Syndrome infiltration of lung fabric. What is infiltration of light tissue
Infiltration -excess penetration and accumulation of effusion in alveoli containing various cellular elements, chemicals (biologically active substances).
Depending on the cause and nature of traffic, infiltration happens:
- inflammatory(with pneumonia, tuberculosis, fibrosing alveolitis, diffuse connective tissue diseases);
- non-inflammatory(with lung cancer, leukose, lightctuity).
Clinical manifestations:
· Cough;
· Shortness of breath;
· Pain in the chest - only when involving in the pathological process of pleura;
· Herakewall - when destruction of light tissue, tuberculosis, staphylococcal pneumonia, lung cancer.
General inspection:
· "Warm cyanosis" caused by respiratory failure;
· Forced position on the patient side with the defeat of the pleura.
Common inspection of the chest:
· Static - asymmetric swelling on the side of the defeat in children;
· Dynamic - the lag of the amazed half in the act of breathing, Tahipne.
Palpation of the chest:
· In the initial and final stages of infiltration - tympanic sound;
· In the stake stage of infiltration - stupid or dull sound.
Topographic percussion:reducing the mobility of the lower moor edge on the side of the lesion.
Auscultation of lungs:
In the initial stage of infiltration:
The emergence of non-corporate attitudes (Crepitatio Indux).
In the patch stage:
Vesicular breathing and attitudes disappear, bronchial breathing appears.
At the stage of resolution (resolution) of infiltrate:
Weakening of vesicular breathing;
Sound crepitation (Crepitatio Redux) + sonorous wet small-pushed wheels;
There may be whistling wheels, the noise of friction of the pleura;
Bronchophony strengthened.
Tool diagnostics:
· The main method of research - radiography of lungs in a straight and lateral projection - the presence of shading;
· Spirography - restrictive type of violation of the function of external respiration, due to respiratory failure or mixed with broncho-prestructive syndrome.
Clinical symptoms of intoxication syndrome:
Complaints:
· General complaints:
Fever;
General weakness, malaise;
Sweating;
Malgia;
· Cardiac complaints - heartbeat, fainting, attacks of suffocation;
· Cerebral complaints - headaches, sleep disorder, nonsense, hallucinations, confusion of consciousness;
· Dyspeptic complaints - a decrease in appetite, nausea, vomiting.
Feature: Pneumonia caused by mycoplasma, chlamydia, legionell, proceed with the predominance of general-cycling syndrome, bright-light manifestations are scarce, so these pneumonia are called "atypical".
Changes detectable with general inspection Patients with pneumonia:
· Consciousness - oppressed to a hypoxic coma with extremely severe pneumonia, acute respiratory failure;
Nonsense, hallucinations in children, alcoholics against the background of intoxication;
· May be forced position on the sick side;
· Cold skin, cyanosis with a marble tint;
· Herpety races on the lips and wings of the nose;
· Forest face, blush on the side of the defeat.
Respiratory Research - manifestations of lung tissue infiltration syndrome.
- Tachycardia, emphasis in pulmonary artery, hypotension.
Laboratory diagnostics of pneumonia:
· Common blood test: leukocytosis, formula shift to the left, toxic neutrophil grain, raising SEE - inflammatory changes;
with viral pneumonia: leukopenia, relative lymphocytosis.
· Biochemical blood test - increasing the level of fibrinogen, positive C - reactive protein - sharp phase indicators; With severe flow - laboratory manifestations of renal, liver failure;
· Immunological examination of blood - with viral, atypical pneumonia - detection of the diagnostic titer of specific antibodies;
· Wet analysis: - general (microscopic): many leukocytes, macrophages, bacterial flora - gram coloring, detection of atypical cells, VK - DIF. diagnostics;
Bacteriology: Verification of the pathogen, definition
its sensitivity to antibiotics; meaningful number
10 5 - 10 7 microbial bodies in 1 ml.
· General urine analysis - may be feverish proteinuria, hematuria.
Tool diagnostics of pneumonia:
· R-graphic of the chest organs in 2 projections - the main method - focal and infiltrative dimming, amplification of the pulmonary pattern;
· R-tomography, computer tomography of the lungs - in abscessive - for differential diagnosis with tuberculosis, lung cancer.
· Bronchoscopy - when suspected of cancer, a foreign body, therapeutic - with abscess.
· ECG - with severe flow to identify signs of overloading right hearts.
· Spirography - with other diseases of the respiratory system.
Basic principles of pneumonia treatment:
· Gentle mode;
· Full nutrition;
Etiotropic: antibacterial, antiviral, fungal, antiprotozoic;
Disintellation - saline solutions;
Pathogenetic - with severe and complicated pneumonia:
anticoagulants (heparin), antimemental preparations (conficilla), glucocorticoids, oxygen therapy, antioxidant therapy, immunocorrective therapy;
Symptomatic therapy: bronchophimatics, mercolics, analgesics, antipyrtic;
· Non-drug treatment:
Physiotherapeutic treatment - UHF, magnetotherapy, laser therapy, EHF therapy;
LFK, respiratory gymnastics.
Pleurisy - This is the inflammation of the pleura with the formation on its surface or accumulation in its cavity.
This is not an independent disease, but a manifestation or complication of many diseases.
The etiopathogenetic classification of pleural lesions:
1. Inflammatory (pleurisy):
a) infectious
b) non-infectious:
· Allergic and autoimmune:
· With rheumatic diseases:
· Fermentogenic: pancreatogenic;
· Traumatic, radiation therapy, burns;
· Uremic.
2. Non-inflammatory:
· Tooth lesions of pleura;
· Stagnation - with left ventricular heart failure;
· Dispensenemic pleural effuses;
· Other forms of accumulation of effusion - hemotorax, chylotorax;
· The presence of air in the pleural cavity is pneumothorax.
By criterion of availability Pleurrites happens:
Dry (fibrinous);
Exudative.
By character Exudent pleurite exudative effusion happens:
Serous;
Serous-fibrinous or hemorrhagic;
Purulent (emmps of pleura).
By flow plerites are:
Subacute;
Chronic.
Pathogenesis:
1. Increase the permeability of the vessels of parietal pleura with excessive heating of fluid, proteins and uniform elements of blood into the pleural cavity;
2. Violation of the resorption of the pleural liquid with a diaphragmal part of the parietal pleura and lymphochok;
3. The combination of the first 2 factors most often.
With moderate exudation in the pleural cavity, a fibrinous pleurisy is formed by the preserved outflow due to the falling out of the fibrin exudate to the surface of the pleura. With pronounced exudation and disturbance of resorption - exudative pleurisy. When the exudate is infected with the glotted flora - Empiama pleura.
Clinical manifestations of fibrinous syndrome (dry) pleuritis:
Complaints: 1) acute pain in the chest, increasing with deep breath, cough, slope into a healthy side;
2) unproductive cough.
With general inspection The forced position on the sick side is revealed.
Inspection of the chest - Takhi-, Hypopeloe, the lag of the affected half of the chest in the act of breathing, reducing the tours of the chest.
Palpation of the chest: Soreness when pressing in the field of pleural overlays. The noise of friction of the pleura can be detected.
Percussian -the limitation of the mobility of the lower edge of the lungs on the lesion side is determined.
Auscultative The sign of fibrinous pleurite is the noise of friction of the pleura.
Clinical manifestations of exudative pleuritis:
Complaints 1) feeling of gravity, overflow in the affected half of the chest;
2) shortness of breath inspiratory;
3) unproductive cough;
4) Fever, oznoby, sweating.
With general inspectiona forced position on the sick side is revealed; With massive population - sitting; "Warm" cyanosis.
Chest inspection:
An increase in the affected half of the chest;
Intercostal expansion and empty
intervals;
The lag of the affected half of the chest in the act of breathing.
Percussian Revealed stupid sound with an oblique upper boundary (Damuazo-Sokolova line).
Auscultation of the lungs.In the field of accumulation of reach, breathing is not determined by its upper boundary, the noise of friction of the pleura may be heard, in the region of the Harland triangle - bronchial breathing. Bronchophony is missing over effusion.
Research of the cardiovascular system:swelling of cervical veins, frequent pulse, tachycardia. The topping push and the boundaries of the relative dullness of the heart are shifted into the "healthy" side. On the side of the lesion, you can reveal the manifestations of the collapse of the lung.
Clinical manifestations of empya pleura The same as with an exudative pleurisite. The peculiarity of the expression of intoxication is a febrile hectic fever, stunning olar, profuse sweating.
Non-inflammatory pleural syndromes:
2.1 Hydrotorax - This is a cluster in the pleural cavity of the distance of a non-inflammatory nature (transudate).
Pathophysiological mechanisms for the occurrence of hydrotorax:
Increased hydrostatic pressure in pulmonary capillaries - in heart failure, hypervolemia, difficulty venous outflow;
Reducing the colloid-oncotic pressure plasma pressure - with nephrotic syndrome, liver failure;
Violation of lymphottock - the syndrome of the vein vein tumors of the pleura, mediastinum.
2.2 Cylotorax- This is a cluster of lymph in the pleural cavity.
Damage to the breast lymphatic duct during operational interventions, chest injuries;
Blockade of the lymphatic system and the mediterranean veins of the tumor or metastases;
2.3 Hemotorax- This is a cluster of blood in the pleural cavity.
Possible reasons Gemotorax:
1) injury and injury of the chest;
2) aortic aneurysm rupture;
3) iatrogenation - with the catheterization of a subclavian vein, transciliation aortography, uncontrolled treatment with anticoagulants;
4) Spontaneous bleeding in patients with hemophilia, thrombocytopenia.
The clinical manifestations of hydrotorax, chylotorax and hemotorecase are due to the presence of pleural effusion and correspond to those in the syndrome of exudative pleuritis. However, there are distinctive features: the absence of intoxication syndrome, when hemotorax - manifestations of postghemorrhagic anemia.
2.4 Syndrome pneumothorax - This is a pathological condition due to the presence of air in the pleural cavity.
Clinical manifestations of pneumothorax syndrome:
Complaints:
1) Pain in the chest - it occurs suddenly when coughing, physical voltage, is intensified with deep breathing;
2) shortness of inspiratory, arises suddenly;
3) unproductive cough.
Sometimes pneumothorax proceeds asymptomatic and is a diagnostic find with a x-ray study.
General inspection. With the rapid development of the pneumothorax, the patient takes the forced position sitting, the skin is wet, cold, pale due to the reflex collapse.
Inspection of the chest. The affected half is increased in volume, lags behind in the act of breathing. Tahipot. Reducing an excursion of the chest.
Permons perk: Over the area of \u200b\u200bthe pneumothorax, a tympanic sound, the lower boundary of the affected lung raised, is limited to the mobility of the lower pulmonary edge.
Auscultation of the lungs: Weakening or lack of vesicular breathing and Bronchophone. On the side of the lesion, you can reveal the manifestations of the lung collapse syndrome.
Research cardiovascular system: swelling of the cervical veins, frequent, small, threaded pulse, tachycardia, the shift of the top shock and the boundaries of the relative dullness of the heart in a healthy side.
2.4 Fibrotorax syndrome is a pathological condition due to obliteration (in advance) of the pleural cavity. Fibrotorax is formed in the outcome of such states as hemotorax, empty, tuberculosis, pectoral operations.
Clinical manifestations of fibrotorax:
Complaints:
1) shortness of breath;
2) periodic pain in the chest, increasing with deep breath, exercise, changing meteo conditions.
Chest inspection: The affected half is reduced in volume, lagged in the act of breathing, the excursion of the chest is limited.
Percussian - Blutuminous sound, reducing the height of the tops and the width of the crennics fields, the lower boundary of the affected lung is raised, reduced the mobility of the lower pulmonary edge.
Auscultation of the lungs - Weakening of vesicular breathing.
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Light infiltration syndrome | |
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The concept of pulmonary infiltration syndrome. The reasons for the appearance of infiltrate. | |
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Inflammatory and non-inflammatory infiltrates | |
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Tumor infiltrates. Lung cancer in the practice of a physician. | |
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Tuberculosis of the lungs in the practice of a physician. Medical tactics for examination and treatment of patients. | |
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Differential diagnosis for lung atelectase | |
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Curacy of patients. Collapse of patients. |
Light infiltration syndrome
Under the infiltrate it is understood as a piece of tissue, characterized by the accumulation of the usually not peculiar cell elements (inflammatory, eosinophilic, tumor), increased volume and increased density. In accordance with this, the following main groups of infiltrates in the lungs are distinguished: infectious-inflammatory, for example, with pneumonia and tuberculosis, allergic and infiltrates during tumors (cancer, leukemic, with malignant lymphomas, etc.).
Differential-diagnostic search differs significantly depending on whether the patient has a false (segmental, polistery) or an unlawful defeat. In this regard, the differential diagnosis is advisable to light separately with equity and unlawful infiltrates.
At the first stage, the doctor should make sure that the patient really has pulmonary infiltrate. The identification of infiltrate is carried out according to clinical and radiological data. Depending on the nature of the pulmonary infiltration (mostly exudative or mainly productive nature), various physical changes in the lungs are observed. The most vivid clinical changes are observed in infectious-inflammatory pulmonary infiltrates, mainly under nonspecific pneumonia: local gain of voice trembling, pointing percussion sound (or stupidity), rigid or bronchial breathing, attitudes. In case of pulmonary infiltrate is predominantly a productive nature, for example, with tumors, as well as in inflammatory infiltrates with impaired bronchial drainage, gaining voice trembling, attitudes and wheezing are not determined, loose breathing listened. In such cases, on the basis of clinical data, it is not possible to determine the pulmonary infiltration.
Radiographic examination is crucial for the establishment of pulmonary infiltration. On the radiograph, the pulmonary infiltrate gives dimme with a diameter of more than 1 cm of weak or average intensity, less often, with extensive, such as equity, infiltrates - dimming of considerable density. The contours of dimming depend on the nature (substrate) of the pathological process, its localization and projection of the study. The structure of blackout at pulmonary infiltrates can be both homogeneous and inhomogeneous, which is determined by the nature of the pathological process, its stage and the presence of complications.
At the second stage of differential diagnostic search, inflammatory and tumor infiltrates are distinguished. Patch inflammatory infiltrates are observed mainly with pneumonia and tuberculosis process. Tumor nature infiltrates usually do not capture a whole share. The shared darkening of tumors is more often observed in the bronchogenic lung cancer, when the tumor stenosis of the bronchus leads to hypoventilation and the atelectasis of the corresponding segment or share with the subsequent development in these areas of the inflammatory process (obstructive pneumonitis). Thus, the lobar processes in pneumonia and tuberculosis should be differentiated with obstructive pneumonitis.
Obstructive pneumonite is diagnosed in the presence of clinical and radiological signs of atelectasis (less often hypoventilation) share or segment in combination with clinical and laboratory signs of the inflammatory process in the lungs. Large importance for diagnosis has bronchoscopy with biopsy suspicious sites.
Inflammatory infiltrates of an unlawful (focal pneumonia, infiltrative tuberculosis of the lung, allergic processes of the lungs) must be differentiated primarily with peripheral lung cancer, which in the radiograph more often gives an infiltrative shadow of the rounded shape.
For peripheral cancer, the inconspicuous start, without increasing temperature, cough and shortness of breath, physical changes in the lungs are scarce or absent. In general blood test, only a moderate increase in ESP is determined in the absence of other changes. The main differential diagnostic differences from inflammatory infiltrates of a rounded form are determined by x-ray examination. Unlike peripheral cancer when focal Pneumonia Typically, the dimming of incorrect shape is determined, which in itself is an important distinctive feature. In rare cases, a piece of homogeneous dimming during focal pneumonia has a rounded shape (spherical pneumonia), while the outdoor dimming contours are fuzzy with a gradual transition to a healthy pulmonary tissue. In contrast, with peripheral cancer, a non-homicidal dimness is more often determined with more clearly smooth or wavy contours, on the outer surface of which short linear shadows leaving into the surrounding pulmonary tissue ("mustache") can be detected. Less sharp external tumor contours are available in the infiltrating growth phase and especially with the complication of the main disease of the perifocal pneumonia. In such cases, when conducting antimicrobial therapy, a decrease in dimming dimensions is traced, but the rounded shadow on the radiograph is preserved. Peripheral lung cancer is inclined to decay with the formation of cavity in the tumor. At the same time, in contrast to the abscessive pneumonia, this cavity is usually located eccentric and does not contain liquids.
For diagnostics uses bronchoscopy with aspiration of the contents of leading bronchi and its subsequent cytological examination.
Limited infiltrates at least need to differentiate with central lung cancer, not complicated by atelectasis, giving a radiograph of an expanded root with uneven outdoor contours by type "rays of the rising sun" or "janitor's beams", as well as with malignant lymphomas, especially lung lymphogranulomatosis.
At the third stage of differential diagnostics, the inflammatory infiltrates are distinguished.
With equity infiltrates, differential diagnosis is carried out mainly between the equity (more often inhibitory) pneumonia, tuberculosis to shake (as an option for infiltrative pulmonary tuberculosis) and caseometric pneumonia.
Tuberculous Lobit and caseometric pneumonia have a lot of common with equity pneumonia: usually acute start, high body temperature, cough, sometimes with blood spray, chest pain, similar physical changes in the lungs, with a x-ray study - darkening of a share with an increase in affected shares. In favor of tuberculosis, it is suggested: 1) the heterogeneity of dimming on the radiograph with the presence of more dense formations and sections of the enlightenment (better visible on the tomogram) and especially focal shadows, both dense and soft due to lymphogenic and bronchogenic surgery of the surrounding infiltration of pulmonary fabric; 2) the detection of mycobacterium tuberculosis in sputum; 3) more frequent absence of leukocytosis and neutrophilic shift to the left in peripheral blood; 4) lack of effect from treatment in "laid" with pneumonia. However, the last position can be used only with the correct definition of the etiology of the equal pneumonia and the appointment of adequate treatment.
More significant differences with the equity, in particular with the brunt, pneumonia has caseometric pneumonia - one of the most severe forms of pulmonary tuberculosis, the frequency of which has increased sharply in recent years. In contrast to the collaboration with caseometric pneumonia, there are pronounced and constant sweating, especially at night (with bruboral pneumonia, sweating appears during the crisis or with an abscessive disease complication), it is usually not observed with strong pain in the chest; After a few days from the beginning of the disease, a large number of greenish (purulent) sputum begins to separate (with truck pneumonia after a short period of separation of rusty sputum, the mocity mucosa is determined in a small amount); The hectic fever is noted (there is no brute pneumonia); With auscultation, usually by the end of the 1st week of the disease are determined by wet wrecks of increased sound. Radiological research data and sputum analysis on mycobacteria of tuberculosis are crucial for diagnosis. Caseous pneumonium X-ray from the first days of the disease is characterized by a non-homogeneous darkening of the loss of the lung (less often 1-2 segments), which consists of merging large, flue-like species of foci or infiltrative focus with the outlined areas of enlightenment due to the rapidly occurring decay. Already a few days later, numerous fresh cavities with john-like outlines are formed at the site of these sites. It is characterized by a rapid transition of the process to a neighboring share or to another easy-to-develop these departments and further development for several days of new drain foci with their subsequent decay.
With inflammatory infiltrates, the differential diagnosis is more often carried out between focal pneumonia and infiltrative tuberculosis of the lung, however, allergic lung lesions should be eliminated. Tuberculosis infiltrates are divided into several types: broncholobular, rounded, cloud-shaped and perissisurite, under which the tuberculous infiltrate is understood, located along a large or small interdepal gap.
Unlike focal pneumonia, when infiltrative tuberculosis is observed:
a more gradual and less noticeable principle of the disease, which is particularly often noted when rounded infiltrate;
the absence or small severity of intoxication syndrome and catarrhal phenomena. In particular, the cough in the patients is not expressed and is the character of "cuffs". Often, with infiltrative tuberculosis, the first clinical syndrome is the hemoptia, which appears as "thunder among the clear sky" and evidence of the decay of infiltrate;
the most frequent localization in the upper share or in the VI segment (focal pneumonia is often localized in the basal segments of the lower share);
frequent detection of the paleness of the face, abundant sweating at night, good tolerability of elevated body temperature (patient often does not feel its increase), poor performer and auscultative data (singular wheezing are more likely, usually after shaking). Note G. R. Rubinstein (1949) that with tuberculosis (more precisely, with its infiltrative form), "much can be seen (meaning when a x-ray study) and little heard", to date, remains relevant;
as a rule, a normal or somewhat increased amount of leukocytes with a trend towards lymphocytosis. However, during focal pneumonia, leukocytosis is absent from almost half of the patients. Therefore, only the detection of leukocytosis above 12 10 9 / l with a pronounced shift of the leukocyte formula to the left and ESO above 40 mm / h may indicate pneumonia;
contact instructions with patients with tuberculosis.
A crucial importance for differential diagnosis has a radiographic study, the detection of mycobacterium tuberculosis in sputum, in some cases - bronchoscopy.
Radiographic differences are reduced to the following. With infiltrative tuberculosis, the shape of the darkening is rounded, less often the cloud-shaped or oblong in the interdole harness (with perisisurite), the contours are more often clear, the intensity is pronounced. For focal pneumonia, the darkening of the wrong shape with blurred contours, weak intensity is characterized. The main difference is the presence against the background of tuberculous infiltrate and in the neighborhood of soft (fresh) or dense focal shadows and the tracks to the root (due to lymphangoita and fibrosis). With pneumonia on the side of the lesion, an extended and infiltrated root is determined. Some importance for the diagnosis has an estimate of the dynamics of infiltration under the influence of non-specific antibiotic therapy.
Allergic lesions of the lungs with which the pneumonium and infiltrative tuberculosis should be differentiated in shape: 1) of eosinophilic pulmonary infiltration (el), also called volatile eli, simple lung eosinophilia or Lefeler syndrome (Lefefler described in 1932); 2) long lung eosinophilia; 3) allergic pneumonitis; 4) Allergic Alveolitis. The need to exclude allergic processes in the lungs is dictated by treatment tasks, since the purpose and especially the help of antibiotics during allergic processes does not simply do not give effect, but leads to a deterioration of the state and often to death.
The greatest complexity is the differential diagnosis with allergic pneumonites, which more often serve as manifestations of drugs, although they can develop when exposed to other allergens. Allergic pneumonites are a localized process in the lungs, more often unilateral, which is impossible to distinguish from pneumonia along clinical and radiographic data. Often amazed pleura with the possible development of traffic. The idea of \u200b\u200bthe allergic nature of the pulmonary process is added: 1) the development of the process against the background of taking medicines (more often preparations of penicillin rows, sulfanimamides, cephalosporins, furazolidone, adelphine, continuing, vitamin B 1, cocarboxylase and many others); 2) an increase in the part of patients with the amount of eosinophils in the peripheral blood and the presence of clinical manifestations of allergies (skin rashes, asthmatic bronchitis, conjunctivitis, etc.), however, in a significant percentage of cases, these features are absent, since the possibility of autonomous response of the lungs as an immunocompetent authority is allowed; 3) the ineffectiveness of antibacterial therapy; 4) improving the state after eliminating contact with suspected allergen, for example, after the abolition of the "guilty" drug; 5) the effectiveness of glucocorticosteroids.
Allergic pneumonitis often enjoyed on the usual pneumonia. In these cases, the antibiotics initially give a certain effect, but then the reverse development of the process is stopped, despite the change of antibiotics (antibiotics); Moreover, the process applies to neighboring lung departments, and sometimes destructive changes are developing and hemochkali appears, which is explained by hemorrhagic vasculitis and microcirculation disorders. The pulmonary destruction during allergic pneumonite develops due to aseptic necrosis and, unlike the abscessive pneumonia, the formation of it is not preceded by separation of purulent sputum, and the cavity itself does not initially contain liquids. In the future, it often occurs its secondary infection with the formation of an abscess.
If the patient has pneumonia, then transfers to the fourth stage - differential diagnosis between various forms of pneumonium on the etiological factor.
2 auscultation. Above the lesion zone is the weakening of vesicular breathing, in the rest of the zones - gain. In Alveoli, a small amount of exudate sonic creed over the lesion zone (index). The noise of friction of the pleura (pleurisy) stage II - the midst (red and gray compelling) percussion. Absolutely stupid percussion sound (both above the cookie) auscultation. Larngo-tracheal breathing is carried out on the surface - such breathing is called bronchial. Small and medium bronets are filled with exudate wet resistant wheezing (medium fine-duct). The rotion of the friction of the pleura is preserved. III Stage - permission. Percussion. The exudate is highlighted in the form of a sputum appears a dull or duty-chosen percussion sound. Topography is similar to that in the I stage. Auscultation. At the beginning - broncho-vesicular breathing (transitional stage, air enters the alveoli), then - more and more vesicular. The abundance of sonorous wet wheezes, at the end - attitudes (Redoks - before recovery). The friction noise of the pleura (which remains after recovery). Lab data and instrumental research methods. Laboratory methods of research OAK: - pronounced NF leukocytosis with a shift to the left - toxic grain of NF-OB (purulent intoxication) - aezinophilia (the oppression of km, prognostically unfavorable sign) - ESO has sharply increased (up to MM / H) OAM. Much significance does not have b / x: nonspecific inflammation markers. - increased content of C-reactive protein (++ / +++) and fibrinogen - disproteinemia (increasing γ-globulin, decrease in albumin) Wet analysis: - At the beginning - mucous-purulent or hemorrhagic, moderate quantity, turbid - microscopy: alveolar macrophages (cover the walls of the alveoli), siderofagged (MF containing HB), a large amount of NF (PNI); If there is a tumor - atypical cells, tumor rapad - fresh unchanged ER; TB - Mycobacteria, lymphocytes Instrumental methods Research Study Functional respiratory function Spirography, pneumotheometry, picofloumometry (jerking, mod, CHA, MAV) - Restrictive type of ventilation violations R-graphics: signs of infiltration - shadow without clear boundaries (blurred), inhomogeneous intensity. In the upper share - most often TB (+ advanced root, track, enlarged lymph nodes) Tumor - SD "middle lobe" (more often on the right) CT and so on. - In suspected of presence of complications (most often - an abscess or exudative pleurisy) The pleural effusion syndrome. Main complaints: shortness of breath, cough, feeling in the chest dyspnea Inspiratory (compression atelectasis) is enhanced in the lying position (therefore patients occupy the forced position of orthopne or lying. on a sick side). Dry cough, quiet (irritation of pleural leaves) Feeling of cutting, pressure, gravity in the chest. General complaints: High fever, pronounced sweating, decline in appetite General inspection Data Conditions Heavy (purulent pleurisy) Position forced - ortopna or lying on a sick side skin - diffuse cyanosis. If the disease is chronic - "drum sticks" and "hourly windows" study of the chest inspection. The chest of irregular shape, asymmetric (the affected half is increased, the lower departments are especially expanded), the interrochemical gaps are expanded and empty. 2.
3 The amazed half lags behind in breathing. Surface breathing, frequent, auxiliary muscles, rhythmic. The ratio of phases inhale and exhalation is not broken. Palpation. When palpation, interrochemical gaps are expanded. Rigid's chest (increased resistance). Voice trembling below the level of liquid accumulation: - with a small amount of liquid weakened; - With a large amount of liquid there is no liquid. In the garland zone (where the lung is pressed to the root) above the compression atelectasis zone, voice trembling is reinforced. There is no change on the healthy side. Auscultation. On a healthy side - reinforced vesicular breathing. On the affected side: if the atelectasis is incomplete - weakened vesicular breathing, if the full compression is bronchial breathing. Tob., Above the damage zone M.B. Weakening or absence of vesicular breathing. Whole crepitate (because around is a dense tissue). Damuazo Line: Kosy - a sign of pleurite, horizontal - a sign of hydrotorax. Damuazo is listened to the noise of friction of the pleura. Laboratory methods for the study of the UAC, OAM: Changes are similar to those in pneumonia, but the analysis of pleural effusion is less pronounced. For the collection of pleural effusion, pleural puncture is carried out. Pleural puncture diagnostic: to differentiate transudate from exudate transudate (horizontally accumulated): hydrotorax, PSN, nephrotic SD, cirrhosis exudate (spacecraft accumulates): Exudative pleurisy for determining the cause of inflammation: bacterial inflammation, TB, carcinomatosis of therapeutic treatment: when cluster\u003e 500 ml liquid. If the liquid reaches the level III of the edge, the pleural puncture is urgent manipulation (prevention of compression atelectasis). Not more than ml are removed simultaneously.! Introduction of medicinal substances (bacterio, tuberculostatics) The imposition of an artificial pneumothorax for causing atelectase cavity falls down and is frozen (when TB cavernose) differences between the transudate from the exudate transdate exudate Physical properties 1. The color is transparent, opaleszing depends on the nature of the shaped elements, no proteins 2. The liquid consistency is the greater in the pus, the thicker 3. Character serous serous-purulent purulent hemorrhagic chileosic 4. The smell without smell depends on the composition (pussy, TB, the decay of the pleural sheets purulent odor) Chemical properties 1. Presence of a protein of finely dispersed,< 30 г/л иммуноглобулины, > 30 g / l of trial of Rivolt "-" single leukocytes 2. Specific density Microscopic examination 3 Rivolt sample "+" (clouding with adding any acid) Multiple leukocytes of NF GNU (pleurite empy
5 Research of sputum: Basic purulent or mucule-purulent spatter, silent, 2 x - 3 x-slave (3 x-slave - Sign of abscess breakthrough): At the bottom - Defrost products of light tissue, microscopically: NF, lymphocytes (TB), ER (decay), Ditrich tubes (Bab - small cavities), lentils (TB), Elastic fibers (disintegration of light tissue) Instrumental research methods 1. Study of the function of external respiration - Restrictive type of ventilation disorders 2. Overview R-graphics: Rominal shadow with Horizontal liquid level 3. Bronchology (Bab) 4. layered R-tomography, layer-by-layer CT 5. Endoscopy: inspection of bronchial wood + biopsy and a study of washing water (search for atypical cells and BC). Elevated airiness syndrome of pulmonary fabric (lung emphysema) increased airiness of the pulmonary tissue or emphysema of the lungs (email) - a pathological condition characterized by the expansion of air spaces located distal than terminal bronchioles, and the reasons for development of the elastic properties of pulmonary fabric. For reasons and mechanisms for the development of EL, are divided into: primary email - it occurs in unaffected lungs due to congenital, genetic anomalies or the impact on them of various pathological factors; Secondary el - arising against the background of other, chronic respiratory diseases, such as HB. The primary email is an independent disease, it was previously called idiopathic, essential ell, because The reasons for its occurrence were not clear. Currently revealed many causal factors of primary email. Endogenous and exogenous factors are distinguished in the development of primary ell. 1. Among endogenous factors, the roles of genetic factors are greatly imported. Among them: Congenital deficiency of ά-1-antitripxin; violation of products and activity of surfactant; Mukopolyachharid violations; Genetic defect of elastin and collagen in the lungs; violation of physiological equilibrium in the system of protease inhibitors; Equilibrium disorder in estrogen-androgens ratio. A) An important place among endogenous factors is given the role of genetic factors, in particular, the deficiency of ά-1-antitripsein. It refers to serum proteins from the group of ά-1-globulin and is a glycoprotein, which accounts for about 90% of the total plasma tripsigning ability. It easily penetrates into the lungs and inhibits trypsin, chymotrypsin, collagenase, elastasia, a number of plant and bacterial proteases. The congenital deficit of ά-1-antitrypsin leads to an excessive action of enzymes, including elastase, the main source of which are neutrophils, it leads to the destruction of (destruction) of interlimoolar partitions and the merger of individual alveoli into larger emphysematous cavities with a gradual decrease in the respiratory surface. B) Another endogenous factor contributing to the development of EL is the violation of the exchange of mucopolysaccharides in the pulmonary tissue, due to the presence of a congenital defect of structural glycoproteins (pulmonary collagen, elastin, proteoglycan), or by changing the properties of the surfactant. C) Endogenous factors include the weakness of the smooth muscle light framework, as a result of which the bronchiole and alveoli conversion occurs in emphysematous cavities, at which initially does not destruction of the interlimoolar partitions. D) a violation of the ratio of androgens and estrogen also provides damaging is on the stroma of light, which partly explains the age and sex features of the development of EL. Estrogens stabilize the lysosomal membranes, have an antiproase effect, stimulate fibroblasts, causing reparation of elastin and collagen. 2. Exogenous factors in the development of primary email: These include: 5
6 (a) Smoking, air pollution, pulmonary infection, as well as allergic conditions. Such components of tobacco smoke and contaminated air, like cadmium, nitrogen oxides, hydrocarbons, weighted dust, etc. lead to the development of email, because On the one hand, these factors activate the activities of alveolar macrophages and neutrophils, which contributes to an increase in the level of neutrophil elastase, on the other hand, the activity of proteolysis inhibitors is reduced, primarily ά-1-antitripsein. This leads to significant damage to elastic fibers and a decrease in the elasticity of pulmonary fabric. In addition, smoking necessitates violations in the oxidant system. In tobacco smoke, oxidants are contained, which suppress the activity of antiolastase inhibitors, inhibit reducing processes in the damaged elastic mild frame. Under the influence of smoking, the content of antioxidants in the blood plasma decreases. All this contributes to the development of EL. Smoking is an important factor in Pathogenesis EL, as it leads to a permanent imbalance of proteases and inhibitors. B) One of the frequent causes of el - pulmonary infection (inflammation of a non-specific nature). Development mechanisms. A good elastic traction of healthy pulmonary fabric holds small and thin walls of terminal bronchioles from falling, acting on them from the inside on the exhale and in the breath. At the same time, on the breath, the elastic thrust of expanding lungs even more stretches on the side of the wall bronchiol, increasing their lumen. If the lungs lose their elasticity, and with it and the strength of elastic thrust, then the walls of bronchi are falling down, and their lumen decreases. In cases of a pronounced decrease in the elastic properties of the pulmonary fabric, even an active breath leading to the stretching of the pulmonary tissue does not lead to the full resort of the bronchiole walls. During the exhalation, on the contrary, the walls bronchiole quickly fall, and their lumen decreases until the onset of such a moment when the further exhalation becomes impossible. Thus, with EL infectious inflammation stimulates the proteolytic activity of macrophages and neutrophils. Bacteria can also be an additional source of proteolytic enzymes, which leads to email. Secondary email is not an independent nosological form, and the syndrome that arises against the background of various lung diseases. A) The main cause of the secondary el is chronic obstructive bronchitis (hob). The development of EL is associated with obstruction, impaired bronchial patency, leading to the emergence of the valve mechanism with air delay. The violation of bronchial patency arises both in the breath and exhale. However, the decrease in the intragenuous pressure on the breath leads to passive stretching of the lumen of the bronchi and to some increase in bronchial passability, and an additional compression is created on the exhalation of a positive intragenum pressure, an additional compression is created. This causes air delay in alveoli and contributes to the increase in pressure in them. An additional increase in effort on exhalation leads to an even greater increase in the intragenic pressure and squeezing small bronchi. When hob, permanent cough and obstruction of small bronchi and bronchiol leads to a constant increase in intrastallyolar pressure. B) bronchial asthma. During the attacks of Ba, there is a short-term expansion of the alveoli, and the repetition of the attacks leads to the loss of elasticity of pulmonary fabric, and, consequently, to the development of EL. The bronchiole walls play the role of the valve, which during the exhalation is closed, as a result of which the alveoli remains constantly inflated increased amounts of residual air. Extended alveoli squeeze the pulmonary capillaries, which causes trophic changes in the pulmonary fabric, the destruction of the fine network of pulmonary capillary vessels, the destruction of the interlimoolar partitions. Alveolas are often stretched so much that, along with the destruction of alveolar partitions, their ruptures are possible. The blown and separation of pulmonary tissue, the destruction and breaks of inter-vololar partitions contribute to the formation of large air cavities - Bull, which, in turn, squeeze another functioning pulmonary tissue and disturb its ventilation and blood circulation. Thus, there is a vicious closed circle of pathological mechanisms for the formation of irreversible changes in the lungs and steady progression of email. S.P. Botkin very accurately noticed that "to restore the destroyed alveoli is also impossible, how to grow a torn finger." As a result, breathing is disturbed, especially the act of exhalation, which becomes active. The chest gradually expands, acquires a barrel-shaped form. Progressive decrease 6.
The 7 general functioning surface of the lungs and the phenomena of secondary bronchial obstruction is carried out to the development of respiratory failure. With an alveolar hypoxia, associated with violation of the ventilation of the alveoli, causes a spasm of pulmonary arterioles. On the other hand, due to structural disorders, the total lumen of the arterial bed is reduced. The combination of these factors underlies the development of pulmonary hypertension. Increased pressure in the pulmonary artery system creates an increased load on the right ventricle of the heart, as a result of which signs of its hypertrophy appear, and later dilatation. Therefore, over time, heart failure also joins the respiratory failure. The phenomena of the secondary obstruction of terminal bronchiol with an email was found to include it in a group of obstructive lung diseases, which also includes BA and obstructive bronchitis. The main complaints of the patient with El - Dyspnea. Dyspnea is a manifestation of respiratory failure, reflects its degree. At first, it happens only during exercise, then appears during walking, especially in cold, crude weather, and sharply increases after coughing - the patient cannot "breathe" (with secondary email). Dyspnea is a non-permanent, changeable ("day for a day not necessary") - today is stronger, tomorrow is weaker. General inspection data. Diffuse cyanosis of the skin and visible mucous membranes, the neck is shortened, the veins of the neck of the swollen. Study of the chest. Inspection. The chest emphysematous (barrel-shaped), the front-rear size is increased, the ribs have a horizontal direction, the intercostal gaps are expanded and smoothed, sometimes even empty. Epigastric angle\u003e 90 o. Included pits sput and filled with extended pulmonary tops. Breathing superficial, difficult, with the participation of auxiliary respiratory muscles. Patients exhale with closed lips, inflating cheeks ("puff"), which reduces the flip of the walls of terminal bronchiol and increases the removal of air from the lungs. Palpation. The chest rigidna due to the loss of elasticity with a pulmonary cloth. Voice trembling is weakened due to increased light airiness. Percussion. Increased lung airiness causes the appearance of tympanic percussion sound, and the decrease in the voltage of the walls of the Alveol gives it a kind of shade, and such a low tympanic chopper sound is called boxes. As a rule, it is determined at email with a comparative percussion. The standing height of the tops of the lungs increases, the landscape fields are wider, the lower boundary of the lungs fall below the norm, the mobility of the lower edge of the lungs is reduced. Auscultation. Uniform weakening of vesicular breathing, it resembles breathing, hearing through cotton ("cotton breathing"). If EL accompanies the inflammatory process in bronchi, it may appear hard breathing, as well as dry and wet wheels. In the emphysema of the lungs, the area of \u200b\u200babsolute dullness of the heart is reduced, and the tones of the heart are muffled, as it is covered with bloated light. The emphasis of the I Tone on La is listened (a sign of increasing pressure in the ICC). Additional research methods for EL. From instrumental research methods, X-ray and spirographic research are the most informative. 1. X-ray study. The main radiological features of EL include: an increase in the transparency of pulmonary fields, the expansion of intercostal intervals, the omission of the lower borders of the lungs, the sluggish mobility of the diaphragm dome, pathognomonic for the email is a diffuse or peripheral device with a simultaneous increase in transparency, an increase in the angles of vessels. 2. Computed tomography - makes it possible to identify bullous formations in the lungs with great accuracy, determine their localization and prevalence. Showing at suspected bullous email. 3. Nuclear magnetic resonance - allows you to estimate the structure of vascular walls, air conductive paths and mediastinal structures. 4. The scanning and scintigraphy of the lungs detect vascular changes in the lungs in emphysema. The scintigraphic picture at EL is characterized by a reduced and uneven distribution of 7
8 radioactive drug, which can be observed in the early stages of EL, when the X-ray picture remains still normal. 5. Bronchoscopy - allows you to detect such a sign of emphysema as trachea hypotension and bronchi 6. Spirography. At EL, there is a resistant reduction in high-speed indicators (the volume of the forced exhalation for 1 s., Tiffno, jerk, increasing the overall and functional residual lung tank). 7. Pneumoscopy - reveals early signs of EL. Early signs of EL referred to a change in the curve "Volume-flow" of the maximum exhalation, expressed in the reduction of the flow and the appearance of concavity, pointing up from the volume axis. Candular deficiency syndrome (CH) I. Acute CH 1. Heart (LPN, LLN, PZHN) 2. Vascular (collapse, fainting, shock) II. Chronic CH 1. Cardiac (LPN, LHN, PZHN, Total CH) 2. Vascular (chronic hypotension) 3. Mixed (cardiovascular) Classification of HSN according to Vasilenko-Strazhestko. 3 Stages: 1. Initial (hidden, latent). Hemodynamics alone is not violated, asymptomatic LV dysfunction. With a significant physical activity - shortness of breath, heartbeat 2. Clinically pronounced stage. A. Hemodynamic disorders in one of the circles of blood circulation. Clinical signs of blood circulation deficiency. B. Heavy circulatory disorders (hemodynamic disorders in both circles) with adequate treatment of symptoms decrease! 3. Finite (dystrophic) stage of irreversible morphological (dystrophic) changes in parenchymal and other internal organs, reduced muscle mass. Functional classes of circulatory insufficiency against the background of treatment it is possible to change the class (and improvement, and deterioration)! The main criterion is the degree of severity of shortness of breath and heartbeat. 1 class. There are no restrictions on physical activity, but with a significant physical exertion, shortness of breath and heartbeat appear, which require a longer period of rest than normal. Grade 2. A minor restriction of physical activity (the patient does not run, but walks on foot). There are no symptoms at rest. The usual physical activity leads to increased fatigue, weakness and requires a long period of rest 3 class. Noticeable restriction of physical activity. Dyspnea and heartbeat appear even with a minor physical exertion. 4th grade. A sharp restriction of physical activity. The slightest physical activity leads to the appearance of shortness of breath and heartbeat. Causes: I. Cardual: myocardial damage. II. Extraacardial: an increased load with which myocardium copes for a long time (compensation) sooner or later decompensation CH increased load of diastolic dysfunction to the heart section flows more blood than normal ( congenital villocks Hearts, all valve deficiencies, BCC: nephrotic SD, anemia, pregnancy); eight
9 Pressure overload (resistance) Systolic dysfunction. Stenosis of valves, arterial gpertenzium (LLN), light hypertension - an increase in pressure in the ICC (PJN) OLDN. Causes: - Stenosis mitral valve - Trombus in LP - Mixoma (tumor) in LP Chlpn. Reason: - Mitral Stenosis of Olzn. Causes: - Myocardial infarction - hypertensive crisis - aortic flavors - rhythm disorders (ventricular fibrillation, full of AV-block) CHLD. Causes: - IBS, cardiosclerosis - GB - deficiency of the mitral valve, all aortic vices. Clinical manifestations of Olpn and Chlpn are the same (pressure in the ICC) - Cardiac Asthma (interstitial stage of elderly). Main SP - Chief: Acute Left Heart Insufficiency Sharp Pressure In the ICC Turning off the pump function of the heart Liquid part of the blood comes out of the vascular channel Overhead tensile tensile violation violation in restrictive type Inspiratory dyspnea of \u200b\u200bgases. Choosing: Inspiratory, arises at the height of physical exertion or at night, the patient occupies a forced position - ortopnoe with lowered legs (blood depositing). In progression: the interstitial edema moves to Alveolar ("Flooding Alveol") separated by serous foamy pink wet, wet large-tape rates appear. The data of the general inspection state is severe consciousness: first initiated (tachipne), then the excitation is replaced by overexcusion and oppression. Behavior is determined by consciousness. Forced position - orthoploa with lowered down legs. The face is thought-out, blue, with severe acricyanosis, the patient "catches" the air open mouth, the wings of the nose are involved in the act of breathing. Study of the chest. Inspection. Breathing is frequent, superficial. Extliented phase inhale. palpation. Voice trembling is enhanced equally on both sides, especially in the lower departments (the edema begins below), the chest in the lower parts of the rigid. Percussion. In the upper departments, a clear light sound, in the lower - dust-tympanic or stupid (the edema of the alveolo wall). Patient in severe condition topographic percussion is not held. Auscultation. In the upper departments - hard breath, in the lower - loose vesicular (corresponds to the dullness zone). At the beginning of the attack, unrivial attitudes, finely and medium-duty wheezes in the lower departments are listened, dry wheels in the upper departments (Otternaya Wall). NB Reflex Euler-Liestranda: Partial pressure of 2 in Alveoli compensatory bronchospasm. The study of blood circulation bodies. Olpn. Inspection. Enhanced abbreviation of LP (a lot of blood, and a narrow hole) in the II-III intercoremores can be seen in the extension of interrochemical gaps. Pressure in the ICC Pulsation of La (II intercostal left) Palpation. In the field of the top of the heart - diastolic jitter ("Cat Murlykanny") percussion. The upper border of the heart is expanded up, the "waist" of the heart is smoothed, the vascular bundle is expanded to the left (due to dilatation of LA). Auscultation. I tone "clapping", II - focus on La, the discovery of the mitral valve (i.e., the "rhythm of gallop"), after which - diastolic decreasing noise. OLZHN. Inspection. Pressure in the ICC Pulsation La (II intercostal left) 9
10 Palpation. The topping push is shifted to the left and down (viorerer), spilled, low, weakened. NB The resistance of the top shock is determined by the cause of percussion. The left limit of the heart is expanded to the left, the vascular bundle is expanded to the left. Auscultation. I tone weakened, accent II tone on La ("Rhythm Galopa"). The top of the III and IV pathological tones are suspended. Rhythmized (compensatory tachycardia). Systolic blood pressure is reduced, diastolic blood pressure is increased, the pulse pressure is reduced. PS with LPNs asymmetric and nehydramine, frequent, weak, small filling, i.e. PS FILIFORMIS, and on the left hand - PS differens (dilated LP squeezes the connective artery). Clinical manifestations of chlpn, chljn: cough, hemoptal, shortness of breath. Gradually, the lungs of the plasma pneumososclerosis of pneumophybresis secondary bronchtic SD cough. Reason: the enemy of the bronchi wall irritation of receptors N. Vagus cough dry, appears in a horizontal position, at night; It is stopped in a position with a highly raised headboard. A serous sprome is separated in the morning (the liquid part of the plasma hearing overnight). If ER is heganized, herlooking appears. (Siderophages are alveolar macrophages containing destroyed HB; "Cells of heart defects"). Dyspnea. Causes: - Ventilation disorders on restrictive type - Dyspacy dishouts (sclerosis) Dyspnea inspiratory, enhanced or occurs in a horizontal position, decreases in a position with a highly elevated headboard. General inspection data. Satisfactory condition. Consciousness is clear. The position is forced - with a highly raised headboard. Corvisar's face: Pastomian, pale gray, with semi-shot centuries, half-open mouth, acrocyanosis (blue lips and uches) and erythrocyanosis (the number of ER extension of the venous network). Skin: diffuse cyanosis + acrocyanosis. Study of the chest. Inspection. The chest of the right shape, symmetrical, both half are equally involved in the act of breathing. Breathing type mixed, breathing frequent, superficial, with the participation of auxiliary muscles. Palpation. The chest rigidna, especially in the lower departments. Voice trembling in the lower parts is reinforced, especially in the morning, after a long time in a horizontal position. Percussion. Light sound dull in the lower departments. Breathing is rigid, in the lower departments - weakened. Dry wheezes are listened in the upper departments, unrivorous crepitiation or wet unrivied wheels in the lower departments. The study of blood circulation bodies. Inspection. Enhanced abbreviation of LP (relative deficiency of the mitral valve) in the II-III inter estreon can be seen in the extension of interrochemical intervals. Pressure in the ICC Pulsation of La (II intercostal left) Palpation. In the field of the top of the heart - diastolic jitter ("Cat Murlykanny") percussion. The upper border of the heart is expanded up, the "waist" of the heart is smoothed, the vascular bundle is expanded to the left (due to dilatation of LA). Auscultation. I tone on the top weakened, II - focus on la, the discovery of the mitral valve. Systolic functional noise (relative deficiency of the mitral valve). With chlpn, tones are nehyrtic (flickering artmy). "Rhythm Galopa does not happen (this is a sign of land)! Clinical manifestations of the Ministry of Affairs Reasons: Thrombosis and Tel and its large branches. Main complaints: Breast pain, shortness of breath, pain in the right hypochondrium (portal hypertension), edema on the legs. NB M.B. Infarction SD sealing light tissue Breast pain caused by a sharp expansion of La Opporting shortness of breath: All the blood remains in the PJ due to the obstacle does not enter into light reduction of vascular beds expressed hypercupnia and hypoxsemia Excessive irritation of DC inspiratory shortness of breath. 10
11 General inspection data. The condition of the heavy consciousness is depressed (Bainbridge reflex: hell, tachycardia, acute vascular failure) Statution forced - ortopnoe with highly raised headboard leather. Pronounced cyanosis in / 2 torso; Cool, wet skin. The study of blood circulation bodies. Inspection. Dilatation of PZ hearty push, true epigastric pulsation Expansion of HPV Empty of the cervical veins, "-" Vyan pulse (does not coincide with a heart impetus). Percussion. Expanding the right border of the heart to the right. Auscultation. I tone is weakened at the 4th point of auscultation (base mesia-shaped process) + There is also a functional systolic noise (relative failure of the tricuspid valve). II tone - sharply metallic, split on la. Liver study. Empty of right hypochondrium, its pain. The liver is enlarged in size, the lower edge is painful (due to the stretching of the glisson capsule). Clinical manifestations of CPZHN Causes: - Stenosis of the tricuspid valve (only congenital vice!) - HNZLE PRESSURE IN MKK (secondary light hypertension) - primary light hypertension (congenital abnormalities of the ICC vessels) at the beginning of hyperfunction then hypertrophy dilatation of PZ NB dilatation of the PJ, developed due to pressure in the ICC - "Light Heart". " Light heart»M.B: Acute (Tala); Subacle (lack of three-dimensional valve, aortic vices, total blood circulation failure); Chronic (easy hypertension) Main complaints: At the beginning - pain in the right hypochondrium (violation of the outflow of venous blood portal hypertension), the outflow of venous blood and from the intestine of the chair disorder (diarrhea / constipation), intestinal dyspepsia is disturbed. Thirst, Oliguria, Nicturia (horizontal position Bleeding in the kidneys) Oliguria + Niccountura \u003d CPJN, polyuria + niccountura \u003d renal failure. Highways on the lower limbs (body weight edema) General complaints: reduced performance, increased fatigue. Total Caudal Reasons: - myocardits, myocardiopathies, myocardiodyatrophy - combined defects of coronary insufficiency syndrome (CN) - acute CN - chronic CN CHN. Causes: - AC (oblicking, stenosing) coronary arteries - IBS; - systemic diseases of Art (vasculitis) - SLE, nodular periaryitis; - pronounced hypertrophy of myocardial LV (GB, aortic vices) muscle thickened, and the diameter of the blood vessels; - Spasm of coronary arteries. The main stages of atherogenesis 1. The wall of the artery is normal (the free current of arterial blood rich about 2) 2. The formation of lipid spots - lipoid (the accumulation of LP in the intima with the formation of lipid spots) 3. Formation of fibrous plaque - liposclerosis (intima thickens, accumulates in it The MMC and the intercellular substance synthesized with them, from which the fibrous tire is formed. Fibrous plaques sharply narrow the clearance of the vessel) 4. Atheroma formation - atheromatosis (decay of the LP complexes in the thickness of the fibrous plaque) 5. Clinical manifestations of the AC: - Fibrous tire destruction (atheromatous ulcer ) eleven
12 - hemorrhage into a stroke of plaque - the formation of thrombotic overlays on the site of the atheromatous plaque at this stage develop thrombosis, embolism, aneurysm of the vessel, blood bleeding (arrosive). Windows Causes: - thrombosis (atherotromboosis) of coronary arteries; - Myocardial infarction; - unstable angina. Nature angina angina - at the height of the physical activity (the need for heart rate in O 2) is distinguished 4 functional class of stress angina: 1 FC: pain when walking distance\u003e 500 meters 2 FC: pain when walking distance 3 FC: Pain when walking on Distance Meters 4 FC: Pain when walking distance<50 метров по ровной местности, в покое ФК отражает степень сужения коронарных артерий!!! Стенокардия напряжения делится на стабильную и нестабильную. Приступы стабильной стенокардии при определенной (одинаковой) физической нагрузке, длятся определенное время, хорошо купируются НГ. Стабильная стенокардия является признаком медленного прогрессирования КН. Первый признак того, что стенокардия становится нестабильной - учащение приступов. Они начинают возникать при меньшей физической нагрузке, плохо купируются НГ. Это признак быстрого прогрессирования КН («прединфарктное состояние»). NB При стенокардии боль всегда терпима стенокардия покоя - признак выраженного сужения коронарных артерий вариантная (вазоспастическая) стенокардия Принцметала. Её причина - коронароспазм. Приступ возникает обычно ночью (повышается тонус парасимпатической НС). Инфаркт миокарда. Клинические варианты 1. типичный (ангинозный) 2. атипичные астматический (ОЛЖН острый отёк лёгких) гастралгический (абдоминальный) - в результате тромбоза огибающей венечной артерии. Проявляется болями в эпигастрии (в большей степени в подложечной области), тошнотой, рвотой, Sp раздражения брюшины. NB при некрозе базальной стенки в процесс вовлекается диафрагма. церебральный (МОК мозгового кровообращения) периферический (боли в зонах Захарьина-Геда) коллаптоидный (ОСН резкое АД) аритмический Боль при инфаркте миокарда: - вся передняя грудная стенка; - иррадиирует более обширно, чем при приступе стенокардии; - более интенсивная, давящая, сжимающая (могут развиться acute psychosis). If pain does not stop, pain shock develops; - NG does not stop; - Loins\u003e 30 minutes. General inspection data. Heavy condition, even if there are no complaints of consciousness - excessive excitement, incl. and motor; Acute Psychosites Position Forced - Orthopnoe with a highly raised headboard face. Pronounced acricyanosis (IOC). Fear of death (ka). Pale skin, cyanotic, with large drops of cold sweat. 12
13 Investigation of blood circulation bodies. PS frequent, irregular, small filling, soft (PS Filiformis). Systolic hell is sharply reduced, diastolic M.B. Increased (at the expense of the spasm of peripheral arterioles). Inspection of the precartial area. The top push is shifted down and left (dilatation of LV), spilled, low (height and strength reduced). There is a pulsation of LA, especially with asthmatic form (pressure in the ICC). Percussion. The left limit of the heart is expanded to the left auscultation. The pace is rapidly (UO Tachycardia), rhythm disorders. I tone on the top is weakened + there is also listened to the III pathological tone (the result of a sharp decrease in the contractility of myocardium). T. Ob., Notes "Rhythm Galopa". II tone on the aorta is weakened, on La Stregnated. Laboratory methods for research OAC: - NF leukocytosis - by the end of the 1st and early 2nd day (inflammatory infiltration around the necrosis zone). By the end of the 1st week, the leukocyte formula is normalized - the acceleration of the ESR after 7-10 days (the deceased CMC is AUTAAG AT generation) OAM: there are no significant changes. b / x: Markers of the destruction of CMC: - KFK (above the norm after 4-6 hours) - LDH-4.5 (above the norm after 6 hours) - ASAT - a slight increase in the end of the 1st day - alto - to a lesser extent - Mioglobin (staining urine in red) - a cardio-specific fraction of troponins of arterial hypertension syndrome. Arterial hypertension syndrome includes all diseases at which there is an episodic or persistent increase in blood pressure. By origin, arterial hypertension can be: primary (essential, hypertensive disease - by definition of domestic authors) - arises regardless of the state of organs participating in the regulation of the vascular tone; Secondary (symptomatic) - arterial hypertension is one of the symptoms of the underlying disease. Essential arterial hypertension (hypertension). Hypertensive disease refers to the so-called diseases of civilization, since the frequency of its prevalence in economically developed states is significantly higher than in developing countries. Pathogenesis. The pathogenesis of primary arterial hypertension is quite complicated, and it can be conditionally divided into 2 links: breakage of the central regulatory mechanisms; breakage of peripheral regulatory mechanisms. Central regulatory mechanisms. I. brain cortex. Brake gamke-eergic brain system. GABA reduces the activity of the processes of excitement in KGM and prevents the development of stagnant foci of excitation. 2. Subcortical brain structures. Adrenergic brain system (catecholamines). Holieregic brain system (acetylcholine) Endorphins synthesis system (endogenous opioids). Biological synthesis system. active amines (serotonin et al.) Release system (minising hormones, regulating the synthesis of trop hormones by hypophysome). 3. The pituitary. System of synthesis of trop hormones (ADG, ACTH, TG, STG). Peripheral regulation mechanisms. 13
14 1. Sympathetic nervous system. Fabric depots norepinephrine (heart muscle and vascular wall) circulating catecholamines. 2. Parasympathetic nervous system. Acetylcholine. 3. Vascular wall. Volumentraceptors. Osmoreceptor. Chemoreceptors. 4. Peripheral. Endocrine organs. Adrenal glands (glucocorticosteroids, mineralocorticoids, adrenaline - cerebral layer and paravertebral chromaffinized cloth). Thyroid gland (T3, T4). fourteen
15 5. Kidneys. South (Renin, angiotensin, pg). The pressing effect on the vascular wall is provided: circulating catecholamines; serotonin; Vasopressin (ADG); ACTH; Ttg; STG; T3 and T4; glucocorticosteroids: aldosterone; Renin, angiotensin II; PG F2A (especially in large quantities is produced in the south of kidneys). The depressor effect on the vascular wall is provided: GABA; acetylcholine; endorphins; PG 12. The basis of increasing blood pressure is a psycho-emotional stress, which is a violation of an adequate response of the body to situationally determined influence. The reaction to external stimuli, as a rule, becomes with a sign "-". This is more often due to the genetic basic properties of the personality. Primary arterial hypertension refer to psychosomatic diseases (displaced emotions). Forming autoagression is aimed at target organs (left ventricle and vascular wall). Adrenaline mainly affects myocardium left ventricle and, to a lesser extent, on a vascular wall. This is realized by hyperfunction of the left ventricle, with an increase in the heart rate, the reduction rate of the left ventricle, the UO, IOC, which leads to a significant increase in the filling of the vessels in systole and is realized as an increase in systolic pressure indicators. 1. Formation or activation of a stagnant focus of excitation in KGM (weakness of the GAmK-Ergic brain system). 2. Activation of central and peripheral pressing mechanisms. 3. Increasing the level of circulating catecholamines, vasopressin, trop hormones of pituitary glands, glucocorticoids. 4. Hyperfunction of the left ventricle, increase the vascular tone. 5. Tachycardia, systolic or diastolic arterial hypertension. At the later stages of the disease, along with an increase in the level of adrenaline, the level of circulating norepinephrine, which mainly has a vasopressor effect and, to a lesser extent, affects the heart muscle. This is accompanied by an increase in OPS. The combination of increased vascular tone and the dyed cardiac emission leads to an increase in and systolic and diastolic blood pressure (systole organic arterial hypertension). Increasing the level of circulating catecholamines activates the south of the kidneys, which is accompanied by an increase in the synthesis of renin, angiotensin and aldosterone. The following stage of the progression of arterial hypertension is connected - salt mechanism. The reabsorption of Na and sodium-dependent H2O in the distal kidney channels increases. This leads to an increase in the BCC. The Na and H2O delay in the vascular wall leads to an increase in its sensitivity to the vasopressor influence of circulating catecholamines. An increase in the synthesis of angiotensin II with hyperrheninemia has a powerful straight vasopressor effect on the vascular wall. At the same time, the content of the SA ions in the MMC vessels increases, which stimulates their reduction and even more increases the vascular tone and the OPS. Systolic blood pressure is maintained due to the increase in UO and IOC. Further increase in the vascular tone determines the further increase in diastolic blood pressure. A resistant systole historical arterial hypertension with systolic and volumetric overload of the left ventricle is formed. Systolic overload is associated with an increase in the OPS, and the volume - with an increase in the BCC. This is accompanied by remodeling resistive vessels and compensatory left ventricular hypertrophy. Clinically manifests itself with bradycardia with an increase in the duration of systole and the diastole of the left ventricle, working against an increased OPS. With the overwork of myocardial left ventricle in it develop dystrophic changesEspecially in the subendocardial departments of the heart muscle due to the emerging relative coronary failure. This leads to the decompensation of the left ventricle with a decrease in cardiac output and a decrease in systolic blood pressure. Developed "decapitated" (diastolic) arterial hypertension. fifteen
16 dilatation Left ventricular (left ventricular deficiency) and the remodeling of the vascular wall determines the violation of the blood supply to the internal organs: the brain, the retina, the kidneys and the heart muscle. Damage to the targets is clinically manifested: angina and high risk of myocardial infarction; chronic cerebrovascular insufficiency with the development of ONMK; intracranial hypertension with the risk of eclampsia development; reduced visual acuity, high risk of hemorrhage development in retina and retinal detachment; Kidney Ischemia ranging into hypertensive nephrolerosis with a high risk of kidney infarction and CPN with appropriate clinical symptoms. According to indicators, the blood pressure is distinguished by 3 versions of arterial hypertension: hyperkinetic (systolic ag) - pulse pressure increases to 60 mm.rt.st. and more. Corresponds to the adrenergic pathogenetic version of the AG. Eukineic (Systole Outolic AG) - pulse pressure does not change significantly. Corresponds to a noradreengic pathogenetic version of AG. Hykokinetic ("decapitated" AG) - The pulse pressure indicators are reduced. Corresponds to the salt pathogenetic version of hypertension on the background of emerging left vehicles. adrenergic arterial hypertension . The main pathogenetic factor is to increase the level of circulating adrenaline. These are situationally due to arterial hypertension in hyperreactors. It is characterized by an unstable flow with a periodic increase in systolic blood pressure. It is implemented due to the activation of the central hemodynamics link with the hyperfunction of the left ventricle. This is predominantly systolic arterial hypertension with adrenergic crises (crises I order): hypercathecholamine, pronounced vegetative symptoms, tachycardia. As a rule, they are not complicated by vascular disasters, easily coupon They are engaged in sedative, psychotropic drugs, to a lesser extent - β-adrenoblockers. They can be observed throughout life, exacerbating in the preclimberic period (connecting hormonal shifts) and in persons the older age (the development of atherosclerotic damage vessels). Noradrenergic arterial hypertension The main pathogenetic factor is to increase the level of circulating norepinephrine, activation of motor centers and peripheral hemodynamics. Most often, drugs are induced by medicines by the destructive adrenaline or decreasing sensitivity of tissue receptors to the circulating adrenaline (Raunatin, Adelganine, Spere, Clofhelin, etc. ). The level of norepinephrine rises gradually and remains for a long time. Developed against the background of hyperfunction of the left ventricle and an increased vascular tone. These are predominantly systole organic arterial hypertension with noradreengic crises (crises II of the order). They are characterized by a slower increase in systolic and diastolic blood pressure, which is preserved within a few hours, days. Poor corrected by drugs. Preparations of pathogenetic action are used. High OPS determines the decrease in heart rate with an increase in the duration of the heart cycle. The risk of developing complications is extremely high: OnMK, acute myocardial infarction, kidney heart attack, retina hemorrhage and retinal detachment. Increases the risk of Development of Olzn, up to the ethics of the lungs. Salt arterial hypertension. The main pathogenetic factor is the primary (gene. Deterministic) or secondary (as a result of the first 2-mechanisms) Raas activation. Water-salt exchange is broken, the BCC increases, the vascular tone increases. This is predominantly diastolic ag with saline (cerebral) crises against the background of systolic and volumetric overload of the left ventricle. The symptoms of the crises are associated with an increase in Hell and VCHD (due to the increase in the volume of the liquor). The brain symptoms of the high risk of eclampsia development, ONMK is revealed. The development of crises is provoked by an improper water-salt regime. Characterized by the "Ring" syndrome. This AG has long been clinically manifested. Maintenance clinical symptoms. Symptomatics is associated with hemodynamics violation and lesion of target organs. 1. Intracranted pain hypertension in the back of the head. Nausea, vomiting at the height of the rise of the PCF. 2. Violation of cerebral blood flow dizziness. Violation of equilibrium. Reduced memory. Astheno-neurotic symptoms. Depressive states. sixteen
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Belarusian State Medical University
On the topic:
"Differential diagnosis for pulmonary infiltration syndrome"
Minsk, 2008.
Infiltrate in Lögk. - This is a plot of light tissue, characterized by the accumulation of usually non-peculiar cellular elements, increased volume and increased density.
According to X-ray research:
1) limited dimming and foci (most often)
2) Round Shadow - Single or Multiple
3) pulmonary dissemination
4) amplification of the pulmonary pattern
Subjective symptoms:
Nonspecific
May indicate the defeat of the respiratory system
More often occurs shortness of breath, cough, chest pain, sputum isolation, hemoplary
Perhaps the presence of only nonspecific symptoms: fatigue, reduced performance, headache, loss of body weight
Perhaps the complete absence of subjective complaints
Physical examination data:
Standing of the patient of half the chest in breathing
Stupid or dull percussion sound
Bronchial breathing (large foci) or weakened vesicular (small)
Additional respiratory noises: Capital, various wheezes, friction noise pleura
1. PNEUMONIA
Pneumonia - acute infectious inflammation of light tissue with mandatory involvement in the process of respiratory departments of lungs
Due to the occurrence:
-- Primary pneumonia
Bacterial (bond and conditional pathogenic strains)
Viral (influenza, RVS, torso)
Ricketsiomic (with ku-fever)
Mushroom (candidis, actinomycetes)
Secondary pneumonia
As a result of circulatory disorders (stagnation)
As a result of changes in the bronchi (peribronoectal, when COPD, with bronchial asthma, bronchuchous cancer)
In the atelectasic zone
After toxic effects (carbon dioxide, Uremia)
Bacterial superinfection (cough, malaria, leptospirosis, leukemia)
When aspiration
Lipoid (after the aspiration of paraffin, oil)
Pneumonian classification
1) Complete-Complete
2) NOZOKOMIAL (INTERBACICAL)
3) Atypical (chlamydia, mycoplasma, legionella) !!! do not confuse Sars. \u003d Torso - caused by coronavirus
4) In persons with immunodeficiency
5) Aspiration
On the volume of pulmonary infiltrate
Share (previously traded)
Focus (\u003d bronchopneumonia, however, the term is recognized as obsolete)
Polycegimentary (term is used in x-ray, not applicable in clinical practice)
Interstitial (not true pneumonia, since there is no defeat of Alveol, currently the term is replaced by "pulmonit")
Suspected of pneumonia:
1. Anamnesis
** Communication with transferred ORVI
** Contact with patient
** Disadvantage, symptoms of general intoxication for several days
** Hyperthermia (subfebrile) for several days
** Perhaps a sharp start or asymptomatic flow - there is no history
2. Complaints:
** Characteristic for intoxication syndrome
** Hypertermia
** Pain in the chest
** Perhaps the complete absence of complaints
2. Infiltrative tuberculosis
Classification:
1. Focular t lung
2. Infiltrative T.
4. Lung tuberculosis
5. Silicotuberculez
6. Casomic pneumonia - as an independent form and how complications t lungs in the phase of acute progression
Suspicion of tuberculosis:
Gradual start
Preceded the period of unmotivated malaise
Subfebrile, cough
Fiscological symptoms are weak
Syndrome of pulmonary infiltration is detected in the region of the top or upper lobe
Darkening is usually homogeneous, but in the removal fabric there are fresh foci
- "Track" to the root
In the roots there are occasional lymph nodes
Casomic pneumonia:
· Progressive course of an exudative-necrotic process
· No tendency to limit
· The presence of massive caseous necrosis with the lesion of the vascular system of lungs
· Massive reproduction of mycobacteria leads to a breakthrough of the Gisto-hematological barrier with the development of baremaemia
· As a result - the dissemination of the specific process
3. Light eosinophilic infiltrate
Clinical classification, 1990
1. Local pulmonary eosinophilite
· Simple lung eosinophilite (Lefeler syndrome), reasons - vegetable allergens, mold mushrooms, Halmintes, medications, food products, Nickel
· Chronic eosinophilic pneumonia (long pulmonary eosinophilitis, Lera-Kindberg syndrome), reasons - mold mushrooms, helminths, medicines, food, domestic tumors (kidneys, prostate), hemoblastosis
2. Light eosinophilite with asthma syndrome, reasons - medicines, helminths, mold mushrooms, food products, cancellation of supporting therapy (GKS), Aspergillla
3. pulmonary eosinophilite with systemic manifestations (hyperoeosinophilic myeloproliferative syndrome), the reason is not known
Clinic
No more often
Possible manifestations characteristic of pneumonia
Infiltrates in lungs are homogeneous, without open circuits and "tracks" to the root
Localize in various parts of the lung
Characteristic to "volatility"
Fast effect GKS.
4. Allergic infiltration in the lung
Occurs when the dust containing in the respiratory tract organic Particles
Often does not have differences from eosinophilic infiltrate
Describes:
- "Light agricultural worker"
- "Empty Birdhouse"
- "Employee of tobacco plantation"
5. Dimming with malignant tumors
Central lung cancer
Peripheral lung cancer, especially the pneumonic form of bronchio-salmon
Metastasis in the lungs - single and multiple, including endobronchial
Lymphoma light
Sarcoma light
Peripheral Cancer:
o burglar, uneven outlines shadow
o The shadow structure is homogeneous or with decay cavities
o surrounding pulmonary fabric intact (mb periccken pneumonia)
o the discharge track to the root no
o often increased mediastinum lymph nodes
o elderly age
o Smoking
o repeated pneumonia of one localization
o Durable cough episodes, incl. unproductive
Metastatic lesions:
Multiple round shades
Need to search primary tumor
More often metastasis the kidney tumor, chorionepitheloma, melanoma, uterine cancer, breast, gastrointestinal tract
6. Dimming with benign tumors
Gamartoma
Adenoma Bronchi.
Chondroma
Nevnomane
Require diff. Diagnostics with malignant, incl. Morphological
Characteristic:
· Single education, exist for a long time
· More often spherical formations with china contours
· There is no "track"
· Surrounding intact
7. Anomalies of the development of lungs
Easy cyst with abnormal blood supply (intra-oxide sequestration of the lung)
Lightweight hypoplasia simple, cystic, incorporated pulmonary cysts
Arteriovenous aneurysms in the lungs
Lymphangectasia and other abnormalities of the lymphatic system
8. Vagnative diseases of the lungs
This is a group of acute inflammatory processes in the LGKY, leaking with fitting, necrosis and destruction.
Terms:
Abscess - Reflected ulotnik, "Multiple abscesses"
Gangrene
Gangrenoz abscess ??? Today there is no definition
Classification:
1. Acute purulent-necrotic destruction of light
Limited GDL (with good bronchial drainage; with insufficient bronchial drainage; with a full impaired bronchial drainage))
Common GND (bronchogenic - pulmonary, pulmonary-pleural; hematogenic - pulmonary, pulmonary-pleural)
Limited gangrene (regressive, progressive)
Common gangrene (progressive)
2. Chronic purulent destruction of lungs
9. Focal pneumosclerosis
Postpnemonic
Posttuberculate
10. Light-style infarction (TEL)
Not developing all patients undergoing TEL
* Diagnosis of the foundation on complaints, history, results instrumental research, incl. ECG, radiography OGK, isotopic scintigraphy lungs, CT
* High reliability of the diagnosis when conducting angiopulmonography and spiral CT with contrasting of the light artery
11. Hemosiderosis of Lögsky
It is rare
Combined with the hemosiderosis of other organs
Repeated hemorrhage in the pulmonary fabric
Hemlochy, anemia
X-ray - bilateral symmetric small-scale changes in lungs
It has a crisis current - crisis lasts from several hours to 1-2 weeks
Hamosiderophages in sputum
Refivid Test
Biopsy Lekhsky
12. Echinococcosis Lögkov
There are no subjective symptoms
Form of cysts round or oval with hawk and protrusion
Shadow outlines are smooth, clear
The structure of one-bottomed, but can be determined by the regional occasion of the capsule or the symptom of the chitin sheath detachment
The surrounding fabric is usually intact
13. Pulzonites for immunopathological diseases
System Vasculitis
Hoodpasher syndrome
Granulomatosis Vegener
Basal pneumophibrosis with systemic sclerosis
14. idiopathic pulmonary fibrosis (FIBROZing Alveolit)
Criteria (2000g):
Big:
The elimination of other interstitial diseases of the lungs
Changes in FVD, including restrictive diseases and gas exchange disorders
Bilateral reticular changes in the basal departments of the lungs with minimal changes in the type of "matte glass", according to CT
There are no signs of alternative diagnosis according to transbronchial biopsy and bronchoalveolar lavage
Small:
Age older 50.
Independent gradual appearance of the dispatch at physical load
Duration of the disease for more than 3 months
Inspiratory attitudes in the basal departments of the lung
4 large + at least 3 small
15. Diaphragmal hernia
Parasezophageal
Axial
16. Sarcoidosis Lekhsky
Unknown etiology
Start gradual, asymptomatic
No signs of intoxication
Normal or subfebrile temperature
Journal Erythema
Negative tuberculin tests
Radiograph is characteristic of tuberculosis
17. Drug toxic pneumopathy
Nitrofuran
Amiodar
Sulfanimida
Salicylate
18. Aspiration of the foreign body
Obbitation of bronchi with the development of atelectasis and pneumonia distal as the place of obstruction
DIIF.Diagnosis with tumor atelectasis
In the case of aspiration of the X-ray contrasting body, it is visualized against the background of infiltrate
19. Pneumoconiosis
Histoplasmas - bilateral small infiltrates ("Snowstorm", "Misel")
Aktinomycets.
20. Alveolar Proteinosis
Belkovo lipoids accumulate in alveoli and bronchioles
X-ray - "Alveol filling syndrome"
A substance giving a chic-positive reaction is detected in the fabric of the lungs in histological examination.
LITERATURE
1. Rainbow N.L. Domestic MN: VS, 2007, 365C
2. Pies K.T. Domestic diseases, M: Eksmo, 2005
3. Sirotko V.L., All about internal diseases: a textbook for graduate students, MN: VS, 2008
Initially, the specialist should determine that the patient really has an infiltrate easy. It is possible to identify it using clinical and X-ray studies. A different type of physical changes in lungs is observed depending on which character is messenger infiltrate.
What is a lung infiltrate
The most pronounced changes in the case of an infectious infection-inflammatory infectious infiltration, mainly at pneumonia of a non-specific type: attitudes, bronchial or hard breathing, dulling or dullness of the percussion sound, reinforced local voice jitter. With productive light infiltrate wheezing and , reinforced voice jitting, in the presence of tumors listened to the breath loose. In this case, according to the results of clinical studies, it is impossible to determine the lung infiltrate.
The decisive stage to confirm the presence of infiltrate in the lungs is the conduct of radiography. If the picture shows the dimming more than 1 cm in the diameter of medium or weak intensity. In rare cases, blackout with a more dense infiltrate.
The contours of dimming directly depend on the projection of the study, the pathological nature of the process and the location of its localization. The structure is homogeneous and inhomogeneous. It is determined by the presence of complications, stage and character of the pathological process.
The second stage of the differential diagnostic study includes finding the boundary between tumor and inflammatory infiltrates. Infiltrate inflammatory type of equity is mainly observed with and pneumonia. Tumor infiltrates do not capture a whole share.
Darkening the share in the presence of tumors is most often observed in the bronchogen cancer in the lung.
In light microorganisms can fall in the following ways:
- contagious;
- airborne droplet;
- lymphogenic;
- hematogenous;
- bronchogeno.
Factors of occurrence
Factors that are able to provoke the development of infiltrate lungs are:
- virus infections;
- supercooling;
- operations;
- elderly age;
- alcohol;
- smoking.
Pneumonian classification
Pneumonia is classified for atypical, non-hospital, community-friendly.
And also conduct their classification and on the following features:
Panelutes of pneumonia in lungs
GR + microorganisms:
- Pool streptococcus up to 4%. Frequent complications of diseases of the type pericarditis, pleurisy and during the seasonal flu epidemic;
- Staphylococcus golden up to 5%. Inclination to destruction, with outbreaks of the epidemic up to 40%;
- Pneumococcus from 70 to 96%.
GR organisms:
Anaerobic type pathogens
It happens very rarely and is accompanied by a felonic wet.
Simplest
It is observed in people after radiation therapy, with immunodeficiency, after transplantation, in a weakened after illness and HIV-infected. Statifia is atelectatic, ethnic, emphysematous. Determined on the smears of Romanovsky - GIMZE.
Viruses
This includes viruses after transplantation, with therapy of suppressive, respiratory and sycital, paragrippa and influenza.
Mycoplasma
Most often are present in places of cluster of people. The discrepancy between the symptoms of lesion of light, catarral phenomena and pronounced intoxication.
Signs of infiltration in light X-rays
It is characterized by infiltration by a moderate increase in the fabric of the lightweight and its increased density. It is for this reason that X-ray signs of infiltration in lungs have their own singles.
When infiltration in light inflammatory type, uneven outlines are observed and the incorrect shape of the dimming. For acute stage Infiltrates in the lungs are observed by the unaware contours of the outline, gradually turning into the cloth, which surrounds the lungs. In chronic inflammation, the contours are served and uneven, but expressed more clearly. With inflammatory form of infiltration in lungs, it is very often possible to see branching light strips - these are bronons filled with air.
Due to the fact that the causative agent causes damage under a number of inflammatory-type diseases on the respiratory organs, fabric necrosis can be observed, which, in turn, significantly increases the severity of the disease.
In order to prevent the development of necrosis and the restoration of the integrity of bronchial and light fabric, you can recommend the following type of treatment: swamp drying, medicinal donel, yarrow, leaves and kidney birch, aloe and medicine medicine.
Symptoms with infiltrate in lungs
Complaints that occur most often with light infiltrate
Most often, with a light infiltrate, such complaints arise:
- Increased sweating;
- Headaches;
- Weakness;
- Chills;
- Increasing body temperature;
- In the chronic form of a light infiltrate, the body's depletion may be observed, and therefore loss.
The cough character is completely dependent on the etiology and stage of light infiltrate, and also on how many changes are related to Plegre and bronchi.
At the initial stage of development of light infiltration, a dry cough is observed, in which the sputum is not expectorated. But after a small amount of time, the scarce wet begins to separate, and in the future the cough is already becoming more productive. Short, weak and unsealing casing can talk about beginner infiltration of lungs, which is located on the periphery of their fabrics.