The state of sanogenesis and pathogenesis in pneumonia. Pathogenesis of pneumonia, features of etiology and forms of disease damage

Pneumonia is an infection of the lungs. It is characterized by the development of inflammation in organ tissue. Its nature may be viral, bacterial, fungal or other. Every year, approximately 500 thousand people worldwide are diagnosed with pneumonia, and 1.5% die due to the disease. Death occurs due to misdiagnosis, when the disease is confused with other disorders and treated incorrectly.

For timely diagnosis It is important to know about the etiology and pathogenesis of pneumonia.

Course of the disease

The pathogenesis of pneumonia is based on damage to the lungs by an infectious pathogen. Usually pathogenic microflora enters different parts of the lung through the bronchi - this is the bronchoorgan route.

The hematogenous route of infection is also common. This pneumonia occurs as a complication of sepsis or other infections.

Lymphogenic pathway - through lymph. It is caused by activation of the microflora of the lungs.

Classification

Specific types of pneumonia are distinguished according to the following groups:

• reasons for development;
• duration of symptoms;
• type of pathogen;
• the route of entry of the microbe into the lungs;
• the focus of the pathology and its prevalence.

Each type inflammatory process characterized by characteristic features and symptoms. In this regard, in order to correctly identify the disorder and prescribe treatment, the specialist first diagnoses the type and establishes the pathogenesis of pneumonia.

The severity of the pathological process largely influences the duration of therapy for pneumonia:

1. Mild form - therapy is implemented within 5 - 10 days.
2. Moderate severity - treatment takes 1 - 2 weeks.
3. Severe form - requires mandatory hospital treatment for 2 - 3 weeks.

Etiology

Pneumonia is characterized by the presence of a large number of causes that can trigger its development. The inflammation may be non-infectious or infectious nature. The disease develops in isolation or as a complication primary disease. Bacterial infection is the most common among all provoking factors. It occurs independently or can be a complication of a viral or bacterial-viral infection.

The main causative agents of pneumonia include:

• Gram-positive pathogens: most often pneumococci - 70 - 95%, staphylococci - no more than 5%, streptococci - 2.5%.
• Gram-negative enterobacteria: Pseudomonas aeruginosa, rod-shaped intestinal bacterium.
• Mycoplasma – from 6 to 20% of cases.
• Viruses, these can be adenoviruses, influenza, herpes viruses - the share of such lesions accounts for 3 - 8%.
• Fungi - candida, yeast, etc.

Non-infectious causes include:

• Inhalation of toxic substances of the asphyxiating type - kerosene, oil, gasoline, chlorophos.
• Chest injuries - blows, bruises, compression.
• The influence of allergens - dust, pollen, pet hair, some medications.
• Burns of the respiratory system.
• Radiation therapy, which is used to treat cancerous tumors.

Factors that increase the risk of infection should also be highlighted. For children it is:

• hereditary disorder of the immune system;
• intrauterine asphyxia or oxygen starvation of the fetus;
• congenital pathologies of the heart or lungs;
• malnutrition;
• birth injuries;
• pneumopathy.

In teenagers:

• smoking;
• the presence of chronic infectious foci in the nasopharynx or nasal cavity;
• caries;
• acquired heart defects;
• poor functioning of the immune system, and therefore frequent damage by bacterial and viral infections.

In adults, pneumonia etiologies include:

• chronic respiratory pathologies of the lungs and bronchi;
• smoking and alcohol abuse;
• decompensated stage of heart failure;
• diseases of the endocrine system;
• drug addiction, in particular snorting drugs through the nose;
• immunodeficiency, which includes HIV and AIDS;
• prolonged forced stay in a lying position, for example, after a stroke;
• complication after chest surgery.
• prolonged forced stay in a supine position, for example, during a stroke;
  as a complication after surgical operations on the chest.

Epidemiology

IN modern world pneumonia ranks 4th - 6th in terms of fatal outcome. The incidence of morbidity in people over 60 years of age is very high. Men are slightly more likely to suffer from this pathology.

The main risk factors are:

• hypothermia;
• age group after 60 years;
• smoking - smoke from cigarettes disrupts the proper functioning of the cilia, it thickens sputum and suppresses the immunity of macrophages, impairs the production of immunoglobulin;
• primary, secondary immunodeficiency;
• periods after surgery, especially when surgical intervention affected the chest cavity or top part abdominal region;
• frequent contact with rodents and birds.

Favorable prognoses in the treatment of pneumonia in most cases depend on the effectiveness of the use of antibiotics and the correct selection of medications and their dosage. Correct diagnosis and appropriate treatment guarantee recovery in 3 to 4 weeks.

If the pathological process is started, complications arise and a protracted form develops, characterized by a high risk of death.

Every person should understand that pneumonia is a serious and dangerous disease, the treatment of which takes a long time. To prevent the development of this condition, it is necessary to properly organize the microclimate in the house, maintain the functioning of the immune system and pay sufficient attention to the state of health.

Pneumonia– an acute infectious-inflammatory disease of the lungs involving all structural elements of the lung tissue with obligatory damage to the alveoli and the development of inflammatory exudation in them.

Epidemiology: the incidence of acute pneumonia is 10.0-13.8 per 1,000 population, among persons > 50 years old - 17 per 1,000.

ThisIology:

A) community-acquired (out-of-hospital) pneumonia:

1. Streptococcus pneumoniae (pneumococcus) – 70-90% of all patients with community-acquired pneumonia

2. Haemophilus influenzae (hemophilus influenzae)

3. Mycoplasma pneumoniae

4. Chlamydia pneumoniae

5. Legionella pneumophila

6. Other pathogens: Moraxella catarralis, Klebsiella pneumoniae, Escherichia coli, Staphylococcus aureus, Streptococcus haemoliticus.

B) Nosocomial (hospital / nosocomial) pneumonia(i.e. pneumonia, Developing 72 hours after hospitalization When excluding infections that were in incubation period at the time the patient is admitted to the hospital And up to 72 hours after discharge):

1. Gram-positive flora: Staphylococcus aureus

2. Gram-negative flora: Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis, Haemophilus influenzae, Enterobacter, Serratia

3. Anaerobic flora: gram-positive (Peptostreptococcus, etc.) and gram-negative (Fusobacterium, Bacteroides, etc.)

The etiology and nature of the course of hospital-acquired pneumonia has a significant impact on Specifics of the medical institution.

B) pneumonia in immunodeficiency states(congenital immunodeficiency, HIV infection, iatrogenic immunosuppression): pneumocystis, pathogenic fungi, cytomegaloviruses.

Factors predisposing to the development of pneumonia:

1) violation of the interaction of the upper respiratory tract and esophagus (alcoholic sleep, anesthesia with intubation, epilepsy, trauma, stroke, gastrointestinal diseases: cancer, esophageal stricture, etc.)

2) diseases of the lungs and chest with a decrease in local protection of the respiratory tract (cystic fibrosis, kyphoscoliosis)

3) infection of the sinuses (frontal, maxillary, etc.)

4) factors that weaken the body (alcoholism, uremia, diabetes, hypothermia, etc.)

5) immunodeficiency conditions, treatment with immunosuppressants

6) travel, contact with birds (chlamydial pneumonia), air conditioners (legionella pneumonia)

Pathogenesis of pneumonia:

1. Penetration of pneumonia pathogens into the respiratory sections of the lungs bronchogenic (most often), hematogenous (with sepsis, tricuspid valve endocarditis, septic thrombophlebitis of the pelvic veins, general infectious diseases), per continuinatem (directly from neighboring affected organs, for example, with a liver abscess), by lymphogenous routes with subsequent adhesion to epithelial cells bronchopulmonary system. In this case, pneumonia develops only when the function of the local bronchopulmonary defense system is impaired, as well as when the general reactivity of the body and nonspecific defense mechanisms decrease.

2. Development of a local inflammatory process under the influence of infection and its spread throughout the lung tissue.

Some microorganisms (pneumococcus, Klebsiella, coli, Haemophilus influenzae) produce substances that increase vascular permeability; as a result, pneumonia, starting from a small focus, then spreads throughout the lung tissue in the form of an “oil stain” through the alveolar pores of Cohn. Other microorganisms (staphylococci, Pseudomonas aeruginosa) secrete exotoxins that destroy lung tissue, resulting in the formation of foci of necrosis, which merge to form abscesses. A major role in the development of pneumonia is played by the production of cytokines by leukocytes (IL-1, 6, 8, etc.), which stimulate the chemotaxis of macrophages and other effector cells.

3. Development of sensitization to infectious agents and immuno-inflammatory reactions(with a hyperergic reaction of the body, it develops lobar pneumonia, with normo- or hypergia - focal pneumonia).

4. Activation of lipid peroxidation and proteolysis in lung tissue, which have a direct damaging effect on the lung tissue and contribute to the development of the inflammatory process in it.

Classification of pneumonia:

I. Etiological groups of pneumonia

II. Epidemiological groups of pneumonia: community-acquired (community-acquired, home-acquired, outpatient); hospital (nosocomial, in-hospital); atypical (i.e. caused by intracellular pathogens - legionella, mycoplasma, chlamydia); pneumonia in patients with immunodeficiency conditions and against the background of neutropenia.

III. By location and extent: unilateral (total, lobar, polysegmental, segmental, central (root) and bilateral.

IV. By severity: severe; moderate severity; mild or abortive

V. According to the presence of complications (pulmonary and extrapulmonary): complicated and uncomplicated

VI. Depending on the phase of the disease: height, resolution, convalescence, prolonged course.

Main clinical manifestations of pneumonia.

You can select a row clinical syndromes pneumonia: 1) intoxication; 2) general inflammatory changes; 3) inflammatory changes in lung tissue; 4) damage to other organs and systems.

1. Pulmonary manifestations of pneumonia:

A) cough– initially dry, for many on the 1st day in the form of frequent coughing, on the 2nd day a cough with difficult-to-discharge sputum of a mucopurulent nature; Patients with lobar pneumonia often have “rusty” sputum due to the appearance of a large number of red blood cells in it.

B) chest pain– most characteristic of lobar pneumonia, caused by the involvement of the pleura (pleuropneumonia) and lower intercostal nerves in the process. The pain appears suddenly, it is quite intense, intensifies with coughing and breathing; in case of severe pain, there is a lag in the corresponding half of the chest in the act of breathing, the patient “spares it” and holds it with his hand. At focal pneumonia pain may be mild or absent.

B) shortness of breath– its severity depends on the extent of pneumonia; with lobar pneumonia, significant tachypnea can be observed for up to 30-40 minutes, while the face is pale, haggard, with the wings of the nose swelling when breathing. Shortness of breath is often combined with a feeling of “chest congestion.”

D) physical signs of local pulmonary inflammation:

1) dullness (shortening) of percussion sound according to the localization of the inflammatory focus (always clearly defined in lobar pneumonia and not always pronounced in focal pneumonia)

3) crepitus, heard above the source of inflammation - resembles a small crackling sound or sound that is heard if you rub a tuft of hair near the ear with your fingers; caused by the walls of the alveoli soaked in inflammatory exudate coming apart during inhalation; heard only during inspiration and not heard during expiration

The onset of pneumonia is characterized by crepitatio indux, it is quiet, heard in a limited area and seems to be coming from afar; The resolution of pneumonia is characterized by crepitatio redux, it is loud, sonorous, heard over a larger area and as if directly above the ear. At the height of pulmonary inflammation, when the alveoli are filled with inflammatory exudate, crepitus is not audible.

4) fine bubbling rales in the projection of the focus of inflammation - characteristic of focal pneumonia, are a reflection of local bronchitis accompanying bronchopneumonia

5) change in vesicular breathing - in the initial stage and the resolution phase of pneumonia, vesicular breathing is weakened, and with lobar pneumonia in the phase of pronounced compaction of the lung tissue, vesicular breathing is not audible.

7) bronchial breathing - heard in the presence of a large area of ​​compaction of the lung tissue and preserved bronchial conductivity.

8) pleural friction noise – determined in pleuropneumonia

2. Extrapulmonary manifestations of pneumonia:

A) fever, chills– lobar pneumonia begins acutely, intense pain in the chest suddenly appears, aggravated by breathing, chills and fever up to 39 ° C and higher are observed; focal pneumonia begins gradually, the temperature increase is gradual, as a rule, no higher than 38.0-38.5 ° C, chills are not natural.

B) intoxication syndrome– general weakness, decreased performance, sweating (usually at night and with minor physical activity), decrease or complete absence appetite, myalgia, arthalgia at the height of fever, headache, in severe cases - confusion, delirium. In severe cases of lobar pneumonia, jaundice is possible (due to impaired liver function due to severe intoxication), short-term diarrhea, proteinuria and cylindruria, and herpes.

Diagnosis of pneumonia.

1. Chest X-ray – the most important method diagnosis of pneumonia.

In the initial stage of pneumonia, there is an increase in the pulmonary pattern of the affected segments.

In the compaction stage - intense darkening of areas of the lung affected by inflammation (areas of infiltration of lung tissue); with lobar pneumonia, the shadow is homogeneous, homogeneous, more intense in the central sections; with focal pneumonia, inflammatory infiltration in the form of separate foci.

In the resolution stage, the size and intensity of the inflammatory infiltration decreases, it gradually disappears, the structure of the lung tissue is restored, but lung root long time may remain expanded.

2. Laboratory inflammation syndrome: leukocytosis, svdig leukocyte formula to the left, toxic granularity of neutrophils, lymphopenia, eosinopenia, increased ESR in the CBC, increased content of a2- and g-globulins, sialic acids, seromucoid, fibrin, haptoglobin, LDH (especially the 3rd fraction), C-reactive protein in the CBC.

Criteria for the severity of pneumonia.

	Severity
	No more than 25		40 or more
			40o and above
Hypoxemia	No cyanosis	Mild cyanosis	Severe cyanosis
		Unsharp	Distinct
Extent of lesion	1-2 segments	1-2 segments on both sides or a whole share	More than 1 share, total; polysegmental

Comparative characteristics of lobar and focal pneumonia.

Signs	Lobar pneumonia	Focal pneumonia
Onset of the disease	Acute, sudden, with high body temperature, chills, chest pain	Gradual, usually after or during a respiratory viral infection
Intoxication syndrome	Significantly expressed	Weakly expressed
	Painful, dry at first, then with rusty sputum	As a rule, painless, with the separation of mucopurulent sputum
Chest pain	Characteristic, quite intense associated with breathing, coughing	Uncharacteristic and non-intense
	Very characteristic	Uncharacteristic
Dullness of percussion sound over the affected area	Very characteristic	Not always observed (depending on the depth of location and size of the inflammatory focus)
Ascultative picture	Crepitation at the beginning of inflammation and in the resolution phase, bronchial breathing at the height of the disease, often pleural friction noise	In a limited area, crepitus is detected, vesicular breathing is weakened, fine bubbling rales are heard
Shortness of breath and cyanosis	Characteristic	Little expressed or absent
Laboratory signs of inflammation	Expressed clearly	Less pronounced
X-ray manifestations	Intense homogeneous darkening of the lung lobe	Spotty focal darkening of varying intensity (in the area of ​​one or several segments)

Complications of pneumonia.

1. Pulmonary: A. parapneumonic pleurisy b. abscess and gangrene of the lung c. bronchial obstruction syndrome, acute respiratory failure.

2. Extrapulmonary: A. acute cor pulmonale b. infectious-toxic shock c. nonspecific myocarditis, endocarditis d. meningitis, meningoencephalitis e. DIC syndrome f. psychoses g. anemia h. acute glomerulonephritis And. toxic hepatitis

Basic principles of treating pneumonia.

1. Treatment regimen : hospitalization (only mild pneumonia is treated outpatiently with proper patient care).

During the entire febrile period and intoxication, as well as until the elimination of complications - bed rest, 3 days after normalization of body temperature and disappearance of intoxication - semi-bed rest, then ward rest.

Required proper care for the patient: a spacious room; good lighting; ventilation; fresh air in the room; careful oral care.

2. Medical nutrition: in an acute febrile period, drink plenty of fluids (cranberry juice, fruit juices) about 2.5-3.0 liters per day; in the first days - a diet of easily digestible foods, compotes, fruits, in the subsequent days - table number 10 or 15; Smoking and alcohol are prohibited.

3. Etiotropic treatment: AB is the basis of treatment acute pneumonia.

Principles of etiotropic therapy of pneumonia:

A) treatment should begin as early as possible, before isolation and identification of the pathogen

B) treatment should be carried out under clinical and bacteriological control with determination of the pathogen and its sensitivity to AB

C) ABs should be prescribed in optimal doses and at such intervals to ensure the creation of therapeutic concentrations in the blood and lung tissue

D) AB treatment should continue until intoxication disappears, body temperature normalizes (at least 3-4 days normal temperature), physical data in the lungs, resorption of inflammatory infiltration in the lungs according to X-ray examination.

D) if there is no effect from AB within 2-3 days, it is changed; in case of severe pneumonia, AB is combined

E) uncontrolled use of antibacterial drugs is unacceptable, since this increases the virulence of infectious agents and creates drug-resistant forms

G) with long-term use of AB, a deficiency of B vitamins may develop as a result of disruption of their synthesis in the intestines, which requires correction of the vitamin imbalance; it is necessary to timely diagnose candidomycosis and intestinal dysbiosis, which can develop during the treatment of AB

H) during treatment it is advisable to monitor indicators immune status, because AB treatment can cause suppression of the immune system.

Algorithm for empirical antibiotic therapy for community-acquired pneumonia (patient age up to 60 years): ampicillin (preferably amoxicillin) 1.0 g 4 times a day, if there is an effect, continue therapy for up to 10-14 days, if not, prescribe options: erythromycin 0.5 g 4 times a day / doxycycline 0.1 g 2 times a day / Biseptol 2 tablets 2 times a day for 3-5 days, if there is an effect, continue therapy for up to 10-14 days, if not, hospitalization in a hospital and rational antibiotic therapy.

Algorithm for empirical antibiotic therapy for community-acquired secondary pneumonia (patient age over 60 years): II generation cephalosporins (cefaclor, cefuroxime) orally or intramuscularly for 3-5 days, if there is an effect, continue therapy for 14-21 days, if not, prescribe options: erythromycin 0.5 g 4 times a day; sumamed 0.5-1.0 g per day for 3-5 days; if there is an effect - continue therapy for 14-21 days, if there is no effect - hospitalization and rational antibiotic therapy.

4. Pathogenetic treatment:

A) restoration of the drainage function of the bronchi: expectorants (bromhexine, ambroxol / lazolvan, bronchicum, licorice root for 5-7 days), mucolytics (acetylcysteine ​​for 2-3 days, but not from the 1st day); in severe cases of the disease - sanitary bronchoscopy with a 1% solution of dioxidine or a 1% solution of furagin.

B) normalization of bronchial muscle tone: in the presence of bronchospasm, bronchodilators are indicated (aminophylline IV drip, prolonged oral theophylline, aerosol b2-adrenergic agonists).

B) immunomodulatory therapy: prodigiosan in gradually increasing doses from 25 to 100 mcg IM with an interval of 3-4 days, course of 4-6 injections; T-activin 100 mcg 1 time every 3-4 days subcutaneously; Thymalin 10-20 mg IM for 5-7 days; sodium nucleinate 0.2 g 3-4 times a day after meals; levamisole (Decaris) 150 mg once a day for 3 days, then a 4-day break; the course is repeated 3 times; adaptogens (Eleutherococcus extract 1 teaspoon 2-3 times a day; ginseng tincture 20-30 drops 3 times a day; Chinese Schisandra tincture 30-40 drops 3 times a day; interferon preparations (contents of 1 amp dissolved in 1 ml isotonic sodium chloride, administered intramuscularly at 1 million IU 1-2 times a day daily or every other day for 10-12 days).

D) antioxidant therapy: vitamin E 1 capsule 2-3 times a day orally for 2-3 weeks; Essentiale 2 capsules 3 times a day during the entire period of the disease; emoxipine 4-6 mc/kg/day IV drip in saline solution.

5. Fight against intoxication: intravenous hemodez drip (400 ml once a day), isotonic sodium chloride solution, 5% glucose solution; drinking plenty of cranberry juice, fruit juices, mineral waters; in case of severe intoxication - plasmapheresis, hemosorption.

6. Symptomatic treatment:

A) antitussives: prescribed in the first days of the disease for a dry cough (Libexin 0.1 g 3-4 times a day, Tusuprex 0.01-0.02 g 3 times a day).

B) antipyretics and painkillers, anti-inflammatory drugs (paracetamol 0.5 g 2-3 times a day; Voltaren 0.025 g 2-3 times a day)

7. Physiotherapy, exercise therapy, breathing exercises : inhalation therapy(bioparox every 4 hours, 4 breaths per inhalation; anti-inflammatory decoctions of chamomile, St. John's wort in the form of inhalations; acetylcysteine); electrophoresis of calcium chloride, potassium iodide, lidase, heparin on the area of ​​the pneumonic focus; UHF electric field in a low-thermal dose, inductothermy, microwave on the inflammatory focus; applications (paraffin, ozokerite, mud) and acupuncture in the resolution phase of pneumonia; Exercise therapy (in the acute period - treatment by position, the patient should lie on the healthy side 3-4 times a day to improve aeration diseased lung, as well as on the abdomen to reduce the formation of pleural adhesions; static breathing exercises followed by the inclusion of exercises for the limbs and torso, training in diaphragmatic breathing); chest massage.

8. Sanatorium treatment and rehabilitation.

In case of non-severe small-focal pneumonia, rehabilitation of patients is limited to treatment in a hospital and observation in a clinic. IN rehabilitation center(department) patients with a history of widespread pneumonia with severe intoxication, hypoxemia, as well as persons with a sluggish course of pneumonia and its complications are sent. Patients who have had pneumonia are sent to local sanatoriums (Belarus, Minsk region, Bug, Alesya, Brest region) and climatic resorts with a dry and warm climate (Yalta, Gurzuf, southern Ukraine).

ITU: approximate timing of VN at mild form acute pneumonia 20-21 days; for moderate forms, 28-29 days; in severe cases, as well as complications: 65-70 days.

Clinical examination: patients who have had pneumonia and are discharged with clinical recovery are observed for 6 months with examinations 1, 3 and 6 months after discharge from the hospital; patients who have had pneumonia with a protracted course and are discharged with residual clinical manifestations of the disease are observed for 12 months with examinations after 1, 3, 6 and 12 months.

Contents of the topic "Pneumonia: etiology (causes), classification, pathogenesis, diagnosis, treatment, prognosis, prevention of pneumonia.":

Pathogenesis of pneumonia development.

In the pathogenesis of Pneumonia (Pn), the main role belongs to the influence of an infectious pathogen entering the lungs from the outside. Most often, microflora enters the respiratory sections of the lungs through the bronchi: inhalation (together with inhaled air) and aspiration (from the nasopharynx or oropharynx). The bronchogenic route of infection is the main one in primary Pneumonia (Pn).

By hematogenous route, the pathogen enters the lungs mainly in secondary Pneumonia (Pn), which develops as a complication of sepsis and general infectious diseases, as well as in the thrombotic genesis of Pneumonia (Pn). Lymphogenous spread of infection with the occurrence of Pneumonia (Pn) is observed only with wounds in chest.

There is also an endogenous mechanism for the development of inflammation in the lung tissue, caused by the activation of the microflora located in the lungs. Its role is great especially in hospital-acquired Pneumonia (Pneumonia). The initial link in the development of pneumonia is the adhesion of microorganisms to the surface of epithelial cells bronchial tree(Scheme 3), which is significantly facilitated by previous dysfunction of the ciliary ciliated epithelium and impaired mucociliary clearance. After adhesion, the next stage in the development of inflammation is the colonization of the microorganism in epithelial cells. Damage to the membrane of these cells promotes intensive production of biologically active substances-cytokines (interleukins 1, 8, 12, etc.).

Under the influence of cytokines, chemotaxis of macrophages, neutrophils and other effector cells taking part in the local inflammatory reaction occurs. In the development of subsequent stages of inflammation, invasion and intracellular persistence of microorganisms and their production of endo- and exotoxins play a significant role. These processes lead to inflammation of the alveoli and bronchioles and the development of clinical manifestations of the disease.

Risk factors play an important role in the development of Pneumonia (Pn). These include age (elderly and children); smoking; chronic diseases lungs, heart, kidneys, gastrointestinal tract; immunodeficiency states; contact with birds, rodents and other animals; travel (trains, train stations, planes, hotels); cooling; formation of closed teams.

In addition to infection, the development of Pn can be facilitated by unfavorable factors of the external and internal environment, under the influence of which there is a decrease in the general nonspecific resistance of the body (suppression of phagocytosis, production of bacteriolysins, etc.) and suppression of local defense mechanisms(impaired mucociliary clearance, decreased phagocytic activity of alveolar macrophages and neutrophils, etc.).

In the pathogenesis of Pneumonia (Pn), a certain importance is attached to allergic and autoallergic reactions. Saprophytes and pathogenic microorganisms, becoming antigens, contribute to the production of antibodies, which are fixed primarily on the cells of the mucous membrane of the respiratory tract. Here an antigen-antibody reaction occurs, which leads to tissue damage and the development of an inflammatory process.

In the presence of common antigenic determinants of microorganisms and lung tissue or when the lung tissue is damaged by viruses, microorganisms, toxins, leading to the manifestation of its antigenic properties, autoallergic processes develop. These processes contribute to a longer existence of pathological changes and a protracted course of the disease. In addition, the protracted course of Pneumonia (Pn) is often caused by associations of microorganisms.

GENERAL PATHOGENESIS AND SANOGENESIS

Pathogenesis is a branch of pathological physiology that studies the mechanisms of occurrence and course of the disease - the relationship of etiological processes occurring in the body with the body’s protective and adaptive reactions to them. In a complex animal organism there are a large number of systems and organs, tissues, the activities of which are closely connected with each other. Under pathological conditions, the relationship between organisms changes significantly. Complex changes that vary depending on the phase of the disease can lead to increased weakening and unusual combinations of functions of various systems and organs. Thus, during illness, the physiological mechanisms of the body work under new conditions, often with unusual strength and in different combinations. Clarification of the pathogenesis of diseases is the main issue of all theoretical medicine and is of great practical importance, because only by knowing the mechanisms of disease development can a doctor consciously and purposefully intervene in its course and rationally treat patients. The study of the pathogenesis of individual diseases, along with elucidation of their etiology, is the most important task pathological physiology. We will talk about the pathogenesis of certain specific diseases for the rest of our life together. Today's lecture is devoted to the most general issues teachings about pathogenesis. Plan: or the first thing we will focus on is the role of the etiological factor in pathogenesis. It is clear that the etiology of the disease and its pathogenesis are very closely related. The etiological factor, based on the definition, not only initiates the onset of the disease, but also gives it a qualitative uniqueness. Such a close connection leads to the fact that some researchers even propose to combine them under the general name “etiopathogenesis.” And until recently, it was generally believed that the causative factor not only begins the disease, it also generates it in all its manifestations throughout the entire course of the disease, i.e. Only the direct and absolute effect of the pathogenic cause on pathogenesis was recognized. However, only with a very large number of pathological processes, the effect of the pathogenic factor on the body is due to internal conditions and the body in the first place and compensatory-adaptive reactions on the part of the body in the second. I'm in in this case I’m talking about diseases that very quickly end in death and are associated with exposure to extremely strong pathogenic agents on the body. Well, for example, the instantaneous evaporation of the human body during the explosion of an atomic bomb. What is this disease? The transition from life to death is always a disease. But in this case, it is a disease that does not have pathogenesis in the generally accepted sense of the word, or pathogenesis that can only be based on the idea of ​​an etiological factor. But I repeat such diseases very few times. In most cases, the pathogenesis and clinical picture of the disease will depend not only on the causative factors, but also on the conditions under which the disease occurred. Conditions, both internal and external: for example: the pathogenesis of pneumonia in a young man and an old man is largely different. The pathogenesis of pneumonia that develops after hypothermia will have its own characteristics, but compared to pneumonia that develops against the background of radiation injury, and therefore treatment in these cases will be different. Moreover, sometimes it is generally impossible to use etiotropic therapy to treat patients (they told you what it is in pharmacology) since the etiological factor often acts on the body for a very short time: for example: in case of burns, injuries. Rational treatment of patients in these cases is possible only if the mechanism and disease are affected, i.e. when using pathogenetic therapy. Schematically, we can distinguish 4 main types of interaction etiological factor: with the body and its influence on pathogenesis.

1. The etiological factor is only an impetus that triggers the pathological process, which then continues to develop under the influence of so-called pathogenetic factors. For example, the effect of heat during burns is short-term. But under the influence of heat, cells die, and from the dead cells a large amount of coagulated proteins, enzymes, including lysosomal ones, and biologically active substances such as histamine, kinins, and electrolytes are released into the tissue. This entire complex of substances causes secondary damage to cells that were not damaged at the time of the burn, and from which new portions of biologically active substances enter the tissue. Thus, although the pathogenic factor itself acts on the body for a short time, its destructive effect is felt in the body over a fairly long period.

2. Second type of interaction. The etiological factor acts throughout the entire course of the disease, which ends when this factor is eliminated. An example of such a disease is scabies.

Type 3 The etiological factor acts during a certain period of the disease, but it does not stop after the pathogenic factor is eliminated. An example is Botkin's disease or infectious jaundice, in which pronounced functional disorders of the liver persist even after the pathogen is removed from the body.

Finally type 4. The etiological factor does not stop its action, but the disease stops. Example: seasickness.

Concluding the conversation about the role of the etiological factor in pathogenesis, it is necessary to distinguish the characteristic change of causes and consequences during each disease. The disease and its pathogenesis can generally be imagined as long chains of events, where the consequence of each previous stage is the cause of the next. For example: intestinal strangulation is the cause of intestinal obstruction, intestinal obstruction is the cause of stagnation of food mass in the intestines, this in turn is the cause of disruption of the digestive process and the development of fermentation and putrefaction processes in the intestines, the accumulation of toxic products of fermentation and putrefaction and their absorption into the blood is the cause intoxication of the body, the cause of the disorder metabolic processes in various tissues and organs of the body, in the central nervous system and cardiovascular system, which in turn is the cause of cardiovascular failure, which is the cause of hypoxia (that is, an inconsistent supply of oxygen to tissues), and hypoxia is the cause of metabolic disorders incompatible with life in all tissues and organs before all in the central nervous system. In this case, I touched upon only one of the causes of the investigative chain in the pathogenesis of intestinal obstruction. So, the pathogenesis of the disease can be represented as a chain of processes linked in time and space by cause-and-effect relationships. However, the significance of the various links for the patient and his doctor in this chain is not the same. In practice, it is very important to identify the main link of pathogenesis, when destroyed, the entire chain disintegrates, and to the elimination of which all the power of therapy should be directed. At first glance, it seems that this main link in pathogenesis is its initial etiological link. In many cases, this turns out to be so. For example, by eliminating intestinal volvulus, we will break the entire pathogenetic chain. By destroying pneumonia in the lungs of a patient with pneumonia, we will stop the development of the disease. But often, the main link of pathogenesis is not chronological and the first. For example, the main link in the pathogenesis of an attack bronchial asthma is a spasm of small bronchioles, which, on the one hand, leads to a lack of supply 02. On the other hand, to a sharp increase in the body’s energy costs for pushing air through the narrowed airways, on the other hand, to a lack of supply or oxygen. Hypoxia develops from which the patient may die. But the spasm of the bronchioles itself is one of the last links of two parallel chains, the beginning of which is sometimes decades apart from the moment of an attack of bronchial asthma. One of these chains is associated with destructive processes in the lungs due to chronic infectious processes. The other chain is caused by an allergic restructuring of the immunocompetent system, again due to prolonged exposure to microflora. A change in cause-and-effect relationships in pathogenesis, in some cases, leads to the formation of so-called pathogenesis circles. For example: Impaired blood supply to the heart. It will lead to the development of one of the clinical forms of coronary heart disease, in which the contractility of the heart decreases, while the amount of blood pumped by the heart into the aorta decreases, which means that both the amount of blood entering the coronary vessels and the contractility of the myocardium decreases. As we have already said, the pathogenesis of the disease is influenced not only by the etiological factor, but also by FEATURES OF THE ORGANISM:

1. its REACTIVITY. 2. The role of the central nervous system, 3. STATE OF ENDOCRINE REGULATION, 4. FEATURES of the state of body tissues.

1) The reactivity of the body is the ability of the body as a whole to respond to the pathogenic influences of the external environment. Because the entire next lecture is devoted to reactivity. I will only say that reactivity can be high, low and perverted. An example of a disease occurring against a background of high reactivity is pneumonia in young people. At the same time, the disease has a very clear clinical picture - high fever, painful breathing, confused consciousness. The outcome of such diseases is most often either full recovery or - death. Pneumonia occurring against a background of reduced reactivity - for example, in old people - will be completely different. Blurred, sluggish symptoms, absence of temperature reaction, absence of pronounced general manifestations. But at the same time, there are active destructive processes in the lungs, becoming protracted and chronic. An example of perverted reactivity is allergic diseases, when the body responds to some pathogenic irritant with a perverted, often unjustifiably violent reaction. It should be remembered that reactivity may change as the disease progresses. Thus, high reactivity can turn into low reactivity or acquire features of perverted reactivity. Role nervous system in pathogenesis. The nervous system has representation in all tissues and organs. With any impact on tissue, the central nervous system is involved in the pathological process. Irritation of the peripheral receptor apparatus leads to excitation of the central nervous system, and subsequently to a general reaction of the body, which is based on a reflex mechanism. Most often, these mechanisms are useful for the body and are aimed at fighting the disease. But sometimes defense mechanisms turn into their opposite - they become the main and strange factors of damage. An example of such a phenomenon is the pathogenesis of pulmonary embolism. With embolism of even a small branch of the pulmonary artery, a reflex spasm of the remaining branches develops pulmonary artery and coronary vessels. At the same time, a reflex expansion of the peripheral vessels of the systemic circulation occurs - pressure drops - collapse - the person dies, with symptoms of acute cardiovascular failure. If, in an experimental animal, the ascending muscles are surgically destroyed, i.e. sensitive nerve bundles lungs, then embolism of the small branches of the pulmonary artery has practically no effect on the general condition of the animal. Not only does it not die, but it doesn’t even stop eating breakfast. Pathological processes can arise through the mechanism of not only unconditioned, but also conditioned reflexes. With repeated combination of a pathogenic factor and an indifferent stimulus (for example, a telephone call), the latter can also become the cause of a disease, which in this case occurs by conditioned reflex. Pathological conditioned reflexes can underlie attacks of bronchial asthma, attacks of angina pectoris, hepatic and renal colic. There is another mechanism for the development of the disease associated with the activity of the central nervous system. Let's say there is an injury - a hip fracture. The hip is not a vital organ, so failure in itself is not life-threatening. However, an intense flow of pain impulses from the area of ​​injury leads to the development of extreme inhibition in the central nervous system, which in turn leads to disorganization of vital functions of the body - such as blood circulation and breathing, and a person dies due to symptoms of cardiovascular failure. All this is called traumatic SHOCK. There are other mechanisms of pathogenesis associated with the activity of the central nervous system, such as the formation of a PATHOLOGICAL DOMINANT underlying the pathogenesis of hypertension, the formation of so-called trace reactions, phase phenomena of the cerebral cortex. Violation of the neurotrophic function of the central nervous system is of great importance. RELATIONSHIP OF GENERAL AND LOCAL IN THE PATHOGENESIS OF THE DISEASE. Naturally, any tissue, any organ functions in the body only if there is a vascular, nervous-humoral connection with the body. Any organ, any tissue in the body acts in close functional connection with all other organs and tissues. Therefore, any pathological process is complex and affects both individual parts of the body, all its systems and organs, and the body as a whole. Any disease is the suffering of the entire organism. However, the ratio and significance of general and local manifestations of the pathological process may be different for different diseases. There are diseases with predominantly general and predominantly local manifestations. At the same time, a local - pathological process - often turns out to be precisely due to the holistic response of the body, which seeks to limit and localize this process. An example of such a restrictive influence of the body is an abscess. Concluding the conversation about the patterns of GENERAL PATHOGENESIS, it is necessary to say that the pathogenesis of many pathological processes is based on the so-called TYPICAL PATHOLOGICAL PROCESSES. What it is. The fact is that the pathogenesis of such diseases as pneumonia, rheumatism, appendicitis and a huge number of others, despite some specific features, has much in common since the basis of these diseases is the same pathological process - inflammation. Inflammation proceeds according to approximately the same laws, regardless of its location. Among other typical pathological processes underlying many diseases, FEVER, edema, ischemia, tumor process, typical metabolic disorders and some others can be caused.

MECHANISM OF RECOVERY

The doctrine of the mechanisms of recovery is called SANOGENESIS from Greek word Sanitas - health. For the first time, I.P. Pavlov gave a clear definition of the recovery process, and he was the first to raise the question of the need to study the recovery process. The entire domestic school of pathophysiology, especially S.M. Speransky, played a very significant role in the development of problems of sanogenesis.

BASIC MECHANISMS OF SANOGENESIS

The process of sanogenesis consists of reactions that restore impaired functions and compensate for pathological disorders. Recovery of the body is carried out due to reactions developing in three main directions.

1. Restoring the structure of damaged tissues i.e. REGENERATION.

2. Restoration of functional connections between various systems and organs of the body that were disrupted during illness.

3. If the regenerative capabilities do not allow the structure of the damaged organ to be completely restored and its function turns out to be defective, then recovery is carried out by creating a fundamentally new system of functional communication between organisms, i.e. COMPENSATORY PROCESSES.

TYPES OF COMPENSATION:

1. Compensation through the reserve capabilities of systems and organs functionally associated with organ damage.

For example, respiratory failure that develops with lung diseases and the associated tissue hypoxia will be compensated by increasing the activity of the cardiovascular system and bone marrow, i.e. a decrease in blood oxygenation in the lungs will be compensated by accelerating the speed of blood flow and the number of red blood cells in the blood.

2. Compensation due to the functional reserves of the most damaged organs. Most organs have reserve functional structures that are not used in the normal state. For example, even with moderate physical activity, no more than 25-30% of the alveoli of the lungs are used. These reserves are naturally put into action in the event that part of the alveoli fails. The liver and kidneys have great reserve capabilities, so when 2/3 of the tissue of each kidney is removed, they cope with their function, and the amount of urine produced remains the same as before the removal.

3. The type of compensation is carried out due to hypertrophy of the damaged organ. Hypertrophy can develop in two ways. Firstly, this is reparative hypertrophy. An example of which is the restoration of circulating blood volume after blood loss due to an increase in the production of red blood cells in bone marrow. Another example of compensation developing due to reparative regeneration is the restoration of the original mass of the liver when 75% of its parenchyma is removed or damaged.

The second type of hypertrophy is caused by an increase in the mass of tissues associated with damaged structures in a functional sense. For example, when defects in the valvular apparatus of the heart occur, it is not the endocardium that hypertrophies, but the myocardium, the heart muscle becomes more powerful, stronger, and due to this, the heart copes with the additional load resulting from the defect in the valvular apparatus.

4. The type of compensation is vicarious hypertrophy and hyperfunction. This type of compensation develops in the case of removal or damage to a paired organ when its function is performed by another, while the functioning organ hypertrophies. So the removal of one lung is completely compensated by the function of the second hypertrophied lung.

In the recovery process, restoration of function is very important, which is achieved through persistent training. The central nervous system has enormous compensatory capabilities and the cortex plays a huge role in this. When the cortex is removed - compensation, the function goes very poorly. Various organs and systems. Of particular importance in this regard is C.N.S. AMPUTATION.

There are three possible ways for pneumonia pathogens to enter the lungs: bronchogenic, the most common, hematogenous and lymphogenous.

The bronchogenic pathway is observed during aspiration of the infectious agent. This is facilitated by various congenital and acquired defects in the elimination of agents: disturbances in mucociliary clearance, defects in the surfactant system of the lung, insufficient phagocytic activity of neutrophils and alveolar macrophages, changes in local and general immunity, tracheobronchial dyskinesia, disturbances in bronchial patency, pleural adhesions with impaired mobility of the lung, dysfunction of the diaphragm , decreased cough reflex and others. Along with the intrakaialicular (along the respiratory tract) spread of the inflammatory process, contact spread of microbes is also possible with pronounced exudation of serous fluid, which carries bacteria, penetrating through the pores in the interalveolar septa. Often there is a combination of both types of distribution infectious process in the lungs.

Hematogenous spread of microbes has been proven in cases of wound sepsis. According to S. S. Weil (1946), in a number of cases of pneumonia in those wounded in the chest, lymphogenous spread of infection occurs due to lymphangitis.

In 1925, A. N. Rubel put forward an allergic theory of the pathogenesis of acute pneumonia, which became widespread and recognized. In accordance with this theory, the pneumonic process goes through two phases: reflex-hyperergic and infectious-allergic. Under the influence of hypothermia or other environmental factors, the immunobiological balance between the macroorganism and the microbes inhabiting the respiratory organs changes. Lung tissue becomes sensitized to bacteria, which leads to the development of local and general allergic reaction underlying pneumonia.

Most researchers believe that the pathogenesis of focal and lobar pneumonia is different. In contrast to focal pneumonia, which is an expression of the body’s normal and hyperergic reaction to an infectious agent, lobar pneumonia is considered as a manifestation of hyperergic reactivity. Sensitization to certain microorganisms occurs in both lobar and focal pneumonia, but the level of specific immunity is higher in patients with lobar pneumonia, which is associated with more significant antigenic irritation and immune defense.

When analyzing the state of the T- and B-immune systems, certain changes were identified that were associated with the clinical features and course of pneumonia. The smallest changes in these systems were noted in patients with favorable course focal pneumonia. In cases of prolonged course, the content of T cells, their functional activity and the amount of immunoglobulins in the blood serum decreased. In patients with lobar pneumonia, pronounced changes in both immune systems were observed, manifested by a significant change in the number of T and B cells (a decrease in T cells and an increase in B cells), a reduced response to phytohemagglutinin and a high content of immunoglobulins. An analysis of the frequency of circulation of immune complexes in the blood of patients made it possible to establish that with lobar pneumonia, immune complexes are present in almost all patients in the acute phase of the disease, and somewhat less frequently with focal pneumonia. It was suggested that the circulation of immune complexes in the blood of patients with acute pneumonia within two to three weeks from the onset of the disease indicates the intensity of immune processes aimed at quickly removing the antigen from the patient’s body and contributes to a faster recovery. The absence of immune complexes at the onset of the disease in the presence of prolonged antigenemia can be considered a manifestation of immune deficiency. In patients with a protracted course of acute pneumonia, a predominance of antigens circulating in the blood over antibodies and significant changes in the complement system were noted. It is suggested that in the absence of a clinical effect during treatment, patients with acute pneumonia almost always have pronounced autoimmune changes or a sharp inhibition of the mechanisms of nonspecific reactivity.

According to A. A. Korovina (1976), the pathophysiological mechanisms of viral influenza pneumonia are associated with a violation of the filtration and excretory function lung tissue under the influence of influenza intoxication. Increased absorption of toxic products from the blood is accompanied by damage to the vascular membrane and the appearance of a nonspecific proliferative reaction in the interstitium. With a malignant course of influenza due to increased permeability blood vessels the pathological process quickly spreads to the alveoli, causing hemorrhagic pneumonia.

Influenza virus and bacterial antigens can reduce the local resistance of the lung to infection by suppressing the phagocytic activity of neutrophils. Staphylococcal antigen and influenza virus inhibit phagocytosis in the acute phase of pneumonia.

The level of lysozyme, complement and P-lysines in the blood largely reflects the nature of the course of pneumonia. IN acute period disease, most patients showed an increase in their level, which reflects the mobilization of nonspecific protective mechanisms. When the clinical manifestations of acute inflammation in the lungs subsided, different levels of these nonspecific protection factors were revealed in patients: from the normal level of all three indicators in patients with a favorable course of acute pneumonia to moderate and severe depression in its protracted course.

In patients with acute pneumonia, according to Barrieti and Gaydos, there are compensatory and adaptive changes in the content of microelements involved in oxygen transport, tissue respiration, detoxification and repair processes. At its height, the concentration of iron in the body is increased, which can be regarded as a protective reaction aimed at normalizing redox processes. An increase in carbonic anhydrase activity in the blood and an increase in zinc content in the body are probably also a protective reaction associated with the resulting oxygen deficiency; An increase in cobalt content in patients with acute pneumonia apparently has a protective and adaptive significance and helps stimulate immunogenesis. Severe disorders of copper metabolism, its endogenous deficiency, observed in the disease, are apparently caused by the fact that copper is a catalyst for many biological processes and is part of a number of oxidative enzymes. All these changes can be considered as one of the links in the pathogenesis of acute pneumonia.

One of the mechanisms of the pathogenesis of the disease is an increase in capillary permeability, which is especially pronounced in patients with lobar pneumonia, complicated by abscess formation. According to the increase in capillary permeability during pneumonia, the activity of lysosomal enzymes in the blood serum increases, which is associated with an increase in the permeability of lysosomal membranes under the influence of bacterial toxins. During treatment, capillary permeability decreases.

The inflammatory process in the lungs of patients leads initially to the breakdown and then to the synthesis of collagen, as evidenced by an increase in the content of hydroxyproline in the blood and urine according to the level of activity of the inflammatory process in the lungs. When the inflammatory process subsides, a further increase in hydroxyproline is explained by an increase in the processes of neoplasm of connective tissue.

In patients with acute pneumonia, a local increase in hemocoagulating and inhibition of fibrinolytic activity was noted, which is one of the mechanisms that contribute to the delimitation of the inflammation zone. The level of fibrinogen in the blood increases, its fibrinolytic activity decreases; at the same time, the concentration of free heparin increases, which leads to compensatory hypocoagulation. In some patients with severe acute pneumonia, hyperfibrinogenemia is combined with thrombocytopenia. This is associated with intravascular platelet aggregation and the development of platelet embolisms, which in some patients culminate in the development of local hemorrhagic necrosis of the lung tissue. The release of serotonin and thromboplastic substances by degrading platelets increases vasospasm and fibrin loss.

The occurrence of pneumonia is influenced by neurotrophic disorders that occur in the lungs and bronchi. The direct impact of infectious agents on various departments nervous system during hematogenous spread and the influence of vegetative and other irritations higher centers nervous system, transmitted through interoreceptor pathways when pathogenic microorganisms damage the mucous membrane of the upper respiratory tract and bronchi. In the development of acute pneumonia important role The effect of bacterial flora on the interoceptor apparatus of the respiratory tract also plays a role, with the occurrence of disturbances in the bronchi and lungs of a reflex nature.