appearance of perivascular accumulations of lymphocytes and other cells.

Phase IV - sclerosis (fibrosis) with the transformation of cells in granulomas into fibroblasts and the gradual formation of a scar.

The heart is the main target organ in rheumatic fever. Deformation of the heart valves leads to the formation of their insufficiency, then to the narrowing and deformation of the atrioventricular orifices.

The development of heart defects often occurs in the form of combined and combined forms.

Classification. The clinical classification according to A. I. Nesterov (1990) takes into account:

1) the phase of the disease (active or inactive, specifying the degree of activity of the process - minimal, medium, high);

2) clinical and anatomical characteristics of damage to the heart and other organs;

3) the nature of the course of the disease (acute, subacute, protracted, continuously relapsing, latent);

4) the state of blood circulation (0, I, IIa, IIb, III degree of violations).

Clinic. The first period is called prerheumatism. It lasts 2-4 weeks from the end of the streptococcal infection to the onset of the manifestations of the disease. Rheumatism never begins at the height of infection.

Appear: malaise, fatigue, loss of appetite, palpitations, tingling in the joints, hyperhidrosis, pallor of the skin. The second period represents a rheumatic attack. Fever with syndromes of damage to the joints, heart (primary rheumatic heart disease) and other organs may appear. The third period represents a long period of clinical manifestations. There is recurrent rheumatic heart disease with progressive heart damage, the formation of complex heart defects.

Primary rheumatic heart disease

Inflammation of all membranes of the heart (pancarditis) is possible, the endocardium and myocardium are most often affected. There is tachycardia, rarely bradycardia. The borders of the heart are normal or moderately enlarged. On auscultation, a muffled I tone is heard, a soft systolic murmur at the apex (associated with myocarditis). Sometimes a third tone may appear. With an increase in the intensity of the noise, the formation of mitral valve insufficiency is possible (not earlier than 6 months from the onset of the attack).

Recurrent rheumatic heart disease

There is a formation of new defects of the valvular endocardium in the form of combined and combined heart defects.

Diagnostic criteria for rheumatism according to Kisel-Jones (modified by the American Rheumatological Association, 1982). There are major and minor criteria for the course of the disease.

Major criteria include: carditis, polyarthritis, chorea, erythema annulare, subcutaneous rheumatic nodules. Minor criteria include: previous rheumatism, arthralgia, fever, elevated ESR, increased C-reactive protein, leukocytosis, prolongation of the PQ interval on the ECG, increased titer of antistreptococcal antibodies in the blood, detection of streptococcal antigen.

In the presence of two major and one or two minor criteria, the diagnosis is considered reliable, in the presence of one major and two minor - probable.

Additional diagnostic study. Of the laboratory parameters, the study of a complete blood count (hypochromic anemia, leukocytosis with a shift to the left, an increase in ESR), a biochemical blood test (the appearance of C-reactive protein, an increase in fibrinogen, dysproteinemia, α₂ hyperglobulinemia, increased content of haptoglobin, ceruloplasmin, acid phosphatase).

An immunological study should be carried out to determine the increase in the titer of antibodies ASH, ASL-O, ASA, myocardial antibodies.

Of the instrumental research methods, an ECG is taken (determination of various arrhythmias, conduction), Doppler echocardiography.

X-ray examination is informative in severe process, when there is an increase in the left heart. At the first attack, changes in the heart are not detected.

Differential diagnostics. Should be done with infectious myocarditis. The disease develops at the height of the infection, it is not characterized by progression, signs of valvulitis.

Of the connective tissue diseases, it is necessary to take into account periarteritis nodosa, systemic lupus erythematosus, scleroderma.

With neurocircular dystonia of the cardiac type, there are diverse complaints, there are no objective signs of the disease.

In the syndrome of primary tuberculosis, there are no radiographic symptoms of the primary complex, antistreptococcal antibodies. Mantoux and Pirquet tests are carried out, tuberculosis mycobacteria in sputum are examined.

Treatment. With active rheumatism, mandatory hospitalization is carried out up to 40-60 days or more.

An appropriate regimen is assigned: in the absence of carditis - half-bed for 7-10 days, then free; in the presence of carditis - strict bed rest for 2-3 weeks, then semi-bed and free.

From nutrition, table No. 10 is prescribed with a protein content of at least 1 g / kg, limiting salt to 6 g / day.

Mandatory early prescription of antibiotics is carried out: benzylpenicillin 1,5-4 million units per day (depending on the degree of activity) for 2 weeks. Then they switch to a prolonged form: bicillin-5, 1,5 million units every 2 weeks for 2 months. After this, antibiotic therapy is carried out every 3 weeks every month for at least 3 years in patients without a history of carditis and for at least 5 years in patients with a history of carditis. If you are allergic to penicillin, antibacterial drugs of other groups are used - macrolides, oral cephalosporins.

Glucocorticoid drugs are prescribed only for severe carditis, acute (less often subacute) course of the disease: prednisolone 20-30 mg / day for 2-3 weeks, then the dose is reduced until the drug is completely discontinued, the course of treatment is 1,5-2 months.

NSAIDs are used as monotherapy, in case of recurrent or prolonged course they are combined with quinoline drugs (delagil, plaquenil for many months).

Of the metabolic drugs, phosphalene, cocarboxylase, a polarizing mixture and antiarrhythmic drugs (for arrhythmias) are used.

With the development of circulatory failure, saluretics are used: hypothiazide, furosemide, uregit, ACE antagonists in a short course.

Flow. If the duration of the disease is up to 6 months, it is considered as acute, more than 6 months - chronic.

Forecast. determined by the condition of the heart. The absence of signs of clinical formation of defects within 6 months is a good prognostic indicator. The formation of a defect within 6 months refers to prognostically unfavorable signs.

Prevention. Primary prevention includes hardening of children from the first months of life, good nutrition, physical education and sports, improvement of living conditions, timely treatment and sanitation of foci of streptococcal infection.

Secondary prevention in patients who have had the first rheumatic attack without carditis is more effective until the age of 18, in patients with carditis with the first attack of rheumatism it is more effective until the age of 25.

In patients with valvular disease, bicillin prophylaxis can be carried out throughout life.

LECTURE No. 8. Mitral valve prolapse

Heart disease is a condition characterized by prolapse of one or both leaflets of the mitral valve into the cavity of the left atrium, which usually occurs in the second half of the ventricular systole (in the exile phase). Prolapse means "bulging".

Etiology. congenital forms noted in the syndromes of Marfan, Emre-Danlos, Holt-Oramp, atrial septal defect, Ebstein's anomaly, Fallot's tetrade.

Possible hereditary pathology of the connective tissue (inheritance by autosomal dominant type).

Acquired Forms noted in ischemic heart disease, rheumatism, neurocirculatory dystonia, hypertrophic cardiomyopathy, thyrotoxicosis, chest trauma.

Pathogenesis. During ventricular systole, blood flows not only into the aorta, but partially back into the left atrium. The amount of reverse blood flow (regurgitation) corresponds to the degree of valvular insufficiency.

Pathological anatomy. More often, prolapse of the anterior leaflet of the mitral valve is noted (44-77%), then the posterior leaflet of the mitral valve (23%) and prolapse of both leaflets of the mitral valve (33%).

Classification. In a clinical setting, mitral valve prolapse is divided into:

1) according to the severity (I - prolapse 3-6 mm, II - prolapse 6-9 mm, III - prolapse more than 9 mm);

2) according to the degree of regurgitation (semi-quantitative assessment in points (1-4));

3) downstream (mild, moderate, severe, asymptomatic (18%)).

Clinic. There are syncopal conditions with lipothymia (sensations preceding loss of consciousness, with a feeling of fear of death), palpitations, interruptions in the work of the heart, stabbing, pressing pains in the heart, shortness of breath.

Accompanying signs are: a narrow shoulder girdle, thin elongated bones, elongated fingers with increased mobility of the joints of the hands, elongated nails, hypomastia in women, unexpressed hair on the chest in men, blond hair, gray-blue eyes.

There are: weakness, fatigue, headache, stabbing pains in the region of the heart, palpitations, fluctuations in blood pressure, dizziness, fainting.

A typical systolic click and late systolic murmur are auscultated. They may not show up at rest. To determine them, it is necessary to conduct a test with exercise or nitroglycerin, since an increase in heart rate reduces the end-diastolic volume.

Rhythm and conduction disturbances may be noted: paroxysmal supraventricular and ventricular tachycardias, extrasystoles, which prevail during wakefulness;

With mitral regurgitation, the frequency of ventricular tachycardia and extrasystoles increases by 2 times, accompanied by the development of circulatory failure, first left ventricular, then total.

Additional diagnostic study. Be sure to conduct an ECG study to identify signs of impaired repolarization, ST wave depression in II, III, aVF left chest leads, T wave inversion, rhythm and conduction disturbances.

Phonocardiographic examination, Holter ECG monitoring for 24-48 hours, echocardiography (to determine signs of prolapse, regurgitation), angiography of the left heart (when deciding on surgical treatment), functional tests with physical activity or nitroglycerin to determine the degree of tolerance.

Flow. Depends on the degree of prolapse of the mitral valve. With asymptomatic and mild course, the disease proceeds for a long time, without progression, with moderate and severe course - for a long time, with progression.

Complications. The main complications include rhythm and conduction disturbances, progression of mitral insufficiency, sudden death (ventricular fibrillation), infective endocarditis, and thromboembolism.

Differential diagnostics. Should be carried out with anomalies in the development of the mitral valve, additional leaflets (up to 3-4), additional chord.

Treatment. With an asymptomatic course and the detection of mitral valve prolapse on echocardiography, it is necessary to conduct periodic examinations every 2-3 years.

β-blockers are used in medium dosage. Antibiotic therapy is used during minor and major surgical interventions to prevent infective endocarditis. Antiarrhythmic drugs Ia (quinidine, novocainamide) are used for supraventricular arrhythmias and group Ib (mexiletine, toklenide) for ventricular arrhythmias. A combination of antiarrhythmic drugs with β-blockers is used. In case of intolerance to drugs, cordarone is prescribed.

Anticoagulant therapy (heparin 40-60 IU/day) is used to prevent thromboembolic complications.

With mitral regurgitation (increasing or severe degree), surgical treatment is performed - mitral valve replacement.

Forecast. With an uncomplicated course, the prognosis is favorable, with a complicated course - serious.

LECTURE No. 9. Mitral valve insufficiency

Incomplete closure of the valves during left ventricular systole as a result of damage to the valvular apparatus. It is rare in isolated form, more often in combination with stenosis of the left atrioventricular orifice.

Etiology. The causes of development may be organic lesions of the valve leaflets or chords in atherosclerosis, rheumatism (up to 75%), infective endocarditis, diffuse connective tissue diseases, less often in visceral forms of rheumatoid arthritis.

Functional lesions are possible: violation of the coordinated function of the muscular apparatus of the valve leaflets, excessive expansion of the left ventricle, annulus fibrosus and circular muscles of the atrioventricular orifice in myocarditis, cardiopathy, myocardial infarction, etc.

Pathogenesis. As a result of incomplete closure of the mitral valve leaflets, blood flows back during systole from the left ventricle to the left atrium. There is a tonogenic dilatation and left atrial hypertrophy (volume overload), an increase in the diastolic volume of the left ventricle, left ventricular hypertrophy. The left atrium loses muscle tone, it increases pressure. Passive (venous) pulmonary hypertension occurs.

The compensatory period is long due to the simultaneous flow of blood into the aorta and pulmonary artery.

Clinic. Clinically, there is an increase in the boundaries of the heart in all directions. An increase in the boundaries of the heart with a decrease in functional activity indicates a relative or muscular insufficiency of the mitral valve.

At the apex, a systolic murmur and a weakening of the I tone are heard, which are more often noted with organic mitral valve insufficiency.

At the first stage, the valve defect is compensated, no complaints are made. With the development of passive (venous) pulmonary hypertension with stagnation in the pulmonary circulation, shortness of breath, attacks of cardiac asthma appear, which ends with the formation of right ventricular failure.

Additional diagnostic study. An ECG study is performed to determine signs of left atrial and left ventricular hypertrophy.

An X-ray examination establishes an increase in the size of the heart, a mitral configuration of the heart, a deviation of the esophagus along a large radius arc, a symptom of a rocker arm.

An echocardiogram is performed to determine the closure of the mitral valve leaflets in systole, a Doppler echocardiogram is performed to determine mitral regurgitation.

Complications. These include pulmonary hypertension, left atrial dilatation.

Treatment. It can be conservative or surgical. Conservative treatment is carried out with the underlying disease and heart failure. Surgical treatment involves mitral valve replacement.

Forecast. Depends on the degree of mitral regurgitation; average life expectancy is about 40 years. With the development of heart failure, the prognosis is unfavorable.

LECTURE No. 10. Mitral stenosis

Mitral stenosis is a heart disease caused by a narrowing of the left atrioventricular orifice, which creates obstacles to the movement of blood from the left atrium to the left ventricle. Women get sick more often.

Etiology. The causes of development are organic lesions (rheumatism), congenital malformations (Lutembashe syndrome - mitral stenosis with simultaneous damage to other organs).

Pathogenesis. There is an fusion of the mitral valve cusps, tendon filaments along the free edge. The area of the mitral orifice decreases (normally 4-6 cm²). In the cavity of the left atrium, pressure rises, the pressure gradient between the left atrium and the left ventricle increases, which facilitates the passage of blood.

Hypertrophy and tonogenic dilatation of the left atrium develop, systole lengthens. The pressure in the pulmonary veins and capillaries, the pulmonary artery increases. There comes a reflex spasm of the pulmonary arterioles (Kitaev's reflex), which leads to an increase in pressure in the pulmonary artery. The load on the right ventricle increases, the emptying of the right atrium becomes difficult. There comes myogenic dilatation of the left atrium, pronounced stagnation in the pulmonary circulation, myogenic dilatation of the right ventricle, hypertrophy of the right atrium.

When the valve opening is reduced to 1,5 cm² development of noticeable hemodynamic disturbances is noted.

Compensation is short-lived, since the load falls on the left atrium and right ventricle.

Clinic. Patients with asthenic physique, are infantile, the skin is pale, cyanosis of the face (facies mitralis) is noted.

Appear: shortness of breath, weakness, palpitations, periodically coughing, sometimes hemoptysis, suffocation at night, occasionally - dysphonia and dysphagia. The borders of the heart are enlarged upward and to the right, a clapping I tone, presystolic murmur, a bifurcation of the II tone, "cat's purr", a weak, irregular pulse are heard.

Additional diagnostic study. The ECG shows P-mitrale - expansion of the P wave and splitting of its apex in I, II left chest leads, lengthening of intra-atrial conduction, left atrial hypertrophy, signs of right ventricular hypertrophy.

X-ray examination establishes an increase in the left atrium, right ventricle, bulging of the left atrial appendage, venous congestion in the lungs and arterial hypertension.

With FCG at the apex, there are: an increase in the amplitude of the I tone (Q interval - I tone less than 0,07 s), mitral valve opening tone (QS) (II tone interval - QS less than 0,12 s), presystolic and mesodiastolic murmurs, an increase in amplitude II tone and its splitting on the pulmonary artery.

An echocardiographic study shows fibrosis of the mitral valve cusps, their unidirectional movement, an increase in the cavity of the left atrium and right ventricle.

When deciding on surgical treatment, angiography is performed.

Complications. These include congestion in the pulmonary circulation, hemoptysis, cardiac asthma, high pulmonary hypertension, pulmonary aneurysm, dilatation of the heart cavities, atrial fibrillation and flutter, thromboembolism, a spherical thrombus in the left atrium, symptoms of compression (recurrent nerve, subclavian artery).

Treatment. Operative is more often performed: mitral commissurotomy. Symptomatic therapy is carried out with circulatory failure and an active rheumatic process.

Forecast. Depends on the stage and complications; on average, 7 years after the appearance of the clinic, patients become disabled, and die over the next 3 years; most die at age 40. With timely commissurotomy and subsequent active antirheumatic therapy, the prognosis is favorable.

LECTURE No. 11. Aortic valve insufficiency

Aortic valve insufficiency is the incomplete closure of the semilunar cusps of the aortic valve, which leads to a backflow of blood from the aorta into the left ventricle during its diastole (aortic regurgitation). Men are more often ill.

Etiology. In the development of the disease, rheumatism, atherosclerosis, infective endocarditis, syphilitic mesaortitis, congenital anomalies, diffuse connective tissue diseases, and injuries are important.

Pathogenesis. As a result of incomplete closure of the aortic valve cusps in diastole, blood flows back from the aorta into the cavity of the left ventricle. There comes a volumetric diastolic overload of the left ventricle, its hypertrophy.

The ejection of blood into the aorta increases. An increase in systolic blood pressure leads to a decrease in diastolic blood pressure. The contractility of the myocardium gradually weakens, myogenic dilatation, decompensation of the left ventricular type occurs.

Valvular (due to the destruction or wrinkling of the valves) and relative (with significant dilatation of the left ventricle with the expansion of the aortic opening) insufficiency of the aortic valve are formed.

Long-term compensation due to the left ventricle.

Clinic. There are no clinical manifestations in the compensation stage. In the stage of circulatory insufficiency, pulsation of large arteries, "carotid dance", Musset's symptom, positive capillary pulse, pulsation of pupils, dizziness, fainting, pain in the heart area are noted.

There is a pronounced cyanosis, an increase in the boundaries of the heart to the left. In the II intercostal space on the left, a diastolic murmur is heard, an enlarged, painful liver is palpated.

Shortness of breath and suffocation occur in the stage of decompensation.

Additional diagnostic study. An ECG examination reveals a shift in the ST interval, the appearance of biphasic or negative T waves (dystrophic changes in the myocardium).

X-ray examination establishes the aortic configuration of the heart, bulging of the IV arch, aortic expansion throughout, its pulsation, "dancing heart", with a free retrocardial space in the I oblique projection, the contrasted esophagus does not deviate.

FCG study at the Botkin point and in the II intercostal space on the right reveals a high-frequency, low-amplitude decreasing noise immediately after the II tone, a decrease in the amplitude of the I tone above the apex and the II tone above the aorta.

Doppler echocardiography determines the change in blood flow velocity.

An echocardiographic study establishes the presence of dilatation, increased mobility of the walls of the left ventricle (volume load), premature closure of the mitral leaflets, diastolic flutter of the mitral leaflets, flutter of the aortic valves, and the absence of their closure in diastole.

Complications. Possible development of heart failure.

Treatment. Conservative treatment involves the treatment of the underlying disease. Cardiac glycosides are used, which are prescribed with caution due to a slowing of the heart rate and an increase in cardiac output (may increase regurgitation), vasodilators for depositing blood in the vascular system and reducing regurgitation (apressin in combination with nitrosorbide).

During surgical treatment, aortic valve replacement is performed.

Flow. In the stage of compensation, the course is long, in the stage of decompensation it is rapidly progressing.

Forecast. The average life expectancy is 20-30 years. With timely treatment, the prognosis is relatively favorable.

LECTURE No. 12. Aortic stenosis

Aortic stenosis is a heart defect caused by narrowing of the aortic orifice, in which blood flows with difficulty from the left ventricle to the aorta. It is rare in isolated form, more often in combination with aortic valve insufficiency. Most often men are ill.

Etiology. In the development of the disease, valvular narrowing of the aorta is important in rheumatism, atherosclerosis, infective endocarditis, gummous syphilis, congenital narrowing of the aortic orifice, or subvalvular (subaortic) narrowing in hypertrophy of the interventricular septum.

Pathogenesis. As a result of the narrowing of the aortic orifice, the systole time of the left ventricle is prolonged. There is an increase in the pressure gradient between the left ventricle and the aorta (more than 40 mm Hg) and left ventricular hypertrophy.

Compensation is long due to the flow of blood into the aorta.

Clinic. There are no clinical manifestations in the compensation stage. With physical exertion, emotional stress, pain in the region of the heart (like angina pectoris), shortness of breath, dizziness, a tendency to faint, headache may appear, which refers to manifestations of the ischemic type.

The skin is pale, the apical impulse is reinforced diffuse, shifted to the left and down, on the handle of the sternum on the right in the II intercostal space and in the jugular fossa, systolic trembling ("cat's purr") is noted.

With a decrease in the contractile function of the left ventricle, attacks of cardiac asthma may occur, which is characteristic of the congestive type.

Additional diagnostic study. An ECG study shows a levogram, signs of overstrain of the left ventricle, there may be a negative T wave, blockade of the left branches of the His bundle.

An x-ray examination determines the aortic configuration of the heart, a rounded apex, narrowing of the retrocardial space due to a hypertrophied and moderately dilated left ventricle.

Echocardiography revealed fibrosis of the valvular leaflets, a decrease in their amplitude of systolic origin.

FCG-study over the aorta is determined diamond-shaped systolic murmur, which is not adjacent to the I tone.

Doppler echocardiography reveals changes in blood flow velocity.

Complications. It is possible to develop left ventricular heart failure, pulmonary edema, as well as conduction disorders (blockade of the left leg of the His bundle, complete AV blockade), coronary insufficiency with angina attacks, myocardial infarction, total heart failure is possible.

Treatment. Conservative treatment consists in the treatment of the underlying disease, angina pectoris (nitrates, calcium channel blockers), heart failure. Surgical treatment consists of aortic commissurotomy, aortic valve replacement.

Forecast. With compensated conditions, the prognosis is favorable, the average life expectancy is 40 years. In decompensated states, the prognosis is serious.

LECTURE No. 13. Tricuspid valve insufficiency

Valve insufficiency - incomplete closure of the valve leaflets, as a result of which part of the blood during systole enters the right atrium from the right ventricle. Relative insufficiency of the tricuspid valve occurs 3 times more often than organic.

Etiology. In the development of the disease are important: organic failure (rheumatism, infective endocarditis) and relative insufficiency with severe dilatation of the right ventricle (mitral stenosis, pulmonary hypertension, cardiosclerosis, pneumosclerosis).

Pathogenesis. During the contraction of the right ventricle, part of the blood returns to the right atrium, which simultaneously receives the usual amount of blood from the vena cava. There is a dilatation of the right atrium with excessive blood flow in diastole to the right ventricle, dilatation and hypertrophy of the right ventricle.).

Decompensation of venous congestion in the systemic circulation develops early.

Clinic. Clinical manifestations of signs of insufficiency of the right side of the heart are characterized by moderate shortness of breath during physical exertion, which does not sharply limit activity (as with mitral stenosis), there is no difficulty in breathing in the supine position. There are: weakness, palpitations, vague pain in the heart, heaviness in the right hypochondrium, dyspeptic disorders, drowsiness, edema.

Expressed cyanosis of the skin and visible mucous membranes (sometimes with an icteric tinge), swelling and pulsation of the jugular veins (positive venous pulse), right ventricular heart beat, epigastric pulsation, pulsation of the liver, anasarca, ascites.

The borders of the heart are enlarged only to the right. Systolic murmur, better heard at the right border of the heart, increases with inspiration, there is no emphasis on the pulmonary artery, arterial pressure is reduced, venous pressure is increased.

Additional diagnostic study. An ECG study shows a rightogram, a negative T wave in II, III standard leads, right chest leads, signs of right atrial hypertrophy, atrial fibrillation, incomplete blockade of the right bundle branch block.

X-ray examination establishes a significant increase in the right ventricle and right atrium, there are no changes in the pulmonary pattern.

In the FCG study in the 5th intercostal space on the right and left of the sternum, immediately after the first tone, a systolic murmur is determined, occupying the entire systole; at the height of forced inspiration with breath holding, its severity increases.

EchoCG study reveals an increase in the amplitude of the opening of the anterior leaflet, dilatation of the cavity of the right ventricle, hyperkinesia of its walls.

Differential diagnostics. Should be done with chronic compressive pericarditis.

Treatment. Used conservative treatment and preventive treatment of congestive circulatory failure.

Forecast. With congestive circulatory failure, the prognosis is poor.

LECTURE No. 14. Atherosclerosis

Atherosclerosis is a disease of the body, the pathomorphological substrate of which is the accumulation of lipids in the inner and middle membranes of large and medium-sized arteries, followed by the deposition of calcium salts and the development of scar connective tissue. Represents one of the most common diseases among the population of developed countries. There are over 30 risk factors for the disease.

Etiology and pathogenesis. Violation of lipid metabolism leads to a change in the metabolism and permeability of the vascular wall. On the surface of the vascular wall, the formation of atherosclerotic plaques, their ulceration, the formation of thrombotic masses on the ulcerated surfaces occurs. Subsequently, the masses formed on the plaques come off, clogging the vessels of small and medium caliber. In the plaques themselves, secondary deposition of calcium salts occurs.

The main types of dyslipoproteinemia (according to G.F. Fredrikson):

1) type 1: increased chylomicron fraction, no risk of atherosclerosis, very rare (1: 1 people);

2) type 2a: increased LDL fraction, high risk of atherosclerosis; hypercholesterolemia can be familial (heterozygous or homozygous high cholesterol) and non-familial (moderate); occurs very often;

3) type 2b: increased fractions of LDL, VLDL (very low density), the risk of atherosclerosis is very high; occurs very often;

4) type 3: increased fractions of DILI (intermediate density), the risk of atherosclerosis is high, the prevalence is 1: 1000-5000 people;

5) type 4: VLDL fraction is increased, the risk of atherosclerosis is moderate, it occurs very often; combined with hypertension;

6) type 5: increased fractions of VLDL and chylomicrons, the risk of atherosclerosis is moderate, very rare.

Clinic. In type 1, eruptive xanthomas, retinal lipid infiltration, recurrent pancreatitis, and hepatosplenomegaly are noted.

In type 2a, there are: lipoid corneal arch, tuberculate and tendon xanthomas, xanthelasmas.

In type 2b, there are: lipoid corneal arch, xanthelasma, hyperuricemia, impaired glucose tolerance.

Type 3 has palmar xanthomas, tuberculate xanthomas.

Type 4 has recurrent pancreatitis.

Type 5 has xanthomas, dyspnea, and hepatosplenomegaly.

Preclinical period characterized by the appearance of complaints of vague pain from the heart, headaches, decreased performance.

Clinical period characterized by the development of severe atherosclerosis of various localizations.

With atherosclerosis of the aorta, systolic murmur is noted along its course. If the ascending aorta or arch is affected, symptomatic hypertension may occur with an increase in systolic pressure with normal or reduced diastolic pressure.

With atherosclerosis of the coronary vessels, clinical manifestations of coronary heart disease are possible.

With atherosclerosis of the cerebral vessels, memory impairment, dizziness, headache develop, in severe cases - a picture of a stroke, cerebral hemorrhage, psychosis.

With atherosclerosis of the renal arteries, there is more often stable arterial hypertension with high numbers.

With atherosclerosis of the arteries of the abdominal cavity, pain, dysfunction of the gastrointestinal tract are noted.

With atherosclerosis of the arteries of the lower extremities, signs of intermittent claudication are determined.

Additional diagnostic study. To determine the type of dyslipoproteinemia, a biochemical study is carried out on the levels of triglycerides, total cholesterol, HDL.

Protein metabolism is being studied, in which dysproteinemia, a decrease in albumin, and an increase in γ-globulin in the sclerotic stage of the disease are noted.

X-ray examination, Doppler echography, which reveals an increase in the speed of propagation of the pulse wave, and angiography, which establishes the presence of atherosclerotic occlusions, are carried out.

Differential diagnostics. It is necessary to exclude secondary dyslipoproteinemia against the background of taking medications, alcoholism, diabetes mellitus, thyroid diseases, nephrotic syndrome, obstructive jaundice.

Treatment. Effective treatment requires lifestyle changes. It is necessary to follow a diet, exercise, monitor body weight, stop smoking.

Initially, diet 1 is prescribed according to nutritional recommendations for atherosclerosis. In the presence of predisposing factors for the development of atherosclerosis, a more rigid diet is prescribed 2 - with familial hypercholesterolemia, the presence of coronary artery disease (coronary heart disease), with the ineffectiveness of the first stage diet. Antioxidants, fish oil are used.

Medical therapy includes taking anion exchange resins (cholestyramine 4 g 2 times a day, colestipol 5 g 2 times a day, may increase to 30 g per day, 1 hour before or after a meal), HMG-CoA reductase inhibitors (statins)inhibitors of cholesterol biosynthesis at a critical stage of the process (mevacor 10-40 mg/day, lovacor 10-40 mg/day, zocor, symbol 5-40 mg/day, lipostat 10-20 mg/day, lescola 20-40 mg/day , lipobaya 100-300 mcg/day, liprimar 10-40 mg/day), nicotinic acid at an initial dose of 100 mg orally 1-3 times a day with meals with a gradual increase (300 mg weekly) to 2-4 g per day, niacinamide (nicotinic acid preparation), fibric acid group drugsthat enhance the catabolism of VLDL (gemfibrozole 600 mg 2 times a day before meals, clofibrate 1 g 2 times a day), drugs with antioxidant properties (probucol - reduces LDL cholesterol - 500 mg 2 times a day with meals).

In severe hypertriglyceridemia) plasmapheresis is indicated.

Forecast. It is serious, especially with damage to the coronary vessels, cerebral vessels, kidneys.

Prevention. In primary prevention, it is necessary to use dietary regulation, limit alcohol intake, smoking, and expand physical activity.

In secondary prevention, an annual determination of the lipid profile is used: at a triglyceride level of more than 400 mg%, LDL is measured, the study is repeated after 1-8 weeks. If the data differ by 30%, the third study is also carried out after 1-8 weeks, the average results of the three measurements are calculated. With an LDL level of less than 100 mg%, an individual diet and physical activity regimen are selected. At the level of LDL more than 100 mg%, drug therapy is prescribed.

LECTURE No. 15. Ischemic heart disease

Ischemic heart disease is myocardial damage caused by a disorder of the coronary circulation, resulting from an imbalance between the coronary blood flow and the metabolic needs of the heart muscle.

Etiology. Atherosclerosis of the coronary arteries, vasospasm, disturbances in the hemostasis system (changes in platelet function, increased blood clotting activity, inhibition of fibrinolysis), an underdeveloped network of collateral circulation, hyperproduction of catecholamines are of primary importance.

Pathogenesis. With angina pectoris, there is a discrepancy between the blood supply to the myocardium and its needs, the development of ischemia. With myocardial infarction, insufficient blood supply to the myocardium occurs with the development of lesions and necrosis in it.

Classification. In clinical practice, the classification of coronary heart disease according to E. I. Chazov (1992) is used:

1) sudden death (primary cardiac arrest);

2) angina pectoris: angina pectoris, first appeared, stable (I-IV FC (functional class), progressive, spontaneous angina pectoris;

3) myocardial infarction: macrofocal (transmural), small focal;

4) postinfarction cardiosclerosis.

Clinic.

Angina pectoris

For the first time angina pectoris characterized by pain syndrome lasting less than 1 month.

With stable angina I functional class pain syndrome occurs during accelerated walking or walking with an average step of up to 1000 m (VEM (veloergometry) - 750 kgm / min.

With stable angina II functional class pain syndrome occurs when walking on flat terrain up to 500 m (VEM - 450 kgm / min).

With stable angina III functional class pain syndrome occurs when walking on flat terrain up to 150-200 m (VEM - 150-300 kgm / min).

With stable angina IV functional class there is an inability to perform any load without an attack of angina pectoris (VEM is not performed).

Progressive angina characterized by a sudden increase in the frequency and duration of seizures with the same degree of physical activity.

Spontaneous (vasospastic or Prinzmetal's variant angina) occurs at night.

With angina pectoris, pain is more often localized behind the sternum with irradiation to the left arm, shoulder blade, neck, sometimes to the left half of the jaw, has a compressive burning character, pain duration from 5-10 minutes to 25-30 minutes. The pain is relieved at rest, after taking nitroglycerin. Possible bradycardia or tachycardia, rise in blood pressure.

Myocardial infarction

The first period represents the period of precursors (prodromal). First-time angina, progressive angina, vasospastic angina may be noted. The most acute period lasts up to 2 hours. The duration of the acute period is up to 8-10 days, there are the following course options:

1) anginal (chest pain for more than 20 minutes), restlessness, cold sticky sweat, nausea, vomiting;

2) gastralgic (pain in the epigastric region);

3) asthmatic (acute left ventricular failure);

4) arrhythmic (acute rhythm disturbances);

5) cerebral (insufficiency of cerebral circulation);

6) asymptomatic (lack of clinical manifestations).

This is followed by a subacute period lasting up to 4-8 weeks. Then the postinfarction period lasting up to 2-6 months develops.

In myocardial infarction, the main syndromes are pain, arrhythmia, circulatory failure, resorption-necrotic.

The pain syndrome differs in intensity, duration (from several hours to a day or more). The pain has a pressing, compressive, cutting, tearing character, is localized more often behind the sternum, less often captures the entire anterior chest wall. The pain radiates to the left shoulder, arm, sometimes jaw, epigastric region, is not removed by nitroglycerin, sometimes by drugs. Patients are excited, experience fear of death. The skin is pale, the mucous membranes are cyanotic, bradycardia develops, more often moderate tachycardia, a short-term increase in blood pressure. Heart sounds are weakened, a proto-diastolic gallop rhythm can be heard.

Additional diagnostic study. A general blood test is mandatory: with angina pectoris it has no diagnostic significance, and with myocardial infarction, manifestations of resorption-necrotic syndrome are noted (an increase in the level of leukocytes in the peripheral blood on the first day, after 2-3 days an increase in ESR with a gradual decrease in the number of leukocytes).

The levels of transaminases specific for myocardial infarction are studied: myoglobin, creatine kinase microfraction (MB-CK mass) - early markers of myocardial damage; troponin, creatine kinase microfraction (MB-CK) - late markers of myocardial damage. With myocardial infarction, there is an increase in transaminase activity, but these indicators do not apply to specific tests. It is necessary to take into account the de Ritis coefficient (AST / ALT ratio), which increases more than 1,33 with myocardial damage.

A biochemical blood test is carried out to determine cholesterol, triglycerides.

ECG study: with angina pectoris, there is no change in the ECG during the pain-free period, with pain, a horizontal displacement of the ST interval below the isoelectric line by more than 1 mm with exertional angina and a rise in the ST segment above the isoline by more than 1 mm with rest angina. With myocardial infarction, a pathological Q wave appears with a depth of more than 1/3R and a width of more than 0,03, there is a shift in the ST interval upward from the isoline and negative T.

In angina pectoris, coronary angiography is recommended.

Stress tests are carried out to determine the functional class of angina pectoris, to resolve expert issues after myocardial infarction.

In the presence of contraindications to stress tests and the establishment of a spasm of the coronary arteries, pharmacological tests are performed.

An echocardiographic study is performed to assess the functional parameters of the heart muscle, to detect hypokinesia and akinesia of the myocardium.

Complications. Early complications include cardiogenic shock, pulmonary edema, rhythm and conduction disturbances, myocardial ruptures (cardiac tamponade), acute cardiac aneurysm, pericarditis, thromboendocarditis, clinical death (ventricular fibrillation).

Late complications are angina pectoris, heart failure, myocardial rupture, thromboembolism, arrhythmias, Dressler's syndrome (pericarditis, pleurisy, pneumonitis), arrhythmias, chronic heart aneurysm.

Treatment. With angina pectoris a pain attack is relieved by taking nitroglycerin, with a progressive form of angina pectoris, vasodilators and non-narcotic analgesics are introduced.

For the prevention of recurrent attacks, it is recommended to limit physical activity, combat hypertension, obesity, diabetes mellitus, hypercholesterolemia, and smoking.

Drug treatment includes the use of long-acting nitrates, nitrate-like agents - nitrong, sustak, sustanite, nitrosorbitol, sydnopharm, erinite. Of the calcium antagonists, cordafen, corinfar, verapamil are used. Of the β-blockers, atenolol, metaprolol (egilok), nebivolol (nebilet), etc. are used. Antiarrhythmic drugs, antispasmodics (if indicated), anabolic agents, prodectin are used.

Surgical treatment includes coronary artery bypass grafting, percutaneous transluminal angioplasty.

With myocardial infarction pain relief is carried out with narcotic analgesics, fentanyl with droperidol, anesthesia with nitrous oxide, epidural anesthesia.

With the duration of the pain syndrome up to 6 hours, thrombolytic and anticoagulant therapy is carried out. It is possible to introduce streptase, streptodecase, heparin, indirect anticoagulants.

Nitrates, β-blockers are used to prevent an increase in the necrosis zone.

In the subacute period, long-acting nitrates, indirect anticoagulants are used to strengthen the coronary circulation.

With the development of complications, their appropriate treatment is carried out.

Flow. With angina pectoris, the course is undulating, depending on the degree and progression of atherosclerosis of the coronary arteries. In myocardial infarction, the course can be uncomplicated, complicated, protracted and recurrent.

Forecast. With angina pectoris, the prognosis depends on the severity of atherosclerosis of the coronary arteries, on the frequency of angina attacks. With myocardial infarction in the absence of complications, the prognosis is favorable, and with complications - serious.

Prevention. Primary prevention includes the following activities: identification of risk factors, rational organization of the regime of work and rest. Secondary prevention includes dispensary observation of persons with unstable forms of angina pectoris, arterial hypertension.

LECTURE No. 16. Dilated (congestive) cardiomyopathy

Cardiomyopathy - diseases of the myocardium of unknown etiology, manifested by cardiomegaly and heart failure, with the exclusion of damage to the heart valves, coronary and pulmonary vessels, arterial hypertension.

Dilated (congestive) cardiomyopathy - damage to cardiomyocytes with the development of their contractile weakness, expansion of the heart cavities and progressive chronic heart failure, resistant to therapy. It is more common in men aged 35-45, but in women the disease is more severe.

Pathogenesis. A hypocirculatory hemodynamic state develops with a decrease in the stroke volume of the heart with increased filling of the heart with blood. Circulatory insufficiency develops as a result of a primary contractile defect in the heart muscle, and myocardial hypertrophy has a secondary compensatory character.

Pathological anatomy. There is a sharp expansion of all cavities of the heart without a significant increase in the thickness of the walls of the ventricles (cor bovinum). The mass of the heart is 2-3 times more than normal. The left ventricle is enlarged compared to the right. The myocardium becomes flabby, dull, areas of hypertrophy and atrophy of cardiomyocytes alternate. The valvular apparatus and coronary vessels do not change. There may be parietal thrombi in the cavities.

Clinic. Extrasystole, ventricular tachycardia appear; atrial fibrillation (an early sign), initially of a paroxysmal type, which quickly becomes permanent. There are signs of circulatory decompensation. Systolic blood pressure decreases while maintaining diastolic blood pressure.

Apical impulse of weak force, spilled; deaf I tone. Due to the increase in end-diastolic pressure, a fourth tone appears in the left ventricle, an accent of the second tone over the pulmonary artery is noted. At the apex of the heart, in the 4th intercostal space on the left side of the sternum, a prolonged systolic murmur appears as a result of mitral regurgitation of blood with the expansion of the mitral orifice or dysfunction of the papillary muscles. Auscultatory signs increase with the progression of heart failure and dilatation of the heart and weaken with improvement in the condition.

The main periods of the disease

В I period there are no asymptomatic complaints. The ejection fraction was reduced to 35%, the end diastolic size of the left ventricle was 6,5 cm.

In II period progressive myocardial damage, symptoms of chronic heart failure appear - NC stage I-II. Ejection fraction 35-25%, end-diastolic size of the left ventricle 7-7,5 cm, volume/weight index of the left ventricle not more than 1,35 mg.

В III period of developed clinical manifestations, a clinic of total heart failure appears - NC IIB-III, severe cardomegaly. Mortality is high from congestive heart failure, thromboembolic complications.

В IV period stabilization occurs complete or significant regression of edema, venous congestion with simultaneous progression of the actual signs of circulatory failure. The inotropic function of the heart and arterial perfusion of organs and tissues decrease, and a small ejection syndrome develops. Index volume / mass of the left ventricle - 1,5 ml / g, ejection fraction up to 20% or less.

В V terminal period there comes a pronounced dystrophy of all internal organs, ischemic damage to the liver, kidneys, dyscirculatory encephalopathy, weight loss due to atrophy of the skeletal muscles, recurrent thromboembolism is possible.

The main criteria for diagnosis are the presence of cardiomegaly, rhythm and conduction disturbances, progressive circulatory failure resistant to cardiotonic therapy, thromboembolic complications.

Additional diagnostic study. It is recommended to conduct a biochemical blood test to establish the presence of dysproteinemia, hypoalbuminemia in congestive heart failure.

An ECG study reveals violations of atrioventricular and intraventricular conduction, repolarization processes (ST segment depression, T wave inversion), high-grade ventricular arrhythmias, atrial fibrillation, pathological Q wave due to severe myocardial fibrosis, complete blockade of the left bundle branch block (in 10% patients); a decrease in the voltage of the R and S waves in standard leads, an increase in the chest leads.

20-hour monitoring of the ECG by Holter, echocardiography is carried out, dilatation of all cavities of the heart, mainly the left ventricle, a decrease in ejection fraction, signs of heart failure: hydropericardium, hydrothorax, increased pressure in the pulmonary artery, ascites, absence of echocardiographic signs of the disease that led to cardiac insufficiency), Doppler echocardiography (mitral and tricuspid regurgitation, intraatrial thrombi (in 25-50%), intraventricular thrombi (in XNUMX%), a significant decrease in systolic function, diastolic dysfunction), x-ray examination (increase in heart size, signs of pulmonary congestion (venous plethora, interstitial pulmonary edema), cavity effusion (hydrothorax, hydropericardium)).

Complications. Complications include a permanent form of atrial fibrillation, thromboembolism.

Differential diagnostics. It is carried out with effusion pericarditis, coronary heart disease, viral myocarditis, alcoholic myocardial dystrophy, rheumatic heart disease, hypertension.

Treatment. In the presence of atrial fibrillation of the tachysystolic form, symptoms of left ventricular failure, cardiac glycosides (digoxin) are used in the treatment.

β-blockers are prescribed after stabilization of the condition with cardiac glycosides and diuretics.

Potassium-sparing diuretics are used (triamterene, veroshpiron, indapamide. If they are used excessively, hypokalemia, a decrease in BCC (circulating blood volume), and a decrease in blood flow to the heart are possible.

ACE inhibitors have a beneficial effect on pre- and afterload with subsequent improvement in hemodynamics.

Additional treatments include peripheral vasodilators. Nitrosorbide reduces preload, lowers the end diastolic pressure in the cavity of the left ventricle, reduces its size.

Antiarrhythmic therapy is also used - cordarone, anticoagulant therapy, blood ultrafiltration to reduce stagnation.

Of the surgical methods of treatment with the ineffectiveness of conservative therapy, implantation of a cardioverter-defibrillator and heart transplantation (with low ejection syndrome and in the period of stabilization) are used.

Flow. The course can be with rapid progression (1-1,5 years), with slow progression or recurrent.

Forecast. Unfavorable, mortality within 5 years is 50%.

LECTURE № 17. Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy - hypertrophy of the walls of the left ventricle (occasionally right) without expansion of the cavity, with increased systolic function and impaired diastolic function. Hypertrophy is more often asymmetric with a predominance of thickening of the interventricular septum, not associated with increased work of the heart. Men get sick 2 times more often.

Pathogenesis. Asymmetric septal hypertrophy leads to dynamic, then fixed obstruction of the outflow tract from the left ventricle. The ability of the myocardium to relax is reduced. The diastolic function of the left ventricle worsens due to calcium overload of the cytoplasm of cardiomyocytes and a decrease in the elastic properties of the myocardium against the background of hypertrophy and cardiosclerosis. Coronary blood flow decreases due to a decrease in the lumen of the intramural arteries against the background of intima proliferation, a decrease in the density of blood vessels per unit volume of a cardiomyocyte, and the lack of complete relaxation during diastole.

Pathological anatomy. There are 4 types of hypertrophic cardiomyopathy: predominant hypertrophy of the upper sections of the interventricular septum, isolated hypertrophy of the interventricular septum throughout, concentric hypertrophy of the left ventricle, hypertrophy of the apex of the heart.

The main hemodynamic options are:

1) obstructive;

2) with permanent obstruction of the outflow tract of the left ventricle (at rest);

3) with latent obstruction (no pressure gradient at rest), obstruction occurs with increased myocardial contractions, a decrease in blood flow to the heart, a decrease in afterload (lowering blood pressure, peripheral resistance);

4) non-obstructive (no pressure gradient).

Clinic. Clinically noted are shortness of breath, aggravated by physical exertion, pain in the region of the heart, muscle weakness, dizziness, fainting, palpitations, attacks of loss of consciousness. The disease can be asymptomatic or vegetative-dystonic. There are no changes in skin color and cyanosis. Pulse of weak systolic filling. Arterial pressure is prone to hypotension, pulse amplitude remains normal or decreases.

The apex beat has a biphasic character, the second wave occurs after overcoming the obstruction. A pre-systolic impulse is possible, coinciding in time with the systole of the left atrium and the sound of the IV tone; a push is possible in the early phase of diastole at the moment of rapid filling of the left ventricle and sounding of the III tone. Double, triple, quarter apex beats represent a symptom pathognomonic for obstructive hypertrophic cardiomyopathy.

During auscultation at the apex and at the Botkin point, a systolic murmur of great variability is heard.

In the non-obstructive form, a secondary origin of cardiomyopathy is possible, since over the years the tendency to cardiac arrhythmias increases, which can be complicated by circulatory decompensation.

Additional diagnostic study. The most diagnostically significant is the ECG study. This study reveals signs of left ventricular hypertrophy; the appearance of atypical Q waves is possible - deep, narrow in leads II, III, aVF, V4, V5; in the inferolateral chest leads, deep Q waves are followed by low R waves and upright T waves; Q waves reflect a sharp thickening of the interventricular septum; possible signs of WPW syndrome, repolarization disorders, ST segment depression, T wave inversion.

To detect ventricular tachycardia, atrial fibrillation, daily Holter ECG monitoring is performed.

Echocardiography reveals changes in the thickness of the interventricular septum, which can reach 1,7-2 cm or more. Hypokinesia or akinesia (due to fibrosis), a decrease in the cavity of the left ventricle (in systole the cavities are in contact), hypertrophy of the basal sections of the interventricular septum are also detected; mitral valve calcification.

Complications. The main types of complications are ventricular fibrillation (risk of sudden death), hemodynamic collapse (during exercise), cardiac asthma, pulmonary edema.

Differential diagnostics. Should be performed with mitral valve prolapse, coronary heart disease, hyperkinetic syndrome, mitral insufficiency, isolated aortic stenosis, congestive cardiomyopathy.

Treatment. β-blockers are prescribed in high doses, which increase the filling of the left ventricle, reduce the pressure gradient and have an antiarrhythmic effect.

Calcium channel blockers are used. Verapamil has a negative inotropic effect on the myocardium, is prescribed 40-80 mg 3-4 times a day. Long-term treatment with this drug can lead to inhibition of automatism, deterioration of atrioventricular nodal conduction, and excessive negative inotropic action. You can not prescribe the drug with a large filling of the left ventricle, with orthopnea, nocturnal paroxysmal dyspnea.

Nifedipine is inappropriate, as it increases the pressure gradient due to a pronounced vasodilating effect (syncope).

Antiarrhythmic drugs are used. Cordarone is prescribed for ventricular arrhythmias: in the first week, 600-800 mg / day, then 150-400 mg daily with a two-day break every week. The effect of the drug occurs after 1-2 weeks and persists for several months after withdrawal. Disopyramide is indicated for supraventricular and ventricular tachycardia.

Physical activity is limited, alcoholic beverages are excluded, and timely antibiotic therapy is carried out for infections.

Cardiotonic agents, diuretics, nitrates, vasodilators are contraindicated in the treatment.

Of the surgical methods of treatment, excision of a part of the interventricular septum and mitral valve replacement are used.

Flow. Relatively favorable, the disease progresses slowly.

Forecast. Severe, annual mortality with obstructive form is about 1,5%, due to congestive insufficiency 0,2%.

LECTURE № 18. Restrictive cardiomyopathy

Restrictive cardiomyopathy is a decrease in myocardial extensibility with limited filling of the left ventricle, a decrease in stroke volume and the development of heart failure. The group with these symptoms includes diseases with obliteration of the cavities of the ventricles, phenomena of atrioventricular regurgitation, parietal thrombosis. The disease is extremely rare, often considered as a complication of endomyocardial (eosinophilic) disease (Leffler's fibroplastic myocarditis) and endocardial fibrosis, fibroelastosis.

Pathological anatomy. The endocardium is primarily affected (except for endomyocardial fibrosis), and the myocardium is involved in later periods of the disease. Connective tissue develops, obliteration of the cavities of the ventricles and the development of parietal thrombosis occur, the proliferation of endothelial cells leads to occlusion of small vessels of the myocardium.

Clinic. Clinical manifestations are characterized by the appearance of complaints of shortness of breath, especially with physical exertion, chest pain, weight loss. In the initial periods, the boundaries of the heart are not changed, in the future there is an increase in the left or right ventricles (where fibrosis predominates), in the later periods there is an increase in toto. At the beginning, the tones are rhythmic, the third tone is heard, above the apex there is a systolic murmur. Symptoms of heart failure increase gradually.

Additional diagnostic study. An ECG study determines changes characteristic of diffuse myocardial damage. X-ray examination reveals dilatation of the heart cavities, venous congestion in the lungs. Echocardiography reveals early rapid filling of the ventricles.

A study of hemodynamic parameters is carried out, which establishes an increase in filling pressure in both ventricles, an increase in end-diastolic pressure in the left ventricle, and pressure in the pulmonary artery.

When ventriculography is determined by increased contraction of the ventricles, smooth contours of the walls, a possible filling defect in the apex during obliteration.

In life, the diagnosis can only be established by endomyocardial biopsy.

Complications. Complications include circulatory failure, thromboembolism, rhythm disturbances (less often than with hypertrophic cardiomyopathy).

Differential diagnostics. Should be performed with amyloidosis, hemochromatosis, sarcoidosis, scleroderma, Abramov-Fiedler idiopathic myocarditis (diagnosis is difficult even with autopsy).

Treatment. In the early stages of the disease in the presence of eosinophilia, corticosteroids are used. Diuretics, vasodilators, anticoagulants (for the prevention of thromboembolism), calcium antagonists are used: they affect the diastolic function of the left ventricle.

Surgical treatment is possible at the stage of fibrosis to remove the altered endocardium, prosthetics of the mitral and tricuspid valves.

Flow. The course of the disease is slowly progressive.

Forecast. With damage to the left ventricle - relatively favorable, with involvement in the process of the valvular apparatus - doubtful.

LECTURE No. 19. Arrhythmias due to impaired impulse formation

1. Sinus tachycardia

Sinus tachycardia - an increase in cardiac activity at rest more than 90 beats per minute with the correct rhythm.

Etiology. It occurs due to an increase in the tone of the sympathetic nervous system (physical activity, fever, intoxication, infections, etc.).

Tachycardias are physiological (with physical exertion, emotions, fear, getting up quickly) and neurogenic (with neuroses).

Tachycardia can be observed in diseases of the cardiovascular system, with drug and toxic effects, with acute and chronic infections and anemia.

Clinic. Complaints are determined by the underlying disease. i tone is enhanced, ii tone is more often weakened, pendulum rhythm and embryocardia are possible.

On the ECG, the heart rate is more than 90 beats per minute, the duration of the RR interval is less than 0,60 s, the rhythm is correct.

Treatment. The intake of tea, coffee, alcohol, spicy food is limited. In the functional form, psychotropic and sedatives, tranquilizers, antipsychotics (meprobamate, diazepam), according to indications, β-blockers (atenolol, egilok in doses that do not reduce the number of heartbeats below 60 beats per minute) are used. In the cardiac form with heart failure, cardiac glycosides and saluretics are used; treatment of the underlying disease.

2. Sinus bradycardia

Sinus bradycardia is a decrease in heart rate below 60, but not less than 40 per minute.

Etiology. The reasons are: an increase in the tone of the vagus nerve, a decrease in the tone of the sympathetic nerve, a direct effect on the cells of the sinus node (hypoxemia, infection).

Bradycardias are functional (vagal) and organic (such as the defeat of the sinus node).

Clinic. The clinic is manifested by palpitations, fainting.

On the ECG, the RR interval is more than 1 s, the rhythm is sinus.

Treatment. With functional bradycardia, treatment is not carried out. With organic bradycardia with a heart rate of less than 40 beats per minute and a tendency to faint, atropine is administered 0,5-1,0 mg intravenously every 3 hours (up to 2 mg) or 0,5-1,0 mg 3-4 times inside, isadrin 1,0-2,0 mg in 500 ml of a 5% glucose solution intravenously, alupent 5-10 mg in 500 ml of physiological saline intravenously or orally, 20 mg 4-8 times a day.

3. Sinus arrhythmia

Sinus arrhythmia - alternating periods of increased and slower heart rate due to uneven generation of an impulse in the sinus node.

Etiology. The reasons are fluctuations in the tone of the vagus during breathing, organic pathology of the heart (CHD, rheumatic heart disease, myocarditis, digitalis intoxication).

Clinic. Arrhythmias are respiratory (physiological) and actually sinus arrhythmias.

On the ECG, there is an irregular sinus rhythm with a difference between the longest and shortest RR intervals of 0,16 s or more.

Treatment. Treatment consists in the treatment of the underlying disease.

4. Sick sinus syndrome

Sick sinus syndrome - paroxysms of supraventricular tachycardia (or atrial fibrillation) followed by a long period of severe sinus bradycardia. Described by B. Lown in 1965.

Etiology. The causes are organic heart damage (acute period of myocardial infarction, atherosclerosis, myocarditis, cardiopathy, digitalis intoxication, antiarrhythmic drugs).

Clinic. Possible sinus bradyarrhythmias, loss of individual sinus complexes with prolonged asystole and subsequent restoration of the rhythm by sinus complexes or due to impulses from the underlying sections (popping complexes).

Depending on the duration of the periods of asystole, there may be dizziness, fainting, Morgagni-Adams-Stokes seizures.

Treatment. With mild bradycardia and passive heterotopic arrhythmias, treatment is not carried out. With attacks of tachyarrhythmias and paroxysmal tachycardia, antiarrhythmic drugs are indicated: aymalin 50 mg intravenously or intramuscularly, novocainamide intravenously or intramuscularly 5 ml of a 10% solution, isoptin intravenously 5-10 mg, inderal (obzidan) 5 mg intravenously carefully, strophanthin 0,5 ml of 0,05% solution intravenously per 20 ml of glucose or isotonic solution. With repeated attacks of asystole, electrical stimulation of the heart is performed.

5. Rhythm of the atrioventricular connection

The rhythm of the atrioventricular connection is the rhythm in which the area of transition of the atrioventricular node into the bundle of His or the trunk of the bundle of His before it branches into branches becomes the pacemaker.

Etiology. The causes are vagotonia (with a healthy heart), medicinal effects and metabolic disorders (digitis intoxication, quinidine, morphine, hyperkalemia, acidosis, hypoxia), organic heart disease (IHD, hypertension, heart defects, myocarditis, rheumatic heart disease, shock).

Clinic. Clinical manifestations are characterized by bradycardia with the correct rhythm of 40-60 beats per minute, enhanced tone I, increased pulsation of the jugular veins.

On the ECG, there is a negative P wave, an unchanged QRST complex.

Treatment. The underlying disease is being treated. Atropine, isadrin, alupent are used. Antiarrhythmic drugs are contraindicated. With hyperkalemia and acidosis, drip administration of sodium bicarbonate and glucose with insulin is carried out. With complete atrioventricular blockade, an artificial pacemaker is implanted.

6. Idioventricular rhythm

Idioventricular rhythm - the pacemaker of the heart becomes the center of the third order with a rare rate of contraction - 20-30 beats per minute.

Etiology. The reason is severe myocardial damage.

On the ECG - altered QRST complexes (as in ventricular extrasystole), negative P waves (coincide with the ventricular complex).

Treatment. The underlying disease is being treated.

7. Extrasystoles

Extrasystoles - contraction of the whole heart or any of its departments under the influence of a premature impulse from the cells of the conduction system of the atria and ventricles.

Etiology. Causes: re-entry of the sinus impulse (local blockade), increased automatism outside the sinus node.

Extrasystoles are of functional genesis (extracardial), organic genesis (for example, ischemic heart disease, heart defects, myocardial damage), toxic genesis (digitis intoxication, adrenaline, nicotine, caffeine, ether, carbon monoxide, etc.), mechanical genesis (catheterization, operations on heart).

Classification. Classification of ventricular extrasystoles (according to Laun).

I degree - single rare monotopic extrasystoles no more than 60 in 1 hour.

II degree - frequent monotopic extrasystoles more than 5 in 1 min.

III degree - frequent polytopic polymorphic extrasystoles.

IV degree - A-group (paired), B-3 and more in a row.

V degree - early extrasystoles of type P to T.

Treatment. It consists in the treatment of the underlying disease. A diet, regimen, hydrotherapy should be used. Sedative drugs, antiarrhythmic treatment (if necessary) are prescribed. With the threat of ventricular fibrillation, lidocaine or novocainamide is indicated intravenously.

8. Paroxysmal tachycardia

Paroxysmal tachycardia is a sudden increase in heart rate as a result of impulses emanating from a focus located outside the sinus node.

Etiology. The causes are strong emotions, nervous tension, overwork, excessive consumption of nicotine, coffee, tea, alcohol, thyrotoxicosis, reflex influences (in diseases of the gastrointestinal tract), WPW and CLC syndrome, myocardial diseases (ischemic heart disease, myocarditis), hypertension , mitral stenosis, digitalis intoxication, hypokalemia.

Treatment. Supraventricular paroxysmal tachycardia is stopped by massage of the carotid sinus zone, using the Valsalva test (pressure on the eyeballs). Inside, 40 mg of propranolol is prescribed, slow intravenous administration of 2-4 ml of a 0,25% solution of isoptin, in the absence of hypotension, 5-10 ml of a 10% solution of novocainamide (preferably with preliminary administration of mezaton or norepinephrine), slow administration of 0,25 -0,5 ml of a 0,05% solution of strophanthin, in the absence of effect - defibrillation.

Relief of an attack of ventricular paroxysmal tachycardia is carried out using electrical impulse therapy, intravenous injection of lidocaine, 5,0-20,0 ml of a 1% solution, then drip at a dose of 500 mg in 500 ml of a 5% glucose solution 3-4 times a day. 1st and 2nd days after rhythm recovery. In non-severe conditions, novocainamide is administered orally 0,75 g and then 0,25 g every 3 hours or intravenously drip 5,0-10,0 ml of a 10% solution in saline or 5% glucose solution (with a decrease in blood pressure in combination with norepinephrine drip). Aymalin, β-blockers; cardiac glycosides are contraindicated.

9. Atrial fibrillation (atrial fibrillation)

Atrial fibrillation (atrial fibrillation) - complete loss of atrial systoles. Up to 350-600 pulses circulate in the myocardium. The rhythm of ventricular contractions is wrong.

Etiology. The causes are organic myocardial damage (IHD, acute myocardial infarction, mitral defects, cardiopathy, myocarditis), thyrotoxicosis.

Pathogenesis. The mechanism of excitation re-entry is micro reentry, stopping the sinus node.

Classification. Atrial fibrillation is paroxysmal, permanent form: tachysystolic (more than 90 beats per minute), normosystolic (60-90 beats per minute), bradysystolic (less than 60 beats per minute).

Clinic. There is general weakness, palpitations, shortness of breath. Auscultation determines the arrhythmia of tones, changes in the volume of tones; pulse deficit. There are no P waves on the ECG, ventricular complexes are irregular, the isoelectric line is wavy.

Complications. Thromboembolism may develop.

Treatment. To stop the attack, sedatives are used, propranolol inside; while maintaining the attack - 4-8 g of potassium chloride diluted in water, intravenous administration of 5,0-10,0 ml of a 10% solution of novocainamide.

In the presence of heart failure in elderly patients, strophanthin is used.

In persistent cases of atrial fibrillation, quinidine and electrical impulse therapy are used.

To prevent seizures, quinidine (0,2 g 2-4 times a day) with propranolol (10-40 mg 2-3 times a day) or delagil with propranolol are used.

With a constant form of atrial fibrillation, cardiac glycosides are prescribed, possibly in combination with β-blockers.

Defibrillation is performed with a recent (up to a year) atrial fibrillation. Contraindications to defibrillation are prolonged arrhythmias, a history of paroxysm, an active inflammatory process, cardiomegaly, severe circulatory failure, and a history of thromboembolism.

10. Atrial flutter

Atrial flutter - rapid, superficial, but the correct rhythm of atrial contraction with a frequency of 200-400 per minute, resulting from the presence of a pathological focus of excitation in the atria. The frequency of contractions of the ventricles is much less.

Etiology. The causes are organic heart disease (valvular disease, coronary artery disease, thyrotoxicosis, rheumatic heart disease, myocarditis, intoxication).

Clinic.

Forms: paroxysmal, constant.

On the ECG, atrial waves in the form of saw teeth.

Treatment. It is carried out similarly to the treatment of atrial fibrillation (atrial fibrillation).

11. Ventricular fibrillation (ventricular fibrillation)

Ventricular fibrillation (ventricular fibrillation) - uncoordinated, asynchronous contractions of individual muscle fibers of the ventricles.

Etiology. The causes are organic heart disease (IHD, acute myocardial infarction, primary circulatory arrest, aortic stenosis, myocarditis), heart failure, postoperative period, hypothermia, WPW syndrome, intoxication, electrical injury.

Pathogenesis. Weak, erratic contractions of the muscle fibers of the ventricles are noted, the aortic semilunar valves do not open. The stroke volume of the heart drops to zero, blood flow to the organs stops. Death occurs within 4-8 minutes.

Clinic. Clinical manifestations are characterized by loss of consciousness, pallor, cold sweat. Arterial pressure drops to zero, heart sounds are not heard, there is no breathing, the pupils are dilated.

On the ECG - large- or small-amplitude random waves follow without intervals;

The onset of death. stage i - reversible state for no more than 8 minutes (clinical death), stage II - biological death.

Resuscitation measures. The patient must be laid on a hard bed, tilt his head back, fix the lower jaw and tongue, clean the oral cavity (dentures). Carrying out artificial ventilation mouth to mouth or mouth to nose and indirect heart massage in the ratio of 2 inhalations and 15 massages (1 resuscitator works) or 1 inhalation and 4 massages (2 resuscitators work).

If it is ineffective, three-time defibrillation of 200 J, 300 J, 360 J is performed. If there is no effect (small-wave fibrillation on the ECG or asystole), 1 ml of a 0,1% solution of adrenaline is injected intravenously or 2 ml endotracheally, after the introduction, defibrillation is repeated.

With successful resuscitation, intravenous administration of 80-120 mg of lidocaine is carried out under the control of acid-base balance, with acidosis - the introduction of sodium bicarbonate.

With unsuccessful resuscitation, repeated administration of adrenaline intravenously by bolus or intratracheal is indicated at the same dosage every 3-5 minutes, followed by defibrillation at 360 J.

CPR must be carried out within 40 minutes.

After resuscitation, lidocaine is administered intramuscularly for 2-3 days every 6-8 hours; over the next 8-18 months, β-blockers are prescribed.

LECTURE No. 20. Arrhythmias due to impaired conduction of impulses

Arrhythmias due to impaired conduction of impulses - conduction disturbances between the sinus node, atria and ventricles.

Etiology. The causes are organic lesions of the heart, increased tone of the cholinergic system, intoxication (digitis, β-blockers).

Conduction disturbances are in the form of:

1) sinoatrial or sinoauricular blockades;

2) violations of intra-atrial conduction;

3) atrioventricular blockades:

a) I degree - deceleration of atrioventricular conduction;

b) II A degree (Mobitz type I) - incomplete blockade;

c) II B degree (Mobitz type II) - incomplete blockade;

d) III degree (complete transverse blockade);

4) intraventricular blockades: complete blockade of the left leg of the bundle of His, complete blockade of the right leg of the bundle of His, incomplete transverse ventricular blockade, complete transverse ventricular blockade;

5) premature excitation of the ventricles (WPW, LGL, CLC syndrome);

6) parasystoles;

7) ectopic activity of centers with exit blockade.

Treatment.

With AV block I degree treatment is not required.

With AV block II-III degree proximal type, verapamil (Isoptin), potassium preparations, cardiac glycosides are used.

With complete AV blockcaused by digitalis, the drug is withdrawn. While maintaining the blockade, 0,5-1,0 ml of a 0,1% solution of atropine is injected intravenously, intramuscularly 5 ml of a 5% solution of unithiol 3-4 times a day.

With sudden onset of complete AV blockade shows the introduction of quinidine, novocainamide, aymaline, allapinin.

With moderate sinoauricular blockade while maintaining the correct rhythm of treatment is not required. In severe cases, atropine, sympathomimetics are used.

With sick sinus syndrome and manifestations of Morgagni-Adams-Stokes syndrome implantation of an artificial pacemaker is indicated.

For ventricular arrhythmias lidocaine, trimecaine, difenin are introduced. Cardiac glycosides are completely contraindicated.

With AV blockade and ventricular disorders quinidine, novocainamide, β-blockers, cordarone, allapinin are used.

WPW Syndrome (Wolff-Parkinson-White)

WPW syndrome (Wolff-Parkinson-White) - shortening of atrioventricular conduction, the appearance of a delta wave (serration) on the ascending knee of the R wave and tachyarrhythmia attacks. Described in 1930, noted in apparently healthy young people with tachycardia attacks.

Etiology. Etiological factors are a short atrioventricular node, the possible presence of two atrioventricular nodes, additional pathways for conducting impulses: Kent's bundle, Maheim's bundle, James's bundle.

Clinic. Clinical manifestations may be absent. It is often an incidental ECG finding. There may be attacks of supraventricular paroxysmal tachycardia, less often attacks of flutter or atrial fibrillation. Sudden death and heart failure are extremely rare.

The ECG shows a negative delta wave in leads II, III, aVF (must be differentiated from posterior diaphragmatic myocardial infarction).

Treatment. With frequent attacks of tachycardia, preventive treatment is carried out.

Syndrome LGL (Launa-Ganong-Levin)

Syndrome LGL (Laun-Ganong-Levin) - shortening of PQ with an unchanged QRS complex, paroxysms of supraventricular tachycardia are possible.

CLC Syndrome (Clerk-Levy-Christerko)

Syndrome CLC (Clerk-Levy-Christerko) - shortening of P-Q with an unchanged QRS complex, ventricular arrhythmias are possible.

Parasystole - the presence of two pacemakers (sinus and ectopic), functioning independently; absent on the ECG: a constant distance from the previous normal ventricular complex to the ectopic one, a constant short interectopic interval, ventricular parasystole is more often noted.

Ectopic activity of centers with exit blockade is a rare variant of parasystole, the ectopic pacemaker has a higher rate than the main one.

LECTURE No. 21. Heart failure

Heart failure is a pathological condition in which the cardiovascular system is unable to provide organs and tissues with the necessary amount of blood both at rest and during exercise.

Etiology. The main reasons for the development of insufficiency are infectious-inflammatory and toxic lesions of the myocardium, impaired blood supply to the myocardium, metabolic disorders, heart pressure overload, volume overload, heart defects such as valvular insufficiency, a combination of heart overload and myocardial damage, and heart rhythm disturbance.

Pathogenesis. In the initial period of heart failure, the functioning of cardiac and extracardiac compensation mechanisms is noted:

1) an increase in the strength of heart contractions (under the influence of the amplifying nerve of the heart);

2) an increase in the number of heart contractions (Bainbridge reflex);

3) decrease in diastolic pressure (as a result of the expansion of arterioles and capillaries);

4) increase in oxygen consumption by tissues;

5) compensation mechanisms are capable of maintaining a sufficient level of hemodynamics for a long time.

Congestive heart failure is caused by:

1) activation of the sympathoadrenal system with the development of tachycardia;

2) myocardial hypertrophy (long-term compensation mechanism);

3) tonogenic dilatation of the heart (Starling mechanism - displacement of myocardial layers relative to each other, leads to increased contractile function of the myocardium, hyperfunction and hypertrophy);

4) an increase in the volume of circulating blood (kidney function, an increase in the production of ACTH and aldosterone, an increase in the number of formed elements due to hypoxia);

5) spasm of the arteries (increased afterload) and congestion in the veins (increased preload);

6) myogenic dilatation;

7) the formation of edema (an increase in hydrostatic pressure in the veins, sodium and water retention, hypoxic capillary porosity, impaired protein synthesis);

8) dystrophic changes in the internal organs.

Table 3. Classification of chronic heart failure (New York Heart Association)

(*FK - functional class)

Clinic. Early stages of heart failure characterized by the appearance of shortness of breath during physical exertion, nocturnal dry cough, nocturia. Auscultatory listening to the gallop rhythm, IV tone.

Acute left ventricular failure (cardiac asthma, pulmonary edema) more often observed in myocardial infarction, hypertension, aortic disease, chronic coronary artery disease. An attack of cardiac asthma develops (severe shortness of breath due to stagnation of blood in the lungs, impaired gas exchange). Shortness of breath occurs more often at rest at night, there is suffocation, severe weakness, cold sweat, cough with difficult to separate mucous sputum, the patient takes a sitting position. Diffuse cyanosis is noted against the background of severe pallor of the skin, hard breathing in the lungs, unsound small and medium bubbling rales in the lower sections. The heart sounds at the apex are weakened, the II tone above the pulmonary artery is increased, the pulse is small, frequent.

With the progression of congestion, pulmonary edema develops - there is an increase in suffocation and coughing, bubbling breathing appears, abundant foamy sputum mixed with blood. In the lungs, profuse wet rales of various sizes are heard in all lung fields; gallop rhythm. The pulse is threadlike, sharply accelerated.

Acute left atrial failure develops with mitral stenosis due to a sharp weakening of the contractility of the left atrium. The clinic is similar to manifestations of acute left ventricular failure.

Acute right heart failure develops with embolism of the pulmonary artery trunk or its branches due to the drift of a blood clot from the veins of the large circle or the right parts of the heart, with pneumothorax, total pneumonia, with gas (decompression sickness) and fat embolism (with fractures of tubular bones). Appear: rapid breathing, cyanosis, cold sweat, pain in the region of the heart, the pulse is small, frequent, blood pressure drops, swelling of the cervical veins, the liver enlarges, edema appears.

Acute vascular insufficiency (fainting, collapse, shock) develops with a decrease in blood mass (blood loss and dehydration), a drop in vascular tone (reflex disorders in trauma, irritation of the serous membranes, myocardial infarction, pulmonary embolism; disorders of innervation of central origin: hypercapnia, acute hypoxia of the interstitial brain, overload, psychogenic reactions; with infections and intoxication). The deposition of a significant part of the blood in the vessels of the abdominal cavity leads to a decrease in the volume of circulating blood, a decrease in pressure.

With fainting, there is a sudden short-term loss of consciousness due to insufficient blood supply to the brain, appear: pallor of the skin, cold sweat, cold extremities, weak or thready pulse, a sharp decrease in blood pressure.

With collapse, there are: dizziness, darkening of the eyes, ringing in the ears, possible loss of consciousness, cold sweat, cold extremities, rapid shallow breathing, small thready pulse, drop in blood pressure; in contrast to fainting, the duration and severity of manifestations are longer.

In shock, the clinical manifestations are similar to collapse, differ in the mechanism of development (associated with trauma, pain, intoxication).

Chronic left ventricular heart failure develops with aortic defects, mitral insufficiency, arterial hypertension, coronary artery disease, diseases with damage to the left ventricle. Appear: shortness of breath, cyanosis, cough; develops congestive bronchitis with sputum, hemoptysis. Harsh breathing is heard in the lungs, in the lower sections there are moist fine and medium bubbling rales, expansion of the heart to the left, tachycardia, accent of the II tone over the pulmonary artery.

Progressive pulmonary hypertension leads to right ventricular failure.

Chronic right ventricular heart failure develops with mitral defects, emphysema, pneumosclerosis, tricuspid valve insufficiency, congenital malformations. There is stagnation of blood in the veins of the systemic circulation, shortness of breath, palpitations, swelling of the legs, pain and heaviness in the right hypochondrium, small diuresis. Expressed acrocyanosis, swelling of the cervical veins, cardiac impulse, epigastric pulsation, expansion of the heart to the right.

There is an increase in the liver, a positive symptom of Plesh (hepatojugular reflux: pressure on the liver increases the swelling of the cervical veins) and venous pulse, ascites, hydrothorax are noted.

An increase in central venous pressure leads to a slowdown in blood flow.

Additional diagnostic study. The colloid-osmotic state of blood is studied: integral indicators of protein and water-electrolyte metabolism, the content of their main components in plasma (electrolytes, non-electrolytes, colloids, plasma volume).

The following indicators are being studied:

1) determination of the volume of fluid spaces (volume of circulating blood);

2) osmotic indicators (serum sodium content, mean erythrocyte volume, osmolarity);

3) dilution or hemoconcentration in the blood - the concentration of hemoglobin in the blood, the hematocrit value, the number of red blood cells in the blood, the concentration of total protein in the serum.

The electrolyte balance of sodium, potassium, calcium, etc. is examined. The ECG reveals signs of overload of the left or right atrium, etc.

EchoCG study determines an increase in cavities, a decrease in myocardial contractility.

X-ray examination establishes the expansion of the cavities of the heart, central and peripheral venous congestion.

Doppler EchoCG study determines the slowing of blood flow, a decrease in stroke and minute blood volumes, and an increase in the mass of circulating blood.

Treatment. A dietary regimen is prescribed (table No. 10) with restriction of liquid and table salt.

To improve the contractile function of the myocardium, cardiac glycosides are prescribed (digitalis, isolanide, digoxin, corglicon, strophanthin, stimulants of β-adrenergic receptors (dopamine, dobutamine), ACE inhibitors (accupro, captopril, berlipril 5).

Normalization of myocardial metabolism is carried out with potassium preparations, ATP, cocarboxylase, B vitamins, inosine; amino acids, anabolic hormones, cozaar, monizol, monocinque.

Diuretics are prescribed - hypothiazide, furosemide, indapamide, triamterene, spironolactone, aldosterone antagonists (veroshpiron).

To improve peripheral circulation, camphor, caffeine, cordiamine preparations, peripheral vasodilators are used: nitroglycerin (for venous vessels), apressin (for arterial vessels), naniprus (mixed action), phosphodiesterase inhibitors (amrinone, milrinone);

Hypoxia should be eliminated using oxygen therapy.

The elimination of stagnation in the small circle is carried out by bloodletting, the use of fast-acting diuretics - uregit, mannitol.

To increase the tone of the cardiovascular system, exercise therapy, massage, carbon dioxide and hydrogen sulfide baths are prescribed.

Forecast. Depends on the severity of the underlying disease and the functional class of heart failure. At stages I and IIA, the prognosis is relatively favorable, at stage IIB - serious, at stage III - unfavorable.

LECTURE No. 22. Pneumonia

Pneumonia is an acute infectious and inflammatory process in the lungs with the involvement of all structural elements of the lung tissue and obligatory damage to the alveoli of the lungs.

Etiology. Pneumonia in all cases is caused by gram-positive or gram-negative microflora. With immunodeficiency pneumonia, Pneumocystis carinii, Cytomega-lovirus, Herpes simplex, and fungi are found. With aspiration pneumonia, anaerobic microorganisms are detected.

Pathogenesis. With community-acquired pneumonia, an airborne route of penetration is observed - inhalation of small drops or aspiration of the secret of the upper respiratory tract containing microorganisms. There is damage to the endothelium of the tracheobronchial tree with a violation of mucociliary clearance and mucociliary barrier. Violated the functioning of macrophages, the secretion of lysozyme and interferon.

RџSЂRё nosocomial pneumonia the cough reflex is suppressed, the mucous membrane of the tracheobronchial tree is damaged during surgery and mechanical ventilation, and there is a sharp decrease in general and local immune defense against the background of immunosuppressive therapy.

Classification. Pneumonia by type is divided into community-acquired, or home, outpatient (acquired outside the hospital), nosocomial, or hospital, nosocomial (acquired in a medical institution), aspiration, in persons with severe immunity defects (congenital immunodeficiency, HIV infection, iatrogenic immunosuppression).

According to the severity of the course, the following pneumonias are distinguished:

1) mild degree: mild intoxication (consciousness is clear, fever up to 38 ° C, tachycardia up to 90 beats per minute, blood pressure is normal), shortness of breath is slight on exertion, not at rest, on the x-ray - the lesion is small;

2) moderate degree: moderate intoxication (clear consciousness, mild euphoria, sweating, weakness, fever up to 39 ° C, tachycardia up to 100 beats per minute, moderate decrease in blood pressure), shortness of breath at rest (number of breaths up to 30 per minute), on X-ray - severe infiltration of the lung tissue;

3) severe degree: severe intoxication (temperature up to 39-40 ° C, weakness, blackout, delirium, tachycardia more than 100 beats per minute, collapse), shortness of breath at rest (30-40 breaths per minute), cyanosis, extensive infiltration on x-ray, complications of pneumonia are frequent. According to the prevalence of pneumonia are lobar, segmental, right-sided, left-sided.

Clinic. high tide It is marked by an acute onset: chills, headache, chest pain when breathing, fever, dry cough, later "rusty" sputum appears. Herpes labialis (nasalis), hyperemia of the cheek on the side of the lesion, swelling of the wings of the nose may appear. When breathing, the affected half of the chest lags behind the healthy one. Percussion determined pulmonary sound with a tympanic tinge. Auscultatory listening to the weakening of vesicular breathing, gentle initial crepitus - crepitus "indux", pleural friction rub.

В compaction stages there is a cough with purulent sputum, persistent fever, shortness of breath, chest pains when breathing and coughing, mental agitation up to psychosis, Herpes, cheek flushing, skin icterus, sclera. Increased voice trembling, bronchophony. Percussion determined dull sound. Bronchial breathing, pleural friction rub are auscultated.

В resolution stages there is a productive cough, a large amount of sputum, body temperature drops. Percussion is determined by dullness with a tympanic shade. Harsh breathing, rough crepitus - "redux" crepitus, sonorous moist rales are auscultated.

Additional diagnostic study. A general blood test is performed (leukocytosis, an increase in ESR), where leukocytosis is detected more than 10-12x10⁹/_л indicates a high probability of a bacterial infection, more than 25x10⁹/_л and leukopenia below 3x10⁹/_л are unfavorable diagnostic features. In a biochemical blood test, dysproteinemia is determined. In arterial blood, hypoxemia is determined with a decrease in oxygen below 60 mm Hg. Art., which is a prognostically unfavorable sign.

Gram-stained bacterioscopy and culture of sputum obtained by deep coughing, determination of antigens, polymerase chain reaction (the method is promising, but cannot be recommended for widespread practice). The pleural fluid is examined (in the presence of pleural effusion - counting leukocytes with a leukocyte formula, determining pH, LDH activity, protein content, Gram smear, culture for aerobes, anaerobes, mycobacteria). Fiberoptic bronchoscopy is also performed with a quantitative assessment of microbial contamination (to exclude pulmonary tuberculosis) and chest x-ray.

Complications. Complications may be pulmonary (pleural effusion, pleural empyema, destruction (abscess formation) of lung tissue, acute respiratory distress syndrome, acute respiratory failure) and extrapulmonary (toxic shock, secondary bacteremia, sepsis, pericarditis, myocarditis, nephritis).

Differential diagnostics. Should be carried out with thromboembolism in the pulmonary artery system, exudative pleurisy, focal tuberculosis, acute abdomen, acute myocardial infarction.

Treatment. The treatment of pneumonia provides for an active and early effect on the pathogen, the use of rational antibacterial therapy, anti-inflammatory treatment through the complex use of physiotherapy and medications (NSAIDs), the elimination of toxemia, the correction of impaired functions of the lungs and other systems (rehabilitation), pathogenetic and symptomatic therapy. Bronchodilators are used in combination with mucolytics to improve the drainage function of the lungs (ambroxol, mucodin, bromhexine, bronchicum, etc.); with bronchial obstruction - bronchodilator drugs with anticholinergic action (atrovent, berodual). Patients are shown early therapeutic breathing exercises (with a decrease in temperature to subfebrile and the absence of hemodynamic disorders), physiotherapy (microwave field on the area of the pneumonic focus) in the absence of contraindications (abscess formation, hemoptysis, suspicion of a tumor or specific process, the presence of severe cardiac pathology). At the end of the course of antibiotic therapy, in the absence of contraindications from the gastrointestinal tract, NSAIDs (non-steroidal anti-inflammatory drugs) are prescribed.

Antibacterial therapy with non-severe pneumonia, it can be completed upon reaching a stable temperature normalization (within 3-4 days); the duration of treatment is usually 7-10 days, with mycoplasma and chlamydial pneumonia - up to 14 days, with staphylococcal or gram-negative pneumonia - from 14 to 21 days, with legionella - 21 days.

Criteria for the sufficiency of antibiotic therapy are body temperature below 37,5 ° C, no intoxication, no respiratory failure, no purulent sputum, normalization of blood counts: leukocytes below 10_л, neutrophils below 80%, young below 6, no negative dynamics on the radiograph.

In severe pneumonia, a two-stage method of using antibiotics is used, the transition from parenteral to oral administration should be carried out as soon as possible, taking into account the clinical condition. The best option is to use two dosage forms of one antibacterial drug.

Transition Criteria (on average 2-3 days after the start of treatment) the following: normalization of temperature (below 37,5 ° C) in two consecutive measurements with an interval of 8 hours, decrease in dyspnea, no impairment of consciousness, positive dynamics of other symptoms of the disease, no violations of gastrointestinal absorption , patient consent to oral treatment.

Flow. The course of the disease can be acute, protracted and chronic. Pneumonia should resolve in 3-4 weeks. Pneumonia that does not resolve for more than 4 weeks and ends in recovery is considered protracted. Long-term (over 8 weeks), chronic inflammatory process in sclerotically altered and (or) carnifying lung tissue with formed irreversible changes in the bronchial tree according to the type of local chronic bronchitis and clinical manifestations of recurrent inflammation in the same affected part of the lung refers to chronic pneumonia .

Forecast. In the absence of complications, the prognosis is favorable, and in the presence of complications, it is determined by them.

Prevention. Preventive measures include the following: hardening of the body, smoking cessation, dispensary observation, vaccination with a 23-valent pneumococcal vaccine S. pneumoniae (all persons over 65 years of age, without immunological disorders, younger than 65 years of age in the presence of severe concomitant diseases).

LECTURE No. 23. Chronic bronchitis

Chronic bronchitis is a diffuse inflammatory and degenerative process in the bronchial mucosa and peribronchial tissue, manifested by persistent or recurrent cough with sputum for at least 3 months a year for 2 years or more.

Etiology. The causative factors are smoking (in smokers, the incidence of chronic bronchitis is 2-5 times higher), infection (viral or bacterial), toxic effects, occupational hazards, α-1-antitrypsin deficiency, household air pollution (combustion products of fossil fuels, food odors). heating devices).

Pathogenesis. There is hyperplasia of the goblet cells of the bronchial glands, hypersecretion of mucus in the bronchi and a change in its properties, inflammatory edema and infiltration of the bronchial mucosa, impaired bronchial patency and drainage function of the bronchi, an imbalance between proteinase inhibitors (α-1-antitrypsin) and proteinases (neutrophil elastase).

Classification. Chronic bronchitis is divided into simple, mucopurulent and mixed. Depending on the characteristics of the clinical course, all forms of chronic bronchitis are differentiated according to the severity of the course, the phase of the disease (exacerbation, remission), as well as complications.

Clinic. When simple chronic bronchitis there is a cough (at first dry in the morning, then with a small amount of mucopurulent sputum up to 20 ml / day), malaise, weakness, fatigue, auscultatory: hard breathing, sometimes weakened; with mucopurulent chronic bronchitis, moist, sonorous fine bubbling rales may occur).

RџSЂRё chronic obstructive bronchitis there is an increase in cough, sputum, shortness of breath, diffuse cyanosis (lips, earlobes, acrocyanosis), rare deep breathing, barrel-shaped chest, percussion: displacement of the borders of the lungs down, their inactivity, box sound. Auscultatory listens to evenly weakened breathing with prolonged expiration, scattered dry buzzing rales, disappearing after coughing. There are 2 variants of the disease: emphysematous (associated with panacytic emphysema) and bronchitis (associated with centriacinar emphysema).

Additional diagnostic study. A general blood test is carried out, where leukocytosis is detected, an increase in ESR in simple and mucopurulent bronchitis during exacerbations, hematocrit in obstructive bronchitis in men is more than 52%, in women more than 47%. An immunological blood test is also carried out (a decrease in the activity of nonspecific and humoral parts of the immune response, an increase in the activity of a cellular link in obstructive bronchitis), a sputum examination (macro- and micro-study - cytology, flora), a calculation of the index of a smoking person (the number of cigarettes smoked per day, multiplied by 12 (number of months in a year); with a value of 160 there is a risk for chronic obstructive bronchitis, more than 200 - classification as "heavy smokers"). The functional state of the lungs is examined (determination of volumetric and speed indicators) - peak flow measurements, spirography, pneumotachometry are used. OVF1 is monitored (long-term re-measurement of the spirometric index): normally, in adulthood, there is an annual drop in OVF1 within 30 ml per year; for patients with chronic obstructive bronchitis, an annual drop in the GFR1 index of more than 50 ml per year is typical. Conduct a bronchological examination (hyperemia, edema, atrophy of the mucosa, the presence of sputum, dyskinesia of the bronchus wall), computed tomography (morphological changes in the lungs, their location, size), ECG (exclusion of cardiac genesis of symptoms, determination of hypertrophy of the right heart - rightogram, deep prong S in V5, V6).

Complications. Complications of the disease can be focal pneumonia, emphysema, respiratory failure, chronic cor pulmonale, secondary erythrocytosis, bronchiectasis;

Differential diagnostics. Should be carried out with chronic pneumonia, tuberculosis, lung cancer, bronchial asthma.

Treatment. Treatment is carried out in the phase of exacerbation and the phase of remission.

В exacerbation phase antibacterial therapy is carried out (in the presence of purulent sputum), M-cholinolytics are prescribed, β₂-agonists, methylxanthines, mucolytics, antihistamines, oxygen therapy, therapeutic bronchoscopy, physiotherapy, exercise therapy, treatment of complications.

В remission phase patients are prescribed bronchodilators (if indicated), mucolytics (used for symptoms of mucostasis), physiotherapy, spa treatment.

Flow. The course of the disease can be recurrent, chronic, progressive.

Prevention. Prevention measures include the following: timely treatment of acute bronchitis and respiratory diseases, early detection and treatment of the initial stages of chronic bronchitis, hardening of the body (air and sun baths, water procedures), measures to combat dust and air pollution in working areas, smoking restriction, sanitation foci of chronic infection.

LECTURE No. 24. Bronchiectasis

Regional expansion of the bronchi with a predominant localization of the process in the lower parts of the lungs, manifested by chronic endobronchial suppuration.

The disease is associated with genetic defects in the development of the bronchi, observed in children and adults. Men get sick more often. Secondary bronchiectasis, in which damage to the lung tissue predominates due to an active inflammatory process, does not belong to bronchiectasis.

Etiology. Etiological factors include bronchopulmonary infections, aspiration of foreign bodies, bronchial stenosis with secretion retention and constant suppuration distal to the stenosis, bronchial malformations, congenital predisposition (Sievert-Kartagener syndrome).

Pathogenesis. Bronchial patency is disturbed (formation of obstructive atelectasis), inflammation of the bronchi occurs, intrabronchial pressure increases, elasticity and mechanical stability of the bronchi decreases, obturation of small bronchi occurs (cystic fibrosis).

Classification. According to the features of clinical manifestations, the disease is divided:

1) according to the form of bronchiectasis (saccular, fusiform, cylindrical, mixed);

2) according to the phase of the disease (exacerbation, remission);

3) by localization (segment, segments, right- or left-sided).

Clinic. The main manifestations of the disease are:

productive cough, mainly in the morning, with the separation of a significant amount of mucopurulent or purulent sputum, hemoptysis, sputum separation depends on the position of the body - it increases in a state of orthopnea. Patients note intoxication, weight loss, fever, puffiness of the face, earthy shade of diffuse cyanosis, retraction of the affected side of the chest. Fingers in the form of drumsticks, nails in the form of watch glasses (a sign of hypoxia). During percussion, a mosaic of percussion sound is determined (a sign of low specificity). Harsh breathing, foci of persistent moist medium and coarse bubbling rales, loud dry rales are auscultated.

Additional diagnostic study. A general blood test is performed, in which anemia, neutrophilic leukocytosis with a shift to the left, and an increase in ESR are noted. Also, a study of a general urine test is carried out (with the development of complications - the appearance of a protein), a biochemical blood test (dysproteinemia: hypoproteinemia, albuminemia, hypergammaglobulinemia), a sputum examination (macro- and microscopic examination of the flora: three-layer, many leukocytes). With bronchoscopy, a lot of sputum is found in the lumen of the bronchi, there is hyperemia of the mucosa, a continuous flow of sputum. With bronchography - bronchiectasis of various forms, with radiography - a decrease in the volume of the affected lung, cellularity of the pulmonary pattern. A functional study of the lungs is being carried out.

Complications. Complications of the disease are pulmonary bleeding, pleural empyema, pyopneumothorax, lung abscesses, amyloidosis of internal organs, cor pulmonale.

Differential diagnosis. Should be carried out with chronic pneumonia, tuberculosis, chronic lung abscess, lung cancer.

Treatment. Patients are shown diet No. 15, active positional drainage according to B. E. Votchal. Antibacterial drugs (parenteral and intrabronchial), repeated sanitation bronchoscopy, bronchodilator therapy, mucolytics, desensitizing agents, anabolic hormones, vitamins (groups B, C) are prescribed; surgical treatment (segmental resection, lobectomy) is indicated for one lobe.

Flow. The course of the disease is progressive, long-term remissions are possible.

Forecast. With a limited lesion, the prognosis is favorable, and with a widespread process and the presence of complications, it is unfavorable.

Prevention. Prevention measures include timely treatment of lung infections, smoking cessation, systematic positional drainage, and treatment of complications.

LECTURE No. 25. Lung abscess

Lung abscess - a limited purulent inflammation of the lung tissue with the destruction of its parenchyma and bronchi, their melting and the formation of a cavity.

Etiology. The etiological factors of abscess are bronchial obstruction by foreign bodies, acute pneumonia, bronchiectasis, chest trauma, hematogenous embolization by infection.

Pathogenesis. There is a penetration of the infectious agent into the lung tissue (bronchogenic, hematogenous, lymphogenous pathways, aspiration of foreign bodies), a violation of the drainage function of the bronchi.

Classification. According to the characteristics of the clinical course, the disease is divided:

1) by origin: acute lung abscess and chronic lung abscess (the course of the process is over 2 months);

2) by localization (segment, segments, right- or left-sided);

3) by complications.

Clinic. In acute lung abscess (AAL) secrete organization period (before opening the cavity - up to 7 days), which is characterized by an acute onset (dry hacking cough, chills), chills changing to pouring sweat (hectic fever), mental disorders, puffiness of the face, flushing of the cheeks, lagging of the affected side of the chest during breathing, local thickening of percussion sound, hard breathing with a bronchial tone, and period after cavity opening, characterized by a sudden discharge of purulent fetid sputum with a full mouth, a drop in temperature, a decrease in intoxication, the appearance of tympanitis is determined percussion over the affected area of the lung, with auscultation, amphoric breathing, moist medium and large bubbling sonorous rales. In chronic lung abscess (CAL), patients have a cough with fetid sputum, hemoptysis, chills, sweating, puffiness of the face, diffuse cyanosis, bad breath, fingers in the form of drumsticks, nails in the form of watch glasses (a sign of hypoxia), over the located auscultated amphoric breathing, moist sonorous fine bubbling rales.

Additional diagnostic study. A general blood test is carried out, in which neutrophilic leukocytosis with a sharp shift to the left is determined during the organization period, increased ESR, and in the period after opening - normalization of indicators; with CAL - neutrophilic leukocytosis with a shift to the left, an increase in ESR. An immunological examination of blood is also carried out (lymphopenia, increased activity of nonspecific and humoral parts of the immune response), sputum examination (macro- and micro-study - cytology, flora, elastic fibers), X-ray examination (during the organization period - massive darkening with fuzzy contours; after opening in bronchus - a cavity with thick, infiltrated walls and with a horizontal level of fluid; with a breakthrough into the pleura - free fluid and gas in the pleural cavity).

Complications. Complications of the disease are sepsis, pyopneumothorax, mediastinal and subcutaneous emphysema, pleural empyema, pulmonary hemorrhage, metastatic brain abscess, cor pulmonale.

Differential diagnostics. Should be carried out with pneumonia (acute and chronic), tuberculosis, lung cancer, sepsis.

Flow. The course can be acute and chronic.

Treatment. Infectious destruction of the lungs is treated only in a hospital, if possible in the department of thoracic surgery. Careful patient care is required, high-quality nutrition with sufficient amounts of protein and vitamins (diet No. 15), infusion of nutrient mixtures, drug treatment that includes antibiotic therapy (parenteral, intravenous), possible introduction into the pulmonary artery, a combination of several types of antibacterial drugs, detoxification therapy (rheopolyglucin, hemodez, hemosorption, ultraviolet autologous blood), bronchospasmolytic therapy, positional drainage, endoscopic bronchial sanitation followed by the introduction of antibiotics, enzymes, antiseptics, blood transfusion (with the development of anemia), the use of heparin (to prevent DIC), mucolytic and expectorant funds.

LECTURE No. 26. Gangrene of the lung

Gangrene of the lung is a progressive necrosis and hypochorous (putrefactive) decay of the lung tissue, not prone to limitation.

Etiology. The causative agents of the disease are non-clostridial anaerobes.

Pathogenesis. Anaerobic bacteria penetrate into the lung tissue, activation of bacterial exotoxins and their direct effect on lung tissue, progressive lung tissue necrosis, vascular thrombosis in the affected area, impaired formation of granulation tissue.

Clinic. The main manifestations of the disease are cough with fetid sputum and fragments of lung tissue, hectic nature of fever, chest pain, shortness of breath, expanding dullness is determined by percussion at the onset of the disease; during the peak - the appearance of areas of tympanitis due to the formation of cavities. On palpation, pain over the affected area (Kissling's symptom) and percussion (Sauerbruch's syndrome) (involvement in the pleura process) is determined, palpation - first, increased voice trembling, then weakening. Auscultatory listening first bronchial breathing, then a sharp weakening of breathing.

Additional diagnostic study. A general blood test is performed, where neutrophilic leukocytosis is determined with a sharp shift to the left, increased ESR. A study of sputum is also carried out (during macro-examination, sputum forms 3 layers: the upper one is foamy, liquid; the middle one is serous; the lower one is fragments of decaying lung tissue; micro-examination is the study of flora, cytology), X-ray examination (massive infiltration without clear boundaries with the presence of multiple confluent cavities irregular shape).

Differential diagnostics. Should be carried out with tuberculosis, lung cancer.

Flow. The course of the disease is severe and progressive.

Treatment. Antibacterial therapy is carried out (parenterally, intravenously), it is possible to introduce into the pulmonary artery. Combine several types of antibacterial drugs. Carry out detoxification therapy (rheopolyglucin, hemodez, hemosorption, ultraviolet autologous blood), bronchospasmolytic therapy, endoscopic bronchial sanitation followed by the introduction of antibiotics, enzymes, antiseptics, blood transfusion (with the development of anemia), heparin is used (to prevent DIC).

Prevention. Preventive measures include adequate treatment of acute pneumonia, adequate bronchial drainage, rehabilitation of chronic infection foci, smoking cessation.

LECTURE No. 27. Pulmonary embolism (PE)

Blockage of the arterial bed of the lung by a thrombus formed in the venous system, right atrium, ventricle of the heart, or other material that has entered these areas.

Etiology. The etiological factor is a venous thrombus (in 85% of cases, the source is in the system of the inferior vena cava, much less often in the right chambers of the heart and veins of the upper extremities). These can be drops of fat, tumor cells, air, parasites, foreign bodies.

К risk factors include old age, atherosclerosis, the presence of malignant tumors, pregnancy, contraceptives, obesity, varicose veins.

Pathogenesis. R. Virchow's triad is characteristic: slowing down of the blood flow rate, increased blood clotting, damage to the vascular wall.

Pulmonary arterial occlusion blocks blood flow in the pulmonary circulation, causes generalized vasospasm of the pulmonary circulation and bronchospasm. Acute pulmonary arterial hypertension develops, overload of the right heart, arrhythmias, ventilation and perfusion of the lungs worsen, accompanied by right-to-left shunting of insufficiently oxygenated blood, myocardial, brain, and kidney ischemia develops.

Classification. According to the features of clinical manifestations, the disease is divided:

1) downstream: acute, subacute, recurrent;

2) according to the affected area: small (up to 25% of the volume of the switched off channel), submassive (up to 26-50%), massive (up to 51-75%), lethal (more than 75%);

3) according to the severity of manifestations.

Clinic. Major Syndromes are the following: pulmonary-pleural (bronchospasm, shortness of breath, cough, hemoptysis, pleural friction noise, the appearance of pleural effusion), cardiac (the appearance of retrosternal pain, tachycardia, accent II tone and noise (systolic and diastolic) over the pulmonary artery, pericardial friction noise, hypotension, swelling of the jugular veins and cyanosis), abdominal (pain in the right upper quadrant of the abdomen), cerebral (loss of consciousness, convulsions, paresis), renal (anuria).

According to the significance and degree of manifestations, the symptoms are distributed in the following sequence: tachycardia, chest pain, shortness of breath, hemoptysis, fever, moist rales, cyanosis, cough, pleural rub, collapse.

Threatening symptoms of PE: fever in the postoperative period (3-10 days), fever in bed rest, unclear dyspnea, chest pain, migrating pneumonia, the appearance of rapidly passing fibrinous pleurisy and the development of pleural effusion, hemoptysis, worsening of the course of the disease.

Additional diagnostic study. A study of sputum (siderophages), a study of the blood coagulation system (moderate hypercoagulation, an increase in the level of platelet β-thromboglobulin and a decrease in antithrombin III), ECG: tachycardia, deviations of the atrial and ventricular vectors to the right, transient blockade of the right leg of the His bundle (changes are present only in 10 -20% of cases), x-ray examination: expansion of the lung root, diffuse depletion of the lung pattern; possible local oligemia, pulmonary infarction, pleural exudates, basally located atelectasis, high standing of the dome of the diaphragm, expansion of the shadow of the heart. Also, patients are shown perfusion scintigraphy (registration of radiation over the lungs after intravenous administration of a colloidal solution of protein labeled with technetium) - with PE, a decrease in radiation, angiopulmonography (contrast X-ray image of the pulmonary vessels) - with PE, filling defects.

Complications. Complications of the disease are shock, pulmonary infarction, lung abscess, fibrinous or hemorrhagic pleurisy, acute and chronic cor pulmonale.

Differential diagnostics. Should be performed with acute myocardial infarction, pneumonia, dissecting aneurysm of the thoracic aorta.

Flow. The course of the disease is associated with the risk of death.

Treatment. When acute PE at the 10st stage, urgent intravenous administration of 000-15 IU of heparin is carried out, sedatives, analgesics are prescribed, oxygen is given. At the II stage, streptokinase (000 IU intravenously drip), vasoactive drugs, antiacidotic therapy, heparin administration (250-000 IU 5000 times a day under control of blood coagulation) are shown. Cardiac glycosides are not used (due to increased pressure in the pulmonary artery). At the III stage, an embolectomy is performed - in the absence of the effect of the I and II stages of treatment and no later than 10 hours from the onset of the disease.

RџSЂRё recurrent PE long-term use of anticoagulants of indirect action (6-12 months) is indicated, the value of the prothrombin index should be in the range of 40-60%, symptomatic therapy, if surgical treatment is ineffective, the imposition of U-shaped sutures on the inferior vena cava or the installation of a Mobin-Uddin filter in it .

Prevention Prevention of the disease is the timely treatment of the threatened contingent, a decrease in the amount of animal fats and cholesterol in food.

LECTURE No. 28. Chronic obstructive pulmonary disease (COPD)

Chronic obstructive pulmonary disease is a heterogeneous group of pulmonary diseases that are combined by a disorder of the function of external respiration of the lungs according to the obstructive type.

They are diagnosed at late stages, when progression becomes inevitable, despite the use of modern treatment programs.

COPD includes chronic diseases of the respiratory system: chronic obstructive bronchitis (88-90%), severe bronchial asthma (8-10%), emphysema (1%).

In the US and UK, the COPD group also includes cystic fibrosis, bronchitis obliterans, and bronchiectasis. With generalized obstruction, differential diagnosis is carried out.

Pathogenesis, clinic, diagnosis and treatment of individual nosological forms of COPD are described independently.

Rehabilitation. For COPD of any severity, a sparing regimen, exercise therapy, physiotherapy, spa treatment are prescribed). Therapy of cardiovascular pathology is shown: angiotensin-converting enzyme inhibitors, calcium channel blockers, diuretics, antiplatelet agents, digoxin (in severe forms of COPD, cor pulmonale).

Management in an outpatient setting.

Early detection of patients is necessary (for mild and moderate course of the disease), early appointment of adequate basic therapy (for mild COPD, 3-week therapy with atrovent is necessary with the possible connection of mucolytics, further prescription of bronchodilators according to indications (weather conditions, nature of work, bad habits), with COPD of moderate and severe course requires a long-term (permanent) intake of bronchodilators (atrovent, berodual 2 doses 3-4 times a day), if necessary, saltos, teopec, teodur, etc. are added, with mucostasis - mucolytics; taking bronchodilators can be discontinued with stabilization of the subjective state and stable stabilization of peak expiratory flow rates for 3 months). Patients are being monitored after ARVI or influenza with a long-lasting cough, unproductive, spastic in nature, not stopped by taking antitussive drugs (appointment of Atrovent for 3 weeks).

LECTURE No. 29. Bronchial asthma

Bronchial asthma is a chronic inflammatory disease of the airways in which many cells and cellular elements play a role. Chronic inflammation causes a concomitant increase in airway hyperresponsiveness, leading to recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, especially at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment.

A similar definition of asthma is presented in the 1995 GINA Working Group report (USA), revised in 2002; GINA - Global Initiative for Asthma, a global strategy for the treatment and prevention of asthma.

Etiology. The causes that cause the development of the disease are divided into internal factors (innate characteristics of the body) and external factors (modify the likelihood of developing the disease in predisposed people).

Pathogenesis. A specific inflammatory process is formed in the bronchial wall in response to damaging risk factors (activated eosinophils, mast cells, macrophages, T-lymphocytes), bronchial obstruction develops, bronchial hyperreactivity increases. An increased predisposition of the bronchi to constriction in response to various triggers is formed, signs of the disease persist in the asymptomatic period. Persistent structural and functional changes are formed, accompanied by remodeling of the airways.

Airway obstruction has 4 forms: acute bronchoconstriction (due to spasm of smooth muscles), subacute (due to swelling of the mucous membrane of the respiratory tract), obstructive (due to the formation of mucous plugs), sclerotic (sclerosis of the bronchial wall with a long and severe course of the disease) (Table 4 ).

Classification. Asthma can be of the following types: with a predominance of an allergic component, non-allergic, mixed.

When making a diagnosis, the etiology, severity of the course, and complications are taken into account.

Clinic. Period of harbingers characterized by a runny nose, sneezing, lacrimation, a feeling of sore throat, paroxysmal cough appears.

В expanded period patients take a forced position (orthopnea), expiratory dyspnea appears, distant dry rales, deep rare breathing, diffuse cyanosis, swelling of the cervical veins, auxiliary muscles participate in the act of breathing, there is an expansion of the intercostal spaces. Percussion is determined by hard breathing, a lot of dry wheezing. Increasing tachycardia.

В permission period there is a cough with hard-to-separate vitreous viscous sputum, distant wheezing disappears. Percussion is determined by the reduction of the box sound. Auscultatory - reduction of dry wheezing.

Additional instrumental study. A general blood test is performed, where leukocytosis, eosinophilia, and an increase in ESR are detected. Allergic status (presence of IgE) is determined, skin tests with allergens are performed. Sputum is examined (macroscopically - viscous, transparent; microscopically - eosinophils, Charcot-Leiden crystals and Kurshman spirals, neutrophils). A functional study of the lungs is carried out (a study of OVF1, FZhEL, PSV), samples with bronchodilators are put (a study of airway hyperreactivity). A non-invasive measurement of airway inflammation markers is carried out (sputum examination for the presence of eosinophils or metachromatic cells after inhalation of hypertonic saline or spontaneously isolated). ECG: overload of the right ventricle.

Complications. Complications of the disease are status asthmaticus (a complication of severe bronchial asthma), pulmonary and pulmonary heart failure, chronic cor pulmonale.

Differential diagnostics. Should be carried out with chronic bronchitis, cardiac asthma, tumors of the trachea, larynx, foreign bodies, cystic fibrosis, bronchiectasis.

Flow. The course of the disease is often progressive, periods of exacerbations and remissions.

Treatment. The goals of management of patients with bronchial asthma are as follows: to achieve and maintain control over the symptoms of the disease, to prevent exacerbation of the disease, to maintain lung function as close to normal as possible, to maintain a normal level of activity, including physical activity, to eliminate the side effects of anti-asthmatic drugs, to prevent the development of irreversible bronchial obstruction, prevention of asthma-related mortality.

Basic principles of management of patients with bronchial asthma: education of patients to form partnerships in the course of their management, assessment and monitoring of the severity of bronchial asthma both by recording symptoms and, if possible, measuring lung function, eliminating exposure to risk factors, developing individual drug therapy plans for long-term management of children and adults, development of individual plans for the relief of exacerbations, ensuring regular follow-up.

Prevention of an asthma attack includes:

1) teaching the patient proper breathing and self-control when feeling worse is the most important factor in managing the patient;

2) elimination of exposure to risk factors.

Treatment is selected based on the severity of the course, the availability of anti-asthma drugs, the individual living conditions of the patient to ensure minimal severity of chronic symptoms, including nocturnal symptoms.

Inhaled glucocorticoids: Becotid, Beclocort, Pulmicort, Ingocort, Becladjet. The route of administration is inhalation.

Systemic glucocorticoids: prednisone, prednisolone, methylprednisolone. They have a minimal mineralocorticoid effect, a relatively short half-life, and a mildly pronounced effect on striated muscles. The route of administration is oral or parenteral.

Cromons: sodium cromoglycate (intal), nedocromil sodium (Tyled).

Stabilize the membrane of mast cells and suppress the mediated release of IgE from them. They are prescribed by inhalation, mainly with mild persistent bronchial asthma.

Methylxanthines: theophylline, eufillin, aminophylline, teodur, teopek, teoteolek, teotard, retophil. They inhibit the activity of phosphodiesterase, are used to control the course of bronchial asthma. The route of administration is oral.

Table 4. Sequence and volume of bronchodilator therapy

After achieving stabilization of bronchial asthma and maintaining it for 3 months, a gradual decrease in maintenance therapy is possible.

Inhaled β₂long-acting agonists: formoterol, salmeterol. The duration of action is more than 12 hours. They relax the smooth muscles of the bronchi, increase mucociliary clearance, reduce vascular permeability, and may reduce the release of mediators from mast cells and basophils.

Inhaled β₂ - short acting agonists: fenoterol, pirbuterol, prokaterol, salbutamol, terbutaline, berotek, asthmapent. The duration of action is from 4 to 6 hours. The route of administration is inhalation.

Oral β₂ - short acting agonists: salbutamol, terbutaline, bambuterol (converts to terbutaline in the body). Relax the smooth muscles of the bronchi, increase mucociliary clearance, reduce vascular permeability, modulate the release of mediators of mast cells and basophils.

Antileukotriene drugs: montelukast, pranlukast, zafirlukast are cysteinyl-leukotriene receptor antagonists, zileuton is a 5-lipoxygenase inhibitor. The 5-lipoxygenase inhibitor inhibits the synthesis of all leukotrienes, cysteinyl leukotriene receptor antagonists block the cisLT1 receptors of the smooth muscles of the bronchi and other cells, inhibit the effects of cysteinyl leukotrienes, which are released from mast cells and eosinophils. The route of administration is oral.

Second generation antihistamines: (n₁ blockers): (acrivastine, astemizole, acelastine, cetirizine, ebastine, fexofenadine, ketotifen, loratadine, mizolastine, terfenadine). Suppress the development of allergic reactions. The route of administration is oral.

Other oral antiallergic drugs: tranilastin, repyrinast, tazanolast, pemirolast, tanned, celatrodast, amlexanox, ibudilast. They suppress the activity of mast cells, influence the synthesis of mediators of inflammation and allergies, act as antagonists of mediators.

Systemic nonsteroidal therapy: troleandomycin, methotrexate, cyclosporine, gold preparations. Include immunomodulators for unwanted effects of glucocorticoids to reduce the need for oral glucocorticoids. They are prescribed only under the supervision of a pulmonologist. The route of administration is oral.

Allergen specific immunotherapy: allergen extracts. The route of administration is subcutaneous, the possibility of sublingual use is being studied.

To quickly eliminate bronchospasm and its symptoms, inhaled β₂-fast-acting agonists (salbutamol, terbutaline, fenoterol, pirbuterol), systemic glucocorticoids, anticholinergics - intratropium bromide - atrovent, oxitropium bromide - troventrol (block the effect of acetylcholine, inhalation route of administration), methylxanthines (short-acting theophylline), oral β₂ short-acting agonists.

With mild suffocation shows inhalation of short-acting β2-agonists (berotek or salbutamol) up to 6 times within an hour, inhalation of anticholinergics (atrovent, troventol) simultaneously or independently, taking methylxanthines (eufillin in tablets) simultaneously or independently.

Relief of moderate suffocation is carried out as a therapy for a mild asthma attack with the addition (optional): aminofillin 2,4% - 10,0 ml intravenously by stream, ephedrine 5% - 0,5 ml subcutaneously, alupent 1 ml intravenously by stream. Corticosteroids are used orally or by infusion (in the absence of effect). If there is no effect, stop the introduction of β₂-agonists.

Forecast. In severe cases - disability.

Prevention. Primary prevention measures include: control of persons with a hereditary predisposition to bronchial asthma, sanitation of foci of infection, smoking cessation, reducing the impact of asthma triggers and reducing the need for drug therapy. Secondary prevention measures include dispensary observation, specific desensitization, anti-relapse treatment, systematic use of bronchodilators, and spa treatment.

LECTURE No. 30. Asthmatic status (complication of severe bronchial asthma)

Etiology. The reasons for the status may be resistance to sympathomimetics and other bronchodilators, rapidly developing total pulmonary obstruction, the development of hypoxia and hypercapnia.

Clinic. There are 3 stages of flow.

At stage 1, there is a discrepancy between distant noises (there are many of them, they are more intense) and auscultatory data (a small amount of scattered dry rales, breathing is weakened), tachycardia, a tendency to increase pressure, resistance to cardiac glycosides, accent and splitting of the II tone over the pulmonary artery, anxiety, tension, asthenia, pale cyanosis.

In stage 2, respiratory failure, tachypnea, oligopnea increase, the sonority and number of dry rales decrease, their disappearance is possible, the formation of a "silent" lung, hypotension, decompensated respiratory acidosis and hypercapnia.

In stage 3, there is pronounced diffuse cyanosis, loss of consciousness with the participation of all reflexes, "silent" lung syndrome, frequent and small pulse, sonorous heart sounds, hypotension, collapse, hypoxic coma is formed.

Treatment. Treatment consists in the rejection of β2-agonists, glucocorticoids (up to 1500 mg per day of prednisone) are administered parenterally and orally, rehydration therapy is performed (up to 3 liters of fluid per day), epidural anesthesia, artificial ventilation of the lungs with bronchoalveolar therapeutic lavage.

LECTURE No. 31. Emphysema

Pulmonary emphysema is a condition characterized by an increase in the size of the air spaces located distal to the terminal or non-respiratory bronchioles, due to the expansion or destruction of their walls.

Etiology. The cause of the disease can be chronic obstructive pulmonary disease (chronic bronchitis, bronchial asthma), chronic pneumonia, pneumoconiosis, tuberculosis.

Pathogenesis. There is a narrowing of the lumen of the bronchi, an increase in intra-alveolar pressure, thinning of the walls of the alveoli, a violation of their trophism, elasticity, development of alveolitis, destruction of the interalveolar septa.

Classification. Emphysema has forms: interstitial, mediastinal, compensatory.

Clinically, pulmonary emphysema is classified:

1) by origin: primary (idiopathic) - hereditary deficiency of α-1-antripsin, α-2-macroglobulin, secondary (due to the development of chronic obstruction of the bronchial lumen);

2) by the nature of development: acute (due to sudden prolonged bronchial obstruction - after an attack of bronchial asthma), chronic (due to the presence of permanent bronchial obstruction);

3) by complications.

Clinic. Primary emphysema occurs in young and middle age, is manifested by shortness of breath (uncaused) of an expiratory nature, an unproductive cough, the appearance of an emphysematous (dyspnea) type of obstruction ("pink puffers" - to combat the collapse of the airways, exhalation is made through lips folded into a tube and is accompanied by a kind of panting).

RџSЂRё secondary emphysema there is a pink complexion, dry cough, with exacerbation of chronic bronchitis with mucopurulent or purulent sputum, expiratory dyspnea; develops gradually, begins to disturb in the 6th-7th decade of life, barrel-shaped chest, retraction of the intercostal spaces during inspiration, participation in breathing of auxiliary muscles, short neck, swelling of the cervical veins, acrocyanosis. There is a bronchial type of obstruction ("cyanotic edema"), patients lose body weight, often sleep sitting. With percussion, a box shade, the lower borders of the lungs are lowered by 1-2 ribs, their mobility is limited, bulging of the tops of the lungs above the collarbones. Auscultatory noted sharply weakened breathing. Cor pulmonale is formed according to the right ventricular type (in the terminal stages), liver enlargement.

Additional diagnostic study. A general blood test is performed, where compensatory erythrocytosis, a moderate increase in ESR are noted. A functional study of the lungs is carried out (determination of volume and speed indicators) - there is a decrease in the forced expiratory rate, a decrease in the Tiffno index, a decrease in lung capacity with an increase in total and residual capacity, a decrease in the diffuse capacity of the lungs). Inhalation tests with bronchodilators are negative. On the ECG - hypertrophy of the right atrium (increased P II-III) and the right ventricle (S I-III). X-ray examination - increased transparency of the lung fields, low standing of the diaphragm, dilated intercostal spaces. The pressure in the pulmonary artery remains at a normal level for a long time or increases only during exercise.

Complications. Complications of the disease are pneumosclerosis, respiratory failure (I-III degree), cor pulmonale.

Treatment. In the presence of a bronchopulmonary infection, antibiotics are prescribed. Bronchodilators are shown (M-anticholinergics, β₂ -agonists, methylxanthines), mucolytics, oxygen therapy, physiotherapy, therapeutic exercises, spa treatment (in the absence of severe pulmonary heart failure).

Prevention. There is no cure for primary pulmonary emphysema. With secondary emphysema, it corresponds to the prevention of chronic bronchitis.

Flow. Chronic, progressive.

Forecast. Adverse.

LECTURE No. 32. Lung cancer

Lung cancer is common, ranging from 20 to 150 cases per 100 population. It mainly affects men aged 000-40 years.

Etiology. The etiology is not known.

The following factors contribute to the occurrence of lung cancer: exposure to carcinogens (nickel, cobalt, iron), inhalation of dust in the mining industry, aromatic substances of products of incomplete combustion of fuel in automobile engines, exposure to tobacco smoke, its passive inhalation, chronic inflammatory processes in the lungs, aggravated heredity , immunodeficiency states.

Pathogenesis. There is an exophytic-endobronchial lesion of the glandular epithelium of large bronchi (1st, 2nd, less often 3rd order), passes to the lung tissue (more often on the right, with localization in the upper lobes, less often in the lower and middle lobes), mediastinal organs, regional lymph nodes. The lumen of the bronchus closes, there is a violation of its patency (obstruction of the bronchus). The corresponding lobe of the lung decreases, the mediastinal organs shift towards the lesion. A secondary inflammatory process develops in the affected area, there is a destruction of pulmonary blood vessels with the development of hemorrhage and extrapulmonary metastasis with damage to the liver, bone marrow, and bone marrow.

Clinic. The main manifestations of lung cancer are as follows: cough associated with the development of reactive bronchitis, then atelectasis of the lungs, perifocal pneumonia, collapse of the lung tissue, the nature of the cough is paroxysmal, pertussis-like, at first dry, later with mucopurulent sputum, mixed with blood (clots, pulmonary hemorrhage) . There is pain in the chest from the damaged side, the intensity of pain increases with the germination of the tumor in the chest wall, the defeat of the ribs, vertebrae with metastases. Shortness of breath increases gradually, is noted with the development of atelectasis of the lungs, massive effusion in the pleura, compression of the mediastinal organs. An increase in body temperature is noted, associated with the inflammatory process, cancer intoxication, and the development of complications. Weakness, sweating, fatigue, weight loss, retraction of the chest wall on the side of the lesion develop.

Percussion is determined by the dullness of the sound over the lesion. Weakened vesicular breathing is auscultated, in the presence of pleural effusion - pleural friction rub.

Additional diagnostic study. A general blood test is performed, in which anemia, neutrophilic leukocytosis with a shift to the left, and an increase in ESR are noted. An immunological blood test is also carried out (an immunodeficiency state, a decrease in the activity of all parts of the immune response), a functional study of the lungs (a decrease in volume and speed indicators), a sputum examination (cytology), an x-ray examination (variability of changes).

With central cancer of the upper lobe and middle lobe bronchi, a darkening of the entire lobe or segment develops with a decrease in the volume of the lobe of the lung. With cancer of the main bronchus, its stenosis appears with the development of hypoectasis, then atelectasis of the entire lobe of the lung with a shift of the mediastinum to the diseased side. Infiltration of the lobe of the lung with the development of perifocal pneumonia refers to a far advanced process with decay, the development of metastases, and secondary bronchiectasis.

With peripheral lung cancer there is a dense rounded shadow with a diameter of 1-5 cm, more often in the upper lobes. Computed tomography is performed (to clarify the location and size of the tumor), diagnostic bronchoscopy (morphological characteristics of the tumor: endobronchial, endophytic or exophytic growth, biopsy sampling).

Complications. Complications of lung cancer are: broncho-obstruction, cor pulmonale, bleeding, metastasis.

Differential diagnostics. Should be carried out with pneumonia, lung abscess, pulmonary tuberculosis, benign lung tumors (lipoma, bronchus chondroma, sclerosing hemangioma, hemarthroma, teratoma), echinococcosis of the lungs, lymphogranulomatosis.

Flow. Rapid progression.

Forecast. Adverse.

Treatment. Shown early surgical treatment, radiation therapy, chemotherapy, symptomatic treatment of complications.

Prevention. Prevention is aimed at reducing dustiness, air pollution, combating occupational hazards, combating smoking, and effective treatment of pneumonia.

LECTURE No. 33. Exogenous allergic alveolitis

Exogenous allergic alveolitis is a group of diseases caused by intense and prolonged inhalation of organic and inorganic dust antigens and characterized by allergic diffuse damage to the alveolar and interstitial structures of the lungs.

Common signs of the disease. The inflammatory process is localized in the alveoli and interstitium of the lungs, and not in the airways. The damaged areas consist of polynuclear and mononuclear infiltrates, sarcoid-like granulomas; in the later stages - the development of interstitial fibrosis. Types III and IV allergic reactions develop.

Etiology. Etiological factors are microorganisms (bacteria, fungi, protozoa) and their metabolic products (proteins, glyco- and lipoproteins, polysaccharides, enzymes, endotoxins), biologically active substances of animal and plant origin, low molecular weight compounds and drugs.

Pathogenesis. Type I pneumocytes are damaged, re-epithelialization of type II pneumocytes is disturbed, and the activity of suppressor T-lymphocytes decreases.

Clinic. Acute stage develops 4-12 hours after contact with the allergen. Chills, fever, cough, shortness of breath, nausea, myalgia and arthralgia (flu-like syndrome) appear, crepitus and moist rales (pneumonia-like syndrome) can be heard in the lungs, there may be a dry unproductive cough with expiratory shortness of breath and dry scattered wheezing (bronchitis syndrome). ), upon repeated contact with the allergen, the symptoms may recur with a subacute (intermittent) course.

In the chronic stage becomes a typical “Monday phenomenon”: acute manifestations are noted on days after rest, disappear by the end of the working week (this form is diagnosed more often), gradually respiratory failure progresses, asthenic syndrome, anorexia, weight loss with the formation of a chronic form, pulmonary hypertension and cor pulmonale are formed .

Additional diagnostic study. A general blood test is performed (neutrophilia, increased ESR, eosinophilia), an immunological blood test (the activity of all parts of the immune response), skin tests with allergens, an inhalation provocative test with an antigen are performed. An x-ray examination is carried out (changes that cannot be explained by other diseases), determination of the function of external respiration: destructive or obstructive types (bronchioloalveolitis) of respiratory failure and impaired diffuse ability leading to hypercapnia, examination of lung tissue biopsies.

Complications. Complications of the disease are respiratory failure, cor pulmonale.

Differential diagnostics. In the acute stage, it should be carried out with ARVI, influenza, acute pneumonia, acute bronchitis. In the chronic stage - with idiopathic fibrosing alveolitis, granulomatous processes in the lungs (tuberculosis, sarcoidosis, Wegener's granulomatosis).

Treatment. In the acute phase, mandatory hospitalization. Glucocorticoid hormones are shown: prednisolone 40-60 mg/day for 1-3 days, followed by a decrease within 3-4 weeks, if hormone therapy is ineffective, immunosuppressants - azathioprine at 150 mg/day for 1-1,5 months, then at 100 mg/day 4 -5 months, then 50 mg / day also 4-5 months, with fibrosis D-penicillamine (cuprenil) 150-200 mg per day for 4-6 months, followed by 100 mg / day for 2 years. Extracorporeal methods are used: plasmapheresis, hemosorption.

Flow. Prolonged, progressive.

Forecast. Relatively favorable.

Prevention. Measures of primary prevention: development of technological processes of production, restriction of work in hazardous industries for patients with bronchopulmonary diseases. Measures of secondary prevention: dispensary observation.

LECTURE No. 34. Fibrous alveolitis

Fibrous alveolitis is characterized by widespread fibrosis of the lungs below the level of the terminal bronchi (respiratory bronchioles and alveoli), leading to the development of an alveolar-capillary block and a sharp decrease in the diffusion capacity of the lungs, manifested by increasing pulmonary insufficiency.

The disease is relatively rare, equally common in men and women, in young and middle age.

Etiology. The etiology of the disease remains unknown. Inheritance is dominant.

Pathogenesis. Interstitial edema and inflammation develop, an irreversible stage of fibrosis is formed, and progressive respiratory failure develops.

Clinic. In the acute form, manifestations of an acute respiratory infection or pneumonia are characteristic, in the chronic form - progressive shortness of breath, unproductive or dry cough, fever to subfebrile (febrile), weakness, fatigue. The severity of shortness of breath and meager physical manifestations do not correspond to each other. Cyanosis, tachypnea, weight loss, change in the terminal phalanges of the fingers (drum sticks, watch glasses) are noted. Percussion is determined by the shortening of the lung sound, especially over the lower sections. Gentle crepitant rales, expressed in the basal regions, tachycardia, accent of the II tone over the pulmonary artery, in the later stages - signs of chronic cor pulmonale are auscultated.

Additional diagnostic study. A complete blood count (moderate leukocytosis, leukopenia, increased ESR, signs of anemia), a biochemical blood test (dysproteinemia, hypergammaglobulinemia), an immunological blood test (an increase in immunoglobulins of classes G and M, the appearance of antinuclear antibodies), an x-ray examination (strengthening and deformation of the lung pattern) are carried out. , its loopiness, nodular focal shadows, a possible decrease in the transparency of the lung tissue), a functional study of the lungs (the presence of a restrictive nature of respiratory disorders), a study of blood gases (a decrease in diffusion capacity).

Complications. Chronic cor pulmonale is the main complication of the disease.

Differential diagnostics. Should be carried out with pulmonary insufficiency, pulmonary heart failure.

Treatment. Shown are corticosteroids (early onset, long-term), a combination of corticosteroids with immunosuppressants. It is possible to use afferent methods (hemosorption, plasmapheresis). During the period of remission, the use of drugs of the aminoquinol series (delagil) is indicated.

Flow. The course of the disease is relapsing and progressive.

Forecast. Unfavorable, average life expectancy 3-5 years.

LECTURE No. 35. Sarcoidosis (Besnier-Beck-Schaumann disease)

Sarcoidosis is the formation of non-caseating epithelial and giant cell granulomas with the greatest localization in the lung tissue. At the same time, intrathoracic lymph nodes, liver, spleen, skin, eyes, nervous system, and heart can be affected.

Etiology. The cause of the disease is not clear.

Pathogenesis. The immunological mechanism of development is the suppression of the T-cell immune response. There is an activation of alveolar macrophages, their accumulation in the form of sarcoid granulomas.

Classification. Sarcoidosis has the following varieties: sarcoidosis of the lungs, sarcoidosis of the lymph nodes, sarcoidosis of the lungs with sarcoidosis of the lymph nodes.

When establishing a diagnosis, the nature of radiological changes is taken into account.

Clinic. At stage I of the disease, weakness, general malaise, subfebrile temperature, sweating, pain in muscles and joints, dry cough, shortness of breath, swelling of the joints appear, erythema nodosum appears on the skin of the extremities. There are no percussion changes. A small amount of dry and wet small bubbling rales is auscultated.

At the II stage of the disease, malaise, weakness, loss of appetite, weight loss, shortness of breath occurs already at rest. Percussion without changes. An increase in the number of dry and wet small bubbling rales, a pleural friction rub is auscultated.

At stage III of the disease, the symptoms of stage II are accompanied by cough with mucopurulent sputum, hemoptysis, cyanosis, and shortness of breath at rest. Auscultatory heard a significant amount of scattered dry and moist rales.

Additional diagnostic study. With a general blood test, there is a slight increase in ESR, lymphopenia, anemia. They conduct a biochemical blood test (dysproteinemia, an increase in α- and γ-globulins, hypercalcemia), an immunological blood test (a decrease in the activity of all parts of the immune response, a decrease in tuberculin sensitivity), a study of the function of external respiration (at stage I - an obstructive type of respiratory impairment; with Stage II - a mixed type of disorder; at stage III - a restrictive type of disorder), x-ray examination (at stage I - a bilateral increase in the size of the hilar intrathoracic lymph nodes, at stage II - the appearance of multiple foci in the lungs, mainly in the middle and lower sections and the root zone , at stage III - pronounced fibrosis, large, confluent focal formations).

Complications. Cardiopulmonary failure is the main complication of the disease.

differential diagnosis. Should be carried out with tuberculous bronchodenitis, lymphogranulomatosis, rheumatism, systemic connective tissue diseases, hepatitis.

Treatment. Patients are shown a diet with a large amount of protein, salt restriction. Glucocorticoids are prescribed (for all forms and stages of the disease), in courses of 3-6 months or more, the initial dose is 30-40 mg, the end of treatment after the clinical and radiological effect, aminoquinolones (delagil), potassium preparations, anabolic steroids (nerabol 5 mg per day). day, retabolil 50 mg 1 time in 2-3 weeks intramuscularly).

Flow. At stage I of the disease, a spontaneous cure is possible, at stage ii - recurrent, a cure is possible, at stage III - a slow progression of the disease.

Forecast. The prognosis is relatively favorable, mortality is from 2 to 5%.

LECTURE No. 36. Chronic cor pulmonale

Hypertrophy and (or) dilatation of the right heart due to pulmonary arterial hypertension due to a respiratory disease.

Etiology. Etiological factors include bronchopulmonary disorders - obstructive and restrictive processes: polycystic lung disease, chronic bronchitis, bronchial asthma, pulmonary emphysema, diffuse pneumofibrosis, pulmonary granulomatosis, vascular lesions - primary pulmonary arterial hypertension, arteritis, repeated pulmonary vascular embolism, lung resection, thoracic lesions -diaphragmatic apparatus; lesions of the spine, chest, their deformation, pleural moorings, obesity.

Pathogenesis. Pathogenetic stages: precapillary hypertension in the pulmonary circulation, right ventricular hypertrophy, right ventricular heart failure, development of pulmonary arterial hypertension, an increase in cardiac output due to an increase in catecholamines caused by hypoxia, an increase in blood viscosity due to erythrocytosis in response to chronic hypoxia, the development of bronchopulmonary anastomoses, an increase in intraalveolar pressure in broncho-obstructive lung diseases.

Classification. The disease is classified as follows:

1) by etiology: bronchopulmonary, thoracophrenic, vascular;

2) downstream: acute (minutes, hours), subacute (days, weeks), chronic (months, years);

3) according to the degree of compensation: compensated, decompensated.

Clinic. The main manifestations of the disease are the following: shortness of breath, cyanosis (appears with II and III degrees of respiratory failure), swelling of the jugular veins, epigastric pulsation, tachycardia, expansion of the boundaries of the heart, especially to the right, deafness of heart tones, emphasis of the II tone over the pulmonary artery, increase and soreness liver, peripheral edema, small diuresis (in a decompensated state).

Additional diagnostic study. A complete blood count (erythrocytosis, normal or reduced ESR), a general urinalysis (the appearance of protein, cylinders during decompensation), a biochemical blood test (dysproteinemia), a functional study of the lungs (allows to distinguish between the degree of respiratory failure) are carried out. On the ECG - signs of cor pulmonale: high P waves in II and III standard leads (P - pulmonale), rightogram, pronounced S wave in I standard lead and left chest leads, the appearance of Q in lead III. A study of hemodynamics is carried out (increased central venous pressure, slowing down the speed of blood flow, increasing the volume of circulating blood). On echocardiography: an increase in thickness in the compensated state and cavity in the decompensated state of the right ventricle. An X-ray examination is also carried out.

Complications. Complications of the disease are pulmonary-cardiac coma (hypercapnic encephalopathy), cough-fainting syndrome (loss of consciousness with convulsions), gastric and duodenal ulcers.

Treatment. Treatment is aimed at treating the underlying disease. In case of infection of the bronchopulmonary apparatus, antibiotics are used, in case of broncho-obstruction - bronchodilators, in case of PE - anticoagulants, fibrinolytic drugs, in case of thoracodiaphragmatic pulmonary heart - artificial ventilation of the lungs. Peripheral vasodilators are used to reduce pulmonary arterial hypertension (nitrates, apressin, calcium channel blockers, β₂adrenomimetics). Oxygen therapy is carried out, bloodletting of 200-300 ml with infusion of low-viscosity solutions (rheopolyglucin) to reduce erythrocytosis, infusion of sodium bicarbonate solution to reduce acidosis. Diuretics are administered, it is possible to use diuretics of different classes simultaneously, vasodilators, antiplatelet drugs, non-steroidal anabolic agents (ATP, riboxin). Remedial gymnastics, massage, postural drainage are shown.

Prevention. Prevention is the prevention and timely treatment of respiratory diseases.

Flow. The course of the disease is chronic and progressive.

Forecast. Adverse.

LECTURE No. 37. Pleurisy

Pleurisy is an inflammatory process in the pleura that develops a second time and is a reflection of an independent disease in the body (tumor, pneumonia, tuberculosis, pancreatitis, trauma, etc.).

Etiology. The etiological factors of the disease are the following: exacerbation of the tuberculosis process in the lungs or intrathoracic lymph nodes, non-specific inflammatory processes in the lungs, rheumatism, collagenoses, heart attacks, lung tumors, chest trauma, acute and chronic infectious diseases (dry pleurisy).

Pathogenesis. There is an excessive accumulation of pleural fluid. This is due to a violation of the ratio between the hydrostatic blood pressure in the capillaries of the pleura and the pleural fluid, an increase in the permeability of the pleura for protein, the ability of the parietal pleura to absorb it through the lymphatic ducts, and a change in the ratio between the oncotic pressure of the plasma and the pleural fluid (normally, the absorption capacity of the pleura is 3 times its secretory capacity).

There are transudates and exudates. The formation of transudate occurs in pathological conditions:

1) with left ventricular failure; with an increase in capillary hydrostatic pressure in the visceral pleura;

2) with right ventricular failure: with an increase in capillary hydrostatic pressure in the parietal pleura;

3) with nephrotoxic syndrome, liver cirrhosis, alimentary cachexia; with a significant decrease in the oncotic pressure of the blood plasma, which leads to a decrease in the absorption capacity of the pleura in relation to the liquid.

The formation of exudate is noted with the direct involvement of the pleura in the inflammatory process or when it is seeded with tumor cells.

Clinic. With dry pleurisy there is pain in the affected half of the chest, aggravated by breathing, coughing; with diaphragmatic pleurisy, pain radiates to the upper half of the abdomen or along the phrenic nerve (to the neck). The pain is most severe in the initial period. Body temperature is normal or subfebrile. The patient spares the affected side, lies on a healthy side. On palpation, soreness and rigidity of the trapezius and pectoralis major muscles are determined (Sternberg and Pottenger symptoms, pain in the hypochondrium), restriction of respiratory mobility of the lungs. Auscultation: breathing is weakened, a pleural friction rub is heard.

With exudative pleurisy there is a high body temperature, severe stabbing pains in the chest, aggravated by deep inspiration, excruciating dry cough, sweating, lack of appetite, shortness of breath, cyanosis, lag of the normal half of the chest during breathing, smoothness of the intercostal spaces. The patient takes a forced position, lies on his sore side. Palpation is determined by the weakening of voice trembling on the affected side. On percussion, dullness of the percussion sound is determined due to the accumulation of fluid with the formation of a characteristic arrangement of exudate in the form of a parabolic curve (Damuazo line). On the diseased side, there is the formation of Garland's triangle with tympanitis (between the spine and the ascending line of dullness), on the healthy side, the Rauchfus-Grokko triangle with dullness of percussion sound. There is a shift of the mediastinal organs to the healthy side due to the high standing of the fluid. On auscultation, a weakening of breathing is heard in the affected area, in the area of Garland's triangle - with a bronchial tinge, a pleural friction rub is heard at the onset of the disease and during resorption of the exudate.

Additional diagnostic study. A general blood test is performed (anemia, leukocytosis, an increase in ESR), a study of the pleural fluid (protein above 3%, relative density above 1,018, positive Rivalt test, many neutrophils in the sediment, straw-yellow color - with exudates, with empyema - pus), x-ray examination: intense darkening with an oblique upper border, shift of the mediastinum to the healthy side - with exudates, limited mobility of the dome of the diaphragm, lowering the transparency of the sinus on the corresponding side.

Complications. Complications of the disease are acute pulmonary heart failure, vascular insufficiency, limited encysted pleurisy, fistulas, adhesions.

Differential diagnostics. Should be carried out with pneumonia, spontaneous pneumothorax, lung cancer, diseases of the osteoarticular and muscular apparatus, tuberculosis.

Treatment. With dry pleurisy, the underlying disease is treated. Analgesics (up to narcotic), non-steroidal anti-inflammatory drugs are introduced.

For pleural effusions the underlying disease is treated, a diet rich in protein, vitamins, limited by salt, liquid is prescribed. Antibacterial drugs are introduced (taking into account the sensitivity of the flora), detoxification therapy (plasma-substituting solutions, vitamins of group B, C), pleural punctures are performed with the evacuation of the pleural fluid. Desensitizing therapy is prescribed.

With hydrothorax (with heart failure) diuretics, peripheral vasodilators, cardiac glycosides are introduced. The physical mode is limited.

For effusions associated with nephrotic syndrome and cirrhosis of the liver, replacement use of protein preparations, salt restriction is carried out.

With pleural empyema antibiotics, drainage of the pleural cavity, replenishment of protein losses are indicated.

For tumor-related effusions, careful intrapleural administration of cytostatics (thiotef, 5-fluorouracil) is carried out.

With recurrent pleural effusions (indomitable pleural effusions) sclerosing therapy is indicated (tetracycline is usually administered, since it causes aseptic inflammation of the pleural sheets, leads to obliteration of the pleural cavity).

With hemothorax consultation with a surgeon is necessary.

Flow. The course of the disease is long, acute, subacute, chronic.

Forecast. The prognosis depends on the underlying disease and the nature of the effusion, more often recovery.

Prevention. Prevention of the disease is aimed at preventing and timely treatment of diseases that can be complicated by inflammatory processes in the pleura, early recognition of the presence of pleural effusion, and its evacuation.

LECTURE No. 38. Diffuse glomerulonephritis

Diffuse glomerulonephritis is an immune-mediated inflammation with a predominant initial glomerular lesion and involvement of all renal structures in the pathological process, clinically manifested by renal and (or) extrarenal symptoms, leading to a secondary shrunken kidney and death from chronic renal failure.

It is divided into acute and chronic glomerulonephritis. True acute glomerulonephritis is only one that is proven by intravital morphological examination. In other cases, chronic glomerulonephritis develops, which has an acute onset.

Etiology. Exogenous factors: bacteria (β-hemolytic streptococcus group A (strains 12, 43, 49), white staphylococcus aureus, bovine corynebacterium, enterococci, typhoid salmonella, pale treponema, diplococci), viruses (cytomegalovirus, herpes simplex viruses, hepatitis B, Epstein-Barr), fungi (Candida albicans), parasites (malarial plasmodium, schistosome, toxoplasma), drugs, poisons, foreign serum.

Endogenous factors: nuclear, brush border antigen, thyroglobulin, immunoglobulins, tumor and embryonic antigens, carcinomatous antigen.

Risk factors: hypothermia

Pathogenesis. There is a passive drift of the immune complex into the glomerulus, its deposition. Antibodies circulating in the blood stream react with a structural antigen or with a triggering non-glomerular autologous or exogenous antigen. There is hyperfiltration, an increase in the transcapillary gradient - the acceleration of sclerosis in the remaining glomeruli.

Clinic. Major Syndromes acute glomerulonephritis are the following: urinary, edematous, hypertensive, nephrotic.

Flow shapes: deployed (cyclic) and monosymptomatic (latent).

Cyclic form never begins at the height of infection, not earlier than 14-25 days after the onset of infection. It is characterized by obligatory cyclicity of the course, it develops acutely, weakness, swelling (mainly of the face), headache, decreased diuresis, urine the color of meat slops, and back pain appear. Arterial hypertension develops (systolic blood pressure does not exceed 180 mm Hg, diastolic blood pressure - 120 mm Hg), tachycardia, there may be signs of acute heart (left ventricular) failure (shortness of breath, cough, attacks of cardiac asthma). There is an expansion of the boundaries of relative cardiac dullness, a systolic murmur at the apex, an accent of the II tone on the aorta, sometimes a gallop rhythm, dry and moist rales in the lungs. Urinary syndrome is characterized by proteinuria, cylindruria, macro- and microhematuria. Proteinuria is associated with gross damage to the vascular wall of the glomerular capillaries, through which albumins, globulins, and fibrinogen are released. Hematuria is a constant symptom. A small number of leukocytes. Edema persists for 10-15 days, disappears by the end of the 3rd week, blood pressure decreases, polyuria develops, urinary syndrome persists for more than 2 months, hypostenuria appears, slight proteinuria may persist for a long time (0,03-0,1 g / day), residual hematuria, leukocyturia disappears at the end of the first month.

For latent form a gradual onset is characteristic, without subjective manifestations, headaches, slight shortness of breath or swelling in the legs are possible, the duration of the condition is up to 2-6 months or more, the presence of an isolated urinary syndrome. Acute nephritis that has not resolved within a year is considered chronic glomerulonephritis.

Major Syndromes chronic glomerulonephritis: urinary, hypertensive, edematous, hyperlipidemia, hypoproteinemia, anemic, chronic renal failure.

Flow shapes: latent, hypertensive, nephrotic, mixed, malignant (subacute), terminal.

The latent form is more often detected by chance, during the clinical examination. Characterized by long-term preservation of working capacity without signs of disease (up to 10-20 years), the presence of isolated urinary syndrome, isohypostenuria, low specific gravity of urine, nocturia, possibly increased blood pressure, hypoproteinemia, hypercholesterolemia, increased ESR.

For a long time, the leading and only symptom of the hypertensive form is arterial hypertension. Initially, hypertension is intermittent in nature, in the future - permanent. On examination, there is an apex beat visible to the eye, an expansion of the relative dullness of the heart to the left, an accent of the II tone over the aorta, a gallop rhythm, with the progression of heart failure, there are manifestations of stagnation in the pulmonary circulation, hemoptysis, attacks of cardiac asthma, rarely - pulmonary edema. The fundus of the eye: neuroretinitis is moderate, only narrowing of the arteries persists for a long time.

RџSЂRё nephrotic form trophic changes appear: dryness of the skin, a decrease in its elasticity, muscle hypotrophy, edema develops due to a decrease in oncotic pressure, at first insignificant in the morning under the eyes, on the ankles, then permanent with a transition to the trunk; hydrothorax, ascites, hydropericardium. There is a dissociation of protein-lipid ratios (hypoproteinemia, hypercholesterolemia), urinary syndrome may appear: hematuria, decreased filtration function, blood pressure does not increase.

For mixed form the severity of edema, urinary syndrome, arterial hypertension, as well as the progressive course and development of renal failure (within 2-5 years) are characteristic.

For malignant (subacute form) characterized by a rapid and persistent decrease in kidney function, increasing changes in the fundus.

terminal form refers to the stage of renal decompensation, associated with insufficiency of nitrogen excretion function. Pronounced nephrotic and hypertensive syndromes, increased levels of urea, creatinine, indican, reduced glomerular filtration, increased filtration fraction.

Additional diagnostic study. A complete blood count (neurophilic leukocytosis, increased ESR, anemia), a biochemical blood test (increased fibrinogen, C-reactive protein, LDH4-5 alkaline phosphatase), and a general urine test are performed.

In acute glomerulonephritis, a decrease in the amount of urine to 400-700 ml / day is characteristic, anuria rarely occurs, protein - from 1 to 10 g / day, albuminuria decreases after 7-10 days, the amount of protein becomes less than 1 g / day, erythrocytes, single hyaline and granular casts, a slight increase in the number of leukocytes, an increase in the specific gravity of urine.

In chronic glomerulonephritis in the stage of renal compensation, there is an increase in the amount of urine, a persistent decrease in specific gravity (isohyposthenuria), nocturia. Insignificant amounts of protein, an increase in erythrocytes, their predominance over leukocytes are noted.

In chronic glomerulonephritis in the stage of renal decompensation, there is a decrease in the amount of urine, an increase in protein, specific gravity, urea, creatinine, and indican in the blood.

The Nechiporenko test is performed (determination of the number of erythrocytes, leukocytes and cylinders in 1 ml of urine: normally, erythrocytes - up to 1000, leukocytes - up to 2000, cylinders - up to 50, with glomerulonephritis, erythrocytes prevail over leukocytes), Kakovsky-Addis test (determination of the number of erythrocytes, leukocytes, cylinders in the daily volume of urine: normal erythrocytes - up to 1, leukocytes - up to 000, cylinders - up to 000, with glomerulonephritis, erythrocytes predominate over leukocytes), urine culture with a quantitative assessment of bacteriuria (if detected in 2 ml urine more than 000 bacteria). They also determine enzymes in the urine: transaminases, redox and their isoforms (LDG000-100), cholinesterases (with glomerulonephritis increase), determination of β₂-microglobulin in urine (β₂-MG) (assessment of the functional state of the kidneys). If the tubules are damaged, protein readsorption is impaired, excretion of β₂-MG increases, no other proteins are detected, the glomeruli are not affected, with an isolated lesion of the glomeruli, the content of β₂-MG is within the normal range, medium molecular weight proteins (albumins) increase, with a mixed process, a simultaneous increase in β is noted₂-MG and albumin.

A Zimnitsky test is carried out to assess the ability of the kidneys to concentrate and dilute urine: under the conditions of normal water and food regimens, 8 portions of urine are collected separately, its quantity and relative density are determined; evaluate daytime (from 8 am to 8 pm) and night (from 8 pm to 8 am) diuresis, dynamics of quantity, relative density of individual portions, nocturia.

In the Folgard concentration test (with dry diet), daily diuresis decreases to 300-500 ml, the specific gravity of urine increases, reaching 4-8 in 1028-1035 hours, not lower than 1025.

Reberg-Tareev test: glomerular filtration rate for creatinine - 80-160 ml / min, tubular reabsorption - 98-99%, with glomerulonephritis, the indicators decrease; in acute glomerulonephritis, the changes are transient; in chronic glomerulonephritis, they are persistent.

An ultrasound examination of the kidneys is mandatory: determining the size of the kidneys, their position, the thickness of the parenchyma to characterize sclerotic processes, deformation of the cavity systems.

A kidney biopsy is performed to clarify the diagnosis of a parenchymal disease; There are 3 types: open (during surgery), semi-open (through a surgical incision of the skin and subcutaneous tissue) and closed, or percutaneous (using a puncture needle). Contraindications: hemorrhagic diathesis, single kidney, polycystic, hydro- and pyelonephritis, severe hypertension, nephrocalcinosis, kidney tumor, negative attitude of the patient.

An immunological blood test is carried out: determining the number of the main immunocompetent forms of lymphocytes, immunoglobulins of classes A, M and J, total complement and the 3rd complement fraction, the number of circulating immune complexes to assess the state of all parts of the immune response, with acute glomerulonephritis and with exacerbation of chronic glomerulonephritis decreases the level of total complement and the 3rd fraction, the number of circulating immune complexes, immunoglobulins of all classes increases, the titer of antistreptolysin O increases.

They also conduct an ECG study (signs of left ventricular hypertrophy), an examination of the fundus (exudation, retinal edema, changes in the papillae of the optic nerve that appear with the development of chronic renal failure).

Complications. Complications in acute glomerulonephritis are acute renal failure, acute heart failure, renal eclampsia. In chronic glomerulonephritis, complications are left ventricular heart failure, chronic renal failure, anemia, uremic stomatitis, gastritis, colitis, bronchitis, polyserositis.

Differential diagnostics. When acute glomerulonephritis differential diagnosis is carried out with chronic glomerulonephritis, collagenosis, bacterial endocarditis, focal nephritis, urological diseases.

RџSЂRё chronic glomerulonephritis differential diagnosis is carried out with hypertension, left ventricular type heart failure, diabetic glomerulosclerosis, liver cirrhosis, amyloidosis, congestive kidney.

Treatment. Patients are shown a diet and regimen: with sufficient kidney function, protein restriction (within 1 g / kg of body weight), with the development of arterial hypertension, salt restriction, with edema - salt and water, restrictions during a pronounced inflammatory process. Glucocorticoids are prescribed (immunosuppressive, anti-inflammatory and desensitizing effect) - an initial dose of 60 mg / day for 3 weeks, then a decrease by 5 mg for 4 days to 40 mg, then by 2,5 mg for 2-3 days, maintenance therapy with persistent urinary syndrome. Cytostatics are administered (with a long process, the presence of a hypertensive syndrome, initial signs of renal failure, with the ineffectiveness of hormone therapy): azathioprine (daily dose of 150 mg), cyclophosphamide (daily dose of 200 mg) to suppress final immune responses; delagin, rezoquin, chloroquine. Also shown are anticoagulants and antiaggregants - heparin 20 thousand units per day for 5 days, then 5 thousand units daily for up to 3-4 weeks, chimes up to 300 mg per day orally on an empty stomach for 6-8 months; in severe renal bleeding aprotinin (antifibrinolytic drug), non-steroidal anti-inflammatory drugs (methindol) 100-150 mg per day for 1-2 months or more in acute glomerulonephritis with nephrotic syndrome. Calcium channel blockers, angiotensin-converting enzyme inhibitors (as pathogenetic therapy), reduction of proteinuria are prescribed.

Symptomatic therapy is carried out: antihypertensive, diuretic drugs, calcium salts, cardiac glycosides, desensitizing agents, large doses of vitamin C are prescribed. In case of uncomplicated AGN, in the first days, complete exclusion of salt, fluid restriction, ascorbic acid, calcium gluconate, if necessary, correction electrolyte disorders. With a persistent course of arterial hypertension, it is necessary to connect pathogenetic, antihypertensive, diuretic therapy. Programmed hemodialysis is carried out (in the absence of the effect of treatment, with an increase in renal failure), plasmapheresis.

Flow. In acute glomerulonephritis, there is usually a complete recovery or recovery with persistent proteinuria. In chronic glomerulonephritis, depending on the form, the course is progressive, with the development of chronic renal failure.

Forecast. In acute glomerulonephritis, the prognosis is favorable (mortality rate is 2%), in chronic glomerulonephritis, it is favorable in the latent form and unfavorable in other forms.

Prevention. Primary prevention measures include sanitation of foci of infection, their adequate treatment, and only appropriate vaccination.

Measures of secondary prevention: dispensary observation, treatment of complications and exacerbations, rational employment.

LECTURE No. 39. Chronic pyelonephritis

Chronic pyelonephritis is an inflammatory process involving the renal pelvis, calyces, and renal parenchyma and predominantly affecting the interstitial tissue.

Etiology. Etiological factors are the old focus of the inflammatory process in the urinary tract, cystitis, pyelitis. The disease can also be the result of untreated acute pyelonephritis.

Pathogenesis. Infection leads to a violation of urodynamics, stagnation of urine in the pelvis. Develop pyelovenous or pyelo-papillary refluxes, impaired lymphatic drainage, stasis, changes in hemodynamics. An inflammatory response develops.

Classification. Flow forms: latent, hypertonic, azotemicheskaya.

Clinic. The disease is detected many years after suffering inflammation of the urogenital area. Women get sick more often. The process can be one- or two-sided. It is characterized by low-symptomatic manifestations, it is possible to establish the disease by chance in the study of urine, an increase in blood pressure. The main symptoms: fatigue, headaches, epigastric pain, subfebrile condition, development of cystitis, dysuria, temperature rises only during exacerbation, chilling; unexplained fevers. Pain in the lumbar region is dull, constant, aggravated by bimanual palpation. Anemia develops even before kidney failure. Arterial hypertension is associated with renal ischemia, for a long time patients are subjectively well tolerated. Polyuria, pollakiuria, nocturia develop.

Additional diagnostic study. A complete blood count is performed (neutrophilic leukocytosis with a shift to the left is noted, an increase in ESR during exacerbation, anemia), a study of a general urinalysis: the specific gravity is reduced, moderate proteinuria, slight cylindruria, microhematuria, severe pyuria - there are many leukocytes, prevail over erythrocytes. With samples of Kakovsky-Addis, Nechiporenko to determine the ratio of erythrocytes, leukocytes, cylinders, an increase in the number of leukocytes is noted. With a latent course, a prednisone or pyrogenal test is indicative (positive, when after the administration of the drug 0,4 x 10⁹/_л and more leukocytes in 1 hour).

They also perform chronocystoscopy, excretory urography (there is a decrease in concentration ability, a violation of the tone of the pelvis, calyces and ureter, expansion of the calyces and pelvis with deformation of the fornixes), ultrasound examination (expansion and deformation of the pelvis, calyces is noted, the structure of the parenchyma changes, echogenicity) and X-ray examination ( visible expansion of the pelvis, necks, change in the structure of the cups, asymmetry of the lesion is characteristic even with a bilateral process).

Complications. Complications of the disease are secondarily wrinkled kidney, chronic renal failure, kidney tumor.

Differential diagnostics. Should be carried out with chronic glomerulonephritis, amyloidosis of the kidneys, nephrosclerosis.

Treatment. Nitropreparations are used: furagin or furadonin 0,1 g 3 times a day, nitroxoline (5-NOC) 0,1 g 4 times a day, nalidixic acid (nevigramon, blacks) 0,5-1 g 4 times a day 2-3 weeks, fast-acting sulfonamides (etazol, urosulfan) 4-6 g per day, prolonged action (biseptol-480) 1-2 g per day up to 2 weeks, sulfalene 0,25 g 1 time per day for a long time time, broad-spectrum antibiotics (with the ineffectiveness of nitrofurans and sulfonamides, with exacerbations), the course should be short, but adequate. Recommend the use of 1,5-2 liters of liquid during the day in the form of water, fruit and vegetable juices, herbal medicine for 2-3 weeks, spa treatment.

Flow. The course of the disease is long, with periods of exacerbations and remissions.

Forecast. The prognosis is favorable for uncomplicated forms, unfavorable for complications.

Prevention. Prevention measures are: timely treatment of acute pyelonephritis, treatment of coprostasis, chronic colitis, cholecystitis, sanitation of the oral cavity, proper nutrition with plenty of vitamins, preventive therapy with herbal preparations.

LECTURE No. 40. Chronic renal failure

Chronic renal failure is a gradually occurring and steadily progressive impairment of kidney function, leading to uremic intoxication.

Etiology. Etiological factors are: chronic glomerulonephritis, chronic pyelonephritis, diabetic glomerulonephritis, amyloidosis, polycystic kidney disease, nephrolithiasis, adenoma, prostate cancer.

Pathogenesis. Pathogenetic mechanisms of the disease: lack of parenchyma regeneration, inevitable structural changes in the parenchyma, a decrease in the number of functioning nephrons, their atrophy and shrinkage, impaired excretory, blood-purifying and homeostatic functions, retention of nitrogenous metabolic products in the blood: urea, uric acid, ammonia, amino acids, creatinine, guanidine, phosphate retention, increased plasma and extracellular fluid potassium levels, hypocalcemia.

Classification. The composition of chronic renal failure includes: chronic uremia, diffuse sclerosing glomerulonephritis, end-stage kidney disease, and other manifestations of chronic renal failure.

Table 5. Stages of chronic renal failure (according to Shulutko B.I., 1994)

Clinic. When subclinical form there is an increase in the amount of fluid you drink (up to 3 liters per day), nocturia (up to 3 times per night), dryness, flabbiness of the skin, its peeling, daytime sleepiness, weakness, fatigue, tinnitus, hearing loss.

RџSЂRё clinical form there are signs of pulmonary heart failure, severe anemia, changes in the liver, gastrointestinal tract without impaired function.

RџSЂRё terminal form intoxication is expressed: slowness, lethargy, drowsiness, puffy face, dry skin, excruciating itching, no sweating, muscle weakness, muscle twitching, large convulsions (due to a decrease in calcium in the blood), deep noisy breathing, chest pain, development of secondary pneumonia, wet wheezing, in the terminal stage - uremic pulmonary edema. Uremic pericarditis develops (auscultatively: pericardial friction rub), hypertensive cardiovascular syndrome, uremic vasculitis, visceritis, hypothermia. Appears anorexia, aversion to food, nausea, vomiting, heaviness, fullness in the epigastrium after eating, thirst. Anemia, toxic leukocytosis with a neutrophilic shift to the left, thrombocytopenia, and a violation of blood coagulation develop. There is damage to the bones, a change in the skeleton, secondary gout, a change in polyuria to oligo- and anuria, the urinary syndrome is slightly expressed.

Additional diagnostic study. A study of blood serum creatinine, a study of nitrogenous metabolic products (residual nitrogen, urea, uric acid), a study of the state of electrolyte and mineral metabolism, an acid-base state, an ultrasound examination of the kidneys, an ECG study are carried out.

Treatment. Patients are shown a diet (physiological, complete) to prevent the breakdown of their own protein, possibly in combination with parenteral administration of anabolic hormones (retabolil 50 mg intramuscularly 1 time in 10-15 days), an extended drinking regimen.

Elimination of hyperkalemia: the introduction of large amounts of glucose 40% - 100 or 200 ml with the addition of 15-20 units of insulin, 10% calcium chloride solution, 3-5% sodium bicarbonate solution (increase in blood potassium levels up to 7 g / day is an absolute indicator for connection to an artificial kidney).

Elimination of hyponatremia: intravenous administration of 10% sodium chloride solution.

Elimination of hypernatremia: the introduction of natridiuretics (10% calcium gluconate solution), tachystin (0,125 mg).

Elimination of acidosis: diet, soda enemas, intravenous administration of alkaline solutions.

Elimination of alkalosis: ammonium or 200 ml of 2% potassium chloride solution;

Elimination of anemia: testosterone 300 mg per week for 3-6 months or sustanon 1 ml intramuscularly 1 time per week; iron preparations only in case of their deficiency, the amino acid histidine, blood transfusion only in case of acute blood loss and hemoglobin level below 60-70 g/l.

Hemodialysis is carried out: hydrocarbonate on capillary dialyzers based on highly permeable cellulose acetate membranes 3-5 times a week for 5 hours. diseases, hemorrhagic syndrome): dialysis fluid is introduced into the peritoneal cavity in small portions for a certain time, and then replaced with a fresh solution. Hemosorption is used: removal of toxic substances from the blood when it passes through a column with activated carbon, the content of toxic substances decreases markedly after 60 hours from the start of the procedure.

To reduce renal hypertension, all antihypertensive drugs are used, a decrease in pressure to normal values is not shown: only to a working level to prevent a decrease in filtration function.

To reduce the edematous syndrome, thiazide derivatives, furosemide with a possible combination with triamterene, veroshpiron are prescribed in the absence of hyperkalemia.

They use herbal preparations (lespenephril (despidoza drug)), kidney transplantation.

Forecast. The prognosis is determined by the phase of renal failure, the rate of its development.

Prevention. Preventive measures: active treatment of underlying diseases, systematic planned secondary prevention of chronic renal failure, clinical examination.

LECTURE No. 41. Systemic lupus erythematosus

Systemic lupus erythematosus is a chronic polysyndromic disease predominantly of young women and girls predisposed to it.

Classification (according to V. A. Nasonova). When making a diagnosis, it is necessary to separate:

1) according to the form of the course: acute, subacute, chronic, with a continuously relapsing course (malignant);

2) according to the degree of activity (see Table 6);

Table 6. Levels of activity of systemic lupus erythematosus

3) by stages: I - initial, II - generalized, III - terminal.

Clinic. When acute course characterized by an acute onset, the development of polysyndromicity over the next 3-6 months (lupus nephritis or CNS damage).

RџSЂRё subacute course the onset is gradual, arthralgia, nonspecific skin lesions are pronounced. The wave-like course is characteristic, the development of polysyndromicity within 2-3 years.

RџSЂRё chronic course for a long time there are relapses of individual syndromes, the development of polysyndromicity at the 5-10th year, the development of deforming polyarthritis at the 10-15th year.

Lupus crises- manifestations of the activity of the lupus process. Characterized by pronounced clinical polysymptomatics, changes in laboratory parameters, general trophic disorders.

Criteria for making a diagnosis (American Rheumatological Association, 1982) are rashes in the zygomatic region ("butterfly"), discoid rash, photosensitivity, ulcers in the oral cavity - mild or painless, arthritis without destruction of cartilage, two or more peripheral joints, serositis (pleurisy, pericarditis), kidney damage (persistent proteinuria, 0,5 g / day or more), neurological disorders (convulsions), hematological disorders, immune disorders, the appearance of antinuclear antibodies with an increase in their titer.

If four or more signs are present, the diagnosis is considered reliable.

Additional diagnostic study. A complete blood count is being studied (anemia, hemoglobin less than 100 g / l, normo- or hypochromic leukopenia, thrombocytopenia, an increase in ESR during exacerbations), a biochemical blood test (dysproteinemia, hypoalbuminemia, an increase in α₂-globulins in the acute period of the disease, γ-globulins in the chronic). Mandatory immunological examination of blood (LE-cells, antibodies to DNA, to native DNA, ribonucleoprotein, other nuclear substances, the study of the level of activity of the immune system: cellular, humoral, non-specific links). A general urine test is also performed (specific gravity, protein, enzyme elements, epithelium, salts), skin biopsy (morphological changes, fixed immune complexes, IgJ and IgM, complement).

Complications. Complications of the disease are chronic renal failure, pulmonary heart failure, acute adrenal insufficiency, cytopenia.

Differential diagnostics. Should be carried out with systemic scleroderma, dermatomyositis, periarteritis nodosa, rheumatic heart disease, bacterial endocarditis, rheumatoid arthritis, hemoblastosis, drug disease.

Treatment. Patients are prescribed glucocorticoids (prednisolone 50-60 mg followed by a decrease of 2,5-5 mg per week) - for many years, immunosuppressants (azathioprine 100-150 mg, 6-mercaptopurine 150-200 mg, leukeran 10-15 mg) - several months, then a maintenance dose of 50-100 mg for many months, complications may develop - leukopenia, thrombocytopenia, infectious complications (pneumonia), dyspepsia. It is possible to use pulse therapy: 1000 mg of methylprednisolone 3 days in a row or 3 times every other day in 100 ml of isotonic sodium chloride solution or 500 mg for 2 times with the addition of 5000 IU of heparin and suprastin; adjunct to conventional hormone therapy. Drugs of the 4-aminoquinoline series (chloroquine, delagil, plaquenil) are used at 0,75 g each, followed by a decrease to 0,25 g - for several years, non-steroidal anti-inflammatory drugs (butadione, indomethacin, etc.) - for several years, anticoagulants (heparin 10 -000 IU under the skin of the abdomen) - several months, antiplatelet agents (chimes 20-000 mg) - several months, plasmapheresis, hemosorption - up to 150-200 sessions.

Forecast. The prognosis of the disease is unfavorable.

LECTURE No. 42. Systemic scleroderma

This disease occurs in young and middle-aged women.

Classification. When refining the forecast, the classification of N. G. Guseva (1988) is used:

1) downstream;

2) according to the stage of the disease;

3) according to the degree of activity (see Table 7).

Table 7. Determination of prognosis in systemic scleroderma

Clinic. The main syndromes are vascular (Raynaud's syndrome), trophic disorders (a symptom of a rat bite, ulcerative lesions), skin (masculine face, skin thickening), musculoskeletal (arthralgia in large joints, polyarthritis, fibrosing myositis, muscle weakness), visceral (lesions heart - non-coronary sclerosis, myocarditis, mitral disease, pericarditis, lungs - pneumosclerosis, digestive tract - dysphagia, gastritis, enteritis; kidneys - chronic nephritis, acute scleroderma nephropathy, nervous system - polyradiculoneuritis, meningoencephalitis), asthenovegetative (weight loss, weakness, increased fatigue , unstable fever).

RџSЂRё chronic course progression of Raynaud's syndrome. Over time, there are changes in the nail phalanges, thickening of the skin, periarticular tissues, the formation of contractures, osteolysis, slowly progressive changes in internal organs.

RџSЂRё subacute course there is a dense swelling of the skin, recurrent polyarthritis, myositis, damage to internal organs.

RџSЂRё acute course - a rapidly progressive variant of the course, fibrinous and visceral lesions already in the first year of the disease, the formation of a scleroderma kidney.

Additional diagnostic study. The examination algorithm corresponds to diagnostic tactics in connective tissue diseases.

Criteria for making a diagnosis are skin changes in the form of dense edema, induration and atrophy, Raynaud's syndrome, osteolysis, soft tissue calcification, musculoskeletal syndrome with the development of contractures, basal pneumonitis, macrofocal cardiosclerosis, lesions of the digestive tract, esophagus, true scleroderma kidney, skin hyperpigmentation, trophic disorders , immune disorders, the appearance of antinuclear antibodies with an increase in their titer.

If four or more signs are present, the diagnosis is considered reliable.

Differential diagnostics. Should be carried out with systemic connective tissue diseases, rheumatoid arthritis, infectious myocarditis, atherosclerotic cardiosclerosis, pneumoconiosis, sarcoidosis, tuberculosis, chronic pneumonia, esophageal cancer.

Treatment. For the treatment of the disease, hormones, immunosuppressants, 4-aminoquinoline drugs, non-steroidal anti-inflammatory drugs, anticoagulants, antiplatelet agents are used - as in other connective tissue diseases, anabolic hormones in cachexia. Physiotherapy is used: electrophoresis with lidase, ultrasound, paraffin applications; massage, physiotherapy exercises, radon, hydrogen sulfide baths in chronic course.

Forecast. In the chronic course, the prognosis is relatively favorable, with stabilization, in the acute and subacute course - unfavorable.

LECTURE No. 43. Nodular periarteritis

Periarteritis nodosa is a systemic necrotizing vasculitis of the arteries of medium and small caliber with the formation of vascular aneurysms and secondary damage to organs and systems.

Men are predominantly ill.

Predisposing factors. Risk factors are drug intolerance, hypersensitivity to food, household and professional influences, cooling and insolation, a history of allergic diseases, arthralgia, myalgia, genetic predisposition to allergic and systemic diseases.

Clinic. The main syndromes of the disease are asthenovegetative (weight loss, undulating fever with high temperatures that do not decrease under the influence of antibiotics, weakness, adynamia), cardiac (coronary insufficiency syndrome, heart attacks are possible), hypertensive (arterial hypertension), pulmonary (pneumonitis, asthmatic syndrome), abdominal (abdominal pain, dyspepsia, bleeding), hepatolienal (more often the liver increases), nephrotic (nephritis, nephrosclerosis with typical clinical manifestations), neurological (polyneuritis), trophic changes (subcutaneous nodules), articular (polyarthralgia), Wegener's syndrome (triad : rhinitis, sinusitis, followed by ulceration of the bones and cartilage of the nose; pulmonary vasculitis; kidney damage with the development of failure).

Course options: acute, subacute, chronically recurrent.

The diagnostic criteria are kidney damage with arterial hypertension, typical abdominal syndrome, combined with dyspeptic disorders, pneumonitis or bronchial asthma with high eosinophilia, cardiac syndrome in the form of coronaritis, polyneuritis.

Three out of five criteria are required for diagnosis.

Additional diagnostic study. Examination algorithm as in systemic connective tissue diseases.

Table 8. Clinical and morphological signs of individual nosological forms of systemic vasculitis (according to E. N. Semenkova, 1988)

Differential diagnostics. Should be carried out with systemic connective tissue diseases, infectious diseases, bacterial endocarditis, appendicitis, intestinal obstruction, ulcer perforation, hemoblastoses (Table 8).

Treatment. Hormone therapy is carried out (prednisolone 30-40 mg for 1-2 months, followed by a dose reduction to a maintenance dose of 10-15 mg, complications may develop - steroid vasculitis), a combination of glucocorticoids with cyclophosphamide and azathioprine - up to several years. Heparin, trental, curantyl (improvement of blood rheological parameters), plasmapheresis, hemosorption up to 5-6 sessions are also used. Physiotherapy procedures are contraindicated. Symptomatic treatment is carried out.

Forecast. The prognosis is unfavorable.

LECTURE No. 44. Rheumatoid arthritis

Rheumatoid arthritis is a chronic systemic connective tissue disease with a progressive lesion of predominantly peripheral (synovial) joints, similar to erosive-destructive polyarthritis.

Classification. When making a diagnosis, a division is made:

1) according to clinical characteristics: poly-, oligo-, monoarthritis, the presence of visceritis, combination with other rheumatic diseases;

2) by the presence of rheumatoid factor: seropositive, seronegative;

3) according to the degree of activity: minimal I, moderate II, maximum III, remission;

4) according to the x-ray stage: I - osteoporosis, II - narrowing of the joint spaces, III - erosion, IV - ankylosis;

5) by functional insufficiency: I degree - professional ability is preserved, II degree - is lost, III degree - the ability to self-service is lost.

Clinic. The main syndromes are articular (damage mainly to small joints of the hands and feet, ulceration of the cartilage of the surface of the joints, deformity, ankylosing, morning stiffness syndrome), cardiac (myocarditis, endocarditis with the formation of a superficial heart disease, pericarditis), pulmonary (adhesive pleurisy, fibrosing pneumonitis) , renal (chronic glomerulonephritis, amyloidosis), trophic disorders (rheumatoid nodules in the periarticular tissues of the affected joints), vascular (digital arteritis in the nail phalanges), asthenovegetative (fever, weight loss), anemic (secondary iron deficiency anemia).

The main clinical forms are articular (the main form of manifestation of the disease - in 80% of cases), benign, articular-visceral, Felty's syndrome (1% of cases - pancytopenia, enlargement of the spleen and peripheral lymph nodes), malignant, rapidly progressive form, Sjögren's syndrome (involvement parenchyma of the salivary and lacrimal glands with subsequent atrophy).

The basis of diagnosis are major and minor criteria.

К big criteria include the following:

1) morning stiffness;

2) pain during movement or soreness of at least one joint;

3) joint swelling;

4) swelling of at least one more joint (established with an interval of no more than 3 months);

5) symmetry of swelling of the joints;

6) subcutaneous nodules;

7) typical radiological changes in the joints with the inclusion of periarticular osteoporosis;

8) rheumatoid factor in the blood;

9) characteristic changes in synovial fluid;

10) characteristic histological changes in the synovial membrane;

11) characteristic histology of rheumatoid nodules.

In the presence of seven criteria, the diagnosis is considered reliable, less than seven criteria - probable.

Small Criteria:

1) subcutaneous rheumatoid nodules;

2) medium or high titers of rheumatoid factor;

3) characteristic radiological changes in the joints;

4) the presence of a symptom of morning stiffness (at least 30 minutes);

5) the presence of a rheumatoid hand (ulnar deviation, "walrus flipper").

If these signs are present, a diagnosis of rheumatoid arthritis can be made.

Additional diagnostic study. The examination algorithm corresponds to that adopted for systemic connective tissue diseases. High titers of rheumatoid factor are found, with x-ray studies - narrowing of the interarticular gaps, erosion, ankylosis.

Complications. Complications are subluxations, ankylosing, bursitis, cysts, secondary iron deficiency anemia, amyloidosis, neurocirculatory dystonia of mixed origin, recurrent iridocyclitis, atrophic changes in regional muscles, secondary infections.

Differential diagnostics. Should be carried out with acute rheumatism, reactive polyarthritis, systemic lupus erythematosus, rheumatoid-like syndromes (Bekhterev's disease, Sjögren's, Reiter's disease, psoriatic arthropathy), deforming osteoarthritis, gout.

Treatment. Non-steroidal anti-inflammatory drugs are prescribed (butadione, indomethacin, voltaren, ortofen, brufen, naproxen, ketoprofen, ponstan, etc.), preference is given to long-acting drugs. Hormone therapy is carried out (corticosteroids, with the ineffectiveness of non-steroidal anti-inflammatory drugs and the ongoing activity of the process - 15-20 mg with a slow decrease and the addition of non-steroidal anti-inflammatory drugs in increasing doses). Cytostatic immunosuppressants are administered (decrease in the formation of immune complexes and rheumatoid factor) - azathioprine pr 50 mg 2-3 times a day, chlorbutin 2 mg 2-3 times a day; D-penicillinamine, cuprenil 0,15-0,3 g 2-3 times a day for 4-5 months, delagil. Basic therapy is carried out with gold preparations (krizanol 2 ml intramuscularly once a week for 1-7 months), aminoquinoline preparations are used: rezoquin, plaquenil 8-0,12 g, 0,25 tablet at night for 1-10 months. Plasmapheresis, hemosorption (to remove immune complexes) is also carried out.

Physiotherapy treatment, physiotherapy exercises, sanatorium treatment, surgical methods of correction are shown - to restore the function of the joints.

Flow. The course of the disease depends on the form: with articular - slowly progressive with gradual deformation of the joints (10-15 years), with articular-visceral - rapidly progressive (2-3 years).

Forecast. With the articular form, the prognosis is favorable, with the articular-visceral form - unfavorable.

Prevention. To prevent the development of relapses of the disease, long-term use of basic drugs, non-steroidal anti-inflammatory drugs is carried out.

LECTURE No. 45. Allergy

Allergy - the appearance of increased sensitivity of the body to the allergen in response to repeated contact with it.

Allergens are antigens that cause allergic reactions. Almost all high- and low-molecular compounds of organic and inorganic nature (antigens and haptens) can acquire the properties of allergens under certain conditions.

Allergens are divided into:

1) household;

2) fungal;

3) animal origin;

4) medicinal;

5) food;

6) microbial;

7) vegetable;

8) simple chemicals.

The intensity of an allergic reaction depends on the nature of the allergen, the exposure dose, the way the antigen enters, the genotype of the individual, and the state of the immune system.

Manifestations of allergenicity depend on environmental factors - air temperature, humidity, wind speed.

Allergic status is associated with a system of histocompatibility antigens:

1) hay fever with HLA-A1, B8;

2) atopic dermatitis with HLA-Bw35;

3) combinations of atopic dermatitis with rhinitis with HLA-Bw40;

4) combinations of atopic dermatitis with bronchial asthma with HLA-B12;

5) atopic eczema with HLA-A1 and HLA-B8 (simultaneously);

6) exogenous allergic alveolitis with HLA-Bw40;

7) genetically determined hyperproduction of IgE with HLA-Dw2. This form is inherited in an autosomal recessive manner and manifests itself during the 1st year of life.

Patterns of the immune response to allergen exposure

There are 3 stages of the immune response:

Stage I - immunological: providing T-lymphocytes with an allergen by macrophages in combination with MHC proteins of class I or II, differentiation of CD4T helpers; increase in antibody titer, interaction of the allergen with antibodies;

Stage II - pathochemical: the release of allergy mediators by various cellular elements - histamine, serotonin, kinins, leukotrienes, prostaglandins, chemotaxis factor, activated complement fractions;

Stage III - pathophysiological: the development of clinical manifestations of allergic reactions.

LECTURE No. 46

Drug disease is associated with the production of antibodies or the appearance of T-lymphocytes specific for the drug or its metabolites.

The first report of drug allergy or serum sickness caused by the administration of horse serum appeared more than 100 years ago. Until the end of the 1930s. (appearance of sulfonamides) complications of drug treatment were observed in 0,5-1,5% of patients. Currently, drug allergy only in patients who are in the hospital occurs in 15-30% of cases.

Reasons for development include repeated use of intolerable drugs: penicillins, chymopapain, immune sera, live viral vaccines, barbiturates, sulfonamides, quinidines, quinine, allopurinol, iodine preparations, hydralazine, timolol, propranolol, cromolyn, nitrofurantoin, isoniazid, gold preparations, carbamazepine, methyldopa , phenacetin, heparin, phenylbutazone, antithyroid drugs, aspirin, indomethacin, opioids, halothane, penicillinamine.

Ways of formation

There are 5 types of drug allergic reactions based on the classification of F. Gell and R. Coombs (1964):

1) anaphylactic: sensitization of the body is associated with hyperproduction of cytophilic IgE, which are quickly fixed by the Fc fragment on tissue basophils - mast cells, to a lesser extent on eosinophils and other cells; this is accompanied by a low plasma IgE concentration. When each antigen molecule binds to two IgE molecules (with an obligatory excess of antibodies), a large amount of biologically active substances is released on the surface of the mast cell;

2) cytotoxic: sensitization is characterized by the production of antibodies against antigens that are direct or secondary components of cell membranes; antibodies are IgJ, less often - IgM. The immunoglobulin molecule binds to an antigen located in the cell membrane, the Fab fragment; free Fc-fragment, its CH2 domain bind complement with the formation of a membrane attack complex, perforation of the cell membrane and its subsequent lysis;

3) immunocomplex: occurs when pathogenic circulating immune complexes (CIC) appear in the plasma; pathogenicity is acquired with the insolubility of the CEC, in the case of complement deficiency, or in violation of their normal clearance by RES cells;

4) cellular (delayed-type hypersensitivity): occurs on allergens that are part of large molecules, which are then phagocytosed by macrophages, without damaging antigenic determinants; they are expressed on the macrophage membrane and combined with their own cellular antigen of the HLA-D clone; information from the antigen on the macrophage is read by T-lymphocytes, a protein is synthesized that is complementary to the antigen structure with its expression on the lymphocyte membrane;

5) immunological stimulation: is a variant of the type 2 reaction, develops when antibodies to cell receptors appear; Immunoglobulin binds to the Fab fragment receptor and activates complement, but the resulting membrane attack complex only stimulates this receptor and the specific function of the cell.

Classification. Complications associated with infusion, transfusion, and therapeutic injections include:

1) anaphylactic shock associated with the introduction of serum;

2) vascular complications associated with infusion, transfusion and therapeutic injection.

The rate of development of allergic reactions. Early allergic reactions (urticaria and anaphylactic shock) develop within 30 minutes after repeated administration of the drug.

Delayed allergic reactions (urticaria, itching, bronzospasm, laryngeal edema) develop 2-72 hours after repeated use of the drug.

Late allergic reactions (maculopapular rash, urticaria, arthralgia, fever) develop no earlier than 72 hours after repeated administration of the drug.

Clinical manifestations. Allergic reactions of immediate type. Caused by many drugs, most often penicillins, develop within 30 minutes after drug administration. Urticaria, Quincke's edema, bronchospasm, anaphylactic shock appear. Rarely, with the introduction of penicillins, Stevens-Johnson syndrome, Lyell's syndrome, interstitial nephritis, systemic vasculitis, hemolytic anemia, neutropenia, neuritis can develop.

Cytotoxic allergic reactions. With this form, hematological disorders develop: autoimmune hemolytic anemia, thrombocytopenia, agranulocytosis. The kidneys are affected: with interstitial nephritis caused by methicillin, antibodies to the basement membrane of the renal tubules appear.

Immune complex allergic reactions. Most often caused by penicillins, heterologous sera. Serum sickness symptoms usually appear 1-3 weeks after serum administration. Urticaria, maculopapular rash, fever, arthralgia (large joints) develop, lymph nodes may increase, glomerulonephritis, peripheral neuropathy, systemic vasculitis, acute inflammatory demyelinating polyradiculoneutropathy may occur. It is possible to develop drug-induced lupus syndrome, vasculitis with symptoms of fever, hemorrhagic rash, more often on the legs, with damage to the kidneys and lungs.

Delayed allergic reactions. These include allergic contact dermatitis (after topical application of drugs), acute pneumonitis, interstitial pneumonitis, encephalomyelitis, interstitial nephritis, drug-induced hepatitis, vasculitis. Acute and interstitial pneumonitis is characterized by fever, dyspnea, cough, eosinophilia, limited or extensive opacities in the lungs, pleural effusion, and respiratory failure.

RџSЂRё additional diagnostic study skin tests are used:

1) in allergic reactions of the immediate type: intradermal injection of the antigen is manifested by hyperemia and a blister at the injection site due to degranulation of mast cells and the release of inflammatory mediators;

2) in delayed-type allergic reactions, skin tests have no diagnostic value;

Application tests reveal sensitization to drugs for topical use only.

The level of specific IgE is determined with the production of a radioallergosorbent test or a histamine release reaction by mast cells.

Immunological determination of specific IgJ and IgM to drugs, fixed in tissues or circulating immune complexes (CIC) is performed.

To identify sensitized T-lymphocytes, the reaction of lymphocyte blast transformation (RBTL) is performed or cytokine production is evaluated. This method is more sensitive than RBTL.

Provocative tests allow you to establish a connection between the use of the drug and the occurrence of an allergic reaction. Due to the high risk of developing severe allergic reactions, samples are used very rarely, only in a hospital.

Complications. These include allergy to drug metabolites, pseudo-allergic reactions.

Differential diagnostics. Should be carried out with the primary side effect of the drug, which develops when using drugs in therapeutic doses and is associated with their direct effect on target organs.

It is necessary to exclude the secondary side effect of the drug as a complication of drug treatment that is not associated with the direct effect of drugs on target organs.

You must also exclude:

1) idiosyncrasy, a qualitatively altered response to the drug, due to non-immune mechanisms;

2) drug intolerance - the appearance of side effects when prescribing drugs in low doses;

3) toxic manifestations that develop with an overdose of the drug;

4) systemic lupus erythematosus;

5) vasculitis;

6) dermatitis, skin diseases.

Treatment. First of all, the drug that caused the allergic reaction is canceled.

In case of a type I allergic reaction, epinephrine, H₁blockers, with allergic reactions II, III and IV types - corticosteroids.

RџSЂRё anaphylactic shock it is necessary to quickly assess the patency of the respiratory tract, indicators of external respiration and hemodynamics. The patient should be laid on his back with raised legs. When breathing and blood circulation stop, immediately begin cardiopulmonary resuscitation.

A tourniquet is applied above the injection site, every 10 minutes it is loosened for 1-2 minutes. A solution of adrenaline 1: 1000 is injected subcutaneously into the shoulder or thigh: for adults - 0,3-0,5 ml, for children - 0,01 ml / kg, if necessary, the administration is repeated after 15-20 minutes.

The injection site of the injected allergenic drug (with the exception of the head, neck, hands and feet) is chipped with 0,1-0,3 ml of adrenaline solution 1: 1000. In case of arterial hypotension, 1 ml of adrenaline solution 1: 1000 is diluted in 10 ml of saline, the resulting solution 1:10 is given intravenously over 000-5 minutes. After that, if necessary, an infusion of adrenaline 10: 1 can be carried out. For this, 1000 ml of adrenaline 1: 1 is diluted in 1000 ml of a 250% glucose solution. The initial rate of administration is 50 μg / min, in the absence of side effects, the rate increases to 1 μg / min.

With coronary heart disease, atherosclerosis of the cerebral vessels in the elderly, side effects of the action of adrenaline may appear.

With cyanosis and severe shortness of breath, oxygen is inhaled at a moderate or high rate (5-10 l / min.) Using a mask or nasal catheter. In chronic obstructive pulmonary diseases, oxygen inhalations are contraindicated, since they lead to depression of the respiratory center.

To prevent the recurrence of symptoms of an anaphylactic reaction, N₁blockers: diphenhydramine - 1-2 mg / kg intravenously (for 5-10 minutes), intramuscularly or orally. A single dose should not exceed 100 mg. Then the drug is taken at 25-50 mg orally every 6 hours for 2 days.

Additionally, N₂- histamine receptor blockers: cimetidine is used at a dose of 300 mg (children 5-10 mg / kg) intravenously slowly, intramuscularly or orally every 6-8 hours, ranitidine at a dose of 50 mg intravenously slowly or intramuscularly every 6-8 hours or 150 mg orally every 12 hours (children 2-4 mg / kg).

If arterial hypotension and respiratory failure persist, the patient is transferred to the intensive care unit, where the following medical measures are taken:

1) intravenous fluid infusion through a catheter with a maximum diameter: 5% glucose solution in 0,45% sodium chloride solution - 2000-3000 ml / m² per day. Within 1 hour, 500-2000 ml of liquid is injected, for children - up to 30 ml / kg. With persistent arterial hypotension, physiological saline, albumin, colloidal solutions are also used;

2) β is used for bronchospasm₂- adrenostimulants: 0,5-1,0 ml of 0,5% salbutamol solution; while maintaining bronchospasm, aminophylline 4-6 mg/kg is administered intravenously over 15-20 minutes;

3) in the absence of the effect of the treatment, adrenostimulants are prescribed: norepinephrine intravenously, 4-8 mg of norepinephrine is dissolved in 1000 ml of a 5% glucose solution in water or saline, the maximum injection rate should not exceed 2 ml / min if the patient takes glucagon , β-blockers are additionally prescribed 5-15 mcg / min intravenously;

4) instead of norepinephrine, dopamine may be prescribed, more often in patients with heart failure: 200 mg of dopamine is dissolved in 500 ml of a 5% glucose solution, administered intravenously at a rate of 0,3-1,2 mg / kg per hour;

5) with a pronounced edema of the upper respiratory tract, tracheal intubation or tracheostomy is indicated;

6) corticosteroids are prescribed early, as they prevent the recurrence of symptoms: hydrocortisone is administered at a dose of 7-10 mg / kg intravenously, then 5 mg / kg intravenously every 6 hours, the duration of treatment is not more than 2-3 days;

7) after stabilization of the condition, the administration of liquid and medication continues for up to several days (depending on the severity of the condition).

Flow. depending on the type of allergic reaction. Recovery is complete.

Death from severe anaphylactic reactions occurs within the first 30 minutes. Complications include the development of myocardial infarction and stroke.

Forecast. With an allergic reaction of type I in case of untimely resuscitation, the prognosis is unfavorable, with allergic reactions of types II, III and IV - favorable.

Prevention. It is necessary to conduct a mandatory collection of an allergic history, to exclude drugs that often cause allergies.

When prescribing drugs, possible cross-reactions should be taken into account, more often developing:

1) between penicillins and cephalosporins;

2) various aminoglycosides (such as streptomycin, kanamycin, neomycin, gentamicin);

3) para-aminobenzene derivatives (such as sulfonamides, sulfonylurea derivatives, thiazide diuretics, procaine, acetylsalicylic acid).

If it is impossible to cancel or replace the drug, provocative tests with a gradual increase in its doses must be carried out.

Usually, the route of administration of the drug is used, which is supposed to be the main one. The drug in increasing doses is prescribed every 15 minutes (Bezredka method). With the development of an anaphylactic reaction during a provocative test, the drug is abandoned.

In life-threatening conditions and the development of an anaphylactic reaction to the drug during a provocative test, when it is impossible to replace the drug with another, desensitization is performed.

For mild to moderate local reactions, the drug is re-introduced at the same dose that caused the reaction, after which the dose is gradually increased.

With an anaphylactic or severe reaction, the dose of the drug is reduced, and then increased more smoothly.

Author: Myshkina A.A.

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